Principles and Practice of Cardiopulmonary Physical Therapy 3rd Edition PDF

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PRINCIPLES AND PRACTICE OF
CARDIOPULMONARY
PHYSICAL THERAPY
THIRD EDITION
PRINCIPLES AND PRACTICE OF
CARDIOPULMONARY
PHYSICAL THERAPY
THIRD EDITION
Edited by:
Donna Frownfelter, MA, PT, CCS, RRT
NovaCare, Inc.
Contract Services
Region 7
Northwestern University
Programs in Physical Therapy
Chicago, IJlinois
Committed to Excellence
Glenview, Illinois
Elizabeth Dean, PhD, PT
Associate Professor
University of British Columbia
School of Rehabilition Sciences
Vancouver, British Columbia
With 22 contributors and 40] illustrations
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THIRD EDITION
Copyright 1996 by Mosby-Year Book, Inc.
Previous editions copyrighted 1978, 1987
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CONTRIBUTORS
Anne Mejia Downs, PT, CCS
Michael Wade Baskin, PT, RRT

OwnerlExecutive Director
Department of Physical and Occupational Therapy
GT Physical Therapy and Rehabilitation
Instructor, Division of Physical Therapy

Department of Medical Allied Health Professions
West Point, Mississippi
School of Medicine
Jean K. Berry, PhD, RN
University of North Carolina
Senior Research Specialist
Chapel Hill, North Carolina
Medical-Surgical Nursing
University of Illinois at Chicago
Willy E. Hammon, BSe, PT
Chicago, Illinois
Chief of Rehabilitative Services
Gary Brooks, MS, PT, CCS
Special Instructor in Physical Therapy
Associate Professor
College of Health
Health and Rehabilitation Sciences
Clinical Instructor, College of Nursing
The University Hospitals
The Sage Colleges
University of Oklahoma Health Sciences Center
Troy, New York
Oklahoma City, Oklahoma
Susan M. Butl er, MMSe, PT, CCS
Scott M. Hasson, EdD, PT
Division of Physical Therapy
Director
Department of Rehabilitation Medicine
Advanced Studies
Maine Medical Center
School of Physical Therapy
Portland, Maine
Texas Woman's University

Houston, Texas
Margaret K. Covey, MS, RN

Senior Research Specialist and Doctoral Candidate
Lyn Hobson, PT, RRT
Medical-Surgical Nursing
Rush-Presbyterian-St. Luke's Medical Center
University of Illinois at Chicago
Chicago, Illinois
Chicago, Illinois
Gail M. Huber, MHPE, PT

L inda D. Cr ane, MMSe, PT, CCS
Instructor
Instructor
Division of Physical Therapy
University of Miami School of Medicine
Chicago, Illinois
Miami, Florida
vi
Preface
Thomas Johnson, MD
Claire Peel, PhD, PT
Associate Professor in Radiological Scienccs
Department of Physical Therapy

and Allied Health Professions
University of Oklahoma Health Sciences Center
School of
Oklahoma Citv. Oklahoma
Creighton
Omaha, Nebraska
PhD
ArthurV.
Associate Professor
of
Susan K.
MS, PT
Rush Medical
Rehabilitation T herapy Services
Illinois
Henry Ford Hospital

Detroit, Michigan
Elizabeth J. Protas,PhD, PT, FACSM

Assistant Dean and Professor
School of
Mary lnaSS l"

President,
Therapy
Texas Woman's University
Physical
Houston, Texas
Illinois
in
MD,
Michael
Assistant Professor of Medicine
Illinois
Rush Medical
'-''''vU,,",V,
Illinois
Mary Mathews, BS, RN, CCRN,RRT

MA,PT
Neonatal and Pediatrics Chest

Coordinator
Assistant Professor
Care Services
Physical
Luke's Medical Center
Program
of Colorado Health Sciences Center
Denver, Colorado
Lisa
Mendelson, MS,
Alexandra J.
CPAN
Practitioner-Teacher, College of
Education Coordinator
Luke's Medical Center
Rush
Rush
Medical Center
University of
Physical
Division
Physical Medicine and Rehabilitation
UIIC<lIW. Illinois
Ann Arbor, Michigan

Victoria A. Moerchen, MS,PT
Doctoral Candidate in Motor Control
of Kinesiology
Maureen
DNSc,R
, FAA
Satellite Site Coordinator

Clinic
Early Intervention
Waisman Center
Adjunct Clinical
Pediatric Consultant and Lecturer
Rush
Madison, Wisconsin
College of Nursing
of Illinois College of
. of Wisconsin
Chicago, Illinois
To our students
Present, and FutureFor T heir Inspiration, Inquiry, and Enthusiasm
CONTEMPORARY DEFINITION OF
CARDIOPULMONARY
PHYSICAL THERAPY
culation,
livery of noninvasive interventions in the
assessment, treatment, and follow-up) of patients with primary or secondary car
diopulmonary dysfunction
from acute, chronic, and acute-on-chronic
conditions, and the cardiopulmonary/cardiovascular manifestations of
disease. CPPT interventions include mobilization,
body positioning,
control, coughing and airway clearance maneuvers, and manual tech

niques. Wherever possible and appropriate, CPPT is applied to
and to
oxygen
or reduce the need for invasive medical

including
Patient education and
patient-driven treatment planning are fundamental
of CPPT. In addi
tion, CPPT has an essential role in the promotion of optimal cardiopulmonary and
cardiovascular health and fitness in the
population.
ix
FOREWORD
Donna Frownfelter and Elizabeth Dean have succeeded in creating a unique set of re
sources for students and clinicians. The importance of the oxygen transport mecha
nism is woven throughout this text and accompanying case study book, Clinical Case
Study Guide. The disruption of the mechanism can create cardiopulmonary dysfunc
tion and can result in reduced function, reduced functional work capacity, and death.
A comprehensive understanding of oxygen transport and the factors that determine
and influence it is therefore essential in order to assess the deficits of the mechanism
and determine treatment interventions.
The third edition of Principles and Practice of Cardiopulmonary Physical Therapy
is not simply a new edition of the former, Chest Physical Therapy and Pulmonary Re
habilitation. It is a totally new textbook, encompassing both the cardiac and pul
monary systems in health and dysfunction. The two previous editions have been
praised for their clinical relevance. The new books go a long way to support the state
of the art clinical practice with documented scientific literature.
The authors have many years of experience teaching undergraduate students as well
as consulting and teaching in professional postgraduate courses. These books have
been written in response to questions and concerns raised by students and clinicians.
This is the only text in which Mary Massery has published her work on neuropul
monary rehabilitation. Several chapters emphasize positioning for respiratory success
and ventilatory strategies to improve rehabilitation potential.
The books are very user-friendly. Each chapter of the text has key terms and questions
for discussion to help the reader focus on the important concepts presented in the chapter.
The combination of the text and case study guide will be an asset in teaching cardiopul
monary physical therapy. However, either book can be effectively used independently of
the other. The case study guide can be of assistance to physical therapists in helping them
focus on patient evaluation, cardiopulmonary dysfunction, and treatment approaches. I
applaud the authors for these new books and would highly recommend them for stu
dents and clinicians.
SaLLy C. Edelsberg, MS, PT

Director and Associate Professor
Northwestern University Medical School
xi
PREFACE
The work that has gone into this third edition has resulted in a completely new book!
When we first discussed the possibilities of a new edition, we knew it would be a total
change from Chest Physical Therapy and Pulmonary Rehabilitation. We wanted to
present a new approach, not just a revision. Elizabeth's research and study of oxygen
transport mechanisms in relation to patient treatment highlighted this concept as the
primary thread that would pull the new book together. The cardiopulmonary system
must be viewed as a whole, interacting with other body systems for optimal function.
Therapy interventions must incorporate cardiopulmonary goals as well as neuromus
cuiar and musculoskeletal goals for patients to reach maximal rehabilitation potential.
We have attempted to pull together physiological as well as clinical data to meet
the changing needs of health care to provide objective documentation for our interven
tions. Yet we were diligent in maintaining a text aimed at the undergraduate student or
practicing therapist with minimal background in cardiopulmonary physical therapy.
To that end we have tried to keep the material readable and very user-friendly. Our
hope is that virtually any question that may arise about treating a patient with car
diopulmonary dysfunction would have some answers in this book.
We both teach undergraduate physical therapy students and thank them for their
input, questions, and concerns about patients with cardiopulmonary dysfunction who
have helped us focus this text to meet students' needs. In addition, through our contin
uing education seminars with postgraduate physical therapists, we have been chal
lenged to apply the concepts in light of the changing health care scene. How can we be
most effective and scientifically correct in choosing treatment techniques that have
demonstrated improvement in the oxygen transport mechanism and patient function?
We always learn when we teach, and we hope to share that learning with others
through this text.
We are excited about being able to present an accompanying text, Clinical Case
Study Guide. We are attempting to show the physiological principles presented in our
text, by identifying real-life case studies that physical therapists deal with every day in
their practice. Our hope is that this will be used widely in teaching physical therapy
students and will facilitate their understanding of how to effectively integrate car
diopulmonary concepts in each of their patients, not just in patients with a primary
cardiopulmonary diagnosis.
To our knowledge, this is the first international book written dealing with car
diopulmonary physical therapy. It is a blend of physiology and international ap
proaches to the patient with cardiopulmonary dysfunction. We have had the privilege
of teaching and consulting internationally and have tried to make this text applicable
to all therapists regardless of their situation and the degree of sophisticated equipment.
xiii
xiv
Preface
hands-on therapy and positioning is the
We realize that in some Third-World

only mode of
available. We believe that this is often all that is needed when
with the proper concepts and thought processes.

We are
new
with the way this edition has come together. We have many
authors who have added
and direction for both cardiac and
monary foci.
We are pleased this is finally completed and thank our families, friends, and colfor
us and
us
the rough times to see this book
Our hope is that this will be a welcome addition to your professional Ii

and we welcome your comments and suggestions for future work.
Donna Frownfelter
Elizabeth Dean
ACKNOWLEDGMENTS
There are so many people that I want to thank and acknowledge for their support and
contributions to this book. First, my family, for their understanding and support dur
ing stressful deadlines and crunch spots. My husband David has been there for me
since I went to physical therapy school and has always encouraged me to do what my
vision led me to do. My three teenagers, Lauren, Daniel, and Kristin, have helped
keep my life on track and grounded in the reality of daily life while taking time to
"smell the roses." You are special gifts to me, and I love you.
To my students, I thank you for your questions, concerns, and wonderings about
what this cardiopulmonary stuff really means to your patients. You wonder if you can
really be a better therapist because you take these things into account in evaluation
and treatment. Please remember the difference between ordinary and extraordinary is
just that little "extra." I believe that is what incorporating cardiopulmonary attention
does; it adds the little extra. Be an extraordinary therapist, no matter what the health
care environment.
To the contributing authors, I thank you for your time and significant effort in
bringing together the literature and clinical aspects of cardiopulmonary physical ther
apy. Your dedication to this project has made it much more than Elizabeth and I
could have done alone. You know how important it is to convey the message of treat
ing the whole patient and helping them reach his or her potential.
To my colleague and soul mate Mary Masse!)/, who I have taught with, travelled
with, given seminars with, laughed with, and cried with, I thank you for all you have
taught me and how special it is to have someone you can always count on to discuss
a difficult patient or a personal issue. We have become quite a team, and I value our
professional and personal relationships. Your contributions to the clinical chapters we
have done together this time have been significant. I look forward to many more pro
jects and fun times together. There is no greater pleasure for a teacher than to see a
former student travel in that teacher's tracks and surpass her. Thanks Spike!
My deepest thanks go to Elizabeth Dean. You have been an incredible colleague
who has given new life to this book. You have, in a gentle way, helped to ensure that
physiologic and scientific evidence be paired with our clinical experience and treat
ment techniques. You have truly brought about a book that I could never have com
pleted alone. Words are not enough to thank you for your commitment to this project
and the countless hours you have spent in a major revision of the former textbook. I
am delighted at what you have done and the depth of knowledge you have brought in
your content and organization of this book. I am honored that you chose this text in
which to share your work, and I have enjoyed working with you and learning from
you. We share a common bond in the relationships we have with our students and our
xv
xvi
Acknowledgements
desire to spread the word about the importance of including cardiopulmonary con
cerns in the patient's evaluation and plan of treatment. We have grown close in the
last 10 years, and I value our friendship as well as our professional work together.
T hank you hardly is enough, but 'Thanks!"
To my friends, family, and fellow workers at NovaCare, Inc. Contract Services, I
thank you for your patience and understanding of the demands on my time and your
encouragement to continue and finish this project. Your support has meant a great deal
and I hope you feel a part of this, for it is because of you this has really happened. I'm
glad to have a work environment that supports personal and professional growth.
To our Mosby staff: Martha Sasser, thanks for your ideas and vision for going with
this new book. You saw the possibilities and were there with other suggestions to
make it even better (even if some of them came when we thought we were donel). To
Kellie W hite, you kept us on track and helped catch up with chapter authors who
needed a nudge and still had time to have Julia Isabelle-quite an accomplishment!
You will now find what we have, that motherhood is often harder than your other
job! Best wishes! To Mamata Reddy and Amy Dubin, you have pushed us through
the editing process with the gentle and firm hand that we needed and with much sup
port and help. Thank you for your cooperation and critical eye in making this an ex
cellent outcome.
Finally, and most importantly, I thank God for the vision, strength, and energy to un
dertake this book and see it through to completion. My involvement in spreading the
word about the need for optimizing the cardiopulmonary system has always felt like a
mission. It has been amazing to me how many therapists don't see the need and how
they can have an "Aha!" experience in a seminar or class, or even just reading this book.
If I can have a small part in that experience, my "mission" has been fulfilled, and for that
I am grateful.
Donna Frownfelter
To Donna, for having made this dream come true. Our working relationship and
friendship began 10 years ago when I first approached Donna to review a manuscript
entitled 'The Pulmonary Effects of Body Positioning," published in Physical Therapy
in 1985. This publication was the stepping stone to a prolonged and ever-growing in
terest in oxygen transport and how it is affected by cardiopulmonary interventions
such as body positioning and mobilization. T he enthusiasm, interest, and support of
Donna and my former graduate student, Jocelyn Ross, have fueled my energies in the
exciting dynamic area of cardiopulmonary physical therapy. My heartfelt gratitude to
you both.
To Daniel Perlman, for your encouragement and support of my liaison with Donna
at the outset and over the years. You knew a good thing when you saw it.
To Doug Frost, for your support in getting this project into the end zone. Thank
you for your support and for being there as the book continued to evolve.
Acknowledgements
To our dedicated contributors, for your expertise, which has contributed to a vol
ume on the principles and practice of cardiopulmonary physical therapy that is on the
cutting edge with respect to the scientific and physiologic literature. Thank you for
your contributions and team effort.
To my cardiopulmonary physical therapy colleagues and students for your inquisi
tiveness and enthusiasm. T hank you all for your inspiration.
And not to forget the Mosby crew-Martha Sasser, Kellie White, Mamata Reddy,
and Amy Dubin-I thank each one of you for your commitment to making this book
the best it can be.
Elizabeth Dean
xvii
CONTENTS
PARTI
Chapter 1
CARDIOPUL MONARY FUNCTION IN HEALTH AND DISEASE, 1

Oxygen Transport: The Basis for Cardiopulmonary Physical
Elizabeth Dean
Therapy, 3
Chapter 2
Cardiopulmonary Anatomy, 23
Elizabeth Dean
Lyn Hobson
Chapter 3
Cardiopulmonary Physiology, 53
Elizabeth Dean
Lyn Hobson
Chapter 4
Cardiopulmonary Pathophysiology, 71
Willy E. Hammon
Scott M. Hasson
Chapter 5
Cardiopulmonary Manifestations of Systemic Conditions, 99
PARTII
CARDIOPULMONARY ASSESSMENT, 1J5
Chapter 6
Measurement and Documentation, 1J7
Claire Peel
Chapter 7
History, 127
Willy E. Hammon
Chapter 8
Pulmonary Function Tests, 145
Donna Frownfelter
Chapter 9
Arterial Blood Gases, 153
Donna Frownfelter
Chapter 10
Principles of Chest X-Ray Interpretation, 159
Elizabeth Dean
Michael Ries
Thomas Johnson
Chapter 11
Electrocardiogram Identification, 169
Gary Brooks
Chapter 12
Multisystem Assessment and Laboratory Investigations, 189
Elizabeth Dean
xix
XX
Contents
Chapter 13
Special Tests, 197
Gail M. Huber
Chapter 14
Clinical Assessment of the Cardiopulmonary System, 209
Susan M. Butler
Chapter 15
Monitoring Systems in the Intensive Care Unit, 229
Elizabeth Dean
PART III
CARDIOPULMONARY PHYSICAL T HERAPY INTERVENT IONS, 249
Chapter 16
Optimizing Treatment Prescription: Relating Treatment
Elizabeth Dean
to the Underlying Pathophysiology, 251
Chapter 17
Mobilization and Exercise, 265
Elizabeth Dean
Chapter 18
Body Positioning, 299
Elizabeth Dean
Chapter 19
Physiological Basis for Airway Clearance Techniques, 321
Anne Mejia Downs
Chapter 20
Clinical Application of Airway Clearance Techniques, 339
Anne Mejia Downs
Chapter 21
Facilitating Airway Clearance With Coughing
Mary Massery
Techniques, 367
Donna Frownfelter
Facilitating Ventilatory Patterns and Breathing
Mary Massery
Strategies, 383
Donna Frownfelter
Exercise Testing and Training: Primary Cardiopulmonary
Susan K. Ludwick
Chapter 22
Chapter 23
Dysfunction, 417
Chapter 24
Exercise Testing and Training: Secondary Cardiovascular
Phyllis G. Krug
Dysfunction, 425
Chapter 25
Respiratory Muscle Weakness and Training, 443
Maureen Shekleton
Jean K. Berry
Margaret K. Covey
Chapter 26
Patient Education, 453
Alexandra J. Sciaky
Contents
PART IV
GUIDELINES FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL
THERAPY: ACUTE CARDIOPULMONARY CONDITIONS, 467
Chapter 27
Acute Medical Conditions, 469
Elizabeth Dean
Willy E. Hammon
Lyn Hobson
Chapter 28
Acute Surgical Conditions, 495
Elizabeth Dean
Mary Mathews
PART V

THERAPY: CHRONIC CARDIOPULMONARY CONDITIONS, 511
Chapter 29
Chronic Primary Cardiopulmonary Dysfunction, 513
Elizabeth Dean
Donna Frownfelter
Chapter 30
Chronic Secondary Cardiopulmonary Dysfunction, 567
Elizabeth Dean
Donna Frownfelter
PART VI

THERAPY: INTENSIVE CARE, 565
Chapter 31
Comprehensive Patient Management in the Intensive
Elizabeth Dean
Care Unit, 567
Chapter 32
Intensive Care Unit Management of Primary
EI izabeth Dean
Cardiopulmonary Dysfunction, 579
Chapter 33
Intensive Care Unit Management of Secondary
Elizabeth Dean
Cardiopulmonary Dysfunction, 599
Chapter 34
Complications, Adult Respiratory Distress Syndrome,

Shock, Sepsis, and Multiorgan System Failure, 617
Elizabeth Dean
xxi
xxii
Contents
PART VII
GUIDELINE S FOR THE DELIVERY OF CARDIOPULMONARY PHYSICAL

THERAPY: SPECIAL CASES, 633
Chapter 35
The Neonatal and Pediatric Patient, 635
Victoria A. Moerchen
Linda D. Crane
Chapter 36
Chapter 37
The Aging Patient, 669
Elizabeth J. Protas
The Patient With Neuromuscular and Musculoskeletal
Mary Massery
Dysfunction, 679
Chapter 38
The Transplant Patient , 703
Susan Scherer
Chapter 39
The Patient in the Community, 721
Donna Frownfelter
PART VIII
RELATED ASPECTS OF CARDIOPULMONARY PHYSICAL THERAPY, 735
Chapter 40
The Art of Positioning and Moving Patients, 737
Mary Massery
Donna Frownfelter
Chapter 41
Respiratory Care Practice Review, 749
Michael Wade Baskin
Chapter 42
Care of the Patient With an Artificial Airway, 761
Lisa Sigg Mendelson
Chapter 43
Respiratory and Cardiovascular Drug Actions, 775
Arthur V. Prancan
GLOSSARY, Gl
INDEX, 11
PAR T
Cardiopulmonary Function
in Health and Disease
CHAPTER
Oxygen Transport: The Basis for

Cardiopulmonary Physical Therapy
Elizabeth Dean
KEY TERMS
Cellular respiration
Gravitational stress
Exercise stress
Oxygen transport pathway
INTRODUCTION
ceptual basis for cardiopulmonary physical therapy
Cardiopulmonary physical therapy is an essential non
practice. Oxygen transport is the basis for life. Impaired
invasive medical intervention that can reverse or miti
or threatened oxygen transport, hence, cardiopul
gate insults to oxygen transport. It can avoid, delay, or
monary dysfunction, is a physical therapy priority.
reduce the need for medical interventions, such as sup
In health, the oxygen transport system is normally
plemental oxygen, intubation, mechanical ventilation,
perturbed by movement and activity, changes in body
suctioning, bronchoscopy, chest tubes, surgery, and
position, and emotional stress. In disease, disruption
medications. A comprehensive understanding of oxy
of or threat to this system is always a medical priority
gen transpol1 and the factors that detelTnine and influ
because of the threat to life or impairment of func
ence it is therefore essential to the comprehensive as
tional capacity.
sessment of oxygen transport and optimal treatment

prescription to effect these outcomes.
The fundamental steps in the oxygen transport

pathway, and their function and interdependence are
This chapter details the oxygen transport system, the
described first. Special attention is given to cellular
pathway, and the component steps that provide a coo-
respiration and the utilization of oxygen during me

3
PART I
Cardiopulmonary Function in Health and Disease
+VC02
+V02
Airways/lungs
('\
('\
g::J
g.
::J
FIGURE 1-1
Scheme of components of ventilatory-cardiovascular-metabolic doupling underlying oxygen
transport. (Modified from Wasserman K et al: Principles of exercise tesling and interpretation,
Philadelphia, 1987, Lea & Febiger.)
tabolism at the cellular level in muscle. Second, the
1992a; Goldring, 1984; Johnson, 1973; Ross, and
factors that normally perturb oxygen transport in
Dean, 1989; Weber et aI, 1983).
health are described, namely gravitational stress sec
Oxygen transpolt variables include oxygen delivery
ondary to changes in body position, exercise stress
(002),
secondary to increased oxygen demand of the work
hancement ratio (OER) or the utilization coefficient.
oxygen consumption
(V02)
and the oxygen en
ing muscles, emotional stress, and arousal. A thor
Oxygen demand is the amount of oxygen required by
ough understanding of the effects of those factors that
the cells for aerobic metabolism. Oxygen demand is
V02;
however, in cases of severe
normally perturb oxygen transport is essential to ac
usually reflected by
curately assess and treat deficits in oxygen transport.
cardiopulmonary dysfunction and compromise to oxy

gen transport,
V02 can fall
short of the demand for oxy
gen. Oxygen transport variables, including the compo
OXYGEN TRANSPORT
nents of
Oxygen transport refers to the delivery of fully oxy
1-2.
002
002, V02,
and the OER, are shown in Figure
is determined by arterial oxygen content and
genated blood to peripheral tissues, the cellular up
cardiac output, oxygen consumption by the arterial and
take of oxygen, the utilization of oxygen from the
venous oxygen content, difference and cardiac output,
blood, and the return of partially desaturated blood to
and oxygen extraction by the ratio of
002 to
\'02.
the lungs. The oxygen transport pathway consists of
Measures and indices of oxygen transport that re
multiple steps ranging from the ambient air to the
flect the function of the component steps of the oxy
perfusion of peripheral tissues with oxygenated arter
gen transpolt pathway are shown in the box above.
ial blood (Figure
1-1).
Oxygen transport has become
the basis for conceptualizing cardiopulmonary func

tion, and diagnosing and managing cardiopulmonary
Energy Transfer and Cellular Oxidation
dysfunction (Dantzker, 1983; Dantzker, Boresman,
Cellular metabolism and survival depend on the con
and Gutierrez, 1991; Dean, 1994a; Dean and Ross,
tinuous s y nthesis and degradation of adenosine
Measures and Indices of the Function of the Steps in the Oxygen Transport Pathway
Control of Ventilation
Physiologic shunt
Systolic and diastolic pulmonary artery pressures
PO. I (central drive to breathe)
Pulmonary capillary blood tlow
Ventilatory responses or hypoxia and hypercapnia
Pulmonary capillary wedge pressure
Pao} and Sa02 responses to exercise
Pulmonary vascular resistance
Inspired Gas
Pulmonary vascular resistance index

Systemic hemodynamic variables
Alveolar oxygen pressure
Heart rate
Alveolar carbon dioxide pressure
Electrocardiogram (ECG)
Alveolar nitrogen pressure
Systemic blood pressure
Hematologic Variables
Mean arterial blood pressure
Hemoglobin
Systemic vascular resistance
Plasma proteins and their concentrations
Systemic vascular resistance index
Red blood cells and count
Central venous pressure
White blood cells and count
Pulmonary artery pressures
Platelets
Wedge pressure
Clotting factors
Blood volume
Clotting times
Cardiac output
Hematocrit
Cardi<lc index
Pao2
Stroke volume
Paco2 (eml tidal CO2)
Stroke index
P(A-a)o2
Shunt fraction
Cao2
Ejection fraction
CV02
Left ventricular work
C(a-v)o2 difference
Right ventricular work
HCo1
Fluid balance
Sa02
Renal output
pH
Creatinine clearance and blood urea nitrogen (BUN)
Paoe/PAo]
Pao2/Flo2
Diffusion
Serum lactate
D (A-a)o2
Pulmonary Variables
Diffusing capacity
Diffusing capacity/alveol<lr volume
Minute ventilation
Tidal volume
Gas Exchange
Respiratory rate
Oxygen consumption (Vo2)
Dead space volume
Carbon dioxide production (VCCl:)
Alveolar volume
Respiratory exchange ratio (Vco}iV02)
Alveolar ventilation
Ventilation and perfusion matching
Distribution of ventilation
Paol/PAol
Static and dynamic lung compliance
P(A-a)o2
Airway resistance
Functional residual capacity
Oxygen Extraction and Utilization
Closing volume
Oxygen extraction ratio (V02/Do2)
Vital capacity
C(a-v)02 difference
Forced expiratory volumes and flows

Other pulmonary volumes, capat:ities, and flow rates
Inspiratory and expiratory pressures
Work ofhreathing
Respiratory muscle strength and endurance
Pulmonary Hemodynamic Variables
Cardiac output
Total perfusion
Distribution of perfusion
P(a-v)o2 differenc e
SV02
Metabolic enzymes at the cellular level
Oxyhemoglobin dissociation
Adequacy of Tissue Perfusion and Oxygen
Transport
Tissue oxygenation
Tissue pH
Anatomic shunt
PART I
Oxygen delivery
Arterial oxygen content
D02
Cardiac output
Oxyhemoglobin + Dissolved oxygen

Hgb
t
1.34
5a02
II
Pa02
0.003
Oxygen consumption
V02
(Arterial oxygen content - Venou s oxygen content)
Oxyhemoglobin
Hgb
1.34
5v02
Cardiac output
Dissolved oxygen
II
Pa02
0.003
Oxygen enhancement ratio

OER
Oxygen consumption
V02
Oxygen delivery
D02
FIGURE 1-2
FOlmulas for determining oxygen delivery
(002),
oxygen consumption
(Vo2),
and oxygen
extraction ratio (OER). (Modified from Epstein CD., Henning R.1.: Oxygen transport variables
in the identification and treatment of tissue hypoxia, Heart Lung
triphosphate (A TP); the major source of energy for
22:328-348, 1993.)
that oxygen delivery is inadequate, nonaerobic (anaer
biological work. Work is performed in biological sys
obic or non-oxygen-requiring) energy-transferring
tems for contraction of skeletal, cardiac, and smooth
processes can also supply ATP. However, supplying
muscle (e.g., exercise, digestion, glandular secretion
energy anaerobically is more costly metabolically, that
and thermoregulation, and nerve impulse transmission)
is, it is not efficient, is limited, and cannot be slistained
(see box below). These processes require a continuous
because of the disruptive effects of lactate, a cellular
supply of A TP, which is made available by aerobic
byproduct of anaerobic metabolism, on physiological
(oxygen requiring) processes primarily. In the event
processes in general. Metabolic acidosis is a conse

quence of lactate accumulation. In critically ill pa
Biological Work Requiring Continuous

Oxygen Supply
Contraction of skeletal muscle
tients, the presence of metabolic acidosis secondary to

anaerobic metabolism can be life-threatening. Pro
longed anaerobic metabolism is lethal in two respects.
First, the patient is increasingly dependent on anaero
Contraction of cardiac muscle
bic metabolism because of inadequate oxygen delivery
Contraction of smooth muscle
to peripheral tissues, and second, acidosis interferes
Nerve impulse transmission

Active cellular metabolic processes
Active pumping mechanisms
with normal cellular processes and homeostasis, which

require an optimal pH of 7.40.
The ATP molecule consists of an adenine and a ri-
Oxygen Transport: The Basis for Cardiopulmonary Physical Therapy
--------------------Lactose
Galactose --+- Galactose- 1 -P

:
t
Glucose- 'I-P
Starch -Maltose Glucose:
__
Sucrose
--- --
- Fructose
-------
Glucose-6-P
(CARBOHYDRATE FOODS)
-
--------------
Fructose-6-P
Fructose- 1 ,6-diP
Glyceraldehyde-3P
Pyn
Pr
in-:
L_____
te= wdale
Acetyl-Co-A -- Fatty acids -- 1 __

F t:_
Amino acids
o
"Glycecol
)+
Citrate
-a
": ;
Ketoglutarate
CO2 + Energy
FIGURE 1-3
Interrelationships among carbohydrate, fat, and protein metabolism and their points of entry
into the Krebs cycle. (Printed with permission from Shepard R.J,:
of exercise,
Physiology and biochemistry
Phi ladelphia, 1985, Praeger Scientific.)
bose molecule with three phosphates attached. Split
electron transfer chain and then use this energy for
ting of the terminal phosphate bond or the two terminal
biological work (Ganong,
phosphate bonds generates considerable amounts of
Carbohydrates, fats, and proteins, ingested from
energy. This energy is used to power various chemical
foodstuffs in the diet, are oxidized to provide the en
1993; Shephard, 1985).
reactions associated with metabolism. These metabolic
ergy for phosphorylation of adenosine diphosphate
processes take place in specialized organelles in the
(ADP), that is, the formation of ATP by combining
cells called mitochondria. The primary pathways that
ADP with phosphate. These substances are broken
are responsible for the formation of ATP are the Krebs
down, and they access the Krebs cycle at the pyruvic
cycle and the electron transfer chain.
acid or acetyl coenzyme A (CoA) levels (Figure
The complex, enzymatically controlled chemical
1-3).
Some amino acids can enter the Krebs cycle directly.
reactions of metabolism are designed to form and
The Krebs cycle degrades acetyl CoA to carbon
conserve energy through the Krebs cycle and the
dioxide (C02) and hydrogen atoms (H2)' The primary
PART I
3ADP
3ATP
Mitochondrion
Shuttle
Krebs cycle
NADH etc.
FIGURE 1-4
Philadelphia, 1985,
and
purpose of this
(Printed with permission from
with the Krebs
Electron transfer chain and its
is to generate hydrogen ions for
the electron transfer chain by two principal electron
Scientific.)
by
energy is primarily
tivity and
aerobic metabolism. Oxygen for this process is pro
acceptors, nicotinamide adenine dinucleotide
vided by the oxygen transport pathway. Carbon com
and flavin adenine dinucleotide (FAD).
pounds that enter the
the numerous reactions of the Krebs
in the form of
and
Cellular oxidation or respiration refers to the func

tion of the electron transfer chain to release energy in
oxidative metabolism
in the form of aerobic glycolysis in the mitochondria

in the
of the cells.
small amounts and to conserve energy in the forma
The Krebs
tion of high energy bonds. It is this process that en
the biochemical
sures a continual energy supply to meet the needs of
cell responsible for harnessing the oxygen for aerobic
metabolism
Three major
supply energy
durations
1-4).
metabolism and
of energy transfer exist to
a continuous supply of oxy

to produce two molecules of
ATP (glycolysis). Glucose is oxidized to
Katch, and Karch, I
though these systems are discrete they
in the mitochondria of the
gen for this process (Shephard, 1985).

cose is
all-out exercise over
and the electron transfer chain are
Cellu
molecules of
yielding a net
lar ATP and creatine phosphate (CP) are immediate
molecules of ATP per molecule of
energy sources for the first 10 seconds of exercise.
pyruvate molecules enter the Krebs
From 30 to 60
are oxidized to
glycolysis
a short
where they
and water. This process
30
term energy source. The ATP-CP system and the
ATP molecules. Hydrogen ions released in the
colytic system are anaerobic processes. As exercise
process are transferred to the electron transfer chain
aerobic
yielding 4 ATP molecules for cellular metabolism.
system oredominates. Thus for sustained ohvsical ac-
Electrons are removed from hydrogen and funnelled
persists for several minutes, the
Sarcoplasmic
reticulum
Triad
j
Mitochondrion
Terminal Transverse
tubule
cisterns
Thick myofilament
Z
line
M
line
Z
line
H zone
I band
I
I band
A band
,
Sarcomere
I band
A band
I
Mi"
.-!n ,n, ,,/ ' . '
.
I band
"
'--11
"
,'"
.
"
'
'
'"''
"
'
, , ,
:
, : ::
:> ,'7:'>
.

, '-"
.
,
. ,
'"
. . . , .. .. , '
"
/ "
. .
"
"
, ,
, "
.
',
,'
'
/ / , " // , .
.- .
... '/ "
.
"
', :> ?::.

.
' .
"
"
'.'
,
,
... ....
,", ' . , ",,',
.. . . _ _
.
"
...
:',', : .
: :
' ::: . :
:: :: :
.
..
.
'.
,' ,
',
11/ . . .. "
_ ._ "
"
" ' // , > '
, . .
. . ' ."
"
"
...
...
, , ,
..
- ... ..
...
."-"
Thin myofilament
I
'
Thick myofilament Cross bridge H z one
,- .
,,,
. '
'''
, ...
Z line
FIGURE 1-5
Schematic of the ultrastructure of a muscle fiber. A, View of muscle mem brane structure and
myofibril arrangement. B, A single functional unit (sarcomere) of a myofibril showing the
interdigitation of the actin and myosin filaments. (Printe d with permission from Tortora, G.J.,
A nagnostakos N.P.: Principles of anatomy and physiology, New York, J 990, Harper & Row.)
10
PART I
Thin
Myosin
(thick)
Thin
FIGURE 1-6
Arrangement of the thick and thin myofilaments. (From Hasson S.: Clinical exercise physiology,
St. Louis, 1994, Mosby.)
down the electron transport chain by specialized elec
anaerobic metabolism can only serve as a shol1-term
tron carrier molecules, cytochromes 1 to S. It is only
energy source.
the last of these cytochromes, cytochrome oxidase,

that can reduce molecular oxygen to water. This
process is driven by a gradient of high-to-Iow poten
tial energy. The energy transferred as electrons are
Muscle Contraction and Metabolism

The basic mechanism for muscle contraction is excita
passed from H2 to O2, and is trapped and conserved
tion contraction coupl ing (Kirchberger,
as high energy phosphate bonds. Oxygen is only in
and Anagnostakos,
volved in these metabolic pathways at the end of the
centrally or through the spinal cord depolarize the
1991; T0I10ra,
1990). Action potentials mediated
electron transfer chain, where oxygen is the final
muscle cell membrane, the sarcolemma, and stimulate
electron acceptor and combines with H2 to form H20.
the release of calcium from the lateral sacs of the sar
More than
coplasmic reticulum, The sarcoplasmic reticulum is an
90% of ATP synthesis takes place through
the electron transfer chain by oxidative reactions
extensive network of invaginations and tubular chan
combined with phosphorylation, that is, oxidative
nels encasing the muscle fibers or myofibrils. The cal
phosphorylation. An individual's peak aerobic capac
cium floods over the myofilaments of the myofibrils.
ity is determined by the availability of oxygen at the
Myofilaments consist of thin and thick fibers, actin,
end of the electron transport chain.
and myosin protein, which interdigitate with each
For each molecule of glucose that is metabolized,
other giving the typical striated appearance to skeletal
1-6). Actin is a helical mole
36 molecules of ATP are produced; four molecules
muscle (Figures I-S and
from substrate phosphorylation (anaerobic), and 32
cule with tropomyosin intertwined along its length.
from oxidative phosphorylation (aerobic). The low
Tropomyosin normally inhibits the interaction of actin
ATP yield from anaerobic metabolism explains why
and myosin. Calcium causes a conformational change
of the tropomyosin molecule that enables troponin,

also distributed along the actin molecule, to combine
11
Principles of Oxygen Transport

A continuous supply of oxygen is needed to meet
with calcium. The combining of calcium and troponin
moment-to-moment demands for oxygen commensu
triggers the movement of actin and myosin. Contrac
rate with changing metabolic demands for energy at
tion involves the attaching and detaching of the
the cellular level in addition to basal metabolic de
myosin heads (cross bridges) to actin in a cyclical
mands (Cone, 1987; Dantzker, 1991; Samsel and
manner, which causes the actin and myosin filaments
Schumacker, 1991). Oxygen transport occurs either
to slide past each other. In this way, the muscle is
by convection or diffusion. Convection of oxygen
shortened without shortening of the myofilaments.
refers to the movement of oxygen from the alveoli to
The energy for muscle contraction in the form of
the tissue capillaries. Convection is primarily deter
ATP is generated within the mitochondria of the my
mined by the hemoglobin concentration, oxygen satu
ofibrils (Shephard, 1985). Myosin ATPase splits ATP
ration, and cardiac output. The diffusion of oxygen
so that the transfer of this energy can be used for
refers to the movement of oxygen from the capillaries
muscle contraction. Specifically, the enzyme ATPase
to the mitochondria. Diffusion is determined by
is activated when actin and myosin are joined. ATP is
metabolic rate, vascular resistance, capillary recruit
then available to bind with the cross bridge, causing
ment, tissue oxygen consumption, and extraction.
it to detach from actin. Relaxation occurs with the
Normally, D02 is regulated by tissue metabolism
cessation of electrical excitation and the rapid re
and the overall demand for oxygen. Typically, DOl is
moval or sequestration of calcium into the lateral sacs
3 to 4 times greater than oxygen demand, and V02 is
of the sarcoplasmic reticulum.
not directly dependent on Do2. In health, the increased
The specific metabolic properties of muscle de
metabolic demands of exercise constitute the greatest
pend on the constituent muscle fiber types (Fox,
challenge to the oxygen transport system. The V02 can
Bowers, and Foss, 1993). The three primary muscle
increase 20 times. In response to increased muscle
fiber groups are fast twitch fibers, slow twitch
metabolism, blood tlow increases to the peripheral
fibers, and intermediate fibers, which have proper
muscles through vasodilatation and capillary recruit
ties of both. The fast twitch fibers (fast glycolytic
ment, thereby increasing the availability of oxygen to
fibers) are recruited during short-term sprint type
the working tissues and its extraction from the arterial
exercise, which relies mainly on anaerobic metabo
blood. As D02 and V02 increase, venous return, stroke
lism. These fibers are well-adapted for rapid force
volume, and heart rate also increase, thereby increas
ful contractions, because they have large amounts
ing cardiac output (CO). The CO can increase more
of myosin ATPase, rapid calcium release and up
than five times in strenuous exercise.
take and high rate of cross bridge cycling. Slow
At rest, regional differences in the proportion of
twitch fibers (slow oxidative fibers) are recruited
CO normally delivered to the body organs reflects dif
during prolonged aerobic exercise. These fibers
ferences in organ functions and is not necessarily
have large amounts of myoglobin, mitochondria,
matched to the metabolic rate (Guyton, 1987). For ex
and myochondrial enzymes. Compared with the fast
ample, the distribution of CO to the kidneys is 20%,
twitch fibers, slow twitch fibers are fatigue-resis
and to the mesenteric, splenic, and portal tissues is
tant. The intermediate fibers have both anaerobic
20% to 30%. Comparatively, muscle at rest is 10%

and the brain and myocardium are less than 5% each.
and aerobic metabolic enzymes, which make these

fibers capable of both types of muscle work. Al
though the characteristics of the fiber types are dis
tinct, activity and exercise recruits both types of
Oxygen Content of the Blood
fibers. Depending on the particular activity or exer
Oxygen is transported in arterial blood to the tissues
cise, one fiber type may be preferentially recruited
in combination with hemoglobin (98%) a n d dis
over the others.
solved in plasma (2%) The majority of oxygen is
12
PART I
carried in the blood by hemoglobin, compared with a

relatively minimal amount of oxygen that is dis
solved in the blood. The oxyhemoglobin dissociation
150
curve represents the relationship between the affinity
A;
of hemoglobin for oxygen and arterial oxygen ten
sion. The affinity of hemoglobin for oxygen depends

on the tissue oxygen demand. In health, exercising
muscle increases the demand for oxygen. The heat of
the working muscles and the acidic environment re
sult in reduced oxyhemoglobin affinity, and in
:100
E
E
d
(/
0....
50
creased oxygen release. This is reflected by a shift to
Gal enp/
Diffusion
o
An
Shunt
Tissues
the right of the oxyhemoglobin dissociation curve

(see Chapter 9). The affinity of hemoglobin and oxy
gen is increased with the cessation of exercise,
which is reflected by a leftward shift of the curve.
o I------
Atmosphere
Mitochondria
FIGURE 1-7
Scheme of oxygen partiaf pressures from air to tissue. The
Oxygen Delivery to the Tissues
cascade reflects the removal of oxygen by the pulmonary
The final steps in oxygen transport involve the disso

ciation of oxygen from hemoglobin and the diffusion
of oxygen from the capillaries to the cells (Schu
macker, Samsel, 1989). Diffusion depends on the
capillary blood and the tissues. Depressions caused by the

effects of diffusion and shunt are also illustrated. (Used
with permission from West lB.: Respiratory p/7ysiology
the essentials, ed 5, Baltimore, 1995, Williams & Wilkins.)
quantity and rate of blood flow, the difference in cap

illary and tissue oxygen pressures, the capillary sur
face area, capillary permeability, and diffusion dis
mitochondria (Guyton, 1991). This decremental Pao2
t a n ce (West, 1 9 95). Wi t h i ncreased metabo lic
profile down the oxygen transport pathway, from the
demand of the tissues, capillary dilatation and recruit
airways to the tissues, is termed the oxygen cascade
ment increase capillary surface area and reduce vas
(Figure 1-7).
cular resistance to flow. Diffusion distance is de

creased, the movement of oxygen into the cell is
facilitated, and the tissue oxygen tension is increased.
Cardiac Output
The two diffusion gradients that determine effec
In addition to arterial oxygen content, CO is a primary
tive oxygen transpolt are between the pulmonary cap
determinant of D02 (Dantzker, 1991). The transport of
illaries and the alveoli, and between the peripheral
oxyhemoglobin to the tissues is dependent on convec
capillaries and the tissue cells. Diffusion of oxygen
tive blood flow by way of CO. The CO is the volume
occurs as the blood moves from the aorta to the arte
of blood pumped from the right or left ventricle per
rioles. The mean oxygen tension in the aorta is about
minute. The components of CO are stroke volume

SV x HR.
95 mm Hg and in the arterioles is 70 to 80 mm Hg.
(SV) and heart rate (HR), that is, CO
The oxygen gradient between the arterioles and the
Stroke volume is the amount of blood ejected from the
cells is the most steep. The mean oxygen pressure is
left ventricle during each ventricular systole or heart
less than 50 mm Hg in the capillaries. The oxygen
beat and is determined by the preload, myocardial dis
tension in the capillaries detennines the rate of diffu
tensibility, myocardial contractility, and afterload. The
sion to the cells. An optimal diffusion gradient main
DDl is optimized in patients by increasing CO through
tains the oxygen tension in the cell between 1 to 10
the therapeutic manipulation of preload, myocardial
mm Hg; oxygen tension is less than 0.5 mm Hg in the
contractility, afterload, and heart rate.
Preload
13
to that consumed. The OER is calculated by dividing
Preload is the end diastolic muscle fiber length of the
V02 by 002. Normally, the OER is 23%.
ventricle before systolic ejection, and reflects the left

ventricular end diastolic volume (LVEDV). The
LVEDV is dependent on venous return, blood vol
Supply-dependent Oxygen Consumption
ume, and left atrial contraction. An increase in ven
Normally, a decrease in 002 does not reduce V02
tricular volume stretches the myocardial fibers and
(Phang, Russell, 1993). With a decrement in 002, the
increases the force of myocardial contraction (Star
tissues extract a proportionate amount of oxygen
ling effect) and stroke volume. This effect is limited
from the blood. In critically ill patients, the 002 may
by the physiologic limits of distension of the my- .

ocardium. Excessive stretching such as in fluid over
be significantly limited to the point where basic

2
metabolic needs for oxygen (300 mllminJM ) are not
load of the heart leads to suboptimal overlap of the
being met (Fenwick et ai, 1990; Lorente et aI, 1991;
actin and myosin filaments, thus impairing rather
Phang, Russell, 1993). The critical level at which V02
than enhancing contractility.
falls is associated with tissue anaerobic metabolism

and the development of lactic acidosis and decreased
pH (Figure 1-8) (Mizock, Falk, 1992; Schumaker,
Afterload
Cain, 1987). Serum lactates correspondingly increase
Afterload is the resistance to ejection during ventricu
and provide a valid index of anaerobic metabolism in
lar systole. Afterload of the left ventricle is primarily
patients with multiorgan system failure.
determined by four factors: the distensibility of the

aorta, vascular resistance, patency of the aortic valve,
and viscosity of the blood.
The Oxygen Transport Pathway

Oxygen transport is dependent on several intercon
necting steps ranging from oxygen-containing air
Myocardial Contractility
being inhaled through the nares to oxygen extraction
Myocardial contractility reflects actin-myosin coupling
at the cellular level in response to metabolic demand
during contraction. Myocardial contractility is assessed
(see Figure I-I , p. 4). These steps provide the mecha
by the ejection fraction, rate of circumferential muscle
nism for ventilatory, cardiovascular, and metabolic
fiber shortening, pressure volume relationships, and the
coupling. In addition, blood is responsible for trans
rate of change of ventricular pressure over time.
porting oxygen within the body, thus its constituents

and consistency directly affect this process.
Oxygen Debt
Tissue oxygen debt or recovery oxygen consumption is
The Quality and Quantity of Blood
the difference between oxygen demand and oxygen
Although not considered a discrete step in the oxygen
consumption. In health, oxygen debt can be sustained
transpolt pathway, blood is the essential medium for
for short periods during intense exercise. Anaerobic me
transporting oxygen. To fulfill this function, blood
tabolism is stimulated to produce ATP under these con
must be delivered in
ditions. In patients, the degree of oxygen debt signifi
proportional to metabolic demands, and have the ap
cantly correlates with survival (Fenwick et aI, 1990).
propriate constituents and consistency. Thus consider
an
adequate yet varying amount
ation of the characteristics of the circulating blood vol

ume is essential to any discussion of oxygen transport.
Oxygen Extraction Ratio or Utilization Coefficient
Blood volume is compartmentalized within the in
The oxygen extraction ratio (OER), or utilization co
travascular compartment such that 70% is contained
efficient, reflects the proportion of oxygen delivered
within the venous compartment, 10% in the systemic
PART I
14
arteries,
15% in the pulmonary circulation, and 5% In

1986). The large volume of
Blood is a viscous fluid composed of cells and
99% of the blood is red blood celis,
the capillalies (Sandler,
plasma. Because
blood contained within the venous circulation permits
the white blood cells play almost no role in determin
adjustments to be made as cardiac output demand
ing the physical characteristics of blood.
changes. The veins constrict, for example, when car
Hematocrit refers to the proportion of blood that is
diac output needs to be increased. When blood vol
38% for women and

42% for men. Blood is several times as viscous as
ume is normal and body fluids are appropriately dis
celis. The normal hematocrit is
t r i b u t e d b e t w e e n t h e i n t r a- a n d e x t r ava scular
water, which increases the difficulty with which
compartments, fluid balance is considered normal.
blood is pumped through the heart and flows through
When these are disrupted, a fluid balance problem
vessels; the greater the number of cells, the greater
exists. In addition, fluid imbalance affects the con
the friction between the layers of blood, which results
centration of electrolytes, and particularly sodium,
in increased viscosity. Thus the viscosity of the blood
which is in the highest concentration in the extracel
increases significantly with increases in hematocrit.
lular fluid. Four primary fluid problems that have im
An increase in hematocrit such as in polycythemia in
plications for oxygen transport are water deficit,
creases blood viscosity several times over. The con
water excess, sodium deficit, and sodium excess (see

Chapter
15). Other ions that are often affected in
fluid and electrolyte imbalance deficits include potas

sium, chloride, calcium, and magnesium (Figure
centration and types of protein in the plasma can also

affect viscosity but to a lesser extent.
In the adult, red blood cells are produced in the
1-8).
marrow of the membranous bones such as the verte
These electrolyte disturbances also contribute to im
brae, sternum, ribs, and pelvis. The production of red
paired oxygen transport by affecting the electrical
blood cells from these sites diminishes with age. Tis
and mechanical behavior of the heart and blood ves
sue oxygenation is the basic regulator of red blood
sels, and hence cardiac output and the distribution of
cell production. Hypoxia stimulates red blood cell
oxygenated arterial blood to the periphery.
production through erythropoietin production in bone

(Guyton,
1991).
Viscosity of the blood has its greatest effect in the

small vessels. Blood flow is considerably reduced in
small vessels, resulting in aggregates of red blood ceils
.Q
c...
E
D02 Dependent
adhering to the vessel walls. This etlect is not offset by
D02 Independent
the tendency of the blood to become less viscous in
I
I
I
I
I
'"
c
o
u
c
Q)
small vessels as a result of the alignment of the blood

cells flowing through, which minimizes the frictional
forces between layers of flowing blood cells. In addi
: Critical D02
tion, in small capillaries, blood cells can become stuck
I
I
I
I
100
200
particularly where the nuclei of endothelial cells pro

300
Oxygen
400
500
600
700
delivery (ml/min)
from the lungs to the tissues. Red blood cells also
(Voz)
and
oxygen delivery (002)' The Dorindependent phase

represents the normal metabolic state. The D02-dependent
phase represents the dependency of Voz on 002 when 002
Falls below the critical 002. (Modified from Phang, P.T.
and Russel, 1.A.: When does V02 depend on D02? Resp
Care 38:
618-630, 1993.)
The major function of the red blood cells is to

transport hemoglobin, which in turn carries oxygen
FIGURE 1-8
Relationship between oxygen consumption
trude and momentarily block blood flow.
contain a large quantity of carbonic anhydrase, which

catalyzes the reaction between COz and HzO. The ra
pidity of this reaction makes it possible for blood to
react with large quantities of CO2 to transport it from
the tissues to the lungs for elimination.
Hemoglobin is contained within red blood cells up
to a concentration of
34 gmll 00 ml of cells. Each
gram of hemoglobin is capable of combining with
15
blood cells. These values vary according to gender,
1-2, p. 6). Therefore in
weight, and other factors. Normally, changes in blood
19 ml of oxygen and in healthy men,
volume reflect deficits and excesses of fluid through
21 ml of oxygen can be carried in the blood, given
imbalances created by losses through the skin and
that the whole blood of women contain
respiratory tract, and through urinary, sweat, and
1.34 ml of oxygen (see Figure

healthy women,
of 14 gmll 00 ml of blood and
an average
16 gmll 00 ml of blood
in men.
fecal losses. Exercise and hot weather are major chal

lenges to fluid balance in health.
Clotting factors of the blood are normally in a pro
The plasma contains large quantities of sodium
portion that does not promote clotting. Factors that
and chloride ions, and small amounts of potassium,
promote coagulation (procoagulants), and factors that
calcium, magnesium, phosphate, sulfate, and organic
inhibit coagulation (anticoagulants) circulate in the
acid ions. In addition, plasma contains a large amount
blood. In the event of a ruptured blood vessel, pro
of protein. The large ionic constituents of the plasma
thrombin is converted to thrombin, which catalyzes
are responsible for regulating intracellular and extra
the transformation of fibrinogen to fibrin threads.
cellular fluid volumes and the osmotic factors that
This fibrin mesh captures platelets, blood cells, and
cause shifts of fluid between the intracellular and ex
plasma to form a blood clot.
tracellular compartments.
The extreme example of abnormal clotting is dis

seminated intravascular coagulation, where both he
mOlThage and coagulation occur simultaneously. The
acute form of this syndrome occurs in critically ill pa
Oxyhemoglobin Dissociation
The demand for oxygen at the cellular level changes
tients with multiorgan system failure. The mechanism
from moment to moment. The properties of oxyhemo
appears to involve tissue factors, factors that damage
globin dissociation ensure that there is a continuous
the blood vessel wall, and factors that increase
supply of oxygen at the cellular level. Oxygen com
1990). The
bines with the hemoglobin molecules in the pul
chronic form of the syndrome occurs in chronic con
monary circulation and then is released in the tissue
platelet aggregation (Green and Esparaz,

ditions such as neoplastic disease.
capillaries in response to a reduced arterial oxygen
Plasma is the extracellular fluid of the blood and

contains
7% proteins, namely albumin, globulin, and
tension. The S-shaped oxyhemoglobin dissociation

curve (see Chapter
9) shifts to the right in response to
fibrinogen. The primary function of the albumin and
reduced tissue pH, increased CO2, increased tempera
to a lesser extent, globulin and fibrinogen, is to create
ture and increased diphosphoglycerate (DPG), a con
osmotic pressure at the capillary membrane and to
stituent of normal blood cells.
prevent fluid leaking into the interstitial spaces. The
The delivery of blood and its ability to effectively
globulins serve as carriers for transporting substances
transport oxygen is central to all steps in the oxygen
in the blood and provide immunity as the antibodies
transport pathway and must be considered at each
that fight infection and toxicity. Fibrinogen is funda
step in clinical problem solving and decision making.
mental to blood clotting. The majority of blood pro

teins, including hemoglobin, are also excellent acid
base buffers and are res ponsi b Ie for
70% of a II
buffering power of whole blood.
(Q) depends on a pressure gradient (P)

and vascular resistance (R), that is, Q
PIR. Hence
Blood flow
blood flow equals the pressure gradient divided by re
Steps in the Oxygen Transport Pathway

Step One: inspired oxygen and quality
of the ambient air
In health, the concentration of inspired oxygen is rel
21 % unless the individual is at al
sistance. The length of a given blood vessel and the vis
atively constant at
cosity of the blood are also detelTninants of blood flow.
titude. In which case, the fraction of inspired oxygen
5,000 ml. Approxi

3,000 ml of this is plasma and 2,000 ml is red
The average blood volume is

mately
is reduced the higher the elevation.

Atmospheric air consists of
79% nitrogen, 20.97%
16
PART I
oxygen and 0.03% CO2. Because nitrogen is not ab
lined with cilia, fine microscopic hair-like projec
sorbed in the lungs, it has a crucial role in maintain
tions, which are responsible for wafting debris, cells,
ing the lung tissue patent. The constituents of the air
and microorganisms away from the lungs into larger
have become an increasingly important social, envi
airways to be removed and evacuated. The airways
ronmental, and health issue because of environmental
are also lined with mucus, which consists of two lay
hazards, pollution, and thinning of the ozone layer re
ers, the upper gel layer and the lower sol layer with
sulting in deterioration of air quality, an increase in
which the cilia communicate.
toxic oxygen free radicals and a reduction in atmos

pheric oxygen pressure.
Step Three: lungs and chest wall
Many factors influence air quality, (e.g., geo
Air entry to the lungs depends on the integrity of the
graphical area, season, urban vs. rural area, high vs.
respiratory muscles, in particular, the diaphragm, the
Jow elevation, home environment, work environment,
lung parenchyma, and the chest wall. Contraction and
indoor vs. outdoor, level of ventilation, air condition
descent of the diaphragm inflates the lungs. The dis
ing, enclosed buildings, areas with high particu late
tribution of ventilation is primarily determined by the
matter, areas with gaseous vapors and toxic-inhaled
negative intrapleural pressure gradient down the
materials, and smoke-filled vs. smoke-free environ
lungs. The negative intrapleural pressure gradient re
ments). Poor air quality contributes to changes in the
sults in uneven ventilation down the lung, and inter
filtering ability of the upper respiratory tract, airway
regional differences (see Chapter 3). However, there
sensitivity, and lung damage, acutely and over time.
are other factors, intraregional differences, that con
Chronic irritation of the lungs from poor air quality
tribute to uneven ventilation within regions of the
can lead to allergies, chronic inflammatory reactions,
lung. These intraregional differences reflect regional
fibrosis, and alveolar capillary membrane thickening.
differences in lung compliance and airway resistance
At the alveolar level, the inspired air is saturated with
(Ross, Dean, 1992). In patients with partially ob
water vapor. In dry environments, however, the upper
structed airways, reduced lung compliance, and in
respiratory tract may become dehydrated, lose its
creased airway resistance increase the time for alveo
protective mucous covering, become eroded, and pro
lar filling. Gas exchange is compromised if there is
vide a portal of infection even though the air is ade
inadequate time for alveolar filling or emptying, that
quately humidified by the time it reaches the lower
is, increased time constants (West, 1995). Different
airways and alveoli.
time constants across lung units contribute to uneven

patterns of ventilation during inspiration. A lung unit
Step Two: airways
with a long time constant is slow to fill and to empty,
The structure of the airways down the respiratory
and may continue to fill when sun'ounding units are
tract change according to their function. The main
emptying. A second factor is altered diffusion dis
airway, the trachea, consists of cartilagenous rings,
tance. In diseases where diffusion distance is i n
connective tissue, and small amounts of smooth mus
creased, ventilation along lung units is uneven.
cle. This structure is essential to provide a firm and
The lungs and the parietal pleura are richly sup
relatively inflexible conduit for air to pass from the
plied with thin-walled lymphatic vessels (Guyton,
nares through the head and neck to the lungs, and
1991). Lymphatic vessels have some smooth muscle
avoid airway collapse. As the airways become
and thus can actively contract to propel lymph fluid
smaller and branch throughout the lung tissue, they
forward. This forward motion is augmented by
consist primarily of smooth muscle. Airway narrow
valves along the lymphatic channels. The rise and
ing, or, obstruction and increased resistance to air
fall of the pleural pressure during respiration com
flow, is caused by multiple factors, including edema,
presses lymphatic vessels with each breath, which
mUCllS, foreign objects, calcification, particulate mat
promotes a continuous flow of lymph. During expi
ter and space-occupying lesions, as well as hyperre
ration and increased intrapleural pressure, fluid is
activity of bronchial smooth muscle. The airways are
forced into the lymphatic vessels. The visceral pleura
continuously drains fluid from the lungs. This cre

ates a negative pressure in the pleural space, keeping
17
Step Five: perfusion

The distribution of blood perfusing the lungs is pri
the lungs expanded. This pressure exceeds the elastic
marily gravity dependent, thus the dependent lung
recoil pressure of the lung parenchyma, which col
fields are perfused to a greater extent than the nonde
lapses the lungs.
pendent lung fields. In the upright lung, the bases are
The peritoneal cavity of the abdomen consists of a

visceral peritoneum containing the viscera and a pari
better perfused than the apices (see Chapter
3). Venti
lation and perfusion matching is optimal in the mid
1985). In health,
etal peritoneum lining the abdominal cavity. Numer
zones of the upright lungs (West,
ous lymphatic channels interconnect the peritoneal
the ventilation to perfusion ratio is a primary determi
cavity and the thoracic duct; some arise from the di
nant of arterial oxygenation. In the upright lung this
aphragm. With cycles of inspiration and expiration,
ratio is
large amounts of lymph are moved from the peri

toneal cavity to the thoracic duct. High venous pres
0.8 in the mid-zone.
Step Six: myocardial function
sures and vascular resistance through the liver can in
Optimal myocardial function and cardiac output de
terfere with normal flu id balance in the peritoneal
pends on the synchronized coupling of electrical ex
cavity. This leads to the transudation of fluid with a
citation of the heart and mechanical contraction. The
high protein content into the abdominal cavity. This
sinoatrial node located in the right atrium is the nor
accumulation of fluid is referred to as ascites. Large
mal pacemaker for the heart and elicits the normal
volumes of fluid can accumulate in the abdominal
sinus rhythm with its component P-QRS-T configura
cavity and significantly compromise cardiopul
tion. This wave of electrical excitation spreads
monary function secondary to increased intraabdomi
throughout the specialized neural conduction system

of the atria, interventricular septum, and the ventri
nal pressure on the underside of the diaphragm.

Optimal diaphragmatic excursion requires a bal
cles, and is followed by contraction of the atria and
ance between thoracic and intraabdominal pressures.
then the ventricles. Contraction of the right and left
Increases in abdominal pressure secondary to factors
ventricles ejects blood into the pulmonary and sys
other than fluid accumulation can impair diaphrag
temic circulations respectively.
matic descent and chest wall expansion, for example,
Cardiac output depends on several factors in ad
gas entrapment, gastrointestinal (GI) obstruction,
dition to the integrity of the conduction system and

the adequacy of myocardial depolarization (dro
space-occupying lesions, and paralytic ileus.
motropic effect). The amount of blood returned to
Step Four: diffusion
the heart (preload), determines the amount ejected
Diffusion of oxygen from the alveolar sacs to the pul
(Starling effect). The distensibility of the ventricles
monary arterial circulation depends on five factors:
to accommodate this blood volume needs to be opti
the area of the alveolar capillary membrane, diffusing
mal, neither too restrictive nor compliant. The con
capacity of the alveolar capillary membrane, pul
tractility of the myocardial muscle must be suffi
monary capillary blood volume, and ventilation and
cient to eject the blood (inotropic effect). And
1993). The transit time of
finally, cardiac output is determined by the aortic
blood at the alveolar capillary membrane is also an
pressure needed to overcome peripheral vascular re
impoltant factor determining diffusion. The blood re
sistance and eject blood into the systemic circula
perfusion ratio (Ganong,
mains in the pulmonary capillaries for
0.75 seconds
tion (afterload).
at rest. The blood is completely saturated within one
The pericardial cavity, like the pleural and peri
third of this time. This provides a safety margin dur
toneal cavities, is a potential space containing a thin
ing exercise or other conditions in which cardiac out
film of fluid. The space normally has a negative
put is increased and the pulmonary capillary transit
pressure. During each expiration, pericardial pres
time is reduced. The blood can normally be fully
sure is increased, and fluid is forced out of the space
oxygenated even with reduced transit time.
into t h e me diastinal lymphatic channels. This
18
PART I
process is normally facilitated with increased volumes
sels, the greater their sensitivity to both exogenous
of blood in the hemt and each ventricular systole.
neural stimulation and endogenous stimulation by cir

culating humoral neurotransmitters such as cate
Step Seven: peripheral circulation
cholamines and local tissue factors. This sensitivity is
Once oxygenated blood is ejected from the heart, the
essential for the moment-to-moment regulation of the
peripheral circulation provides a conduit for supply
peripheral circulation with respect to tissue perfusion
ing this blood to metabolically active tissue. Blood
and oxygenation, commensurate with tissue meta
vessels throughout the body are arranged both in se
bolic demands, and control of total peripheral resis
ries and in parallel. The arteries and capillaries are
tance and systemic blood pressure.
designed to advance blood to pelfuse the tissues with

oxygenated blood. The vasculature is architected so
that the proximal large al1eries have a higher propor
Step fight: tissue extraction
and utilization of oxygen
tion of connective tissue and elastic elements than
Perfusion of the tissues with oxygenated blood is the
distal medium and small arteries, which have a pro
p r i n c i p a l goal of t he oxygen transport system
gressively higher proportion of smooth muscle. This
(Dantzker, 1993). Oxygen is continually being used
structure enables the large proximal arteries to with
by all cells in the body, thus it diffuses out of the cir
stand high pressure when blood is ejected during ven
culation and through cell membranes very rapidly to
tricular systole. Considerable potential energy is
meet metabolic needs. Diffusion occurs down a gra
stored within the elastic walls of these blood vessels
dient from areas of high to low oxygen pressure. The
as the heart contracts. During diastole, the forward
distance between the capillaries and the cells is vari
propulsion of blood is facilitated with the elastic re
able, thus a significant safety factor is required to en
coil of these large vessels. The thin-walled muscular
sure adequate arterial oxygen tensions. Intracellular
arterioles serve as the stopcocks of the circulation and
P02 ranges from 5 to 60 mm Hg, with an average of
regulate blood flow through regional vascular beds
23 mm Hg (Guyton, 1991). Given that only 3 mm
and maintain peripheral vascular resistance to regu
Hg of oxygen pressure are needed to support metab
late systemic blood pressure. Blood flow through
olism, 23 mm Hg of oxygen pressure provide an ade
these regional vascular beds is determined by neural
quate safety margin. Thcsc mechanisms ensure an
and humoral stimulation, and by local tissue factors.
optimal oxygen supply over a wide range of varying
Blood pressure control is primarily regulated b y
oxygen demands in health and in the event of im
neural stimulation of the peripheral circulation and
paired oxygen delivery because of illness. Normally,
these vascular beds.
the rate of oxygen extraction by the cells is regulated
The microcirculation consists of the precapillary ar
by oxygen demand by the cells, that is, the rate at
teriole, the capillary, and the venule. The Starling effect
which ADP is formed from A TP and not by the
govems the balance of hydrostatic and oncotic pres
availability of oxygen.
sures within the capillary and the surrounding tissue.

The balance of these pressures is 0.3
The adequacy of the quality and quantity of the mi
Hg; its net ef
tochondrial enzymes, required to support the Krebs
fect is a small outward filtration of fluid from the mi
cycle and electron transfer chain, and the availability
mrn
crovasculature into the interstitial space (see Chapter 3).
of myoglobin may be limiting factors in the oxygen
Any excess fluid or loss of plasma protein is drained
transport pathway secondary to nutritional deficits and
into the sun'ounding lymphatic vessels, which usually
muscle enzyme deficiencies. Myoglobin is a compara
has a small negative pressure as does the interstitium.
ble protein to hemoglobin that is localized within
The integlity of the microcirculation is essential to reg
muscle mitochondria. Myoglobin combines reversibly
ulate the diffusion of oxygen across the tissue capillary
with oxygen to provide an immediate source of oxy
membrane, and to remove CO2 and waste products.

The greater the muscular component of blood ves
gen with increased metabolic demands and facilitate

oxygen transfer within the mitochondria.
Normally, the amount of oxygen extracted by the
19
ergy expenditure, and thus increase rate of metabolism.
tissues is 23%, that is, the ratio of oxygen consumed
Several factors related to disease can significantly
to oxygen delivered. Thus this ratio ensures that con
increase oxygen consumption and metabolic rate over
siderably greater amounts of oxygen can be extracted
and above BMR. Such factors include fever, the dis
during periods of increased metabolic demand.
ease process itself, the process of healing and recov

ery from injury or disease, thermoregulatory distur
Step Nine: return of partially desaturated
bance, reduced arousal, increased arousal resulting
blood and C02 to the lungs
from anxiety and pain, sleep loss, medical and surgi
Partially desaturated blood and CO2 are removed
cal interventions, fluid imbalance, and medications
from the cells via the venous circulation to the right
Dean, 1994b). These factors may contribute to a sys
side of the heart and lungs. C02 diffuses across the
temic increase in BMR or may reflect local changes in
alveolar capillary membrane and is eliminated from
tissue metabolism. Autoregulation of the regional vas
the body through the respiratory system, and the de
cular beds promotes increased regional blood flow in
oxygenated venous blood is reoxygenated. The oxy
accordance with their local tissue metabolic demand.
gen transport cycle repeats itself and is sensitively
Because gravitational stress and exercise stress are
tuned to adjust to changes in the metabolic demand of
fundamental to normal cardiopulmonary function and
the various organ systems, such as digestion in the GI
oxygen transport, the effects of gravity and exercise are
system, and cardiac and muscle work during exercise.
highlighted. It should be emphasized that the effects of
Factors that intelfere with tissue oxygenation and
gravity on fluid shifts and the systeIllic effects of exer
the capacity of the tissue to use oxygen include ab
cise are physiologically distinct, that is, exposing an in
normal oxygen demands, reduced hemoglobin and
dividual to a gravitational stress does not adapt that in
myoglobin levels, edema, and poisoning of the cellu
dividual to an exercise stress and vice versa. These two
lar enzymes (Kariman, Burns, 1985).
factors also augment arousal, through stimulation of the

reticular activating system in the brain stem and the au
tonomic nervous system (ANS), which when de
FACTORS THAT NORMALLY PERTURB
pressed, significantly compromises oxygen transport in
OXYGEN TRANSPORT
patient populations. The impact of emotional stress on
Basal metabolic rate (BMR) reflects the rate of me
oxygen transport is discussed briefly. These concepts
tabolism when the individual is in a completely
are described fUlther in Chapters 17 and L8.
rested state, that is, no food intake within several

hours, after a good night's sleep, no arousing or dis
tressing emotional stimulation, and at a comfortable
ambient temperature. Normally, the BMR is constant
Gravitational Stress
Humans are designed to function in a I G gravita
within and between individuals if measured under
tional field. Given that 60% of the body weigllt is
standardized conditions. This rate reflects resting en
fluid contained within the intra- and extravascular
ergy expenditure of the body's cells to maintain rest
compartments, and that this fluid has considerable
ing function, including the work of breathing; heart,
mass, changes in body position result in significant

fluid shifts instantaneously and threaten hemody
renal, and brain function; and thermoregulation.

Normally, over the Course of the day, the human
namic stability (Dean, Ross, 1992a; Dean, Ross,
body is exposed to fluctuations in ambient temperature
1992b). To maintain consciousness and normal body
and humidity, ingestion states, activity and exercise
function during changes in body position, the heart
levels (exercise stress), body positions and body posi
and peripheral vasculature are designed to detect
tion changes (gravitational stress), emotional states
these fluid shifts and accommodate quickly to avoid
(emotional stress) and states of arousal. These factors
deleterious functional consequences (e.g., reduced
significantly influence oxygen consumption and en
stroke volume, CO, circulating blood volume, and
20
PART I
cerebral perfusion). The preservation of the f1uid
The oxygen transport system is designed to deliver
regulating mechanisms is essential to counter the he
oxygen from the ambient air to every cell in the body
modynamic effects of changing body position. This
to support cellular respiration, that is, the metabolic
capacity is quickly lost with recumbency and is the
utilization of oxygen at the cellular level. Blood is the
primary cause of bed rest deconditioning in patient
essential medium in which cellular and noncellular
1966;
components transport oxygen from the cardiopul
1985). Restoration of gravitational stress
monary unit to the peripheral tissues. The fundamental
and older populations (Chase, Grave, Rowell,

Winslow,
with upright positioning is the only means by which
steps in the oxygen transport pathway were described.
these fluid-regulating mechanisms can be maintained
These steps included the quality of the ambient air, the
and orthostatic intolerance and its short- and long
airways, lungs, chest wall, pulmonary circulation, lym
term sequelae averted.
phatics, he31t, peripheral circulation, and the peripheral

tissues of the organs of the body.
In health, the most significant factors that perturb
Exercise Stress
oxygen transport are changes in gravitational stress
Exercise constitutes the greatest perturbation to home
secondary to changes in body position, exercise stress
ostasis and oxygen transport in humans. Cardiac output
secondary to increased oxygen demand of working
can increase five times to adjust to the metabolic de
muscles, arousal, and emotional stress. A thorough
mands of exercise stress. All steps in the oxygen trans
understanding of the normal effects of gravitational
port pathway are affected by exercise stress. Ventilation
and exercise stress and arousal is essential to under
is increased, and ventilation and perfusion matching is
stand deficits in oxygen transport. In disease, numer
optimized to maximize oxygenation of blood. Heart
ous factors impair and threaten oxygen transport, that
rate and stroke volume are increased to effect greater
is, underlying pathophysiology, restricted mobility,
cardiac output of oxygenated blood to the tissues. At
recumbency, factors related to the patient's care, and
the tissue level, oxygen extraction is enhanced.
factors related to the individual (see Chapter
16).
Thus the physical therapist needs a detailed under

standing of these concepts to diagnose these deficits
Emotional Stress
and prescribe efficacious treatments.
The body responds to emotional stress similar to ex

ercise stress with the sympathetic stress reaction. Per
ceived threat, the basis of emotional stress, triggers
the fight, flight, or fright mechanism and a series of
sympathetically mediated physiological responses.
This reaction that prepares the body for flight in
cludes an increase in heart rate, blood pressure, CO,
blood glucose, muscle strength, mental alertness, cel
REVIEW QUESTIONS
1. Describe the oxygen transport pathway, its steps
and their interdependence.

2. Describe the physiological processes of energy
transfer and cellular oxidation.

3. Explain oxygen transport with respect to oxygen
lular metabolism, and increased local blood flow to
delivery, uptake and utilization and the interrela
specific muscle groups, as well as inhibition of invol
tionship among these processes.
untary function.
4. Outline the factors that perturb oxygen transport
in health.
SUMMARY
This chapter described the oxygen transport system,
its component steps, and their interdependence. This
framework provides a conceptual basis for the prac
tice of cardiopulmonary physical therapy.
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Dean, E., & Ross, 1. (1992b). Oxygen transport. The basis for con
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Cardiopulmonary Anatomy
Elizabeth Dean
Lyn Hobson
KEY TERMS
Cardiopulmonary unit
Peripheral circulation
Heart
Pulmonary circulation
Heart-lung interdependence
Respiratory muscles
Lymphatic circulation
Thoracic cavity
Parenchyma
Tracheobronchial tree
INTRODUCTION
This chapter presents the anatomy of the car
The heart lies in series with the lungs, constituting
diopulmonary system, including the skeletal features
the cardiopulmonary unit, the central component of
of t h e t horacic cavity; muscles of respiration;
the oxygen transport pathway (Scharf and Cassidy,
anatomy
1989; Weber et ai, 1983). Virtually all the blood re
parenchyma; basic anatomy of the heart; and periph
of t h e tracheobronchial tree; lung
turned to the right side of the heart passes through
eral, pulmonary, and lymphatic circulations (Berne
the lungs and is delivered to the left side of the heart
and Levy, 1992; Burton and Hodgkin, 1984; Ganong,
for ejection to the systemic, coronary, and bron
1993; Guyton, 1991; Katz, 1992; Murray, 1986; Mur
chopulmonary circulations. Because of this interrela
ray and Nadel, 1988; Nunn, 1993; West, 1991; West,
tionship, changes in either lung or heart function can
1995; and Williams et ai, 1989).
exert changes in the function of the other organ. A

detailed understanding of the anatomy of the heart
and lungs, and how these organs work synergisti
THORAX
cally is essential to the practice of cardiopulmonary
The bony thorax covers and protects the principal or
physical therapy.
gans of respiration and circulation, as well as the
23
24
PART I
FIGURE 2-2
The relationship of the lungs to the bony thorax (posterior
view).
FIGURE 2-1
The relationship of the bony thorax and lungs to the
abdominal contents (anterior view).
level with the second costal cartilages. The bifurca

tion of the trachea into the right and left mainstem
bronchi al s o occurs at t h e sternal ang le. The
liver and the stomach (Figures 2-1 and 2-2). The pos
manubrium and body are joined by fibrocartilage,
terior surface is formed by the 12 thoracic vertebrae
which may ossify in later life.
and the posterior part of the 12 ribs. The anterior sur
The body of the sternum is twice as long as the
face is formed by the sternum and the costal carti
manubrium. It is a relatively thin bone and can be
lage. The lateral surfaces are formed by the ribs. At
easily pierced by needles for bone marrow aspira
birth, the thorax is nearly circular, but during child
tions. The heart is located beneath and to the left of
hood and adolescence, it becomes more elliptical
the lower one third of the body of the sternum. Al
until adulthood. It is wider from side to side than it is
though it is attached by cartilage to the ribs, this por
from front to back.
tion of the sternum is flexible and can be depressed

without breaking. This maneuver is used, with care,
in closed cardiac massage to artificially circulate
Sternum
blood to the brain and extremities. The lower margin
The sternum, or breastbone, is a flat bone with three
of the body is attached to the xiphoid process by fi
parts: the manubrium, body, and xiphoid process.
brocartilage. This bone is the smallest of the three
The manubrium is the widest and thickest bone of the
parts of the sternum and usually fuses with the body
sternum. Its upper border is scalloped by a central
of the sternum in later life.
jugular notch, which can be palpated, and two clavic

ular notches that house the clavicles. Its lower border
articulates with the upper border of the body at a
Ribs
slight angle, the sternal angle or angle of Louis. This
A large portion of the bony thoracic cage is formed
angle can be easily palpated, is a landmark located
by 12 ribs located on either side of the sternum. The
between thoracic vertebrae T4 and TS, and is on a
first seven ribs connect posteriorly with the vertebral
25
FIGURE 2-3
The movements of the r ibs. A, "Bucket handle," lower rib. B, "Pump handle," first rib.
column and anteriorly through costal cartilages with
MOVEMENTS OF THE THORAX
the sternum. These are known as the true ribs. The re
The frequency of movement of the bony thorax joints
maining five ribs are known as the false ribs. The
is greater than that of almost any other combination
first three have their cartilage attached to the cartilage
of joints in the body. Two types of movements have
of the rib above. The last two are free or floating ribs.
been described-the pump-handle movement and the
The ribs increase in length from the first to the sev
bucket-handle movement (Figure 2-3) (Cherniack
enth rib, and then decrease to the twelfth rib. They
and Cherniack, 1983). The upper ribs are limited in
also increase in obliquity until the ninth rib and then
their ability to move. Each pair swings like a pump
decrease in obliquity to the twelfth rib.
handle, with elevation thrusting the sternum forward.
Each rib has a small head and a short neck that ar
This forward movement increases the anteroposterior
ticulate with two thoracic vertebrae. The shaft of the
diameter and the depth of the thorax and is called the
rib curves gently from the neck to a sudden sharp
pump-handle movement. In the lower ribs, there is
bend, the angle of the rib. Fractures often occur at
little antero-posterior movement. During inspiration,
this site. A costal groove is located on the lower bor
the ribs swing outward and upward, each pushing
der of the shaft of the ribs. This groove houses the in
against the rib above during elevation. This bucket
tercostal nerves and vessels. Chest tubes and needles
handle movement increases the transverse diameter
are inserted above the ribs to avoid these vessels and
of the thoracic cage. Thus during inspiration, the tho
nerves. The ribs are separated from each other by the
rax increases its volume by increasing its anteropos
intercostal spaces that contain the intercostal muscles.
terior and transverse diameters.
26
PART I
MUSCLES OF RESPIRATION
Inspiration
Inspiration is an active movement involving the con
traction of the diaphragm and intercostals. Additional
muscles may come into play during exertion in
health. In disease, the role of these accessory muscles
of inspiration may have an important role even at
rest. The accessory muscles include the sternocleido
mastoids, scalenes, serratus anterior, pectoralis major
and minor, trapezius, and erector spinae. The degree
to which these accessory muscles are used by the pa
tient is dependent on the severity of cardiopulmonary
distress (Clemente,
and Williams et ai,
1985; Murray and Nadel, 1988;

1989).
Diaphragm
The diaphragm is the principal muscle of respiration.
During quiet breathing, the diaphragm contributes ap
proximately two thirds of the tidal volume in the sit
ting or standing positions, and approximately three
fourths of the tidal volume in the supine position. It is
also estimated that two thirds of the vital capacity in
all positions is contributed by the diaphragm.
The diaphragm is a large, dome-shaped muscle
that separates the thoracic and abdominal cavities. Its
FIGURE 2-4
upper surface supports the pericardium (with which it
The diaphragm from below.
is partially blended), heart, pleurae, and lungs. Its

lower surface is almost completely covered by the
peritoneum and overlies the liver, kidneys, suprarenal
2-4). This large
lumbar vertebrae and extends upward to the central
muscle can be divided into right and left halves. Each
tendon. The central tendon is a thin, strong aponeuro
glands, stomach, and spleen (Figure
half is made up of three parts-sternal, lumbar, and
sis situated near the center of the muscle, somewhat
costal. These three parts are inserted into the central
closer to the front of the body. It resembles a trefoil
tendon, which lies just below the heart. The sternal
leaf with three divisions or leaflets. The right leaflet
part arises from the back of the xiphoid process and
is the largest, the middle is the next largest, and the
descends to the central tendon. On each side is a
left leaflet is the smallest.
small gap, the sternocostal triangle, which is located
Major vessels traverse the diaphragm through one
between the sternal and costal parts. It transmits the
of three openings (see Figure
superior epigastric vessels and is often the site of di
opening is located to the right of the midline in the
2-4). The vena caval
aphragmatic hernias. The costal parts form the right
central tendon and contains branches of the right
and left domes. They arise from the inner surfaces of
phrenic nerve and the inferior vena cava. The
the lower four ribs and the lower six costal cartilages.
esophageal opening is located to the left of the mid
They interdigitate and transverse the abdomen to in
line and contains the esophagus, the vagal nerve
sert into the anterolateral part of the central tendon.
trunks and branches of the gastric vessels. The aortic
The lumbar part arises from the bodies of the upper
opening is located in the midline and contains the
27
--------
?
I t.
\ ff
'---
-----
FIGURE 2-5
When the patient is lying on side, the dome of the diaphragm on the lower side rises fUI1her in the
thorax than the dome on the upper side.
aorta, thoracic duct, and sometimes the azygos vein.
in this POSItIon. On x-ray, the position of the di
The diaphragm is also pierced by branches of the left
aphragm can indicate whether the film was taken dur
phrenic nerve, small veins, and lymph vessels.
ing inspiration or expiration, and may also indicate
The position of the diaphragm and its range of
pathology in the lungs, pleurae, or abdomen.
movement vary with posture, the degree of distention
Each half of the diaphragm is innervated by a sep
of the stomach, size of the intestines, size of the liver,
arate nerve-the phrenic nerve on that side. Al
and obesity. The average movement of the diaphragm
though the halves contract simultaneously, it is pos
12.5 mm on the right and 12
sible for half of the muscle to be paralyzed without
mm on the left. This can increase to a maximum of
affecting the other half. Generally, the paralyzed half
in quiet respiration is
28 mm on the left during in
remains at the normal level during rest. However,
creased ventilation. The posture of the individual de
with deep inspiration, the paralyzed half is pulled up
30 mm on the right and
termines the position of the diaphragm. In the supine
by the negative pressure in the thorax. A special x
position, the resting level of the diaphragm rises. The
ray, moving fluoroscopy, is used to determine paral
greatest respiratory excursions during normal breath
ysis of the diaphragm.
ing occur in this position. Howevcr, the lung volumes
Contraction of the diaphragm increases the tho
are decreased because of the elevated position of the
racic volume vertically and transversely. The central
abdominal organs. fn a sitting or upright position, the
tendon is drawn down by the diaphragm as it con
dome of the diaphragm is pulled down by the abdom
tracts. As the dome descends, abdominal organs are
inal organs, allowing a larger lung volume. For this
pushed forward, as far as the abdominal walls will
reason, individuals who are short of breath are more
allow. When the dome can descend no farther, the
side-lying po
costal fibers of the diaphragm contract to increase the
sition, the dome of the diaphragm on the lower side
thoracic diameter of the thorax. This occurs because
rises farther into the thorax than the dome on the
the fibers of the costal part of the diaphragm run ver
comfortable sitting than reclining. fn
upper side (Figure 2-5). The abdominal organs have a
tically from their attachment at the costal margin.
tendency to fall forward out of the way, allowing
Thus contraction of these fibers elevates and everts
greater excursion of the dome on the lower side. fn
the ribs (Figure 2-6). If the diaphragm is in a low po
contrast, the upper side moves little with respiration
sition, it will change the angle of pull of the muscle's
28
PART I
.-;;/
"W.M
FIGURE 2-6
Contraction of the costal fibers of the diaphragm causes rib eversion and elevation.
costal fibers. Contraction of these fibers creates a
muscle forward to the sternum. There are II external
horizontal pull, which causes the lateral diameter to
intercostal muscles on each side of the sternum. They
become smaller as the ribs are pulled in toward the
are thicker posteriorly than anteriorly, and thicker
central tendon.
than the internal intercostal muscles. They are inner
As the diaphragm descends, it compresses the ab
vated by the intercostal nerves, and contraction draws
dominal organs, increasing intraabdominal pressure.
the lower rib up and out toward the upper rib. This
At the same time, the intrathoracic pressure decreases
action increases the volume of the thoracic cavity.
as the lung volume is increased by the descending di
There are also 11 internal intercostals per side.
aphragm. Inspiratory airflow occurs as a result of this
These are considered primarily expiratory in function.
decrease in intrathoracic pressure (see Chapter 3).
Studies have shown that the intercartilaginous or
The pressure gradient between the abdominal and
parasternal portion of the internal intercostals con
thoracic cavities also facilitates the return of blood to
tracts with the external intercostals during inspiration
the right side of the heart.
to help elevate the ribs. Besides their respiratory func
Movement of the diaphragm can be controlled to
tions, the intercostal muscles contract to prevent the
some extent voluntarily. Vocalists spend years learn
intercostal spaces from being drawn in or bulged out
ing to manipulate their diaphragms to produce the
during respiratory activity.
controlled sounds during singing. The diaphragm mo

mentarily ceases movement when a person holds his
Sternocleidomastoid
or her breath. The diaphragm is invol untarily in
The sternocleidomastoids (SCMs) are strong neck
volved in parturition, bearing down in bowel move
muscles arising from two h e a d s , one from the
ments, laughing, crying, and vomiting. Hiccups are
manubrium and one from the medial part of the clavi
spasmodic, sharp contractions of the diaphragm that
cle (see Figure 2-7, p. 29). These two heads fuse into
may indicate disease (e.g., a subphrenic abscess) if
one muscle mass that is inserted behind the ear into the
mastoid process. It is innervated by the accessory
they persist.
nerve and the second cervical nerve. There are two of
Intercostals
these muscles, one on each side of the neck. When one
The external intercostals extend from the tubercles
SCM contracts, it tilts the head toward the shoulder of
of the ribs, above, down, and forward to the costo
the same side and rotates the face toward the opposite
chondral junction of the ribs below, where they be
shoulder. If the two SCM muscles contract together,
come continuous with the anterior intercostal mem
they pull the head forward into flexion. When the head
brane (Figure 2-7). This membrane extends the
is fixed, they assist in elevating the sternum, increasing
29
Obllquus internus abdomlnis
Transversus abdomlnlS ......
FIGURE 2-7
Respiratory muscles (anterior view).

the anteroposterior (AP) diameter of the thorax.
and inferiorly to the upper surface of the first two
The SCMs are the most important accessory mus
ribs (see Figure 2-7). They are innervated by related
cles of inspiration. Their contractions can be ob
cervical spinal nerves. These muscles are primarily
served in all patients during forced inspiration and in
supportive neck muscles, but they can assist in res
all patients who are dyspneic. These muscles become
piration through reverse action. When their superior
visually predominant in patients who are chronically
attachment is fixed, the scalenes act as accessory
dyspneic (sec Chapter 4).
respiratory muscles and elevate the first two ribs

during inspiration.
Scalenes
The anterior, medial, a n d posterior scalenes are
Serratus Anterior
three separate muscles that are considered as a func
The sen-atus anterior arises from the outer surfaces of
tional unit. They are attached superiorly to the trans
the first eight or nine ribs. It curves backward, forming
verse processes of the lower five cervical vertebrae
a sheet of muscle that inserts into the medial border of
30
PART I
the scapula. It is innervated by the long thoracic nerve
f"
(cervical nerves CS, C6, and C7). There are two of

these muscles, one on each side of the body. Normally,
they assist in forward pushing of the arm (as in boxing
or punching). When the scapulae are fixed, they act as
accessory respiratory muscles and elevate the ribs to
which they are attached.
Pectoralis Major
The pectoralis major is a large muscle arising from
the clavicle, the sternum, and the cartilages of all the
true ribs (see Figure 2-7, p. 29). This muscle sweeps
across the anterior chest to insert into the intertuber
cular sulcus of the humerus. It is innervated by the
lateral and medial pectoral nerves and cervical nerves
CS, C6, C7, C8, and Tl. There are two of these mus
cles, one on each side of the body. This muscle acts

to rotate the humerus medially and to draw the arm
across the chest. In climbing and pull-ups, it draws
the trunk toward the arms. In forced inspiration when
the arms are fixed, it draws the ribs toward the arms,
thereby increasing thoracic diameter.
Pectoralis Minor
The pectoralis minor is a thin muscle originating from
the outer surfaces of the third, fourth, and fifth ribs
near their cartilages. It inserts into the coracoid process
of the scapula. It is innervated by the pectoral nerves
FIGURE 2-8
Respiratory muscles (posterior view).
(cervical nerves C6, C7, and C8). There are two of

these muscles, one on each side of the body. They con
tract with the serratus anterior to draw the scapulae to
ward the chest. During deep inspiration, they contract
the spine of the scapula. Its lower belly arises from

the supraspinous ligaments and the spines of the
to elevate the ribs to which they are attached.
lower thoracic region, and runs upward to be in
Trapezius
serted into the lower border of the spine of the
The trapezius consists of two muscles that form a
scapula. This large muscle is innervated by the ex
huge diamond-shaped sheet extending from the head
ternal or spinal part of the accessory nerve and cer
down the back and out to both shoulders (Figure 2-
vical nerves C3 and C4. Its main function is to ro
8). Its upper belly originates from the external oc
tate the scapulae in elevating the arms and to control
cipital protuberance and curves around the side of
their gravitational descent. It also braces the scapu
the neck to insert into the posterior border of the
lae and raises them, as in shrugging the shoulders.
clavicle. The middle part of the muscle arises from a
Its ability to stabilize the scapulae makes it an im
thin
portant accessory muscle in respiration. This stabi
diamond-shaped
tendinous
s h e et,
the
supraspinous ligaments and the spines o f the upper
lization enables the serratus anterior and pectoralis
thoracic region, and runs horizontally to insert into
minor to elevate the ribs.
Cardiopulmonar)' Anatomy
31
Obliquus Intemus Abdominis
Erector Spinae
The erector spinae is a large muscle extending from
This muscle originates from the lumbar fascia, the an
the sacrum to the skull (see Figure 2-8, p. 30). It orig
terior two thirds of the iliac crest, and the lateral two
thirds of the inguinal ligament (see Figure 2-7, p. 29).
Its post eri or fibers run almost vertically upward to in
inates from the sacrum, iliac crest,
and the spines of

the lower thoracic and lumbar vertebrae. It separates
into a lateral iliocostalis, an intermediate longissimus,
selt into the lower borders of the last three ribs. The
and a medial spinalis column. This muscle mass in
other fibers join an aponeurosis attached to the costal
serts into various ribs and vertebral processes all the
margin above, the linea alba in the midline and the
way up to the skull. It is innervated by the related
pubic crest below. It is innervated by the lower six tho
spinal nerves. These muscles extend, laterally flex,
racic nerves and the first lumbar spinal nerves.
and rotate the vertebral column. They are considered

accessory respiratory muscles through their extension
of the vertebral column. In deep inspiration, these
Transversus Abdominis
The transversus abdominis arises from the inner sur
muscles extend the vertebral column, allowing fur
face of the lower six costal caltilages, the lumbar fas
ther elevation of the ribs.
cia, the anterior two thirds of the iliac crest, and the
lateral one third of the inguinal ligament (see Figure
2-7, p. 29). It nms across the abdomen horizontally to
Expiration
insert into the ap one ur osi s extending to the linea

alba. It is innervated by the lower si x thoracic nerves
,
Expiration is a passive process,
occurring when the in

tercostals and diaphragm relax. Their relaxation al
and the first lumbar spinal nerves.
lows the ribs to drop to their preinspiratory position

and the diaphragm to rise. These activities compress
the lungs, raising intrathoracic pressure above atmos
pheric pressure, and thereby contributing to air flow
out of the lungs.
Action of the Abdominal Muscles

These four muscles work together to provide a firm but
flexible wall to keep the abdominal viscera in position.
The abdominal muscles exert
a compressing force on
the abdomen when the thorax and pelvis are fixed. This
Rectus Abdominis
force can be used in defecation, urination, parturition,
The rectus abdominis rises from the pubic crest and
and vomiting. In forced expiration, the abdominal mus
extends upward to insert into the xiphoid process
cles help force the diaphragm back to its resting posi
and the costal margin of the fifth, sixth, and seventh
tion and thus force air from the lungs. If the pelvis and
costal cartilages (see Figure 2-7, p. 29). It is inner
vertebral column are fixed, the obJiquus externus abdo
vated by related spinal nerves, and its action is con
minis aids expiration further by depressing and com
sidered within the context of the other abdominal
pressing the lower part of the thorax. Patients with

chronic obstructive pulmonary disease (COPD) have
muscles.
difficulty in exhalation, which causes them to trap air in
Ob/iquus Extemus Abdominis
their lungs. The continued contraction of the abdominal
This muscle arises in an oblique line from the fifth
muscles throughout exhalation helps them force this air
costal cartilage to the twelfth rib (see Figure 2-7,
from the lungs. The abdominal muscles also play an
p. 29). Its posterior fibers attach in an almost vertical
impOltant role in coughing. First, a large volume of air
line with the iliac crest. The other fibers extend down
is inhaled, and the glottis is
and forward to attach to the front of the xiphoid
muscles contract, raising intrathoracic pressure. When
process, the linea alba, and below with the pubic
the glottis opens, the large difference in intrathoracic
symphysis. It is innervated by the

spinal nerves.
lower six thoracic
closed. Then the abdominal
and atmospheric pressure causes the air to be expelled

forcefully at tremendous flow rates (tussive blast).
32
PART I
Patients with weak abdominal muscles (from neuro
upper ribs move forward and upward (Cherniack and
muscular diseases, paraplegia, quadriplegia or exten
Cherniack,
sive abdominal surgery) often have ineffective coughs

(see Chapters
28 and 33).
1983).
Quiet expiration is passive and involves no mus

cular contraction although some electrical activity
The four abdominal muscles have many other
can be detected. The inspiratory muscles relax, caus
nonrespiratory functions both individually and as a
ing intrathoracic pressure to be raised as the ribs and
group; these are not discussed here.
diaphragm compress the lungs by returning to their

preinspiratory positions. This increased pressure al
internaiintercostais
lows air flow from the lungs.
There are II internal intercostal muscles on each side
In forced inspiration, a large number of accessory
of the thorax. Each muscle arises from the floor of
muscles may contract in addition to the normal in
the costal groove and cartilage, and passes inferiorly
spiratory muscles mentioned. The erector spinae
and posteriorly to insert on the upper border of the rib
contract to extend the vertebral column. This exten
below. These internal intercostals extend from the
sion permits greater elevation of the ribs during in
sternum anteriorly, around the thorax to the posterior
s piration. Va rious back muscles ( e .g., erector
costal angle. They are generally divided into two
spinae, trapezius, and rhomboids) contract to stabi
parts-the interosseous portion located between the
lize the vertebral column, head, neck, and scapulae.
sloping parts of the ribs, and the intercartilaginous
This enables accessory respiratory muscles to assist
portions located between costal carti lages. As dis
inspiration through reverse action. The SCM raises
cussed previously, the intercartilaginous portions are
the sternum. The scalenes elevate the first two ribs.
considered inspiratory in function. Contraction of the
The serratus anterior, pectoralis major, and pec
interosseous portions of the intercostals depresses the
toralis minor assist in elevating the ribs bilaterally.
ribs and may aid in forceful exhalation. This muscle
All these accessory muscles tend to elevate the ribs,
is innervated by the adjacent intercostal nerves.
thus increasing the AP diameter but not the trans

verse diameter of the thorax. (In fact, the transverse
diameter does increase slightly as a result of the in
SUMMARY OF RESPIRATORY MOVEMENTS
creased strength of the contraction of the normal in
In quiet inspiration, the diaphragm, external inter
spiratory muscles.) The marked increase in AP di
costals, and intercartilaginous portions of the internal
ameter in relation to transverse diameter creates an
intercostals are the primary muscles that contract.
impression of
The diaphragm contracts first and then descends, en
accessory muscles.
en
bloc breathing in the patient using
larging the thoracic cage vertically. When abdominal
In forced expiration, the interosseous portion of
contents prevent its further descent, the costal fibers
the internal intercostals and the abdominal muscles
of the diaphragm contract, causing the lower ribs to
contract to force air out of the lungs. Forced expira
swing up and out to the side (bucket-handle move
tion can be slow and prolonged (as in patients with
ment). This lateral rib movement is assisted by the
COPD) or rapid and expulsive (as in a cough). If the
external intercostals and the intercartilaginous portion
abdominal contractions are strong enough, the trunk
of the internal intercostals. The transverse diameter of
flexes during exhalation. This flexion further com
the thorax is increased by this bucket-handle move
presses the lungs, forcing more air from them.
ment. Finally, the upper ribs move forward and up

ward (pump-handle movement) also through contrac
tion
of
their
external
intercostals
and
the
intercartilaginous portions of the internal intercostals.

This increases the AP diameter of the thorax. During
UPPER AIRWAYS
Nose
quiet inspiration, the epigastric area protrudes, then
Noses vary in size and shape with individuals and na
the ribs swing up and out laterally, and finally the
tionalities. Its framework is comprised of bony and
cartilaginous parts. The upper one third IS primarily
33
are covered with a thin, yellow olfactory mucous
bony and contains the nasal bones, the fr ontal
membrane that consists of bipolar nerve cells that are
processes of the maxillae and the nasal part of the
olfactory in function. Only a portion of inspired air
frontal bone. Its lower two thirds are cartilaginous
reaches the olfactory region to provide a sense of
and contain the septal, lateral, and major and minor
smell. When people smell something specific, they
alar nasal cartilages. The nasal cavity is divided into
sniff
right and left halves by the nasal septum. This cavity
it comes in contact with the olfactory region.
This action lifts the inspired air so that more of
extends from the nostrils to the posterior apertures of
The anterior portion (vestibule) of the nasal cavity
the nose in the nasopharynx. The lateral walls of the
(Figure 2-9) is lined with skin and coarse hairs (vibris
cavity are irregular as a result of projecting superior,
sae) that entrap inhaled patticies. The rest of the cavity
middle, and inferior nasal chonchae. There is a mea
and sinuses (with the exception of the olfactory region)
tus located beneath or lateral to each choncha through
are lined with respiratory mucous membrane. This
which the sinuses drain. The chonchae increase the
membrane is composed of pseudostratified columnar
sUlface area of the nose for maximum contact w ith
ciliated epithelium (Figure 2-10). It contains goblet
inspired air. The superior chonchae and adjacent sep
cells, as well as mucous and serous glands that produce
tal wall are referred to as the olfactory region. They
secrete mucus and serous secretions. These secretions
Vestibule 01 nasal cavity
FIGURE 2-9
Sagittal section of the head and neck.
34
PART I
FIGURE 2-10
B, Normal movements of cilia.
A, Pseudostrmified columnar ciliated
and bacteria. This mucus is then
walls are lined
the cilia at a rate of 5 to 15
swept to the
The
where it is swallowed or
and stratified squamous in the oral

parts.
mucous membrane is vascular, with arterial blood sup

plied by branches of the internal and external carotid
arteries. Venous
occurs
the anterior
The nasopharynx is a continuation of the nasal
2-9, p.
cavitIes
It lies behind the nose
facial veins. The mucous membrane is thickest over the
and above the soft palate. With the exception of the
chonchae. As air is inhaled, it passes around and over
soft
the chonchae, whose vascular moist surfaces heat, hu
never
its walls are immovable, so its
is
as is the oral and laryngeal phar
midify, and filter the inspired air. The mucous mem
ynx. The nasopharynx communicates with the nasal
brane may become swollen and irritated in upper
cavity
infections and may secrete copious amounts of
the posterior apertures of
the nose. It communicates with the
mucus. Because this membrane is continuous with si
pharynx through an opening, the
nuses, auditory tubes and lacrimal canaliculi, people
This opening is closed by elevations of the soft palate
isthmus.
suffering f r o m colds often complain of sinus

headaches, watery eyes,
and other
The oral pharynx extends from the soft palate to
Secretions are often so copious that the nasal passages
p. 33). It opens into the
the ep!.r10ttis (see
become comDletelv blocked.
the oropharyngeal isthmus.

walls lie on the bodies of the second and
third cervical vertebrae. Laterally, two masses of
Pharynx
lymphoid tissue-the
is an oval fibromuscular sac located
The
behind the nasal cavity, mouth, and larynx. It is ap
12 to 14 cm long and extends from the

base of the skull to the esophagus below, at the level
of the cricoid
the sixth cervical
be seen.
These tonsils form part of a circular band of lym

into the diges
phoid tissue surrounding the

t!ve and
tracts.
The laryngopharynx lies behind the larynx and ex

tends from the
above to the inlet of the
vertebra. Anteriorly, it opens into the nasal cavity
esophagus below
(nasophar ynx), mouth (oral pharynx) and larynx
to sixth cervical vertebrae lie behind the laryngeal
Figure
p.
The fourth
35
a n d the cartilages of the larynx (e.g., thyroid,

cricoid, epiglottic, right and left arytenoids, cornic
ulates, and cuneiforms). The thyroid cartilage is the
largest. It has a V-shaped notch in its upper one
third, which projects forward, forming the "Adam's
apple." The entire cartilage is pulled up in swal
lowing, with the upper part of the cartilage passing
beneath the hyoid bone. The cricoid cartilage is
shaped like a signet ring, with the signet part facing
the posterior. The anterior part of the carti lage is
easily palpated just below the thyroid cartilage. It is
thicker and more prominent than the tracheal rings,
FIGURE 2-11
which lie below. It is the only cartilage that com
Visualization of the larynx via a laryngoscope.
pletely circles the airway. The cricoid cartilage is

connected to the thyroid cartilage by the cricothy
roid membrane. (This membrane is often punctured
pharynx. In front of the laryngopharynx are the
to establish an airway in an emergency when the
epiglottis, the inlet of the larynx and the posterior
upper airway is obstructed.) The epiglottic cartilage

is the elastic skele ton of the epiglottis. It is a
surfaces of the arytenoid and cricoid cartilages.
leaflike structure attached by ligaments to the hyoid

bone anteriorly and the thyroid cartilage below. It is
Larynx
considered a vestigial structure, and its removal
The larynx is a complex structure composed of carti
causes little effect. Finally, the arytenoid cartilages
lages and cords moved by sensitive muscles (Figure
are two small pyramid-shaped cartilages that articu
2-11), and is located between the trachea and laryn
late with the posterior part of the cricoid cartilage.
gopharynx, for which it forms an anterior wall. It acts
The vocal cords attach from these cartilages to the
as a sphincteric valve with its rapid closure, prevent
thyroid cartilage.
ing food, liquids, and foreign objects from entering
The true vocal cords (or vocal folds) are two
the airway. It controls airflow, and at times closes so
pearly white folds of mucous membrane that stretch
that thoracic pressure may be raised and the upper
from the arytenoid cartilage to the thyroid cartilage.
airways cleared by a propulsive cough when the lar
The space between the true vocal cords is called the
ynx opens. Expiratory airflow vibrates as it passes
rima glottidis. It changes shape with movement of the
over the contracting vocal chords, producing the
cords but is generally triangular when the cords are
sounds used for speech. (The larynx is not essential
open. The rima glottidis and the true vocal cords are
for speech. Humans can speak by learning to dilate
grouped together under the term glottis. The glottis is
the upper part of the esophagus so that air vibrates as
the narrowest part of the adult airway.
it passes over; this is called esophageal speech).
Just above the true vocal cords are two shallow
In adult men, the larynx is situated opposite the
grooves in the mucous membrane lining of the larynx.
third, fourth and fifth cervical veltebrae; it is situated
These grooves (ventricles of the larynx) contain nu
somewhat higher in women and children. In children,
merous glands that secrete the mucus that covers the
the larynx is essentially the same in girls and boys. At
larynx. The false vocal cords (vestibular or ventricular
puberty, the male larynx increases in size consider
folds) lie just above the venuicles of the larynx. They
ably until its AP diameter is almost doubled. All the
are two soft, pink masses of mucous membrane raised
cartilages enlarge, with the thyroid cartilage becom
slightly from the laryngeal wall. They extend from the
ing prominent anteriorly.
thyroid cartilage to the arytenoids. The false cords are
The laryngeal skeleton contains the hyoid bone
not as well developed as the true cords and do not
36
PART I
approximate completely during phonation. However,

their closure can help protect the airway from aspira
tion of foreign material.
There are two main groups of muscles that control
the opening and closing of the glottis-the abductors
and adductors. The posterior cricoarytenoid muscle is
the most important muscle in the larynx, since it is the
only abductor of the vocal folds. It is vital for respira
tion. Contraction of this muscle separates the vocal
folds and widens the lumen of the glottis. There are
eight adductors of the vocal folds: (I) aryepiglottic,
(2) thyroepiglottic, (3) thyroarytenoid, (4) vocalis,
(5) cricothyroid, (6) lateral cricoarytenoid, (7) trans
verse arytenoid and (8) oblique arytenoid muscles.
Contraction of these muscles results in approximation
of the vocal cords and narrowing of the glottis. The
adductors of the cords are important in protecting the
lower airways. Their contraction prevents fluids, food,
and other substances from being aspirated. All the in
trinsic laryngeal muscles are innervated by the recur
rent laryngeal nerve (a branch of the vagus nerve)
with the exception of the cricothyroid muscle, which
is supplied by the external branch of the superior la
ryngeal nerve (also a branch of the vagus nerve).
The mucous membrane of the larynx is continu
ous with that of the laryngopharynx above and the
trachea below. It lines the cavity of the larynx and
the structures found within. On the anterior surface
and upper h a l f of the posterior surface of the
epiglottis, and the vocal folds, the mucous mem
brane is stratified squamous epithelium. The rest of
the laryngeal mucosa is ciliated columnar epithe
lium. The mucous membrane of the larynx has
many mucous glands. They are especially numerous
in the epiglottis, in front of the arytenoid cartilages
and in the ventricles of the larynx. Some taste buds
are also located on the epiglottis and irregularly
throughout the rest of the larynx.
LOWER AIRWAYS
Trachea
The trachea is a semi-rigid, cartilaginous tube approx
imately 10 to II cm long and 2.5 cm wide. It lies in
front of the esophagus, descending with a slight incli
nation to the right from the level of the cricoid carti

lage (see Figure 2-11, p. 35, and Figure 2-12). It trav
els behind the sternum into the thorax to the sternal
angle (opposite the fifth thoracic veltebra), where it
divides to form the right and left main-stem bronchi.
The tracheal wall is strengthened by 16 to 20 horse
shoe-shaped cartilaginous rings. The open P3lts of the
tracheal rings are completed by fibrous and elastic tis
sue and unstriated transverse muscle. This part of the
ring faces the posterior and is very flexible. It indents
or curves inward during coughing. which increases
the velocity of expelled air. These cartilages lie hori
zontally one above the other, separated by narrow
bands of connective tissue. The trachea is lengthened
during hyperextension of the head; swallowing, which
raises the trachea; and inspiration, when the lungs ex
pand and pull the trachea downward. Its cross-sec
tional area becomes smaller with contraction of the
unstriated transverse muscle fibers that complete the
tracheal rings.
The mucous membrane of the trachea also con
tains columnar ciliated epithelium and goblet cells.
Each ciliated epithelial eel I contains approximately
275 cilia. These structures beat rapidly in a coordi
nated and unidirectional manner, propelling a sheet
of mucus cephalad from the lower respiratory tract to
the pharynx, where it is swallowed or expectorated.
The cilia beat in this layer of mucus with a strong,
forceful forward stroke, followed by a slow ineffec
tive backward stroke that returns the cilia to their
starting position. This propelling of mucus by the
cilia (mucociliary escalator) is essential. When cilia
are paralyzed by smoke, alcohol, dehydration, anes
thesia, starvation, or hypoxia, mucus begins to accu
mulate in distal, gravity-dependent airways, causing
infiltrates and eventually localized areas of collapse
referred to as atelectasis.
The number of mucus-containing goblet cells is
approximately equal to the number of ciliated epithe
lial cells. Reserve cells lie beneath the ciliated and
goblet cells. These reserve cells can differentiate into
either goblet cclls or ciliated cells. Beneath the re
serve cells lie the gland cells. There are approxi
mately 40 times more gland cells than goblet cells.
Mucus is composed of 95% water, 2% glycoprotein,
I % carbohydrate, trace amounts of lipid, deoxyri
37
Apical
Apical
Anterior
Anterior
??'fjfjl;ff?-
Posterior
Apical-posterior
Llnguta
Posterior
Anterior
Anterior
Posterior
FIGURE 2-12
Tracheobronchial tree (a three-quarter view, rotated toward the right side).
dead tissue celis, phagocytes,
main-stem bronchus. The azygos vein arches over the
leukocytes, erythrocytes, and entrapped foreign parti
bonucleic acid
right main-stem bronchus, the right pulmonary artery
(DNA),
cles. Mucus lines the airways from the trachea to the
lies beneath. The right main-stem bronchus divides to
alveoli. Two separate layers have been observed-the
form the right upper lobe bronchus, the right middle
sol layer, which lies on the mucosal surface and con
lobe bronchus and the right lower lobe bronchus. The
tains high concentrations of water, and the gel layer,
right upp e r l o b e d i v i d e s i n t o th r e e s e gm e n t al
which is more supelficial and more viscous because
bronchi-apical, posterior, and anterior. The apical
of its lower concentration of water.
bronchus runs almost vertically toward the apex of
The right main-stem bronchus appears to be an ex
the lung. The posterior bronchus is directed posteri
tension of the trachea, being wider, shorter, and more
orly in a horizontal direction, while the anterior
vertical than the left main-stem bronchus. Its greater
bronchus is directed anteriorly in an almost horizon
width and more vertical course cause a majority of
tal direction. The right middle lobe bronchus divides
aspirated foreign material to pass through the right
about
10
mm below the right upper lobe bronchus
38
PART I
and descends downward anterolateraJly. The right
cross-sectional area increases because of the increased
lower lobe bronchus divides into five segmental
number of divisions of the airways. The mucous
bronchi. The apical or superior bronchus runs almost
membrane is essentially the same, with helical carti
horizontally, posteriorly. The medial or cardiac
laginous plates and cilia becoming more sparse. These
bronchus descends downward medially toward the
changes continue throughout the eighth to eleventh
heart. The anterior basal bronchus descends anteri
generations, which are referred to as bronchioles.
orly. The lateral basal bronchus descends laterally
The terminal bronchioles extend from the twelfth
and the posterior bronchus descends posteriorly. Note
to the sixteenth generation. The diameter of these air
that each segment describes its position.
ways is approximately I mm. Cartilage is no longer
The left main-stem bronchus is narrower and runs
present to provide structural rigidity. The airways are
more horizontally than the right main-stem bronchus.
embedded directly in the lung parenchyma, and it is
The aortic arch passes over it, while the esophagus,
the elastic properties of this parenchyma that keep
descending aorta, and thoracic duct lie behind it. The
these lower airways open. Strong helical muscle
left pulmonary artery lies anteriorly and above the
bands are present, and their contraction forms longi
left main-s t e m b r o n c h u s . T h e l e f t m a i n-stem
tudinal folds in the mucosa that sharply decrease the
bronchus has two major divisions-the left upper
diameter of these airways. The epithelium of the ter
lobe bronchus and the left lower lobe bronchus. The
minal bronchioles is cuboidal and no longer ciliated.
left upper lobe bronchus has three major segmental
The cross-sectional area of the airways increases
bronchi. The anterior bronchus ascends at approxi
sharply at this level, as the diameter of the terminal
mately a 45-degree angle. The apical-posterior
bronchioles ceases to decrease as markedly with each
bronchus has two branches; one runs vertically and
generation. All the airways to this level (I to 16 gen
the other posteriorly toward the apex of the left lung.
erations) are considered conducting airways, because
The lingular bronchus descends anterolaterally, much
their purpose is to transport gas to the respiratory
like the right middle lobe bronchus of the right lung.
bronchioles and alveoli, where gas exchange occurs.
The right lower lobe bronchus divides into four seg
The conducting airways receive their arterial blood
mental bronchi. The superior or apical bronchus runs
from the bronchial circulation (branches of the de
posteriorly in a horizontal direction. The anterior
scending aorta). Airways from below this point re
bronchus descends anteriorly. The lateral bronchus
ceive their arterial blood from the pulmonary arteries.
descends laterally, while the posterior bronchus de
The respiratory bronchioles extend from the sev
scends posteriorly. Again the segments describe their
enteenth to the nineteenth generation. They are con
anatomical position.
sidered a transitional zone between bronchioles and
The bronchi of the airways continue to divide until
alveoli. Their walls contain cuboidal epithelium inter
there are approximately 23 generations (Table 2-1).
spersed with some alveoli. The number of alveoli in
The main, lobar, and segmental bronchi are made up
creases with each generation. The walls of the bron
of the first four generations. The walls contain U
chioles are also buried in the lung parenchyma. The
shaped cartilage in the main bronchi. This cartilage
airways depend on traction of this parenchyma to
becomes less well-defined and more irregularly
maintain their lumen. Muscle bands are also present
shaped as the bronchi continue to divide. In the seg
between alveoli.
mental bronchi the walls are formed by irregularly
Alveolar ducts extend from the twentieth to the
shaped helical plates with bands of bronchial muscle.
twenty-second generation. Their walls are composed
The mucous membrane of these airways is essentially
entirely of alveoli, which are separated from one an
the same as in the trachea, but the cells become more
other by their septae. Septae contain smooth muscle,
cuboidal in the lower divisions.
elastic and collagen fibers, nerves, and capillaries.
The subsegmental bronchi extend from the fifth to
The twenty-third generation of air passages is
the seventh generation. The diameter of these airways
called alveolar sacs. They are essentially the same as
becomes progressively smaller, although the total
alveolar ducts, except that they end as blind pouches.
TABLE 21
Structural Characteristics of the Air Passages
GENERATION
(MEAN)
NUMBER
Trachea
MEAN
DIAMETER AREA
(MM)
SUPPLIED
18
CARTILAGE
MUSCLE
Both lungs
13
EPITHELIUM
end of
Individual
EMPLACEMENT
Links open
U-shaped
Main bronchi
NUTRITION
cartilage
lungs
Within
connective
2
Lobar bronchi
Segmental bronchi
4
5
16
32
4
3
2,000
4,000
1
1
Small bronchi
Bronchioles
11
12
and terminal
bronchioles
16
65,000
tissue
Lobes
Segments
sheath
IlTegular
Helical
shaped
bands
and
Secondary
helical
lobules
plates
From the
Columnar
ciliated
alongside
bronchial
arterial
circulation
vessels
Strong
helical
0.5
muscle
Embedded
bands
Cubiodal
directly in
the lung
17
Respiratory
bronchioles
130,000
19
500,000
20
1,000,000
Muscle
0.5
Primary
Absent
lobes
Alveolar sacs
1
22
23
flat
between
between
Thin bands
1
4,000,000
8,000,000
ill
0.3
0.3
Alveoli
From Weibel MorphometlY of the human lung. New York, 1963, Springer. Used with permission.
w
(0
Cubiodal to
band
alveolar
Alveolar ducts
parenchyma
From the
the alveoli
pulmonary
circulation
F01TI1S the
alveolar
lung
septa
parenchyma
Alveolar
epithelium
PART I
40
(Actually, communication occurs between "blind
Other cells located in the distal airways that are
pouches" in the form of the pores of Kohn's, which
important in the defense of the lung are the lympho
are channels ill alveolar walls,. and Lambert's canals,
cytes a n d p o l y m o r p h o n ucl ear l e ukoc ytes. I m
which are communications between bronchioles and
murioglobulins (IgA, IgG, and IgM) in the blood
alveoli. These communications are thought to be re
serum appear to enhance the engulfing activity of the
sponsible for the rapid spread of lung infection. They
macrophages. There are two types of lymphocytes
also provide collateral ventilation to alveoli, whose
found in the lung-the B-Iymphocyte and the T-Iym
bronchi are obstructed. Although this ventilation does
phocyte. The B-lymphocytes produce gamma globu
little to arterialize blood, it does help prevent collapse
lin antibodies to fight lung infections, whereas the T
of these alveoli.) Each alveolar sac contains approxi
lymphoc ytes r e l e a s e a s u b s t a n c e that attracts
mately 17 alveoli. There are about 300 million alveoli
macrophages to the site of the infection. The poly
in an adult man, 85% to 95% of which are covered
morphonuclear leukocytes are important in engulfing
with pulmonary capillaries. Alveolar epithelium is
and killing blood-borne gram-negative organisms.
composed of two cell types. Type I cells, squamous

pneumocytes, have broad thin extensions that cover
about 95'!c of the alveolar surface. Type II cells, the
LUNGS
granular pneumocytes, are more numerous than type
Two lungs, each covered with its pleurae-the vis
I cells but occupy less than 5% of the alveolar sur
ceral pleura and the parietal pleura-lie within the
face. This is because of their small, cuboidal shape.
thoracic cavity. Each lung is attached to the heart and
These cells are responsible for the production of sur
the trachea by its root and the pulmonary ligament. It
factant, a phospholipid that lines the alveoli. SUlfac
is otherwise free in the thoracic cavity. The lungs are
tant keeps alveoli expanded by lowering their surface
light, soft spongy organs, whose color darkens with
tension. Type II cells have been shown to be the pri
age as they become impregnated with inhaled dust.
mary cells involved in repair of the alveolar epithe
They are covered with the visceral pleura, a thin, glis
lium. (This has been shown in experiments where O2
tening serous membrane that covers all sUlfaces of the
toxicity was induced in monkeys and in numerous
lung. The visceral pleura reflects and continues on the
other conditions where type I cells were destroyed.)
med iasti num and inner thoracic wall, where it be
Type III cells, alveolar brush cells, are rare and are
comes known as the parietal pleura. The space be
found only occasionally in humans.
tween the two pleurae is minuscule and contains a

alveolar
negative pressure at all times, which helps keep the
macrophage, is found within the alveolus. These cells
lungs inflated. A small amount of pleural fluid lubri
An
additional
type
of
cell,
the
are thought to originate from stem cell precursors in
cates the two pleurae as they slide over each other
the bone marrow and reach the lung through the
during breathing. In disease, fluid, tumor cells. or air
blood stream. They are large, mononuclear, ameboid
may invade the pleural space and collapse the under
cells that roam in the alveoli, alveolar ducts, and
lying lung. Each lung ha an apex, base, arid three sur
alveolar sacs. They contain Iysosomes, which are ca
faces (costal, medial, and diaphragmatic). There are
pable of killing engulfed bacteria. (Studies show
also three borders (anterior, inferior, and posterior).
them to be most effective i n neutralizing inhaled
Each lung is divided by fissures into separate lobes. In
gram-positive organisms.) They also engulf foreign
the right lung the oblique fissure separates the lower
matter and are either transported to the lymphatic
lobe from the middle, whereas the horizontal fissure
system or migrate to the terminal bronchioles where
separates the upper lobe from the middle. The right
they attach themselves to the mucus. They are then
lung is heavier and wider than the left lung. It is also

'
shorter because of the location of the right lobe of the
carried by the mucus to larger airways and eventually

to the pharynx. Since cilia are not present below the
Jiver. The left lung is divided into upper and lower
eleventh generation of air passages, clearance of mat
lobes by the oblique fissure. It is longcr and thinner
ter and bacteria from these areas is largely dependent
than the right lung, because the hem1 and pericardium
on the macrophages.
are located in the left thorax. Numerous structures
41
enter the lung at the hilus, or root of the lung, includ
rior angle of the scapula with the arm at rest. The in
ing the main-stem bronchus, the pulmonary artery,
ferior border joins the posterior medial border of the
pulmonary veins, bronchial artelies and veins, nerves,
lung 2 cm lateral to the tenth thoracic vertebra. The
and lymph vessels. The root, or hilus, of the lungs lies
posterior medial border runs 2 cm lateral to the verte
opposite the bodies of the fifth, sixth, and seventh tho
bral column from the seventh cervical vertebra to the
racic veltebrae. The lungs are connected to the upper
tenth thoracic vertebra.

The left lung is generally smaller than the right
airways by the trachea and main-stem bronchi.
and accommodates the position of the heart. The me

dial border on the anterior aspect runs from the ster
Surface markings
noclavicular joint to the middle of the sternal angle,
Surface markings of the lungs can be outlined over
down the midline of the sternum to the fourth costal
the chest with a basic knowledge of bony landmarks
cartilage. A lateral indentation of about 1 \/2 in forms
and gross anatomy of each lung (Table 2-2, and Fig
the cardiac notch at the level of the fifth and sixth
ures 2-13, 2-14, and 2-15). The apices of both lungs
costal cartilages. The courses of the inferior and me
extend 1 in above the clavicles at the medial ends.
dial borders on the posterior aspect are similar in the
The anterior medial border of the right lung runs
left and right lungs. In the left lung, however, the in
from the sternoclavicular joint, to the sternal angle
ferior border crosses at the level of the tenth thoracic
downward to the xiphisternum. The inferior border
vertebra, not the twelfth observed in the right lung.
runs from the xiphisternum laterally to the sixth rib in
The position of the fissures of the lungs can be
the midclavicular line, the eighth rib in the midaxil
outlined over the chest wall. In both lungs, the
lary line, and the tenth rib in the midscapular line.
oblique fissure begins between the second to fourth
The midscapular line runs downward from the infe-
thoracic vertebrae. This can be roughly estimated by
Apical
Apical post.
AnI. basal
BRONCHOPULMONARY
SURFACE MARKINGS
SEGMENTS
FIGURE 2-13
Surface markings of the lungs (anterior aspect). The underlying bronchopulmonary segments are
also shown. (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and
disease, ed 3, Philadelphia, 1983, WB Saunders.)
42
PART I
TABLE 2-2
Anatomical Arrangement of the Bronchopulmonary Se.gments
LOBE
RIGHT LUNG:
BRONCHOPULMONARY SEGMENTS
LOBE
LEFT LUNG:
BRONCHOPULMONARY SEGMENTS
Upper
Apical-extends above the
Upper
Apical posterior-extcnds above the

clavicle anteriorly; occupies
clavicle anteriorly; smaller area
comparablc area as the apical and
posteriorly
posterior segments of the right lung

Anterior---occupies area between the
Anterior---occupies area between the
clavicle and horizontal fissure
clavicle and theborder of the lingula

(comparable line to the horizontal
fissure of the right lung)
Posterior-remainder of upper lobe

on the posterior aspect down
to the oblique fissure
Middle
Lateral-extends medially
(Lingula)'"
from junction of the two fissures
Superior---occupies upper half of the

lingula
Inferior---occupies lower half of the
at the third intercostal space to
lingula
occupy one third the anterior

SlIrface of the lobe
Medial-occupies the remaining
anterior surface of the lobe
Lower
(Base)
Anterior---occupics basal area
Lower
beneath the oblique fissure anteriorly
(Base)
Supelior---occupies half the area from
Anterior---occupies area inferior to the

oblique fissure anteriorly
Superior---occupic.' onc third of the
the oblique fissure downward*
basal area posteriorly from the oblique
on the posterior aspect
tissure downward
Lateral-extends from the junction
Lateral-occupies the lateral half of the
of the middle lobe over the
remaining two thirds of the left lower
midaxillary area to occupy one third
lobe beneath the superior scgment on
the area inferior to the superior
the posterior aspect
segment on the posterior a pect

Posterior---occupies two thirds
Posterior---occupies the medial ponion
of the area posteriorly beneath
of the remaining two thirds of the left
the superior segment
ower lobe beneath the superior
Medial-occupies a space on
segment on the posterior aspect
the inner aspect of the righl base+
'This segmenl can be drained preferentially when the patient lies prone.
j"
Medial basal
segent has
therefore, cannot be directly auscultated. This segment

s e gment because of the comparable angle ur its bronchus.
no direct exposure to the chest wall,
when the patienl is positioned for the left lateral basal
i:
Superiur segmenls abo called apical.
Lingula is not an anatomically uislinct area comp<lred with the right middle lobe; rather, it
is Hn<llo mical l y
preferenlially dr<lins
pari of the left upper lobe.
--
.....
- 4th rib
-Xiphi
sternal
j u nc t io n
i
Mi d ax llary line
8th rib
SURFACE MARKINGS
FIGURE 214
SUlface markings of the lungs (lateral aspect). (Printed with permission from Cherniak RM,
Cherniack L: Respiration in health and disease, ed 3, Philadelphia, 1983, WB Saunders.)
ji.' J/J
}:o
l'
'-.r'
T2(spine)
Apical
l
i
Lat. basal
BRONCHOPULMONARY
SURFACE MARKINGS
SEGMENTS
FIGURE 215
Surface markings of the lungs (posterior aspect). The underlying bronchopulmonary segments are
also shown. (Printed with permission from Cherniak RM, Cherniack L: Respiration in health and
disease, ed 3, Philadelphia, 1983, WB Saunders.)
43
44
PART I
following a line continuous with the medial border
heart is rotated to the left in the chest, resulting in the
of the abducted scapula, around the midaxillary line
right side of the heart being foremost. Thus joining
at the fifth rib, and terminating at the sixth costal
the two uppermost points outlines the level of the
cartilage anteriorly. The horizontal fissure of the
atria and joining the two lower points represents the
right lung originates from the oblique fissure at the
margin of the right ventricle.
level of about the fourth intercostal space in the mi
The heart as a whole is freely movable within the
daxillary line, and courses medially and slightly up
pericardial cavity, changing position during both con
ward over the fourth rib anteriorly. The left lung has
traction and respiration. During contraction, the apex
no horizontal fissure.
moves forward, strikes the chest and imparts the chest

and apex beat, which may be felt and seen. Abnormal
position of the apex beat can indicate cardiac enlarge
Bronchopulmonary Segments
ment or displacement. During breathing, the move
The bronchopulmonary segments lie within the
ments of the diaphragm determine the position of the
three lobes of the right lung and the two lobes of the
heart. This is because of the attachment of the central
left lung. There are 10 bronchopulmonary segments
tendon of the diaphragm to the pericardium. Changes
on the right and eight on the left. Brief anatomic de
in position during quiet breathing are hardly notice
scriptions of the position of each lobe are provided
able, but with deep inspirations, the downwal'd excur
in Table 2-2, p. 42. Figure 2-13, p. 41, illustrates the
sion of the diaphragm causes the heart to descend and
surface markings on the anterior view of the lungs
rotate to the right. The opposite occurs during expira
and the position of the various bronchopulmonary
tion. Pathology of the lungs can also change the posi
segments within the major anatomic divisions pro
tion of the heart. Atelectasis shifts the heart to the
vided by the fissures. Figure 2-14, p. 43, shows
same side. In tension pneumothorax, where air enters
some of these features from the lateral views. Figure
the chest usually through an opening in the chest wall
2-15, p.43 illustrates the surface markings and bron
and cannot escape, the positive pressure shifts the
chopulmonary segments of the posterior aspect of
heart away from the side of the pathology.

The heart is enclosed by the pericardium, whose
the lungs.
two surfaces can be visualized by considering the

heart as a fist that is plunged into a large balloon. The
HEART
outer surface, a tough fibrous membrane, is called the
The herut is a conical, hollow muscular pump enclosed
fibrous pericardium. It encases the heart and the or
in a fibroserous sac, the pericardium. Its size is closely
gans and terminations of the great vessels. This mem
related to body size and corresponds remarkably to the
brane is so unyielding that when fluid accumulates
size of an individual's clenched fist. It is positioned in
rapidly in the pericardial cavity, it can compress the
the center of the chest behind the lower half of the ster
heart and impede venous return. When this occurs
num. The largest portion of the heart lies to the left of
often, a window is cut in the pericardium, allowing
the midsternal line; the apex is found approximately 9
the fluid to escape. The inner surface, the serous peri
cm to the left in the fifth intercostal space.
cardium, is a serous membrane that lines the fibrous
The surface markings of the heart can be traced by
pericardium. Ten to 20 ml of clear pericardial fluid
joining four points over the anterior chest wall. On
separates and moistens the two pericardial surfaces.
the right, the heart extends from the third to the sixth
The pericardium with its fluid minimizes friction dur
costal caltilages at a distance of about to to 15 mm
ing contraction. It also holds the heart in position and
from the sternum. On the left, the heart extends from
prevents dilation. The serous pericardium consists of
the second costal cartilage to the fifth intercostal
an outer layer, the parietal layer, and an inner layer
space 12 to 15 mm, and 9 cm from the left sternal
the visceral layer, or epicardium.
border, respectively. Joining the two points on the
The heart is divided into right and left halves by an
left side outlines the left atrium and ventricle. The
obliquely placed longitudinal septum (Figure 2-16).
45
Superior vena cava .......

Pulmonary veins
Pulmonary veins
Atrium
Pulmonary valve
t <?t@iW._ Ventricle
..
FIGURE 2-16
Blood flow of the heart.
Each half has two chambers-the atrium, which re
amount of work they perform. The ventricles do more
ceives blood from veins, and the ventricles, which
work than the atria, and their walls are thicker. The
eject blood into the arteries. The sllperior vena cava,
pressure in the aorta is higher than that in the pul
inferior vena cava, and intrinsic veins of the heart de
monary trunk. This requires greater work from the
posit venous blood into the right atrium. Blood then
left ventricle, so its walls are twice as thick as those
passes through the tricllspid valve to the right ventri
of the right ventricle. The innermost layer, the endo
cle. The right ventticle projects the blood through the
cardium, is the smooth endothelial lining of the inte
pulmonary valve into the pulmonary arteries, which
rior of the heart. *
are the only arteries in the body containing deoxy

genated blood. Pulmonary veins return the blood to
the left atrium and from there, it passes through the
Heart Valves
mitral valve to the left ventricle. From the left ventri
The four valves of the heart, although delicate in ap
cle it is ejected through the aortic valve into the main
pearance, are designed to withstand repetitive clo
artery of the body-the aorta.
sures a g a i n st h i g h pressures (se e F i g u r e 2-16)
The heart is divided into three layers-the epi
(French, Criley, 1983). Normally, they operate for
cardium, myocardium, and endocardium. The outer
more than 80 years without need of repair or replace
most layer, the epicardium, is visceral pericardium
ment. The tricuspid and mitral valves function differ
and is often infiltrated with fat. The coronary blood
en tly from the other valves of the h e art. Bei n g
vessels that nourish tile heart run in this layer before

entering the myocardium. The myocardium consists
of cardiac muscle fibers. The thickness of the layers
of cardiac muscle fibers is directly proportional to the
"For additional information o f tbe
refer
clinical aspects o f heart
And reol i et ai, 1991; Goldberger, 1990;

Sokolow, Mcilroy, Cheitlin, 1990; and Gray s Anatomy.
anatomy,
10
'
46
PART I
located between the atria and ventricles, they must ef
free edges of these valves project into the lumen of
fect a precise closure within a contracting cavity.
the vessels. At the end of systole, blood in the aorta
During diastole, the two leaflets or cusps of the
and pulmonary artery forces the cusps of the valves
mitral valve and the three cusps of the tricuspid valve
shut. These valves are attached in such a manner
relax into the cavities of the ventricles, allowing
that they cannot be everted into the ventricles by in
blood to flow between the two chambers. As the ven
creased pressure in the vessels. During diastole, the
tricular chambers fill with blood, the cusps of the
cusps support the column of blood filling the ven
valves are forced up into a closed position. Fibrous
tricles. Contraction of the ventricles during systole
cords, the chordae tendinae, are located on the ven
increases pressure within the ventricular chambers,
tricular surfaces of these cusps. These cords connect
forcing the cusps to open and allow blood flow into
the cusps of the valve with the papillary muscles of
the vessels.
the ventricular walls. As pressure builds in the ven
The arterial supply of the heart muscle is derived
tricular chambers, contraction of these muscles pre
from the right and left coronary arteries, which
vents the cusps from being forced up into the atria.
arise from the aortic sinuses (Figure
Dysfunction or rupture of the chordae tendinae or the
coronary artery (LCA) divides into the anterior de
papillary muscles may undermine the SUppOlt of one
scending artery a n d the left circumflex artery.
2- 17). The left
or more valve cusps, producing regurgitation from
These arteries supply most of the left ventricle, the
the ventricles to the atria.
left atrium, most of the ventricular septum and, in
The pUlmonic and aortic valves are similar in ap
45% of people, the sinoatrial (SA) node. The right
pearance but the aortic cusps are slightly thicker
coronary artery (RCA) supplies most of the right
than the pulmo ic cusps. Each valve has three fi
ventricle, the atrioventricular (A V) node and, in
brous cusps, the bases of which are firmly attached
55% of people, the SA node. Infarction of these ar
to the root of the aorta or the pulmonary artery. The
teries or their branches can thus cause interruption
----
Circumflex branch
Interventricular branch (posterior descending) /
FIGURE 2-17
Blood supply of the heart.
47
or cessation of the conduction system and death of
node retains its position as pacer of the heru1 as long as
the myocardial muscle in the area supplied by the
it generates impulses at a faster rate than any other pru1
artery. The severity of the infarction is dependent
of the myocardium and as long as these impulses are
on the size of the artery and the importance of the
rapidly conducted from the atria to the ventricles. Nor
area it supplies.
mal impulse formation may be interrupted by vascular
The heart is drained by a number of veins. Most of
lesions (occlusion of the coronary arteries) or by car
the veins of the heart enter the coronary sinus, which
diac disease (pericarditis). The SA node is especiaUy
then empties into the right atrium. A small portion of
susceptible to pericarditis and all other surface cardiac
veins, the thebesian veins, empty directly into the
diseases because of its superticiaJ position immediately
right and left ventricles.
beneath the epicardium.

The muscle fibers of the heart are self-excitatory,
which enables the heart to rhythmically and automati
Innervation
cally contract. The normal pacemaker of the heart is
Innervation of the heart involves a complex balance be
the sinoatrial node located in the posterior wall of the
tween its intrinsic automaticity and extrinsic nerves
right atrium. The concentric waves of excitation sent
(Figure 2-18). The SA and A V nodes provide the heart
out by the SA node must travel through the A V node
with an inherent ability for spontaneous rhythmic initia
to reach the ventricles. This node is located in the floor
tion of the cardiac impulse. The rate of this impulse for
of the light atrium, just above the insertion of the tri
mation is regulated by the autonomic nervous system
cuspid valve. Its main function is to cause a 0.04 sec
(ANS), which also influences other phases of the car
ond delay in the atrioventricular transmissions. This
diac cycle. It controls the rate of spread of the excitation
has two advantages. It postpones ventricular excitation
impulse and the contractility of both atria and ventricles.
until the atria have had time to eject their contents into
The ANS extends its influence to the heaIl via the
the ventricles. It also limits the number of signals that
vagus nerve (parasympathetic) and upper thoracic

nerves (sympathetic). These nerves mingle together
around the root and arch of the aorta near the tracheal
bifurcation, forming the cardiac plexus. Extensions
from the cardiac plexus richly supply the SA and A V
nodes. They are so well-mingled that scientists are un
able to determine which nerves supply which parts of
the heart. Stimulation of the sympathetic nervous sys
tem causes acceleration of the discharge rate in the SA
node, increase in A V nodal conduction, and increase
in the contractile force of both atrial and ventricular
muscles. Stimulation of the vagus nerve causes car
diac slowing and decreased A V nodal conduction.
Thus the parasympathetic system decelerates heart
rate and the sympathetic system accelerates heart rate.
Intrinsic innervation of the heart centers around the
SA node, which lies near the junction of the superior
vena cava and the right atrium. It is the normal pace
maker of the heart, sending concentric waves of excita
tion throughout the atrium. Without neural influence,
impulse formation from this node would be greater than
100 beats/minute. However, vagal influence decreases
FIGURE 2-18
the impulse formation to 60-90 beats/minute. The SA
Electrical conduction of the heart.
48
PART I
can be transmitted by the A V node. The A V node also
tion, the QRS complex indicates ventricular depolar

ization and the T-wave indicates ventricular repolar
has its own inherent rhythmicity, firing at a much
(40-60
beats/minute). Its
ization. There is no wave indicating atrial repolariza
main pathology is a result of occlusion of the right
tion, since this is embedded in the QRS complex
slower rate than the SA node
coronary artery, which supplies the AV node in
90%
(Andreoli et aI,
of the cases. From the A V node arises a triangular
of the Electtical Excitation of the Heart and ECG In
His. This bundle divides in the ventricular septum into
Conover,
group of fibers known as the AV bundle or bundle of
terpretation, Chapter II; Dubin,
1989;
Marriott,
1989; and Wagner, 1994.
two branches-the left bundle branch and the right

bundle branch. Each of these bundles continues to di
SYSTEMIC CIRCULATION
vide into many fine strands that spread across the ven
The systemic vascular system is a complex series of
tricles. At the end of the bundle's ramifications are

Purkinje's fibers, which are continuous with the car
blood vessels throughout the entire body. It conveys
diac muscle. The waves of excitation pass through the
nutrition and oxygen to all tissues of the body and car
bundle of His, down the bundle branches, and through
ries away their waste products. The driving force for
the Purkinje fibers, which permeate the ventricles and
this system is the heart. The vascular system can be
cause them to contract. This wave of depolarization
considered to have two major components-the periph
gives rise to the normal P-QRS-T configuration of the
eral and pulmonary circulations (Schlant et aI,
electrocardiogram (ECG) tracing (Figure 2- 19) (see
Chapter
II).
Blood vessels are designed to forward oxygenated

blood from the heart during systolic ejection of the
The P-wave indicates atrial depolariza
b =J==1--+-t----t-11r-I
L-1-+-+--l--+++-+--i--t i-ll rQO.2
1.
L-t-+
t-t-tTRl--r1!-t1l-r.o.4 l1
1
L -++rt ti T1 w
1
J
lj 4-1
-titti-r rT- I
I
.+ST
m
second
s con
l-+-+----t-
PR se ment
g
-rl II
I'
II
I
'
PI
I
I---+-+-+-t-.iI
I t- I i
t-
5 mm
0.5 mv
mm
'
I_
I-.II I1 [ffiI l'
It
se ment
g
I
r-
I
! 111 0
I
I
I
l ]1
-+---r---,-,--:
L-+r-
-t-"t-I-+-+1
\41 rr-4
PR interval I I !... I.
I
J 1 J -J IOR S.1nterva
' .1
1---+-+-+-t -1"-11T1 '1 II 1 l 1 1
I
, 1
U
.
I, !I
I
I
l ..l -J
I
I I
OTI interval
L.i+-t--+-t-t
i
I I
I
FIGURE 2-19
A normal ECG showing characteristic waves, intervals, and segments.
49
left ventricle, perfuse the vascular beds commensu
veins. These veins branch and become increasingly
rate with their metabolic needs and remove metabolic
larger. Blood flow through the veins is largely depen
excreta. Anatomically, the proximal vessels have a
dent on muscular or visceral action or pressures.
higher proportion of connective tissue and elastin to
These pressures are intermittent and, were it not for
withstand high pulse pressures (e.g., the aorta, which
double-cusp valves located within the veins, blood
carries blood to the head, viscera, and limbs). In addi
would flow backward when the pressure ceases. In the
tion, potential energy is stored in the walls of the
extremities, muscular contractions move blood into
larger vessels during systole. During diastole, the
the trunk. In the pelvic and abdominal region, blood
elastic recoil of these vessels maintains the forward
flow is dependent on intraabdominal pressure exceed
motion of the blood between ventricular systoles. The
ing intrathoracic pressure. Blood flows through the
medium-size blood vessels have comparable propor
trunk in veins that become increasingly larger until
tions of connective tissue and elastin to smooth mus
they finally enter the supelior and inferior vena cavae.
cle. As the blood vessels become smaller, smooth

muscle predominates. The arterioles are primarily
smooth muscle and their diameter can alter signifi
PULMONARY CIRCULATION
cantly. They regulate the blood flow to regional tis
The vena cavae empty directly into the right atrium.
sue beds and are also responsible for regulating total
Blood flow from the right side of the heart through
peripheral resistance and systemic blood pressure.
the lungs is known as the pulmonary circulation. The
They are called the stopcocks of the circulation.
quantity of blood flowing through the pulmonary cir
Many factors (e.g., nervous impulses, hormonal stim
culation is approximately equal to that flowing
ulation, drugs, oxygen, and carbon dioxide concentra
through systemic circulation. Blood flows from the
tions) determine the degree of contraction of vascular
right ventricle into the pulmonary artery, which di
smooth muscle and whether contraction occurs lo
vides into right and left branches 4 cm from the ven
cally or throughout the entire body.
tricle. These branches then separate, one going to
Arterioles branch to form the smallest vessels, the
each lung, where they continue to divide into smaller
capillaries, which consist of a single layer of endothe
arteries. The pulmonary arteries and arterioles are
lial cells forming lumen just large enough for the red
much shorter, have thinner walls and larger diame
blood cells to roll along. The capillary bed is enormous;
ters, and are more distensible than their systemic
its capacity far exceeding 5 L. Its network is finer and
counterparts. This gives the pulmonary system a
denser in active tissue like muscle and brain, and less
compliance as great as that of the systemic arterial
dense in less active tissue such as tendon. Gas ex
system, thereby allowing the pulmonary arteries to
change occurs in the capillary bed, where the red blood
accommodate the stroke volume output of the right
cells give up their oxygen, and blood plasma t:ransudes
ventricle. Pulmonary vascular resistance and arterial
capillary walls, carrying nutrition to tissue.
pressure are one sixth that of the systemic system
The microcirculation specifically consists of the

metarterioles, the capillary bed, and the venules. The
20110 mm Hg com
120/80 mm Hg systemically).
(pulmonary arterial pressure is

pared with
capillary wall is a semipermeable membrane that is re
P u l m o n a r y c a p i l l a r i e s are s h o r t a n d a r i s e
sponsible for the transfer of oxygen, nutrients, and
abruptly from much larger arterioles. They form a
waste between the circulation and the interstitial fluid
dense network over the walls of the alveoli, making
3). The capillary pores selectively
a minimum distance over which gas exchange oc
(see Chapters 1 and
allow different-size molecules to pass through them.
curs. The pulmonary veins are also very short but
This is an essential feature that regulates the move
have distensibility characteristics similar to those of
ment of fluid in and out of the intra- and extravascular
the systemic system. Unlike systemic veins, these
compartments. This process is fundamental to main
veins have no valves. Pulmonary veins act as a ca
taining and regulating normal hemodynamics.
pacitance vessel, or a blood reservoir for the left
Capillaries form venules, which are the smallest
atrium. Contraction of smooth muscle in the veins
50
PART I
Cardiopulmonal'Y Function in Health and Disease
makes the reservoir constrict. This increases blood
ture of the bony
volume in relation to the internal volume of the
sociated with the chest wall and of the diaphragm.
vessels. The pulmonary veins become larger until

converge into two veins from each
which
the muscles of respiration as
The upper and lower

scribed, a s well as the
bronchial tree to the
then carry oxygenated blood to the left atrium.
The lung
is defined anatomically in terms of dis

crete bronchopulmonary segments contained within
LYMPHATIC CIRCULATION
three major divisions of each
The lymphatic circulation
an additional
route for fluid t o be returned from the interstitium

to the systemic circulation, and thus has a central
of interstitial fluid
role in the
defined
The specific sur
the lung fissures and the
landmarks for the bronchopulmonary segments were

emphasized. The basic anatomy of the heart was de
and
scribed. The structure of the
the fluid that flows in the
Special ref
monary circulations was also
is interstitial fluid with similar composition t o

tissue fluid. T h e lymphatics remove excess fluid,
large
face
ns, and other large molecules away

lit
from the interstitial spaces. Although
erence was made to the lymphatic circulation and its

central role in the regulation of capillary fluid
of cardiopulmonary
namics. A detailed
anatomy is fundamental to the
base un
tle protein leaks from the capillaries into the sur
the assessment and management of car
rounding tissue. the absence of its immediate re
diopUlmonary dysfunction and impaired oxygen

by physical therapists.
moval is
all areas of the body drain into a network
of
channels. From the lower portion of the
body, and left head and
excess tissue fluid and
drain into the thoracic duct, which empties

into the venous circulation at the junction of the left
REVIEW QUESTIONS
1. Describe the thorax and its movements.
2. Describe the respiratory muscles and their func
internal jugular vein and subclavian vein.

from the right side of the head,
of the
which
tion of the
arm, and
thorax drain into the
from the
monary and
of the body drains
into the inguinal and abdominal lymphatic channels.

The pressure in the lymphatic
which helps to
"dry." The lymph vessels are thin-walled with some
the heart to the pul

circulations.
5. Describe the movement of deoxygenated blood

from the oerioherv back to the heart.
is
the interstitium
of oxygen from the atmos
4. Describe the movement of oxygenated blood
vein and subclavian
vein. Lymph from the lower
the
phere to the alveolar capillary membrane.
lymph duct,
into the venous circulation at the junc

internal
tion.
3.
6.
\Jrnnh"tlr
circulation and
its physiological
smooth muscle and thus can contract to propel their

contents. In addition,
vessels have valves to
facilitate the forward motion and to minimize retro

movement of lymph.
References
Andreoli,
K.G., Fowkes. Y.K., Zipes, D.P., & Wallace, A G,

.
(199!). Comprehensive cardiac c are (7th ed,). Sl. LOllis:

Mosby.
SUMMARY
Berne. R.M"
This chapter reviewed the anatomy of the cardiopul

monary system. The anatomical features of the respi
ratory pump were described with respect to the struc
& Levy, M.N. (1992). Cardiovascular physiology
(6th ed,). St Louis: CY Mosby,
G.G., & Hodgkin. J.E. (1984). Respiratorv care: A gllide

18 Lippincott.
Chemiack, R.M., & Cherniack, L (1983), Respiration in Health
and Disease (3rd ed,), Philadelphia: WB Saunders.
Bunon,
to clinical practice (2nd ed.). Philadelphia:
Clemente, CD. (Ed,). (1985), Anatomy of Ihe humon body (30th

ed,), Philadelphia: Lea & Febiger.
51
Scharf, S,M & Cassidy. S,S. (Eds,), (1989). Hear/-lung interac

tions in health and disease. New York: Marcel Dekker,
Dubin, D, (1989) Rapid interpretation of EKGs (4th ed,), Tampa,
Sokolow, M" McIlroy, M.B" & Cheitlin. M,D, (1990), Clinical

cardiology (5th cd,). Norwalk, Conn.: Appleton & Lange,
Florida: Cover Publishing,

French, W,G" & Criley, I.M, (Eds,). (1983), Practical cardiology:
Schlant, R,C" Alexander, R,W., O'Rourke, RA" Roberts, R
..
&
New York: John Wiley &
Sonnenblick, E,H, (Eds.). (1994), Hurst's lhe hearl, orteries
Ganong, W,F, (1993), Review of medical physiology (l6th ed,),
Wagoer, G,S, (1994), Marrioll's practical electrocardiography
Ischemic and valvular hearl
and veins (8th ed,). New York: McGraw,Hill.
Sons,
(9th ed.), Baltimore: Williams & Wilkins,
Los Altos, Calif.: Lange Medical Publications.

Goldberger, E, (1990), Essentials of clinical cardiology, Philadel
phia: JB Lippincott,
Weber, KT, Jaoicki, J.S" Shroff, S,G" & Likoff. MJ. (1983), The
cardiopulmonary unit. The body's gas transport system, Clinics
Guyton, A,C, (1991), Textbook of medical physiology (8th cd,),
in chest medicille, 4, 101-110,
Weibel, E,R. (1963), Morphometry of the human lung, New York:
Philadelphia: WB Saunders,
Katz, A.M. (1992), Physiology of the heart (2nd cd.). New York:
Raven Press,
Springer-Verlag,
West, lB, (Ed,), (199l), Best and Taylor's physiological basis of
Marriott, H.1.L, & Conover, M,B, (1989), Advanced concepts in
medical practice (12th cd,). Baltimore: Williams & Wilkins,
West, lB. (1995), Respiratory physiology-the essentials (5th ed,),
arrhythmias (2nd ed,), St. Louis: Mosby,
Murray, J,E (1986), Till? normal lung. Philadelphia: WE Saunders,

Murray, J.P., & Nadel, I.A, (1988). Textbook of respiratory medi
Baltimore: Williams & Wilkins,

Williams, P,L, Warwick, R., Dyson, M., & Bannister, LH,
(1989), G r a y
cine, Philadelphia: WB Saunders,
Nunn, lE (1993), Applied respiratory physiology (4th ed.), Lon
Churchill Livingsione,
don: BUllerworths,
a n atomy (37th
E d i n b u r gh:
Cardiopulmonary Physiology
Elizabeth Dean
Lyn Hobson
KEY TERMS
Control of breathing
Oxyhemoglobin dissociation
Control of the heart
Respiratory mechanics
Diffusion
Ventilation and petfusion matching
Electromechanical coupling
Ventilation perfusion
Gas exchange
INTROOUCTION
CONTROL OF BREATHING
This chapter reviews the basics of cardiopulmonary
The act of breathing is a natural process to which
physiology. A thorough understanding of normal
most of us give little thought. Unconsciously, it ad
physiology provides a basis for understanding the
justs to various degrees of activity, maintaining opti
deficits of cardiopulmonary dysfunction and adapta
mum arterial levels of POl and Peo2, whether we are
tion to it, and conducting a thorough assessment and
resting or physically active. Sighing, yawning, hiccup
prescribing treatment (Bates, 1989; Berne and Levy,
ing, laughing, and vo mitin g are all involuntary acts
1992; Clemente, 1985; Goldberger, 1990; Guyton,
using respiratory muscles. Br athing is also under our
1991; Katz, 1992; Murray and Nadel, 1988; Nunn,
voluntary control. A person can stop it temporarily by
1993, Sch31f and Cassidy, 1989; Schlant, Alexander,
holding his or her breath or can increase it by rapidly
O'Rourke, Roberts, and Sonnenblick, 1994; Sokolow,
panting until he or she faints (from cerebral vascular
McIlroy, and Cheitlin, 1990; and West, 1995.
constriction as a result of a decrease in arterial Peo2).

53
PART I
54
InhitJl/lon
S/imv/olion
:;::rJ
MEDULLA .
:,
t ::"
',
Expir%ry -..Ce//s
yj
jl
pulmonory streICh receptors
ororecePlors
emasenSilive
Cells
--.
-"
.--
to Insptrotory tnt
_
__
_
:d
iralOry
Cells
______
--------===-
ca rotid and aortic cl1emoreceplors
to exptrotory tntereostols
I"
mo
FIGURE 3-1
Control of breathing.
Exhalation is used in singing, speaking, coughing, and
longed inspiratory gasps (apneustic breathing) occur.
blowing, whereas inspiration is used for sniffing and
The pneumotaxic center is in the upper one third
sucking. Parturition, defecation, and the Valsalva ma
of the pons. It maintains the normal pattern of respi
neuver are all performed while voluntarily holding our
ration, balancing inspiration, and expiration by in
breath. These activities are directed by control centers
hibiting either the apneustic center or the inspiratory
located in the brain. The centers integrate a multitude
component of the medullary center.
of chemical, reflex, and physical stimuli before trans

mitting impulses to the respiratory muscles. The cere
bral hemispheres control voluntary respiratory activ
i t y , whereas i n v oluntary respiratory activity i s
controlled b y centers located i n the pons and medulla
(Figure
3-1).
Central Chemoreceptors
These receptors are located on the ventral lateral sur
faces of the upper medulla. They are bathed in the
cerebrospinal fluid (CSF), which is separated from
blood by the blood-brain barrier. Although this bar
rier is relatively impermeable to hydrogen (H) and bi
Medullary and Pontine Respiratory Centers
carbonate (HC03) ions. Carbon dioxide (C02) diffuses
The respiratory center in the medulla is in the reticu
through the barrier easily. Increased stimulation of
lar formation. It contains the minimum number of
central chemoreceptors by a rising arterial PC02 re
neurons necessary for the basic sequence of inspira
sults in increased rate and depth of ventilation.
tion and expiration. Although this center is capable of

maintaining some degree of respiratory activity, these
respirations are not normal in character.
Peripheral Chemoreceptors
The apneustic center is in the middle and lower
These receptors are located in the carotid bodies,
pons. If uncontrolled by the pneumotaxic center, pro
which lie in the bifurcations of the common carotid
55
artery and in the aortic bodies located above and
tory time. Receptors for this reflex are thought to
below the aortic arch. These bodies receive blood
lie in the smooth muscle of airways from the tra
from small branches of the vessels on which they are
chea to the bronchioles. In humans, it takes a lung
located. The receptors respond to an increase in arter
inflation of more than 800 ml above func tional
ial Peo2 by increasing ventilation but are much less
residual capacity to activate the reflex and delay the
important in their response to Peo2 than are the cen
next breath.
tral chemoreceptors.
The main role of the peripheral chemoreceptors is
to respond to hypoxemia by increasing ventilation. If
Cough Reflex
arterial Peo2 is normal, the P02 must drop to 50 mm
Mechanical or chemical stimuli to the larynx, trachea,
Hg before ventilation increases. A rising Pe02 causes
carina, and lower bronchi result in a reflex cough and
the peripheral chemoreceptors to respond more quickly
bronchoconstriction. The high velocity created by the
to a decreasing Po2. In some patients with severe lung
cough sweeps mucus and other irritants up toward the
disease, this response to hypoxemia (the hypoxic
pharynx (see Chapter 21).
drive) becomes very important. These patients often

have a permanently elevated Peo2 (C02 retention). The
CSF in these patients compensates for a chronically el
Stretch Reflex
evated arterial Peo2, by returning the pH of the CSF to
The intercostal muscles and the diaphragm contain
near normal values. When these patients have lost the
sensory muscle spindles that respond to elongation. A
ability to stimulate ventilation in response to an ele
signal is sent to the spinal cord and anterior horn
vated Peo2, arterial hypoxemia becomes the major
motor neurons. These neurons signal more muscle
stimulus to ventilation (hypoxic drive).
fibers to contract (recruitment) and thus increase the

strength of the contraction. Theoretically, such a
stretch reflex may be useful when there is an increase
REFLEXES
in airway resistance or a decrease in lung compliance.

Stretching the ribs and the diaphragm may activate the
Hering-Breuer Reflex
stretch reflex and help the patient take a deep breath.
Hering and Breuer noted in 1868 that distention of
The fundamental pathways of the stretch reflex are
anesthetized animal lungs caused a decrease in the
shown in Figure 3-2. Research is needed, however,
frequency of inspiration and an increase in expira-
to establish the therapeutic role of propriocepti ve
SPINDLE
AFFERENT
MUSCLE SPINDLE
FIGURE 3-2
Stretch reflex.
56
PART I
neurofacilitation techniques based on stretch reflex
creasing alveolar pressure. The increased alveolar
theory in altering pulmonary funclion.
pressure contributes to air flowing from the lungs.

Normally, expiration is a passive process reflecting
elastic recoil of the lung parenchyma.
Joint and Muscle Receptors

Peripheral joints and muscles of the limbs are believed
to have receptors that respond to movement and en
hance ventilation in preparation for activity. Ventila
tion has also been shown to be stimulated by a similar
Resistance to Breathing
Compliance
The inner walls of the thorax, lined with parietal
reflex in humans and anesthetized animals in response
pleura, and the parenchyma of the lung, enclosed in
to passive movement of the limbs. The precise path
visceral pleura, lie in close proximity to one another.
ways for these reflexes have not been well-established.
The pleurae are separated by a potential space con

taining a small amount of pleural fluid. Muscular
contraction of the intercostals and the diaphragm me
Mechanoreceptors
chanically enlarges the thorax. The lungs are en
Changes in systemic blood pressure cause correspond
larged at this time because of their close proximity to
ing changes in pressure receptors in the carotid and
the thorax. The healthy lung resists this enlargement
aortic sinuses. Increase in blood pressure causes me
and tries to pull away from the chest wall. The ease
chanical distortion of the receptors in these sinuses,
with which the lungs are inflated during inspiration is
producing reflex hypoventilation. Conversely, a reduc
known as compliance and is defined as the volume
tion in blood pressure can result in hyperventilation.
change per unit of pressure change. The normal lung

is very distensible or compliant. It can become more
rigid and less compliant in diseases that cause alveo
MECHANICAL FACTORS IN BREATHING
lar, interstitial or pleural fibrosis, and alveolar edema.
The flow of air into the lungs is a result of pressure
Compliance increases with age and in emphysema.
differences between the lungs and the atmosphere. In
The elastic recoil or compliance of the lung is also
normal breathing, for inspiration to occur, alveolar
dependent on a special surface fluid caJled surfactant,
pressure must be less than atmospheric pressure.
which lines the alveoli. This fluid increases compli
Muscular contraction of the respiratory muscles low
ance by lowering the surface tension of the alveoli,
ers alveolar pressure and enlarges the thorax (Gold
thereby reducing the muscular effort necessary to
man, j 979). The decreased pressure causes air to
ventilate the lungs and keep them expanded. It is a
flow from the atmosphere into the lungs. Patients
complex lipoprotein that is thought to be produced in
2). A decrease
who are unable to create adequate negative pressure
the type II alveolar cells (see Chapter
may have to be mechanically ventilated. The ventila
in surfactant causes the alveoli to collapse. Reex
tors create a positive pressure (greater than atmos
panding these alveoli requires a tremendous amount
pheric pressure) that forces air into the lungs where
of work on the part of the patient. The patient may
there is atmospheric pressure. The iron lung used dur
become fatigued and need mechanical ventilation.
ing the poliomyelitis epidemic of the 1950s assisted
This occurs in respiratory distress syndrome of the
ventilation using cycles of negative pressure to inflate
premature infant (previously called hyaline mem
the lungs.
brane disease) and in adult respiratory distress syn
Ex halation occurs when alveolar pressure is
drome. In another disease, alveolar proteinosis, there
greater than atmospheric pressure. At the cessation of
is excessive accumulation of protein in the alveolar
inspiration, the respiratory muscles return to their
spaces. This may be because of excessive production
resting positions. The diaphragm rises, compressing
of surfactant or deficient removal of surfactant by
the lungs and increasing alveolar pressure. As the in
alveolar macrophages.
tercostals relax, the ribs drop back to their preinspira
The elastic properties of the lung tend to collapse
tory position, further compressing the lungs and in
the lung if not counterbalanced by external forces.
57
FIGURE 3-3
Various relationships between the lungs and the thorax. At. The size the lungs would assume if
they were not acted on by the elastic recoil of the thoracic wall. A2, nOlmal size of lungs within the
thorax BI, The size the thorax would assume if it were not acted on by elastic recoil of the lungs.
B2, Normal position of the chest wall when acted on by elastic recoil of the lungs C, The normal
relationship of lung to thorax. 0, The positions assumed by the lung and thorax in a tension
pneumothorax.
The tissues of the thoracic wall also have elastic re
posed by the usual elastic forces of the lungs, which
coil, which cause it to expand considerably if unop
have been damaged by disease.
posed. These two forces oppose each other, keeping

the lungs expanded and the thoracic cage in a neutral
position. If these forces are interrupted (as in pneu
mothorax), the lung collapses and the thoracic wall
expands (Figure
3-3). Similarly, the overinflated, bar
Pressure Volume Relationships

Pressure volume curves help to define the elastic
properties of the chest wall and lungs (Cherniack,
1983; Co m r o e, Fo r s t e r, Dub o i s ,
1986). The elasticity of the
rel-shaped chest of the patient with chronic obstruc
Ch e r n i a ck,
tive pulmonary disease (COPD) is explained in part
Briscoe, and Carlsen,
by the elastic tension of the chest wall being unop
respiratory system as a whole is the sum of its two
PART I
58
and therefore functional residual

100
90
*
(3
;t
<l(
()
curve also shows the range of lung volumes,
60
cally tidal volume, over which the energy
.f . }
'1
30
ff
0
f-
process. The pressure volume
70
50
Z
:::>
-'
-'
is
lar work is required to effect inspiration,
80
>f-
is the rest
system. Active muscu
ing volume of the
20
RESIDU
VOLUME --
10
-10
+10
+20
ture for breathing is most economicaL In other words,

result from relatively small
volume
,U,C"ONAC
RESIDUAL
CAPACITY
in pressure as noted from the sloDe of the

curve over tidal volume,
In lung
this balance of forces is disrupted

More work and more energy are re-
to sustain the
+30
less able to
PRESSURE (em, H20)
chest
FIGURE 3-4
effort. The
or both.
put more energy into the
The relaxation pressure curve. The pressure in the lung at
is
on normal elastic recoil of either the

to
function. The limits of respiratory excur
any volume reflects elastic forces of the lung and chest
sion are determined
wall.
both elastic and muscular
forces. At total lung
the elastic forces of the

are balanced
the inspiratory
muscle force. At residual volume, the elastic forces of

components, the
and the chest wall.
The so-called relaxation pressure curve is shown in
the chest wall are balanced
3-4. The curve illustrates the static pressure

of the
the maximum
tory muscle force. This volume excursion from total

capacity to residual volume reflects vital
chest wall, and the combination of the
the elastic forces
the curves
two measured at given lung volumes, Functional
of the lungs and chest wall are
residual capacity reflects the balance o f elastic
helpful in understanding the effect of lung dysfunction
forces exerted
the chest wall and the lungs, This
is an
and management of pa
The relaxation pressure curve
static
is determined
by the balance of forces between the chest wall and

the lungs, The chest wall and
and Ket
the characteristic
the chest wall,
the excursion
111
lungs. At the other extreme is the effect of a
and the volume in the
in the
in
of the chest as a result of reduced elastic recoil of the
pressure measurements, This means that the

muscles are
1983). For
barrel chest reflects the unopposed elastic forces of
tients with cardiopulmonary dysfunction.
at a
on pulmonary function and on the clinical presenta

tion of the patient (Burrows, Knudson,
point with significant
for the clinical
they are
wound to the chest wall, which

trapleural pressure
exert elastic
the in
that normally keeps the
and the chest wall contained. The re
forces that oppose each other. The chest wall at
sult of such a puncture is to produce a
tempts to pull the lung out and the lungs
where the lung collapses down to the hilum and the
to
recoil and pull in the chest wall. The curves labeled

and chest wall are theoretical and illustrate the
elastic force exerted
each when permitted to act
chest wall sorinQs outward (see FiQure 3-3, p. 57),
Airway ReSistance
unopposed by the other. Normally, these two forces
The flow of air into the lungs
are exerted together and
the pressure volume re
ferences and on the resistance to flow by the airways,
laxation curve, It can be seen that at functional resid
Resistance is defined as the pressure difference re
ual caoacitv (FRO. these forces are in equilibrium,
quired for one unit flow
on pressure dif
The air passages in
59
other obstructions. In normal lungs, airflow is a combi
LAMINAR
nation of laminar and turbulent flow and is known as
,)
( [)
tracheobronchial flow.
The airways are distensible and compressible, and
thus are susceptible to outside pressures. As these pres
sures compress the airways, they alter the airway resis
tance. Transmural pressure is the difference between
TURBULENT
, ,;:
the pressures in the airways and the pressures sur
'-.=C)Jl 2,)
rounding the airways. In erect humans, there is a

higher transmural pressure at the apices of the lungs
than at the bases. This expands the alveoli at the apices
relative to those at the bases. Although the alveoli in
the apices have a greater volume at end expiration, the
alveoli in the bases are better ventilated. This is be
cause the alveoli in the bases operate at lower trans
mural pressures and thus accommodate a greater vol
ume during inspiration than those at higher pressures.
Airway resistance decreases during inspiration as a
FIGURE 3-5
result of widening of the airways. During expiration,
The different types of airflow seen within the
airways narrow, thus increasing resistance. The posi
tracheobronchial tree.
tive alveolar pressure that occurs during expiration

partially compresses the airways. If these airways have
lost their structural support as a result of disease, they
humans are divided into upper and lower airways (see
may collapse and trap air distally (as in emphysema).
Chapter 2). The upper airways are responsible for 45%

of airway resistance. The resistance to airflow by the
lower airways depends on many factors and is there
VENTILATION
fore difficult to predict. The branching of the lower air
Ventilation is the process by which air moves into the
ways is irregular, and the diameter of the lumen may
lungs. The volume of air inhaled can be measured
vary because of external pressures, and contraction or
with a spirometer. The various lung capacities and
relaxation of bronchial or bronchiolar smooth muscle.
volumes are defined in chapter 8.
The lumen diameter may also decrease as a re.sult of
Regional differences in ventilation exist through
mucosal congestion, edema, or mucus. Any of these
out the lung. Studies using radioactive inert gas have
changes in the airway diameter may cause an increase
shown that when the gas is inhaled by an individual
in airway resistance. Flow of air through these airways
in the seated position, and measurements are taken
3-5). Lami
with a radiation counter over the chest wall, radiation
nar flow is a streamlined flow where resistance occurs
counts are greatest in the lower lung fields, interme
can be either laminar or turbulent (Figure
mainly between the sides of the tubes and the air mole
diate in the midlung fields, and lowest in the upper
cules. It tends to be cone-shaped, with the molecules in
lung fields. This effect is position or gravity depen
contact with the walls of the tubes moving more
dent. In the supine position, the apices and bases are
slowly than the molecules in the middle of the tube.
ventilated comparably, and the lowermost lung fields
Turbulent flow occurs when there are frequent molec
are better ventilated than the uppermost lung fields.
ular collisions in addition to the resistance of the sides
Similarly, in the lateral or sidelying position, the
of the tubes seen in laminar flow. This type of flow oc
lower lung fields are preferentially ventilated com
curs at high flow rates and in airways where there are
pared with the upper lung fields (see Chapter
irregularities caused by mucus, exudate, tumor, and
18).
The causes of regional differences in ventilation
60
PART I
can be explained in terms of the anatomy of the lung
greater volume change in relation to resting volume
and mechanics of breathing. An intrapleural pressure
which effects greater overall ventilation compared
gradient exists down the lung. In the upright position,
with the upper lung fields. In summary, ventilation is
the intrapleural pressure tends to be more negative at
favored in the lowermost lung fields regardless of the
the top of the lung, and becomes progressively less
position of the body.
negative toward the bottom of the lung. This pressure

gradient is thought to reflect the weight of the sus
pended lung. The more negative intrapleural pressure
DIFFUSION
at the top of the lung results in relatively greater ex
Once air has reached the alveoli, it must cross the
pansion of that area and a larger resting alveolar vol
alveolar-capillary (A-C) membrane (Figure
ume. The expanding pressure in the bottom of the
gases must cross through the surfactant lining, the
lung, however, is relatively small and hence has a
alveolar epithelial membrane and the capillary en
3-6). The
smaller resting alveolar volume. This distinction be
dothelial membrane. Oxygen has to travel further
tween the upper and lower lung fields is fundamental
through a layer of plasma, the erythrocyte membrane
to understanding differences in regional ventilation.
and intracellular fluid in the erythrocyte, until it en
The regional differences in resting alveolar volume
counters a hemoglobin molecule. This distance is ac
should not be confused with regional differences in
tually small in normal lungs, but in disease states, it
ventilation volume. Ventilation refers to volume
may increase. The alveolar wall and the capillary
change as a function of resting volume. The relatively
membrane often become thickened. Fluid, edema, or
higher resting volume in the upper lung fields renders
exudate may separate the two membranes. These
it stiffer or less compliant compared with the low
conditions are often first detected when arterial P02
lung volumes and greater compliance in the lower
becomes chronically lower than normal. Oxygen dif
lung fields. The lower lung fields therefore exhibit a
fuses slowly through the A-C membrane in compari-
".<
.rlfflllll".
FIGURE 3-6
The components of the alveolar-capillary membrane.
son to CO2 diffusion. As a result, patients with diffu
61
or poorly oxygenated lung areas. Although hypoxic
sion problems frequently have hypoxemia with a nor
vasoconstriction may have an important role to im
mal Pe02. Sarcoidosis, berylliosis, asbestosis, sclero
prove the efficiency of the lungs as a gas exchanger,
derma, and pulmonary edema are some diseases that
this mechanism may be potentially deleterious to a
decrease the diffusing capacity of the gases. The ca
patient who has reduced arterial oxygen pressure sec
pacity may also decrease in emphysema because of a
ondary to pulmonary pathology.

The acid base balance of the blood also affects
decrease in surface area for gas exchange.
pulmonary blood flow. A low blood pH or acidemia,

for example, potentiates pulmonary vasoconstriction.
PERFUSION
Thus impaired ventilatory function can disturb blood
Pelfusion of the lung refers to the blood flow of the
gas composition and in turn, acid base balance. This
pulmonary circulation available for gas exchange.
effect can be amplified because of the cyclic reaction
The pulmonary circulation operates at relatively low
of pH on pulmonary vasoconstriction. Consideration
pressures compared with the systemic circulation. For
of these basic physiologic mechanisms are tanta
this reason, the walls of the blood vessels in the pul
mount to optimizing physical therapy intervention.
monary circulation are significantly thinner than

comparable vessels in the systemic circulation. Pul
monary arterial pressure is low, because perfusion of
the top of the lung is the most distal area. Compared
Ventilation and Perfusion Matching

It is essential that ventilated areas of the lung are in
with the systemic circulation, there is little require
contact with peIfused areas of the lung to effect nor
ment for significant regional differences in perfusion.
mal gas exchange. Conditions that alter the ventila
Hydrostatic pressure has a significant effect on per
tion or perfusion of part of the lung also affect the gas
fusion of the lowcr lobes. The hydrostatic pressure re
exchange in that portion of the lung. Uneven ventila
flects the effect of gravity on the blood, tending to
tion occurs where there is uneven compliance or un
favor peIfusion of the lower lung fields. This fact has
even airway resistance in different parts of the lung.
been substantiated using radioactive tracers in the pul
The lung is more compliant, that is, easier to inflate
monary circulation and measuring radiation counts
at low lung volumes. In the upright position, the
over the lung fields. The nonuniformity of peIfusion
apices have a higher resting volume because of a
reflects the interaction of alveolar, arterial, and venous
more negative intrapleural pressure than the bases,
pressures down the lung. Normally, blood flow is de
which renders the apices less compliant than the
termined by the arterial venous pressure gradient. In
bases with relatively low resting volumes. Ventilation
the lungs, there are regional differences in alveolar
as previously described is favored in the lower lung
pressure that can exert an effect on the arterial venous
regions rather than the apices. Uneven airway resis
pressure gradient. For example, in the upper lung
tance may result from airway narrowing (bron
fields, alveolar pressure approximates atmospheric
choconstriction in asthma, mucous plugs, edema,
pressure, which overrides the arterial pressure and ef
tumor,) or collapse from external pressures as with
fectively closes the pulmonary capillaries. In the lower
tumors or emphysema). Uneven compliance may also
lung fields, the opposite occurs. The relatively low vol
result from fibrosis, emphysema, pleural thickening,
ume of air in the alveoli is oveITidden by the greater
effusions, or pulmonary edema.
capillary hydrostatic pressure. Thus the capillary pres
Nonuniform peIfusion or blood flow can be a re

sult of gravity, regional differences in intrapleural
sure effectively overcomes the alveolar pressure.

Pulmonary blood vessels constrict in response to
pressure, regional changes in alveolar pressure, and
low arterial pressures of oxygen. This is termed hy
obstruction or blockage of part of the pulmonary cir
poxic vasoconstriction. Hypoxic vasoconstriction in
culation. Gravity increases blood flow in the depen
the lung is believed to serve as an adaptive mecha
dent portions of the lung and decreases it in the non
nism for diverting blood away from underventilated
dependent portions of the lung. Regional differences
62
PART [
ZONE I
ZONEm
FIGURE 3-7
The perfusion of the lung is dependent on posture. In the
upright position three areas can be seen. Zone III has
perfusion in excess of ventilation, in Zone II perfusion and
ventilation are fairly equal and in Zone I ventilation occurs
in excess of perfusion.
in intrapleural pressure change the transmural pres

sure of blood vessels and thereby the amount of
blood flowing through those vessels. Changes i n
a lveolar pressure also affect the amount o f blood
flowing through the vessels. Overexpanded alveoli
can compress blood vessels, while underexpanded
alveoli may allow more blood to flow through those
vessels. Blood clots, fat, parasites, or tumor cells may
constrict or block part of the pulmonary circulation.
As discussed previously, gravity tends to pull
blood into the dependent positions of the lung (Figure
3-7). In erect humans, therefore, there is greater
blood flow at the bases of the lung. In places, the ar
terial blood pressure exceeds the alveolar pressure
and causes compression or collapse of the airways
(Figure 3-8). Blood flow to the apices is decreased
because of gravity. Alveoli in this region are more
fully expanded as a result of high transmural pres
FIGURE 3-8
Relationship between the size of the airways and the
amount of perfusion in the area in the upright position.
A, Perfusion is decreased in the apices due to gravity. This

enables the alveoli to fully expand. This expansion may
compress blood ves els and thereby fUl1her decrease blood
sures and may further decrease blood flow by com
flow. B, Perfusion is increased in the bases of the lungs due
pressing blood vessels. It follows that the areas of op
to gravity. The enlarged vessels prevent full expansion of
timal gas exchange occur where there is the greatest
alveoli and may in fact compress them to a smaller size.
CardiopuLmonary Physiology
FIGURE 3-9
The effect of positioning on perfusion of the lung. Note that gravity-dependent segments have the
greatest amount of perfusion.
B
A
FIGURE 3-10
A, Normal alveolus. B, Dead space. C, Shunt.
63
64
PART I
Cardiopulmonary Function in Healt.h and Disease
amount of perfusion and ventilation. This occurs to
ues of POl and PC02. Therefore the lungs must be able
ward the base of the lungs in erect humans. Changes
to supply four parts ventilation to about five parts
in posture cause changes in perfusion and ventilation.
perfusion. When the ratio is not uniform throughout
Generally, greater air exchange occurs toward the
the lung, the arterial blood cannot contain normal
gravity-dependent areas. In side lying, there is greater
blood gas values. Regions with low ratios (perfusion
gas exchange in the dependent lung (Figure
3-9).
in excess of ventilation) act as a shunt, while regions
In normal lungs, there is an optimal ratio or
with high ratios (ventilation in excess of perfusion)
matching of gas and blood. This ratio of ventilation

to perfusion is
3-10). Hypoxemia results
act as dead space (Figure
0.8 to maintain normal blood gas val-
if regions of abnormal V:Q ratio predominate. An
\\tntilation-Perfusion Ratio
o
4
v
Apex
Blood flow
Base
.05
Distance Down Lung
.10
1/min, % Lung
.15
Iume
FIGURE 3-11
The effect of gravity on ventilation, perfusion and ventilation-perfusion matching (V/Q ratio).
PO?
,W
ALVEOLAR
pco
.L
_ _ _ _
'
Apex
Po,
'
A
_
pco
:::'2::
Base
'd----
DEAD SPACE
t=oo
NORMAL
*::::1:;
SHUNT
*=0
Distance Down Lung

FIGURE 3-12
Schemata showing the effect of gravity on ventilation and perfusion down the upright lung.
elevation in arterial Peo2 may also occur unless the
65
COORDINATION OF CARDIAC EVENTS
patient increases ventilation. Therapists who are posi
The mechanical activity of the heart is precisely regu
tioning patients with cardiopulmonary pathology may
lated with the electrical activity of the heart to effect
find that their patients experience greater distress
optimal cardiac output to the organs of the body (An
when placed in certain positions. Such position-de
dreoli, Fowkes, Zipes, and Wallace,
pendent distress can be explained by ventilation-per
1991; Dubin,
1989; Wagner, 1994). The electrical and mechanical
fusion inequalities that cause poor gas exchange in
events of the cardiac cycle are summarized in Figure
the dependent lung.
3-13. These events include the spread of the wave of
The relationship of ventilation and perfusion in the
electrical excitation throughout the myocardium, the
lung is summarized in the following figures. Figure
resulting sequence of contraction of the atria and ven
3-11 shows increases in ventilation and peifusion down
tricles followed by dynamic changes in pressure and
the upright lung. Optimal ventilation and perfusion
blood volume in the heart chambers, the heart sounds
matching, V:Q occurs in the mid-lung zones. In the up

right position, ventilation is in excess of pelfusion in
the apices, and perfusion is in excess of ventilation in
0. 4
120
right lung, and their effect on alveolar gas. Specifically,

Figure
(seconds)
TIME
the bases. Figures 3-12 illustrate the effects of shunt

and physiologic dead space on V:Q matching in the up
0,
3-12 shows a schematic representation of re
100
gional differences in ventilation and perfusion in the

upper, middle, and lower zones of the upright lung.
These gradients are reflected in the alveolar P02 and
80
W
a:
60
::J
(/)
(/)
Peo2 levels associated with alveolar dead space of the
W
a:
c..
apices, appropriate ventilation-perfusion matching in

the mid-lung, and shunt in the bases.
0.6
0.8
.. .
.. ....... .
.. :: .... . .
... .. .
. b
..
E.
c
I
Ventricle
40
d
20
Atrium
DIASTOLE
a:
::s E
CARDIAC REflEXES
The heart behaves automatically, thus is termed a
functional syncytium. Three primary reflexes enable
the heart to increase stroke volume and cardiac out
put with moment-to-moment changes in myocardial
demand (French and Ct'iley,
120
::J
Ow
80
a:
f-::J
z..J
wO
40
HEART
SOUNDS
1983).
-fl
__
__
________
4th R
The first reflex is the Starling effect which refers

to the increased force of contraction that occurs with
ECG
increased venous return (preload). The second reflex,
the Anrep effect, refers to the increase in ventricular

contractile force as a result of an increase in aortic
pressure (afterload). And third, the Bowdich effect
refers to the corresponding increase in heart rate
when myocardial contractile force increases. The in
tegrated function of these three reflexes ensures that
FIGURE 3-13
Summary of electrical and mechanical events of the heart.
A, Atrial systole. B, Isovolumetric contraction. C, Ejection.
D, Isovolumetric relaxation. E, Rapid inflow, diastasis, and
active rapid filling. Note relationship of ventricular pressure
cardiac output adjusts as de mands on the heart
and volume.
change, that is in health, primarily in response to ex
(b)
ercise, body position and emotional stress.
semilunar valves;
(a) closure of the
atrioventricular valves;
opening of the semilunar valves;
(d)
(c) closure
of the
opening of the atrioventricular valves.
66
PART I
takes
of these events. The cardiac
and the
0.8 second in a heart
Myocardial Depolarization
at 75 beats/min. Ventric
ular systole or ejection takes about one-third of this
Ventricular Contraction
time. Its onset and termination are marked respec

by closure and
of the atrioventricular
valves (mitral and tricuspid). Diastole, or the period
Tricuspid and Mitral Valves Close
between successive ventricular systoles in whieh the

ventricles fill with blood, takes two thirds of the 0.8
second of each cardiac
Pressure Increases and

Pulmonary
Aortic Pressure
Phases of Systole and Diastole

Ventricular systole normally has three phases: isovol
period, and
umctric contraction
a slower
Pulmonic and Aortic Valves Open
period. Ventricular diastole also has
three phases: passive

slower filling
diastasis (a
and active
is Completed; Pressure
Below
Pulmonary and Aortic Pressure
phase.
Heart Sounds
Pulmonic
duration sound (SI) followed by a

slower duration sound
sounds of LUB-dub. S I is associated with closure of

is associated with c1o
Tricuspid and Mitral
sure of the semilunar valves. In inspiration, the aortic

valve closes several milliseconds before the pulmonic
valve, resulting in a splitting of the second heart
venous return and
increase, hence pulmonary
heart volume
is prolonged in this
Myocardial Depolarization
and closure of the pulmonary valve is deOther variations in splitting of
occur with
pathology. The presence of a third (S3) or fourth

heart sound is usually considered abnormal.
associated with the
is usu
Open
Diastolic Filling
S2. During inspiration, intrathoracic pressure becomes

more
tiC Valves Close
Ventricular Pressure Falls Below Atrial Pressure
that resembles the phonic
the atrioventricular valves.
The heart sounds are described as a low-pitched long
FIGURE 3-14
The sequence of pressure
in the hearl
the
cardiac
phase, and
with the active rapid-filling phase.

heart are responsible for the
and
of the
valves. Coordinated valve opening and closure are im
Volume and Pressure Changes
portant in promoting the forward movement of blood
Changes in the ventricular volume curve and aortic
and
pressure wave reflect
in atrial and ventricular
pump resulting from valvular
of blood
and diastole (Ganong, 1993;
ventricular contraction.
of blood
pressure during
mechanical
of the heart
Guyton, 1991). The sequence of events appears in a
in the retrograde direction gives rise to heart murmurs
tlow chart in Figure 3-14. Pressure gradients within the
audible on auscultation of the heart (Goldberger. 1990).
67
fluid to be filtered out of the systemic circulation
TABLE 3-1
into the interstitium. Table
Balance of Forces Moving Fluid
3-1 illustrates the mean
pressures determining normal fluid dynamics across
In and Out of the Capillary
capillary membranes.
mmHg
TRANSPORT OF OXYGEN BY THE BLOOD
Mean forces moving fluid out of capillary

17.0
6.3
5.0
28.3
Mean capillary pressure

Negative interstitial pressure
Oncotic interstitial pressure
TOTAL OUTWARD PRESSURE
Plasma oncotic pressure
28.0
28.0
TOTAL INWARD PRESSURE
OUTW ARD PRESSURE - INW ARD

=
with hemoglobin to form oxyhemoglobin (West,
1995). A small proportion of oxygen is dissolved in

the plasma. The use of the hemoglobin molecule as
Mean forces moving fluid into capillary
PRESSURE
Once oxygen reaches the blood, it rapidly combines
NET OUTW ARD PRESSURE
0.3
an oxygen carrier allows for greater availability and

efficiency of oxygen delivery to the tissues in re
sponse to changes in metabolism. Saturation of the
oxygen-carrying sites on the hemoglobin molecule is
curvilinearly related to the partial pressure of oxygen
in the tissues. This relationship is called the oxyhe
moglobin dissociation curve and is a sigmoid or S
3-15). The hemoglobin of arter

98% or almost completely saturated with
shaped curve (Figure

ial blood is
Peripheral Circulation
oxygen. Under normal circumstances, arterial blood
The purpose of the peripheral circulation including
is mixed with a small proportion of venous blood
the microcirculation at the tissue level is to provide
from the coronary and pulmonary circulation, result
100%. The graph
saturated oxygenated blood and remove partially de
ing in arterial saturation of less than
saturated blood. The microcirculation within each
shows a range of partial pressures of oxygen that may
organ regulated the blood flow both exogenously via
exist in the tissues. At relatively high arterial oxygen
the neurological system and endogenously via the hu
pressures, the oxygen saturation is high. This reflects
moral system commensurate with the metabolic
high association or low dissociation between oxygen
2). The four
and hemoglobin. Saturation does not fall significantly
needs of that tissue bed (see Chapter
80
50 mm Hg, al1er
principal factors that determine the movement of
until the partial pressure of oxygen falls below
fluid in the microcirculation include the following:
mm Hg. Even at P02 levels of 40 to
1. The capillary hydrostatic pressure from the

blood pressure, which tends to move blood
ial saturation is still
75%. This suggests an enormous
capacity of the oxyhemoglobin dissociation system to
across the capillary membrane out of the circu
meet the varying needs of different tissues without
lation into the interstitium
severely compromising arterial saturation. A P02 of
2. The capillary oncotic pressure from the pro
less than
50%, for example, has a profound effect on
teins within the blood vessels, which tends to
arterial saturation. This demonstrates an adaptive re
retain fluid in the circulation
sponse of hemoglobin dissociation to respond to low
3. The interstitial hydrostatic pressure, which
oxygen tissue pressures by greater dissociation of
tends to move fluid back into the circulation
oxygen from hemoglobin as the need arises. As the
4. The interstitial oncotic pressure, which tends
P02 improves as a result of increased supply of oxy
to draw fluid out of the circulation into the
gen or decreased demand, the affinity between oxy
interstitium
gen and hemoglobin increases, and arterial saturation
The net forces acting on the capillary fluid are

nearly in equilibrium with a slight tendency for
increases. Thus oxygen is not released unless there is

a need for greater oxygen delivery to the tissues.
68
PART I
ARTERIAL OXYGENATION
C\J
0
75
Z
0
i=
0:::
::J
(f)
0
20
27
80
60
40
PARTIAL
PRESSURE
100
02
FIGURE 3-15
The oxyhemoglobin dissociation curve.
Different conditions can increase or decrease he
Anemia (reduced red blood cell count and hemo
moglobin affinity for oxygen and thereby cause a shift
globin) and polycythemia (excess red blood cells and
in the oxyhemoglobin dissociation curve (West, 1995)
hemoglobin) produce changes in oxygen content of
(Figure 3-15). A shift to the right results in decreased
the blood as well as saturation. Anemia shifts the
oxygen affinity and greater dissociation of oxygen and
curve to the right and lowers the maximal saturation
hemoglobin. In this instance, for any given partial
achievable. Polycythemia has the opposite effect. The
pressure of oxygen, there is a lower saturation than
curve is shifted to the left and maximal saturation ap
normal. This means that there is more oxygen avail
proaches 100%.
able to the tissues. Shifts in the curve to the right

occur with increasing concentration of hydrogen ions
(i.e., decreasing pH), increasing Peo2, increasing tem
TRANSPORT OF CARBON DIOXIDE
peratures, and increasing levels of 2,3-DPG (diphos
CO2 is an acid produced by cells as a result of cell
phoglycerate), a byproduct of red blood cell metabo
metabolism. It is carried in various forms by venous
l i s m . W e s t ( 19 9 5 ) s u g g e s t s , "A simple way t o
blood to the lungs, where it is eliminated. Most of the
remember these shifts i s that an exercising muscle (in
CO2 added to plasma diffuses into the red blood cells,
creased metabolic demand), is acid, hypercarbic, (hy
where it is buffered and returned to the plasma to be
percapnic) and hot, and it benefits from increased un
carried to the lungs. The buffering mechanism is so

.
effective that large changes in dissolved CO2 can
loading of oxygen from its capillaries."

A shift of the curve to the left results in increased
occur with small changes in blood pH.
oxygen affinity. Thus for any given partial pressure
The transport of CO2 has an important role in the
of oxygen, there is a higher saturation than normal.
acid-base status of the blood and maintenance of nor
This means that there is less oxygen available to the
mal homeostasis (Comroe, Forster, Dubois, Briscoe,
tissues. This occurs in alkalemia, hypothermia, and
and Carlsen,
decreased 2,3-DPG.
carbonic acid per day. (Carbonic acid is broken down
1986). The lung excretes 10,000 mEg of
69
into water and CO2. The CO2 is buffered and elimi
globin dissociation ensures adequate oxygen delivery
nated through the lungs.) The kidney can excrete only
to the tissues once oxygen has diffused through the
100 mEq per day of acids. Therefore alterations in
alveolar capillary membrane into the circulation.
alveolar ventilation can have profound effects on the
Transport of CO2 and its buffering mechanisms are
body's acid-base status. A decrease in the lung's abil
central to acid base balance and normal homeostasis.
ity to ventilate causes a sharp rise in Peo2 and a drop

in pH. This causes an acute respiratory acidosis. If
this change occurs gradually, the pH will remain
REVIEW QUESTIONS
within normal limits while the Peo2 is elevated. This
I. Describe the control of breathing.
is known as a compensated respiratory acidosis. Hy
2. Explain respiratory mechanics with respect to
perventilation or excessive ventilation causes rapid

elimination of C02 from the blood. This results in a
decreased Peo2 and an increased pH and is known as
an acute respiratory alkalosis. Again, if the change
occurs gradually, the pH remains within normal lim
airway resistance and lung compliance.

3. Describe the distributions of ventilation, perfu
sion and diffusion.
4. Explain the determinants of ventilation and per
fusion matching.
its even though the Peol is decreased. This is a com
S. Describe electromechanical coupling in the heart.
pensated respiratory alkalosis.
6. Describe oxyhemoglobin dissociation and the

oxyhemoglobin dissociation curve.
SUMMARY
This chapter presented an overview of cardiopul
monary physiology with respect to breathing control,
both central and peripheral mechanisms such as mus
cle, joint, and lung and chest wall stretch receptors, in
volved with the regulation of respiration. Mechanical
factors of breathing, chest wall and lung compliance,
and airway resistance are described. The elastic prop
erties of the respiratory system, that is, chest wall and
lungs, are ret1ected in the pressure volume relaxation
curve. This curve has important implications for the
clinical presentation of the patient with cardiopul
monary dysfunction, and in particular, the efficiency
and energy requirement of the respiratory system.
Ventilation and pelfusion matching is the basis of gas
exchange and the adequacy of lung function. Many
factors in addition to disease, however, can affect ven
REFERENCES
Andreoli, K.G., Fowkes, V.K., Zipes, D .P.,
Mosby.
Bates, D.V. (1989). Respiratory Junction
Berne, R.M.,
& Levy, M.N. (1992).
pling of electrical and mechanical events in the heart

to effect cardiac output are described.
Arterial P02 and Peo2 are normal! y maintained
within certain prescribed limits. In health, oxyhemo
& Keitel, L.J. (1983).
Res
piratory disorders: A pathophysiologic approach (2nd ed.).
Chicago: Year Book Medical.

Cherniack, R.M.,
& Cherniack, L. (1983).
Respiration in health
and disease ( 3rd ed.). Philadelphia : WB Saunders.
Clemente, C.D. (Ed.). (1985). Anatomy oj the human body (30th

ed.). Philadelphia: Lea and Febiger.
Comroe,
J.H., Jr., Forster, R.E., Il, Dubois, A.B., Briscoe, W.A., &
Carlsen, E. (1986). The lung; Clinical physiology and pul

monary Junction tests (3rd ed.). Chicago: Year Book Medical.
Dubin, D. (1989). Rapid interpretation oj EKGs (4th ed.). Tampa,
FL: Cover.
diac output, hence, adequate oxygen delivery to the
Cardiovascular physiology
Burrows, B., Knudson, R.J., Quan, SF,
French, W.G.,
vital organs and peripheral tissues. The optimal cou
disease. (3rd ed.).
(6th ed.). St Louis: CV Mosby.
position, breathing at low lung volumes and smoking

The purpose of the heart is to provide an adequate car
ill
Philadelphia: WB Saunders.
tilation and perfusion matching, including age, body

history. The relationship of such factors are discussed.
& Wallace, A.G.
(Eds.). (1991). Comprehensive cardiac care (7th ed.). SI Louis:
& Criley, J.M. (Eds.). (1983).
Practical cardiology:
Ischemic and valvular heart disease. New York: John Wiley
and Sons.
Ganong, W. F. (1993). Review oj medical physiology (16th ed.).
Los Altos: Lange Medical Publications.
Goldberger, E. (1990). Essentials oj clinical cardiology. Philadel
phia: JB Lippincott.
Goldman, M. (1979). Mechanical interaction between diaphragm
and rib cage. American Review oj Respiratory Disease,
I 19(Part 2), 23-26.
PART I
70
Guyton, A,C, (l99J), Textbook of medical physiology. (8th ed,j,

Raven Press.
Murray, IF, & Nadel, l.A. (1988). Textbook of respiratory medi
cine Philadelphia: W.s. Saunders,
ed.). Baltimore: Williams and Wilkins.
Nunn, J.F ([993). Applied respiralory physiology (4th ed,). Lon
West, 1.B. ([992), Pulmonary pathophysiology: The essenlials (4th
00.). Baltimore: Williams and Wilkins.
don: Butterworths.
Scharf, S,M" & Cassidy S.S, (Eds,), (1989). Hearl-lung interac
in health and disease. New York: Marcel-Dekker, Inc.
West, .l.B. (1991). Best and Taylor's physiological basis of med

ical praclice (12th ed.J. Baltimore: Williams and Wilkins.
Schlant, R,C., Alexander, R.W., O'Rourke, R.A., Robens, R., &

Sonnenblick, E. H. (Eds.J. (1994). Hurst's lite heart: Arleries
and
& Cheitlin, M.D. (1990), Clinical
(5th 00.), Norwalk: Appleton & Lange.

Wagner, G.S. (J994), Marrioll's practical electrocardiography
(9th ed,). Baltimore: Williams and Wilkins.
West, J.B. (1995). Respiratory physiology-The essen/ials (5th
cardiology
Katz, A,M, (1992). Physiology of Ihe hearl (2nd ed.) New York:
tions
Sokolow, M., McIlroy, M.B"
veins (8th ed.J. New York: McGraw-Hill.
Cardiopulmonary Pathophysiology
Willy E. Hammon
Scott Hasson
KEY TERMS
Angina
Fibrosis
Bronchiectasis
Myocardial infarction
Coronary artery disease
Obstructive lung disease
Emphysema
Restrictive lung disease
INTRODUCTION
formance. The parameters affected by CAD can be the
The first part of this chapter, beginning with obstruc
volume of blood pumped and the heart rate. The
tive lung disease, describes the pathophysiology of
major purposes of this portion of the chapter are to de
chronic pulmonary disease. Chronic pulmonary dis
scribe the etiologic factors of clinical syndromes asso
ease can be categorized broadly into obstructive and
ciated with CAD, briefly describe medical treatment,
restrictive disorders.
and discuss issues of prognosis.
Obstructive disorders are characterized by a de

creased rate of airflow during expiration (as a result
of increased airway resistance). Restrictive disorders
OBSTRUCTIVE LUNG DISEASE
are conditions in which the inspiratory capacity of the
Several abbreviations can be found in the literature
lungs is restricted to less than the predicted normal.
for a pulmonary disorder characterized by increased

airway resistance, particularly noticeable by a pro
Overlap between the two categories does exist.

The second part of this chapter, beginning with
longed forced expiration. Some of these are chronic
coronary artery disease (CAD), describes the patho
obstructive pulmonary disease (COPD), chronic ob
physiology of cardiovascular disease. Cardiovascular
structive airway disease (COAD), chronic airway ob
disease is also known primarily as CAD, and is mani
struction (CAO), and chronic obstructive lung disease
fested in various clinical syndromes. CAD is an ather
(COLD) (Fishman,
1988).
osclerotic process that occurs in the right and left
The first part of this chapter describes chronic
coronary aJ1eries, which ultimately affects heart per-
bronchitis, emphysema, asthma, and bronchiectasis

71
72
PART I
individually. With the possible exception of asthma
susceptible to rcspiratory infections, and it takes them
and bronchiectasis, however, it is unusual in the clini
longcr to recovcr from these infections. In addition, the
cal setting to find a patient with only one of these con
ilTitation of smoke in the tracheobronchial trec causes
ditions. Most patients have some combination of
bronchoconstriction. Although smoking is the most
chronic bronchitis, emphysema, and asthma, and in
common cause of chronic bronchitis, other agents that
this chapter, these individuals are referred to as having
have been implicated are air pollution, bronchial infec
COPD. These patients have intermittent episodes of
tions, and certain occupations.
wheezing, along with a variable degree of chronic
These patients are referred to as "blue bloaters,"
bronchitis and emphysema (Hodgkin, 1975). Radio
because they usually have stocky body build and are
logically, they may have hyperinfiated lungs, flattened
"blue" as a result of hypoxemia (Dornhorst, 1955;
diaphragms, and an enlarged right ventricle as a result
Filley et ai, 1968; Fishman, 1988; Nash, Briscoe,
of increased pulmonary artery pressure. Other findings
and COUlnand, 1965. Although many of these pa
vary from patient to patient, depending on the predom
tients have a high arterial partial pressure of carbon
inant disease process contributing to their COPD.
dioxide (Pac02), the pH is normalized by renal re
COPD is very common. In 1994 the American
tention of bicarbonate (HC03). In the patient with
Lung Association (ALA) estimated that 14.2 million
chronic bronchitis, bone marrow tries to compensate
Americans have COPD. In the United States alone,
for chronic hypoxemia by increased production of
health care costs for COPD exceed $7.6 billion annu
red blood cells, leading to p olycythemia (Snider,
ally. Deaths from COPD numbered more than 85,000
Faling, and Rennard, 1994). Polycythemia, in turn,
in 1991; it is the fourth leading cause of death in the
makes the blood more viscous, forcing the heart to
United States.
work even harder to pump it. Long-term hypoxemia

leads to increased pulmonary artery pressure and
right ventricular hypertrophy.
Chronic Bronchitis
Individuals with bronchitis often expectorate mu
Chronic bronchitis is a disease characterized by a
coid brownish-colored sputum. In an exacerbation,
cough producing sputum for at least 3 months and for 2
usually from infection, they have an even greater
consecutive years (American Thoracic Society, 1962).
amount of purulent sputum. Ventilation-perfusion ab
Pathologically, there is an increase in the size of
normalities are common, which increase hypoxemia
the tracheobronchial mucous glands (increased Reid
and Paco2 retention (Rochester and Brown, 1976).
index) and goblet cell hyperplasia (Mitchell, 1968;
The respiratory rate increases, as does the use of ac
Reid, 1960; Stoller and Wiedemann, 1990). Mucous
cessory muscles. The resultant increased work of
cell metaplasia of bronchial epithelium results in a
breathing requires greater oxygen consumption by
decreased number of cilia. Ciliary dysfunction and
these muscles, with a greater production of carbon
disruption of the continuity of the mucous blanket are
dioxide (C02) than the respiratory system can ade
common. In the peripheral airways, bronchiolitis,
quately meet. This contributes to a further drop in the
bronchiolar narrowing, and increased amounts of
arterial partial pressure of oxygen (Pao2) and a rise in
mucus are observed (Cosio, 1978; Wright, 1992).
Paco2. The hypoxemia and acidemia increase pul
The cause of chronic bronchitis is believed to be re
monary vessel constriction, which raises pulmonary
lated to long-term in-itation of the tracheobronchial tree.
artery pressure and ultimately leads to right heart fail
The most common cause of irritation is cigarette smok
ure (cor pulmonale).
ing (US Surgeon General, 1984). Inhaled cigarette
In the following example, a patient is admitted to
smoke stimulates the goblet cells and mucous glands to
the hospital with an exacerbation of chronic bronchi
secrete more mucus. This smoke also inhibits ciliary
tis and presents the following picture: he is of stocky
action. The hypersecretion of mucus and impaired cilia
body build, his color is dusky, and he breathes with
lead to a cllronic productive cough. The fact that smok
moderate-to-marked use of the respiratory accessory
ers secrete an abnormal amount of mucus makes them
muscles, depending on the degree of respiratory dis
tress.
may be audible or noted by ausculta
and Rennard,
on the degree of respiratory dis
sent, also
tress. Edema in the extremities
iJ"'''''''''U
in the
and neck vein distention reflect decom

cor pulmonale. The
may report that

w i th i n c r e a s e d
There are two main

ular and panlobular
color) or decreased amounts of sputum
in
Arterial blood gases
creased retention of
Emphysema
a change in normal
this b r e athing difficu

amounts o f secretions
of emphysema-centrilob
1976; ThurJbeck, I
It
that centrilobular
has been
20 times more common than panlobular

both types are often found in the same pair
show the individual with bronchitis to have a lowered

and a lowered
Pao2, a raised
function tests indicate a reduced vital

forced
v o lume in I second
maximum voluntary ventilation and diffus

capacity, as well as an increased functional resid
ual
73
1983). Diuretics and
retractions may be pre
tion. Intercostal (or
ankle
and residual volume.
As its name implies, centrilobular emphysema is

characterized
destruction of the respiratory bron
chiole, edema,
and thickened bronchi
olar walls. These changes are more common and

more marked in the upper lobes and superior seg
an exacerbation, these
are usually
1963). This
ments of the lower lobes
fluids, antibiotics, bron
form of emphysema is found more often in men than
chodilator and low-flow oxygen. CO!1iocosteroids may
in women, is rare among nonsmokers, and is com
be administered. Some
mon among
treated with intravenous
with increased secre
tions respond to chest physical therapy and bronchial
with chronic bronchitis.
Pan lobular emphysema, on the other hand, is
Alveoli
___
FIGURE 4-1
A, Panlobular
is characterized by a destructive enlargement of the alveoli, B, A nonnal
respiratory bronchiole and alveoli.

and destmction of the
Centrilobular emphysema is characterized

bronchiole.
a selective
74
PART I
characterized by destructive enlargement of the alve

oli, distal to the terminal bronchiole (Figure
4-1).
It
(Figure
1976).
4-2) (Reid, 1967; Thurlbeck, 1991; Thurlbeck,
It is thought that bullae develop from a coales
most often involves the lower lobes. This type of em
cence of adjacent areas of emphysema or an obstruc
physema is also found in subjects that have alphaJ
tion of the conducting airways that permits the flow of
antitripsin deficiency. Airway obstruction in these in
air into the alveoli during inspiration but does not
dividuals is caused by loss of lung elastic recoil or
allow air to flow out again during expiration. This
radial traction on the bronchioles. When individuals
causes the alveoli to become hyperinflated and even
with normal lungs inhale, the airways are stretched
tually leads to destruction of the alveolar walls with a
open by the enlarging elastic lung, and during exhala
resultant enlarged air space in the lung parenchyma.
tion the airways are narrowed as a result of the de
These bullae can be more than
creasing stretch of the lung. However, the lungs of
by compression, can compromise the function of the
10
cm in diameter, and
4-3).
patients with panlobular emphysema have decreased
remaining lung tissue (Figure
elasticity because of disruption and destruction of
surgical intervention to remove the bulla is often nec
If this happens,
surrounding alveolar walls. This in turn leaves the
essary. Pneumothorax, a serious complication, can re
bronchiole unsupported and vulnerable to collapse
sult from the rupture of one of these bullae.
during exhalation.
The emphysema patient's most common com
Bullae, emphysematous spaces larger than I cm in
plaint is dyspnea. Physically, these patients appear
diameter, may be found in patients with emphysema
thin and have an increased anteroposterior chest di-
FIGURE 4-2
A, AP chest film reveals bullous emphysema with multiple, thin, rounded fibrotic lucencies. B, The
spot film bronchogram of the left midlung field shows intact bronchi and distal emphysematous blebs.
(Courtesy of T. H. Johnson, M.D.)
75
ameter. Typically, they breathe using the accessory
heart (Figure 4-4). Pulmonary function tests show a
muscles of inspiration. These patients are often seen
decreased vital capacity, FEY"
leaning forward, resting their forearms on their knees
ventilation and a greatly reduced diffusing capacity.
or sitting with their arms extended at their sides and
The total lung capacity is increased, while the resid
pushing down against the bed or chair to elevate their
ual volume and functional residual capacity are even
maximum voluntary
shoulders and improve the effectiveness of the acces
more increased. Arterial blood gases reflect a mildly
sory muscles of inspiration. They may breathe
or moderately lowered Pao2, a normal or slightly
through pursed lips during the expiratory phase of
raised Pacol and a normal pH. These patients, unlike
breathing. These patients have been referred to as
patients with chronic bronchitis, normally will de
"pink puffers" because of the increased respiratory
velop heart failure in the end stage of the disease
work they must do to maintain relatively normal
(Figure 4-5).
blood gases (Dornhorst, 1955; Filley et aI, 1968;
Treatment of progressive emphysema that requires
Fishman, 1988; Nash, Briscoe, and Cournand, 1965).
hospitalization often includes IY fluids, antibiotics,
On auscultation, decreased breath sounds can be
and low-flow oxygen (Snider, Faling, and Rennard,
noted throughout most or all of the lung fields. Radi
1994). Some of these patients also receive bron
ologically, the emphysema patient has overinflated
chodilators, corticosteroids, diuretics, and digitalis.
lungs, a flattened diaphragm, and a small, elongated
Pursed-lip breathing can relieve dyspnea and improve
FIGURE 4-3
A, AP and B, lateral views of the chest of a patient with advanced bullous emphysematous changes.
Note the bullae in the upper lung fields. The lateral film reveals an increased A-P diameter of the thorax,
flattening of the diaphragms and in increased anterior clear space. (Collrtesy of T. H. Johnson,
M.D.)
76
PART I
FIGURE 4-4
A, AP chest film reveals the increased lucency of lung fields and flattening of the diaphragm of
emphysema. The vascular structures are crowded mediaHy. B, Lateral chest film reveals an
increased AP diameter and flattening of the diaphragms. There is an increase in the anterior clear
space. These are all findings of emphysema. (Courtesy of T. H. Johnson,
M.D.)
arterial blood gasses (Muller, Petty, and Filley, 1970;
these and other factors in producing emphysema is
Petty and Guthrie, 1974).
still not well understood.
The cause of emphysema is uncel1ain. It is known

that the incidence of emphysema increases with age. It
Prognosis of chronic bronchitis and emphysema
is most often found in chronic bronchitics, and there is
Chronic bronchitis and emphysema are marked by a
no question that emphysema is more prevalent in cig
progressive loss of lung function. At the end of 5
arette smokers than in nonsmokers (US Surgeon Gen
years, patients with COPD have a death rate four to
eral, 1984). The risk of developing COPD is 30 times
five times greater than the normal expected value.
greater in smokers than nonsmokers (Fielding, 1985).
Death rates reported by various studies depend on the
There also seems to be an hereditary factor, evident in
method of selection of patients, types of diagnostic
the severe panlobular emphysema that patients with
tests and other criteria (Anthonisen, 1989; Bousky et
an alpha,-antitrypsin deficiency develop relatively
ai, 1964; Kanner et ai, 1983; Kanner and Renzetti,
early in life, even though they m a y never h ave
1984). One study reported a 3-year overall mortality
smoked (Eriksson, 1965; Tobin, Cook, and Hutchin
rate of 23%, with patient age and the initial FEY I
son, 1983). Repeated lower respiratory tract infections
value being the most accurate predictors of death
may also play a role. However, the interrelationship of
(Anthonisen, Wright, and Hodgkin, 1986). In general,
77
gestive heart failure (CHF), which is secondary to cor

pulmonale; respiratory failure; pneumonia; bronchi
olitis; and pulmonary embolism.
Asthma
Asthma is a disease characterized by an increased re
sponsiveness of the trachea and bronchi to various
stimuli, and is manifested by widespread narrowing
of the airways that changes in severity either sponta
neously or as a result of treatment. During an asthma
attack, the lumen of the airways is narrowed or is oc
cluded by a combination of bronchial smooth muscle
spasm, inflammation of the mucosa, and an overpro
duction of a viscous, tenacious mucus.
Asthma is certainly a widespread disease in the
world today. Its incidence is about 3% to 7% in
adults (Barnes, 1993; National Asthma Education
Program, 1991). It is found more often in individuals
under age 25, where estimates of prevalence vary
from 5% to 15% (Williams and McNicol, 1969).
FIGURE 4-5
The chest film reveals peripheral emphysematous lucency.
About 80% of children with asthma do not have
The hilar areas are tremendously enlarged by the
asthma after the age of 10.
pulmonary arteries in a typical cor pulmonale
Asthma that begins in patients under the age of 35
configuration. Cardiomegaly is also present. (Courtesy
is usually allergic or extrinsic. These asthma attacks
ofT. H. 10hnson, M.D.)
are precipitated when an individual comes in contact

with a specific substance to which that person is sen
sitive, such as pollens or household dust (see box 4-1
the death rates 5 years after diagnosis are 20% to
below). Often people with asthma are allergic to a
55%. Other investigators reported an overall mortal
number of substances, not only one or two.
ity of 47 percent at the end of 5 years (Burrows, and
If a patient's first asthma attack occurs after the
Earle, 1969). They believed a 5-year survival rate can
age of 35, usually there is evidence of chronic airway
be estimated as follows: 80% in patients with an
obstruction with intermittent episodes of acute bron
FEY I close to 1.0 L; and 40% for patients with an
chospasm. These individuals, whose attacks are not
FEY I less than 0.75 L. However, if the above flow
triggered by specific substances, are referred to as
rates are found in patients with complications of rest
having nonallergic or intrinsic asthma (see b o x
ing tachycardia, chronic hypercapnia and a severely
below). Chronic bronchitis i s commonly found i n this
impaired diffusing capacity, the survival rates should
group, and this is the type of individual often seen in
be reduced by 25%. Other factors that have been as
the hospital setting.
sociated with a poor prognosis are cor pulmonale,
The individual with an acute asthma attack usually
weight loss, radiologic evidence of emphysema, a
has been awakened at night or early in the morning with
dyspneic onset, polycythemia, and Hoover's sign (an
one or more of the following symptoms: cough, dysp
inward movement of the ribs on inspiration)
nea, wheezing, or chest tightness (McFadden, 1988). In
(Mitchell, Webb, and Filley, 1964; Renzetti, 1967).
fact, nocturnal awakenings are such a common occur
The most common cause of death in patients with
rence with asthma, that their absence from the history
COPD (in descending order of frequency) are con
causes even experienced clinicians to doubt the diagno
78
PART I
Factors That May Precipitate an Asthma Attack

Allergic or extrinsic asthma
Pollen (especially ragweed)
Animals
Feathers
Molds
Household dust
Food
Nonallergic or intrinsic asthma
Inhaled irritants
Cigarette smoke
Dust
Pollution
Chemicals
Weather
High humidity
Cold air
Respiratory infections
Common cold
Bacterial bronchitis
Drugs
Aspirin
Emotions
Stress
Exercise
FIGURE 4-6
A patient in respiratory distress during an acute asthma
attack. Note the marked use of the stcrnocleidomastoids
and other accessory muscles during inspiration.
sis (Turner-Warwick,
(988). The patient has a rapid
rate of breathing and is using the accessory respiratory

muscle (Figure
4-6). The expiratory phase of breathing
high PacD2, a low Pao2, and a pH of less than

Fadden and Lyons,
7.30 (Mc
1968).
Medical management of acute asthma has three
(2) mobilization of
(3) maintenance of alveolar ventila
is prolonged with audible wheezing and rhonchi. How
goals: ( l ) relief of bronchospasm,
ever, when severe obstruction is present, the chest be
secretions, and
1976). The patient may cough
tion. Th e r e f ore m o s t hospitalized patients with
often, though unproductively, and may complain of
asthma are treated with IV fluids, bronchodilators,
tightness in his chest. Radiologically, the lungs may ap
supplemental oxygen, and corticosteroids.
comes silent (Gold,
pear hyperinflated or show small atelectatic areas from
An asthma attack that persists for hours and is unre
retained secretions. The degree of tachypnea, hyperin
sponsive to medical management is referred to as sta
flation, accessory muscle use, and pulsus paradoxus
tus asthmaticus. The patient may appear dehydrated,
(difference in systolic blood pressure during inspiration
cyanotic, and near exhaustion from labored breathing.
and expiration) are useful guides for determining the
In contrast to the audible whcczing and rhonchi heard
degree of airway obstruction present (Woolcock,
1994).
early in the attack, the chest now has greatly dimin
Early in the attack, arterial blood gases reflect slight hy
ished or absent breath sounds. Status asthmaticus re
poxemia and a low Paco2 (from hyperventilation). If the
sults in a significant death rate and is regarded as a
attack progresses, the PaD2 continues to fall as the PacD2
medical emergency. Bilateral manual lower chest com
climbs above the normal range. As obstruction becomes
pression assists expiration and has value as an emer
severe, deterioration of the patient occurs, evident by a
gency treatment of asthma (Fisher, Bowery, and Ladd
79
FIGURE 4-7
Gross specimen of lung showing large mucus plug within the bronchial tree of a patient who died
from status asthmaticus. (Courtesy of J. J. Coalson, Ph.D.)
Hudson, 1989; Watts, 1989). Patients in respiratory
bronchial lumen, further contributing to the stasis of

secretions. Although the alveoli are overinflated, the
failure may require mechanical ventilation.

Studies that examine the lungs of patients who die
from status asthmaticus find lungs that are signifi
cantly hyperinflated and do not deflate even when
the thorax is opened (Huber and Koessler, 1922;
permanent destructive changes found in emphysema

are not present.
Prognosis of asthma
Dunnill, 1960; Saetta et ai, 1991). Examination of
Most studies following children with asthma for a
the airways reveals a mucosa that is edematous and
number of years report a death rate of about 1 %
inflamed. Characteristic of asthma, the basement
(Ogilvie, 1962). One large study of 1,000 people with
membrane is thickened. The mucous glands are en
asthma of all ages in England reported a mortality of
larged, and there is an increase in the number of gob
7% as a result of asthma or its complications. This
let cells. Evidence of bronchospasm is seen by the
study reported that 2% of the patients with intermit
hypertrophied and thickened smooth muscle. The lu
tent asthma died, compared with 9% of those with
mens of most bronchioles, down to the terminal
continuous asthma. During the 1960s, there was a
bronchioles, are filled with viscous, sticky mucus
sharp increase in the number of deaths among people
(Figure 4-7). It is evident that the occluded bronchi
with asthma reported by countries around the world.
oles have caused death by asphyxiation. Secretions
At the peak of this increase, England and Wales re
in the tracheobronchial tree of the patient with
ported that 7% of the deaths in children between 10
asthma are a combination of mucus, secreted by the
and 14 years of age were attributable to asthma. This
mucous glands, and an exudate from the dilated cap
reflected a 700% increase in only 7 years. Some med
illaries just below the basement membranae. It has
ical authorities feel this increase in deaths was related
been shown that cilia do not sweep the mucoserous
to widespread use or abuse of certain pressurized
t1uid nearly as effectively as pure mucus. In addition,
aerosol nebulizers containing isoproterenol, but this
sheets of ciliated epithelium have been shed into the
has been disputed (Gandevia, 1973). In 1987 there
80
PART I
were more than 4,300 deaths from asthma in the Un
bronchi to resemble varicose veins (Figure 4-8). Sac
tied States, 31% more than in 1980 (McFadden and
cular (or cystic) bronchiectasis refers to airways that
Gilbert, 1992).
have intermittent sphcrical ballooning (Figure 4-9).

Bronchiectasis is usually localized in a few seg
ments or in an entire lobe of the lung. Most com
Bronchiectasis
monly, it is unilateral (although 40% to 50% of the
Bronchiectasis is defined as an abnormal dilation of
cases are bilateral) and affects the basal segments of
medium-size bronchi and bronchioles (about the
the lower lobes. When the left lower lobe is involved,
fourth to ninth generations), generally associated with
it is not unusual to find bronchiectasis in the lingula of
a previous, chronic necrotizing infection within these
the left upper lobe as well. Interestingly, bronchiecta
passages. Ordinarily, there is sufficient cartilage
sis of the right middle lobe is relatively common in
within the walls of the larger bronchi to protect them
older adults and can contribute to both hemoptysis
from dilation.
and repeated infections of this lobe. Upper lobe
The airway deformities can be classified into three
bronchiectasis generally involves the apical and poste
types (Reid, 1950; Luce, 1994). Cylindrical (or longi
rior scgments and is usually caused by tuberculosis or
tudinal) bronchiectasis is the most common type,
bronchopulmonary aspergillosis.
with a uniform dilation of the airways. Varicose
Pathologically, the mucosa appears edematous and
bronchiectasis refers to a greater dilation than in
ulcerated. Destruction of the elastic and muscular
cylindrical bronchiectasis, causing the walls of the
structures of the airway walls is evident with resultant
FIGURE 4-8
A, AP chest film of a bronchogram with cylindrical and varicose bronchiectasis in the lower lung
fields. B, Close-up view of cylindrical and varicose bronchiectatic changes in the left lower lobe.
(Courtesy of T. H. Johnson, M.D.)
81
dilation and fibrosis. The walls are lined with hyper
Obstruction can cause bronchiectasis by collaps
plastic, nonciliated, mucus-secreting cells that have
ing lung tissue (atelectasis) distal to the obstruction
replaced the nOImal ciliated epithelium. This change
(Barker and Bardana, 1988). The increased negative
is significant, because it interrupts the mucociliary
pressure in the chest (from the collapsed lung) exerts
blanket and causes pooling of infected secretions,
a greater traction on the airways, causing them to ex
which further damage and irritate the bronchial wall
pand and to become distorted. Secretions are re
(Barker and Bardana, 1988; Currie et ai, 1987).
tained, and if the obstruction is prolonged, an infec
The etiology of bronchiectasis is related to ob
tio.u occurs that begins to destroy the walls of the
struction of the airways and respiratory infections
bronchi, as described above. There has been a signifi
(Luce, 1994; Simpson, 1975). Some 60% of the cases
c a n t reduction in the n u m b e r of p a t i e n t s w i t h
of bronchiectasis are preceded by an acute respiratory
bronchiectasis since the introduction o f antibiotics to
infection. The infection involves the bronchial walls.
treat respiratory infections.
Portions of the mucosa are destroyed and are re
Twenty-four-hour sputum volume has been used
placed by fibrous tissue. The radial traction of the
as an indicator of severity of disease to categorize pa
lung parenchyma on the damaged bronchi causes the
tients with bronchiectasis (Ellis et aI, 1981). Those
involved airways to become permanently dilated and
producing less than 10 ml per day have been catego
distorted (Barker and Bmdana, 1988). These areas,
rized as having mild bronchiectasis, to to I SO ml as
devoid of normal ciliated cells, contain secretions
moderate bronchiectasis and greater than I SO ml as
that eventually become chronically infected.
having severe bronchiectasis.
FIGURE 4-9
A, AP chest film of a bronchogram shows saccular bronchiectasis. B, Close-up view of
bronchiectatic areas with grapelike saccular bronchiectasis. (Courtesy of T. H. Johnson,
M.D.)
82
PART I
P atients w ith severe, diffuse, long-standing

bronchiectasis are rare today. Physically, they are ema
ciated, and as many as 25% of them may have clubbed
fingers. A chronic cough, with expectoration of un
pleasant-tasting, purulent sputum is typical in these pa
tients. When this sputum is collected and allowed to
stand, it may separate into three distinct layers: the up
permost layer is frothy, the middle layer is serous or
mucopurulent, and the lowest layer is purulent and
may contain small grayish or yellowish plugs (Dit
trich's plugs). Changes of body position, while sleep
ing or on arising, often stimulate coughing as the
pooled secretions again spill onto the mucosa of nor
mal, larger airways. These individuals may have cor
pulmonale from fibrosis that has extended to involve
the pulmonary capillary bed. Patients with widespread
bronchiectasis appear dyspneic and have increased
work of breathing as a result of hypoxemia and hyper
capnia from ventilation-perfusion mismatching. Anas
tomosis of the bronchial and pulmonary vascular sys
tems causes shunting of the systemic blood from the
hypertrophied bronchial arteries. It also may contribute
to a decreased capability to take oxygen into the in
volved segments of the lung (Liebow, Hales, and Lind
skog, 1949; Luce, 1994).
Most patients complain of relatively few symp
toms, except during a respiratory infection when they
have an increased cough and sputum production. The
amount of sputum expectorated and the severity of
the cough vary from patient to patient, according to
the amount of involvement. Hemoptysis does occur
in about half of the older patients, evidently because
of erosion of enlarged bronchial arteries that accom
pany the dilated bronchi.
Effective postural drainage, percussion, vibration,
and the forced expiratory technique (FET) are impor
tant in the management of bronchiectasis (Gallon,
1991; van Hengstum et aI, 1988; Sutton, 1983; Ver
boom, Bakker, and Sterk, 1986) (see Chapter 20). ,It
should be done as frequently as indicated in patients
with a productive cough. Postural drainage should be
done I hour before retiring at night to facilitate the ex
pectoration of secretions that would interfere with rest
by stimulating violent coughing when the patient
changes positions. It should also be done on arising in
the morning to clear the lungs of secretions that have
accumulated overnight. Therapists teaching the pa

tient postural drainage positions devised to drain the
involved segments should keep in mind that this dis
ease causes distortion and dilation of the bronchi;
hence the traditional positions found in books may be
of limited value in determining the precise segment of
the lung that is the source of the secretions. If the in
volvement is in the lower lobes, the patient should be
placed in the Trendelenburg position and should be
gradually rotated from lying on one side, to supine, to
lying on the opposite side, and prone, if tolerated,
while doing the FET and/or receiving percussion and
vibration 5 to to minutes per segment over all sur
faces of the lower lobe being treated. A similar proce
dure may be followed while sitting if the upper lobes
require drainage, but these segments rarely require
drainage, since they usually drain during the course of
the day while the individual is in a more or less erect
position. Positions that are especially productive
should be emphasized and drained longer. The patient
should be instructed to do the postural drainage even
if the treatment seems unproductive. Secretions may
be mobilized during treatment and it can take several
minutes for the remaining cilia to sweep the mucus far
enough up the tracheobronchial tree to be expecto
rated or swallowed.
Pulmonary function tests of patients with localized
bronchiectasis show few or no abnormalities. How
ever, in more widespread disease, there is a reduction
in the FEV I, maximum midexpiratory flow rate, max
imal voluntary ventilation (MVV), diffusing capacity,
and an increase in the residual volume (Luce, 1994).
Hospitalized patients with bronchiectasis may be
treated with postural drainage, percussion, vibration,
and/or the forced expiratory technique, intravenous
fluids, antibiotics, supplemental oxygen and other
medications (Stoller and Wiedemann, 1990; Luce,
1994). Long-term medical management may include
a broad-spectrum antibiotic taken orally 10 to 14
days per month, low-flow oxygen for hypoxemia,
postural drainage, avoidance of bronchial irritants
(e.g., cigarette smoke and air pollution) and other
measurers. Some patients may have surgical resection
if their area of involvement is quite limited or to con
trol hemoptysis. It is most important that these pa
tients drink large volumes of water each day (2 to
3 L) to keep their secretions thin so they can be ex
83
spondylitis can cause lung restriction. Obesity and as
pectorated more easily (unless fluid intake is limited
cites, by limiting diaphragmatic movement, can also
for cardiac reasons).
produce a restrictive defect.

Pulmonary function tests generally show a de
Prognosis of bronchiectasis
creased vital capacity, inspiratory capacity, and total
Before the antibiotic era, the prognosis for individuals
lung capacity, whereas the residual volume can be
with bronchiectasis was poor. As might be expected,
normal or reduced. If the restriction is pulmonary in
infection was usually the precipitating cause of death.
origin, there is a reduction in the lung compliance
However, at the present time, the prognosis of patients
and the diffusing capacity.
with proper medical management is much improved
Many of these restrictive disorders are discussed
(Sanderson et aI, 1974; Ellis et ai, 1981). Most studies
in Chapter 5. Since obstructive lung diseases are en
show that about 75% of the patients have an improved
countered much more often than restrictive disorders,
symptom complex since diagnosis and lead relatively
they have been discussed in greater detail. The fol
normal lives. Cor pulmonale, a complication of dif
lowing is a brief examination of some of the restric
fuse, long-standing bronchiectasis, accounts for about
tive lung diseases.
50% of the deaths (Konietzki, Carton, and Leroy,

1969). Pneumonia and hemorrhage are less common
causes of death. With modern therapy, only a few pa
Diffuse Interstitial Pulmonary Fibrosis
tients succumb to respiratory infections or their com
This disease is known as diffuse interstitial pul
plications. Few children who develop bronchiectasis
monary fibrosis (IPF) in the United States and cryp
live beyond their 40s. Repeated bronchopulmonary in
togenic fibrosing alveolitis in Europe (Reynolds, and
fections can contribute to worsening pulmonary func
Matthay, 1990). IPF represents a common histologic
tion and an earlier death. Before the antimicrobial era,
response to a wide variety of insults (Weg, 1982).
most patients with untreated, widespread, severe
Initially, some type of injury to the pulmonary
bronchiectasis died within 25 years. Today prognosis
parenchyma causes an influx of inflammatory and
for each individual depends on the extent of the dis
immune cells, resulting in a diffuse inflammatory
ease process at the time of diagnosis and on proper
process distal to the terminal bronchiole (alveolitis).
medical management. Patients with moderate, local
This can progress to subacute interstitial disease with
ized disease, if treated properly, may have a relatively
the presence of acute and chronic inflammatory ceUs.
normal life expectancy.
Chronic disease is manifest by thickened alveolar

walls and progression to fibrosis.
The etiologic factors of this condition are uncer
RESTRICTIVE lUNG DISEASE
tain. Similar conditions can be produced by certain
A restrictive disease is characterized by lungs that are
drugs or poisons and are found in patients with
prevented from expanding fully. Normally during in
rheumatoid arthritis and systemic sclerosis. There
spiration, the diaphragm descends, the dimension of
appears to be a genetic factor, since twins, siblings,
the chest increases laterally and anteriorly, and the
and other members of the same family have been re
lung tissue expands as it fills with air. Hence an ab
ported with diffuse interstitial pulmonary fibrosis.
normality in any of these areas can produce a restric
This condition has also been reported in a few indi
tive pattern. For example, a decrease in compliance
viduals with Raynaud's phenomenon, ulcerative col
or elasticity of the lung parenchyma, such as intersti
itis, and other diseases, but their exact relationship
tial fibrosis, sarcoidosis, pneumoconiosis, and sclero
remains unclear.
derma, can produce this defect. Pleural abnormalities
The most common early symptoms are fatigue,
such as pleural effusion (by direct compression) can
dyspnea on exertion, and a chronic unproductive
prevent the lungs from expanding fully. Thoracic
cough. As the disease progresses, the patient becomes
changes such as kyphoscoliosis and ankylosing
steadily more dyspneic and cyanotic. On auscultation,
84
PART I
one notes sharply crackling rales. Chest expansion is
Since a pattern of DIP is commonly seen along with
reduced and clubbing of the digits is often present.
usual interstitial fibrosis (UIP) or IPF, some believe
The chest x-ray usually indicates diffuse reticu

lar markings, most prominent in the lower lung
that DIP likely represents an earlier and more re

versible stage of IPF.
fields. Sometimes, a gallium citrate Ga 67 isotope
Cortiocosteroids are the mainstay of treatment for
scan of the lungs is conducted to assess the overall
IPF (Reynolds and Matthay, 1990). A trial of im
inflammation of the lung parenchyma (Line et ai,
munosuppressive therapy is almost a l ways pre
1978; Turner-Warwick and Haslam, 1987).
scribed for a period of time. Obj ective measures
Pulmonary function tests show a reduced vital ca
such as blood counts, erythrocyte sedimentation rate,
pacity and total lung capacity with no impaired flow
pulmonary function testing, particularly exercise
rates (Keogh and Crys tal, 1980; Reynolds and
tests with measurement of arterial oxygen desatura
Matthay, 1990). Compliance is markedly reduced to
tion and diffusing capacity BAL fluid analysis and
less than half of the predicted value. A reduced diffus
the patient's symptoms must demonstrate improve
ing capacity is the earliest and most consistent change.
ment or the medication should be discontinued. A
At first, the arterial Pa02 may be normal at rest but
composite clinical roentgenographic, physiological
may drop significantly with exercise. The Paco2 is re
score (CRP score) of eight variables has been devel
duced as a result of hyperventilation, and the pH is
oped that allows quantification of the clinical course
kept normal by renal compensation. Later the Pao2 is
and the re sponse to therapy in individual patients
markedly reduced because of the thickened alveolar
(Watters et ai, 1986). If effective, medications are
membrane and ventilation-perfusion mismatching.
usually continued for a year and then a decision is
Bronchoalveolar lavage (BAL) is often used to as
made about continuing or tapering the dosage.
sess the amount of inflanunation and the accumulation
Individuals who are not responsive to corticos
of immune effector cells and proteins in the alveoli
teroids may be placed on other immunosuppressive
(Crystal, et ai, 1981; Rudd, Halslam, and Turner-War
drugs such as cyclophosphamide, azathioprine, or
wick, 198]). The technique consists of wedging a
penicillamine (Turner-Warwick, 1987; Reynolds and
fiberoptic bronchoscope in a sublobar airway, then in
Matthay, 1990). Penicillamine is more effective in
fusing 20 to 50 ml aliquots of saline into the periph
patients with connective tissue diseases and intersti
eral airway, which are immediately aspirated by sy
tial fibrosis other than those with IPF.
ringe. A total of 150 to 300 ml is ins tilled and
Patients should stop smoking at once. Supplemen
recovered. The fluid and cells are analyzed (Reynolds,
tal oxygen is important with exercise as there is a
1987). High-intensity alveolitis is defined by 10% or
characteristic significant fall in arterial oxygen ten
more polymorphonuclear granulocytes (PMNs) in
sion ( Pa02) (Hammon a n d Mc C a f f ree,
BAL cell differential counts; low-intensity alveolitis
Reynolds and Matthay, 1990). Individuals that re
consists of 10% PMNs or less (Reynolds, 1986).
quire more than 4 L flow/min by nasal prongs may
1985;
Lung biopsies that demonstrate an abundance of
prefer direct administration of oxygen into the tra
inflammatory cells suggest early disease, whereas a
chea. In addition to supplying higher concentrations
prevalence of fibrosis is indicative of advanced dis
of oxygen to the lungs, many patients prefer the cos
ease. A distinct category of IPF has been described
metic effective of not wearing obvious nasal prongs.
and may be clinically useful (Liebow, Steer, and
Patients that have refractory disease limited to the
Billingsley, 1965). Desquamative interstitial pneu
lungs may be candidates for single or double lung trans
monitis (DIP) is characterized by an intraalveolar ac
plantation. There have been significant advances in the
cumulation of mononuclear cells, relatively intact
success of lung transplantation in recent years (Toronto
alveolar walls without destruction or fibrinous exu
Lung Transplant Group, 1988) (see Chapter 38).
dates (numerous inflammatory cells with little or no
Individuals with the subacute form described by
fibrosis). This pattern has correlated with a more be
Hamman and Rich usually die within 6 months
nign course and a better response to corticosteroids.
(Hamman, 1944). Patients with the chronic form,
Cardiopulmonary Pathophysiolog)'
85
treated with steroids, may survive for as long as 15
complex. Over time, it can eventually result in a form
years. Untreated, these patients most often die within
of interstitial pu lmonary fibrosis with honeycombed
I to 4 years. Cause of death is usually related to res
lung changes on chest x-ray and a restrictive pattern
piratory or heart failure, although an unexpected
on pulmonary function tests.
number have died from adenocarcinoma and undif

ferentiated or alveolar cell carcinoma of the lung.
This disease is more common in women (Seder

linic, Sicilian, and Gaensler, 1988). Their symptoms
include an acute respiratory illness with fever, night
sweats, weight loss, and dyspnea. It can be confused
Pulmonary Infiltrates With Eosinophilia
with tuberculosis, but these patients deteriorate when
Eosinophils are commonly present in lung tissue as
treated with antituberculosis drugs. This disease must
part of the body's cellular response to a variety of
also be differentiated from eosinophilic granuloma
agents and systemic immunologic diseases (Butter
and the desquamative form of idiopathic interstitial
worth and David, 1981). They are present in the air
pneumonitis. Dense infiltrates located in the periph
ways and lung tissue of patients with idiopathic pul
ery of the lung on chest x-ray provide an important
monary fibrosis. In interstitial lung disease that
clue. Often, a lung biopsy is necessary to confirm the
appears to have an allergic component (e.g., hypersen
diagnosis. Treatment with cortiocosteroids produces
sitivity pneumonitis, drug-induced lung syndromes,
a striking improvement in the patient's symptoms and
sarcoidosis) eosinophils are a minor component of tis
chest x-ray in just a few weeks.
sue reaction. However, in certain primary or systemic

diseases, eosinophils can be the most conspicuous in
Eosinophilic granuloma
flammatory cell present in the lung. These conditions
Eosinophilic granuloma (or histiocytosis X) can ei
can be grouped t o g ether and referred to a s
ther be a unifocal disease effecting only the lungs or
eosinophilic syndromes (Crofton e t aI, 1952). Consid
a multifocal disease involving the bones of the skull,
erable overlapping exists among these syndromes as
mandible, vertebra, pelvis, ribs, and extremities
their etiologic factors and pathogenesis remains
(Groopman and Golde, J 981; Marcy and Reynolds,

1985). Lung involvement is characterized by an inter
poorly understood (Reynolds and Matthay, 1990).
stitial granuloma composed of moderately large, pale
Simple pulmonary eosinophilia
histiocytes and eosinophils, and arteriolitis with
This is a self-limiting disease with chest x-ray
eosinophils. The histiocytic process with eosinophils
demonstrating migratory, fleeting areas of pulmonary
then involves bronchioles, alveolar ducts, and alveo
infiltrates located in the periphery of the lungs along
lar septa, which results in their destruction. The pro
with minimal respiratory symptoms and blood
liferative endarteritis causes necrosis.
eosinophilia (Crofton et aI, 1952). Certain drugs such
This disease most commonly effects men in their
as sulfonamides have been implicated as a cause
30s or 40s. They usually have symptoms of fatigue,
(Reynolds and Matthay, 1990). This disease is also
malaise, weight loss, a nonproductive cough, dyspnea
referred to as Loeffler's pneumonia and the PIE syr
on exertion, and chest pain, sometimes related to a
drome (peripheral infiltrates with blood eosinophilia)
pneumothorax or rib lesions. The chest radiograph
(Crofton et aI, 1952). If the Jisease is related to an al
often indicates a diffuse micronodular and interstitial
lergic rcsponse LO microfilaria, human parasites (e.g.,
infiltrate initially involving the middle and lower
Ascaris lum.briocoides, Strongyloides stercoralis), or
lung fields. In more advanced disease, small cystic
cat and dog parasites (ascarids) that produce visceral
areas develop in the infiltrate, producing a honey
larva migrans, it is termed tropical eosinophilia.
comb pattern. Spontaneous pneumothorax is a com

plication in approximately 25% of cases.
Prolonged pulmonary eosinophilia
The course of the disease varies (Reynolds and
As implied by the name, this disease is more chronic
Matthay, 1990). Spontaneous regression with residual
than the simple form, with a more severe symptom
symptoms may occur in 10% to 25% of cases. In
86
PART I
many patients, the disease stabilizes or "burns out,"
findings may include fine inspiratory rales, dullness to
leaving them with a moderate pulmonary impairment
percussion and, in the later stages, cyanosis and club
as a result of fibrosis, cystic lung changes and a re
bing. Pulmonary function studies usually show a de
strictive defect on pulmonary function tests. Dyspnea
creased vital capacity, functional residual capacity arid
on exertion is common. Some patients have persistent
diffusing capacity. Arterial blood gases indicate a low
bronchitis. Cortiocosteroids are not particularly effec
Pao2, especially during exercise, with normal Paco2,
tive. Treatment is mainly symptomatic, with judicious
and pH (Rogers et aI, 1978).
use of antibiotics and bronchodilators. Occasionally,
The treatment of choice for patients with moderate
progressive pulmonary disease leads to cor pulmonale
to severe dyspnea on exertion from alveolar pro
and respiratory failure.
teinosis is bronchial alveolar lavage (Rogers and

Tatum, 1970; Rogers, Graunstein, and Shuman
1972). The patient is taken to the operating room
Pulmonary Alveolar Proteinosis
where, after general anesthesia and placement of a
Pulmonary alveolar proteinosis is a rare disease of
double-lumen tube (which isolates each lung), the pa
unknown origin, characterized by alveoli filled with
tient is turned in the lateral decubitus position with
lipid-rich "proteinaceous" material and no abnormal
the lung to be lavaged downward. The double-lumen
ity of the alveolar wall, interstitial spaces, conducting
tube enables the patient to be ventilated by the upper
airways or pleural surfaces. Most often it is found in
most lung while the lower lung is carefully filled with
men between the ages of 30 and SO, although it has
saline to the functional residual capacity. Then an ad
been reported in patients of all ages and both sexes.
ditional 300 to 500 ml saline are alternately allowed
The most common symptoms are progressive dysp

nea and weight loss, with cough, hemoptysis and chest
pain reported less frequently (Claypool, Rogers, and
Matuschak, 1984). Chest x-ray reveals diffuse bilateral
(commonly perihilar) opacities (Figure 4-10). Physical
FIGURE 4-10
FIGURE 4-11
Pulmonary alveolar proteinosis. PA chest film demonstrates
A patient with pulmonary alveolar proteinosis in the
an irregular, patchy, poorly defined confluence of acinar
operating room undergoing bronchial alveolar lavage of her
shadows which are symmetrical in both lower lung fields.
left lung. Percussion is done over the left lung as the saline
The appearance is very similar to pulmonary edema.
runs out, increasing the amount of proteinaceous material
(Courtesy of T. H. Johnson,
M.D.)
removed during this procedure.
87
1990). If the patient is assessed during
to mn into and out of the ung by gravitational flow.
and Matthay,
As the saline flows out, percussion is done over the
an acute episode of pulmonary hemorrhage, fine rales
lung being lavaged, and this grcatly increases the
and dullness to percussion are present on physical ex-
amount of proteinaceous material washed from the
amination. An enlarged liver, spleen, and lymph
lung (Figure
4-1 J). The effectiveness of mechanical
nodes may be noted on palpation in
20% to 25% of
percussion, manual vibration, and manual percussion
cases. The chest x-ray during acute episodes show
in removing the material from involved lungs has
'Dac naI consolidation for 2 to 3 days, then a reticular

pattern identical to other interstitial diseases. The
been compared and manual percussion has been

found to be superior (Hammon,
1983; Hammon ,/'
'-i
chest x-ray usually returns to normal in lO to
12 days.
1986; Hammon, McCaf1993). In this procedure, a patient is usually lavaged with 20 to 30 L saline and is
However, after recurrent episodes with hemosiderin
then taken to the recovery room and later back to his
dicate a decreased diffusing capacity, with or without
Freeman, and McCaffree,
free, and Cucchiara,
or her own room. After
2 or 3 days, the procedure is
repeated on the opposite lung.
deposited in the interstitial spaces, there is progres

sive interstitial fibrosis .. Pulmonary function tests ina fall in the patient's resting Pa02.
The hemorrhage is ordinarily confined to the pe-
Most patients have significant clinical improve
ripheral airspaces. Interestingly, massive blood loss
ment following bronchial alveolar lavage, and many
into lung tissue can occur without hemoptysis or no-
have an improvement in their chest x-rays (Claypool,
ticeable blood in the trachea or major bronchi
Rogers, and Matuschak,
1984). After lavage, for rea
(Reynolds and Matthay,
1990). Sputum samples of
sons that are unclear, the material may reaccumulate
BAL
slowly o r not at all. Some patients d o have sponta
macrophages. After recurrent episodes of hemoptysis,
neous remissions without undergoing lavage.
interstitial fibrosis is present in most cases.
Before bronchial alveolar lavage was done on

these patients, almost all children with alveolar pro-
f l uid
may
c o n t ain
hemosi d e r i n-l a d e n
The prognosis of IPH is variable with death occurring somewhere between
2Y2 to 20 years after the
20% to 25% of the adults died
onset of symptoms. Permanent remissions may occur
or cor pulmonale. Some
5 years, usually because of respiratory failure

60% to 70% improved
treatment has been shown to effectively alter the out-
greatly or recovered. The effect that bronchial alveo
come of this disease.
teinosis died, and

within
with or without corticosteroid administration. No
lar lavage has on the long-term outcome remains to

be seen, but present results are encouraging (Clay
pool, Rogers, and Matuschak,
1984).
Sarcoidosis
Sarcoidosis is a granulomatous disorder of unknown
origin that can effect multiple body systems (Mitchell
IdiopathiC Pulmonary Hemosiderosis
and Scadding,
1974). Typically, initial findings can
Idiopathic pulmonary hemosiderosis (IPH) is a dis
include bilateral hilar adenopathy, pulmonary infiltra
ease of unknown origin and is characterized by re
tion and skin or eye lesions (Sharma,
peated episodes of pulmonary hemorrhage, iron-defi
lungs are the organs most often involved and some
1977). The
ciency anemia, and in long-term patients, pulmonary
20% to 50% of these patients first seek medical atten
1962). IPH is
tion because of respiratory symptoms. It affects
insufficiency (Soergel and Sommers,
10 to 20 times more often than whites and
most commonly found in children under the age of
blacks
10. In children, it is found with equal frequency in
women twice as often as men. It usually occurs in the
both genders, but in adults, it is twice as common in
third or fourth decade of life.

The intrathoracic changes can be classified into
men as it is women.
This disease has an insidious onset. The patient
four stages (Siltzbach et aI,
1974; Weg, 1982). In the
has symptoms of weakness, anemia, pallor, lethargy,
first stage, the patient is asymptomatic, with the chest
and occasionally, a nonproductive cough (Reynolds
x-ray showing bilateral hilar adenopathy and right
88
PART I
FIGURE 4-12
A, Sarcoidosis in its first stage is manifested by bilateral hilar adenopathy. Usually there are no
significant physical symptoms. B, Disseminated sarcoidosis (third stage) reveals widespread
parenchymal changes with scarring. The hilar adenopathy is usually decreased. (Courtesy of
T. H. Johnson, M.D.)
paratracheal adenopathy (Figure 4- J 2, A). In the second
the lungs and pleurae. The most common thoracic
stage a diffuse pulmonary infiltration is found along
complication of RA is pleurisy, with or without
with the bilateral hilar adenopathy. Interstitial infiltra
pleural effusions. Although RA occurs twice as often
tion or fibrosis, without hilar adenopathy, characterizes
in women, pleuritis has a striking predilection for men
the third stage (Figure 4-12, B). In the fourth stage, em
(Reynolds and Matthay, 1990). Pleural disease is one
physematous changes, cysts, and bullae are found.
manifestation of RA, occasionaJJy causing fibrothorax
I n 60% to 90% of t h e s e p a t i e n t s w i t h h i l a r
and restrictive lung disease that requires decortication.
adenopathy, the disease spontaneously regresses over
Interstitial lung disease, indicated by abnormal pul
a period of I to 2 years. About one third of the pa
monary function tests demonstrating a restrictive venti
tients with sarcoidosis involving the lungs also have a
latory impairment and a reduced ventilatory capacity, is
spontaneous regression, usually leaving some resid
evident in about 40% of RA patients (Frank et ai,
ual fibrosis. The remaining two thirds that have
1973). It is also more prevalent in men. The chest x-ray
chronic sarcoidosis have progressive pulmonary im
demonstrates diffuse interstitial infiltrates, especially in
pairment, along with a variable degree of involve
the lung bases. Pulmonary nodules, which are patho
ment of the heart, liver, spleen, lymph nodes, mus
logically identical to the subcutaneous nodules found in
cles, bones, and central nervous system (CNS).
RA, may also oceur and cavitate (Weg, 1982).
Most patients with sarcoidosis need no treatment.
C o al miners with RA may have chest x - rays
Corticosteroids, although controversial, are the most
demonstrating rounded densities that evolve rapidly
effective forms of therapy for patients with sarcoido
and undergo cavitation (Caplan's syndrome) in con
sis that requires treatment (DeRemee, 1977; Turner
trast to the massive fibrosis found in coal miners'
Warwick et ai, 1986).
pneumoconiosis (Caplan, 1953).
Rheumatoid Arthritis
SystemiC lupus Erythematosus (SlE)
Rheumatoid arthritis (RA) is a systemic disease that
Although systemic lupus erythematosus (SLE) is a
principally involves the joints but also often affects
systemic collagen vascular disease, some 50% to
90% of these patients have pleural or pulmonary in

volvement (Hunninghake and Fauci, 1979). Pleuritic
89
group, progression results in death after several years.

Women seem to have a poorer prognosis than men.
chest pain often signals polyserositis associated with

SLE. Pleural effusions are a manifestation of poly
serositis and are present in
40% to 60% of individuals
with SLE. Most often they are bilateral.
Atherosclerosis
Patients with pulmonary involvement present with

dyspnea on exertion and cough productive of mucoid
sputum (Weg,
CORONARY ARTERY DISEASE
1982). Rarely do SLE patients com
Pathophysiology
To discuss CAD the process of atherosclerosis must
plain of supine dyspnea, which suggests diaphrag
first be described. Although the specific pathogenesis
matic paralysis or a diffuse myopathy of the di
of atherosclerosis is not known, it is hypothesized
aphragm (Gibson, Edmonds, and Hughes,
1977).
that the process is initiated by trauma to the intima of
The chest x-ray usually indicates patchy, nonspe
the arterial wall. The trauma may be related to vari
cific densities and/or basilar linear or platelike atelec
ous primary risk factors such as: high blood pressure
tasis. Pleural effusions and pulmonary infiltrates are
and cigarette smoking.
common, whereas diffuse interstitial fibrosis is rarely

seen (Hunninghake and Fauci,
1979).
High blood pressure has been indicated as a poten

tial trauma inducer, since increased pressure and turbu
Pulmonary function tests often indicate a restric
lence may damage the endothelial cells of the intima,
tive pattem with a decreased diffusing capacity and a
thus exposing the media to the circulation. The media,

which is composed primarily of smooth muscle is
reduced arterial oxygen saturation.
thought to be the origin of the atherosclerotic lesion.

Cigarette smoking has also been indicated as a po
Progressive SystemiC Sclerosis (Scleroderma)
tential trauma inducer. However, the hypothesized
Progressive systemic sclerosis (scleroderma) is a rare
mode of injury is different than that observed with in
disease that causes thickening and fibrosis of the con
creased blood pressure. Cigarette smoke is high in
nective tissue of mUltiple parts of the body with re
carbon monoxide and hydrocarbons that are carried
placement of many elements of the connective tissue
by the red blood cells and the plasma. It is thought
by colloidal collagen. The skin is most often in
that the hydrocarbons or carbon monoxide bind to the
volved, although the lungs, heart, kidney, bones, and
endothelial cells, causing damage and possibly death
other parts of the body can also be affected.
to these cells.
Approximately one half to two thirds of the pa
Once the media is sufficiently exposed to the circu
tients with progressive systemic sclerosis have pul
lation the process of atherosclerosis is initiated.
monary involvement (Reynolds and Matthay,
1990).
Platelets aggregate at the injury site and release sub
Many of these patients with pulmonary involve
stances that induce endothelial and smooth muscle
ment are asymptomatic, although symptoms can in
cell replication. It is at this site that fatty streaks and
clude weight loss, progressive dyspnea, low-grade
fibrous plaques are developed. The cause of fatty
fever, and cough (sometimes producing mucoid spu
streak development is that low-density lipoproteins
tum). Chest x-ray shows a characteristic fibrosis of the
(LDLs) deposit fat into the smooth muscle of the
mid and lower lung fields. Auscultation often reveals
media. Why this occurs is unknown, but apparently is
bibasilar rales. Pulmonary function tests reveal a re
related to the smooth muscle cell proliferation and

perhaps increased need for energy. The initial fatty
strictive defect with impaired diffusion.

D-penicil lamine is the best treatment for pul
streaks are generally only slightly raised and do not
monary involvement in patients with progressive sys
imperil circulation. However, when a fibrous plaque
temic sclerosis (DeClerk et ai,
1987).
develops, the characteristic impingement of the vessel
Prognosis of patients with only skin and joint in
lumen occurs. The plaque is somewhat hard and con
volvement is much better than for those that have in
sists of connective "scar-like" tissue, smooth muscle
volvement of the heart, lungs and kidneys. In the latter
and fat. Finally, the plaque may undergo calcification
90
PART I
or lead to hemorrhaging if the vessel wall necroses.
angina, the episodes are more frequent and the dura
The result is decreased blood flow (ischemia) and
tion of each event is usually greater than 15 min
oxygenation (hypoxia), or complete lack of blood
utes. In addition the intensity or the pain may be
flow and oxygen (anoxia) to the target organ.
more severe. Unstable angina is usually an indicator

of CAD progression. Individuals with unstable
Risk factors
angina are at greater risk to have
As described above high blood pressure, cigarette
farction
myocardial in
(MI). Unstable angina is less responsive to
smoking and hyperlipidemia are direct or primary
treatment using rest and sublingual nitrates. Often
risk factors for causing atherosclerosis. Secondary
times, the individual must be hospitalized and
risk factors are age, gender, race, obesity, stress, and
treated with IV nitrates.
activity level. Several risk factors are modifiable and

i n c l u d e: (I) h y pertension,
(2) h y pe r l i p idemia,
Variant angina
(3) smoking, (4) obesity, (5) stress level, and activity
Variant angina occurs while the individual is at rest,
level. It is interesting to note that the "big three" pri
usually during waking and often at the same time pe
mary risk factors are all modifiable by the individual.
riod. Exertion does not influence variant angina.
Reducing risk factors can reduce the probability of
However, the angina may benefit from rest and sub
CAD by five- to ten-fold (Ornish et aI, 1990).
lingual nitrates. Like unstable angina the pain is in

tense and of longer duration and likely to lead to an
CLINICAL SYNDROMES ASSOCIATED WITH CAD
MI. In addition, arrhythmias are more likely to occur

with an individual who has variant angina, as com
pared with exertion related angina (i.e., stable and un
Angina Pectoris
stable). Stable and unstable angina are believed to be
Angina pectoris is defined as chest pain that is related
caused primari Iy by progressive arterial occlusion
to ischemia of the myocardium. However, the pain
and ischemia. It is believed that variant angina is
referred from ischemia may be in the left shoulder,
caused by a combination of occlusion and coronary
jaw, or between the shoulder blades. Angina can be
artery spasm. Therefore variant angina has been suc
classified as stable, unstable, or variant.
cessfully treated with calcium channel blockers.
Prognosis of angina
Stable angina
Stable angina generally occurs during physical effort
Individuals do not die from angina. The progression
but may be related to stress. The individual is able to
of atherosclerosis of coronary arteries is a change
describe what type and intensity of activity causes the
from the clinical signs of angina to MI, which is dis
angina. Stable angina is characterized by substernal,
cussed on p. 91. However, even though there is no
usually nonradiating pain that lasts between 5 to 15
risk for mortality from angina, an individual's
minutes after the offending incident. Care would in
lifestyle can change drastically. People with angina
volve sublingual nitrates and cessation of the activity
may be fearful of being active and may deny that
causing the angina. Usually the angina subsides com
they are having exertion-related chest pain. Denial of
pletely with treatment. However, angina brought
CAD, depression and anger are common manifesta
about by emotional stress is more difficult to treat,
tion for individuals with angina, though it has rarely
since the stress cannot be stopped as easily as cessa
been studied (Beckham et ai, 1994). The result of
tion of exercise.
angina (diagnosed or undiagnosed and denied) can be

depression and potentially further decline in physical
Unstable angina
activity. Although rest is an important aspect of treat
Unstable angina also occurs during physical exer
ment, it is well-documented that even low levels of
tion or psychological stress. The major difference
activity can modify several risk factors and arrest the
between stable and unstable angina is the frequency,
progression of the disease process (Niebauer et ai,
duration and intensity of the pain. In unstable
1995). Research is sti II underway to determine if
CAD is reversible when lifestyle adjustments are ini

tiated (Ornish et ai, 1990; Schuler et ai, 1992).
Myocardial Infarction
MI is defined as necrosis of a portion of the my
ocardium. The death of the myocardium occurs as a
result of ischemia and anoxia. The vessels affected
are the right and left coronary arteries. The right
coronary artery supplies portions of the inferior sec
tion of the left ventricle and the posterior section.
The left coronary artery branches and forms the cir
cumflex and anterior descending arteries. The cir
cumflex supplies the lateral portion of the left ventri
cle, while the anterior descending artery supplies the
anterior portion. In addition, the right coronary
artery supplies the right atrium atrial-ventricular
(AV) bundle and the right ventricle. The left coro
nary artery supplies the left atrium and the primary
portion of the conduction pathway. Generally, the
clinical symptoms are similar to that of angina, with
emphasis on extreme pressure as well as tightness
over the sternum region. In addition, pain can radiate
to the jaw, upper back, and shoulders (with left more
frequent than right).
MIs can be classified into categories by size, loca
tion, and degree of myocardial wall involvement. The
terms small and large are often used to describe MIs.
However, degrees of complication are also used in
conjunction with size. MIs can be described as un
complicated and complicated based on size of the MI
and recovery of the patient. Location indicates the
portion of the heart involved and also what coronary
artery or branch that is at fault. As described above,
the general regions of the heart are anterior, posterior,
lateral, and inferior. Finally, MIs are classified by the
extent of the wall damage. A transmural infarct (or
full wall) extends from the endocardi um to the epi
cardium. There is the potential that only a small por
tion of the ventricle wall is affected, such as just
below the epicardium (subepicardial) and just below
the endocardium (subendocardial).
Uncomplicated myocardial infarction

An uncomplicated MI is described as a small infarc
tion with no complications during recovery. UsuaUy
the result is full recovery without a significant de
Cardiopulmonat'y Pathophysiology
91
crease in cardiac performance at rest and during mini

mal to moderate activity (Cahalin, 1994). However
the location and the extent of the MI is also critical.
MIs located in the inferior portion of the heart are the
least significant, and partial wall thickness is less sig
nificant than a transmural MY.
Treatment, The treatment for an uncomplicated MI is
initially like the complicated MI, where the patient is
cared for in the coronary care unit. The medical treat
ment is designed to decrease myocardial work and
oxygen demand. Therefore patients are on oxygen
and administered vasodilators (nitroglycerin) to in
crease myocardial blood flow and analgesics to help
further reduce ischemic pain. In addition, to reduce
contractility of the myocardium, calcium channel
blockers or beta-blockers are administered. Finally,
antiarrhythmia medication may be prescribed if an
aberrant cardiac rhythm is present or is highly proba
ble to occur.
Since the course is uncomplicated, this means
that a patient's stay in the coronary care unit may be
only 2 to 3 days, with a total hospital stay of 7 to 10
days. Treatment following leU discharge is oriented
toward increasing physical activity and in educating
the patient and family in risk factor reduction.
This process is described as cardiac rehabilitation
Phase 1.
Complicated myocardial infarction

A complicated MI is different from an uncomplicated
case since the patient may have one, a combination,
or all four of the following conditions/complications:
(I) arrhythmia, (2) heart failure, (3) thrombosis, and
(4) damage to heart structures.
Arrhythmias. Arrhythmias occur in 95% of all pa
tients with MIs. The type and severity of the arrhyth
mia is dependent on the extent of myocardial damage
and the location of the damage. As described earlier,
the uncomplicated MI patient usually has a small area
of the myocardium involved; thus the potential ar
rhythmias are less dangerous and occurrence is less
common. Arrythmias that are life-threatening include
(I) complete A V heart block, (2) ventricular paced

arrhytlImia, and (3) ventricular tachycardia, including
ventricular flutter and fibrillation. In these conditions,
either the heart rate is too slow and thus cardiac out
put is impaired, or the heart rate is too rapid with
92
PART I
poor stroke volume and ejection fraction, and again
considered a distinct possibility in all surgical, MI,
impaired cardiac output. Treatment of the above con
and gunshot patients.
ditions is immediate and requires drugs and poten
Heart wall or mural wall thromhosis can lead to an
tially, electrical shock (for flutter/fibrillation). Usu
emboli lodging in the brain, intestine, kidney, artery
ally, an artificial pacemaker is implanted once the
to the extremities, or any location in the systemic ar
patient is stabilized.
terial circulation. Usually mural thrombosis do not
Heart failure. Another complication following MI is
affect the pulmonary system, since even the smallest
heart failure. Heart failure is a condition where the
fragments are caught in capillary beds and do not
heart is weakened and is unable to produce a signifi
enter into the venous system.
cant cardiac output to meet the bodies need for oxy
Structural damage. The last complication is structural
gen, nutrition, and removal of waste products. When
damage to critical myocardial tissue that affects heart
the heart experiences ischemia the myocardium con
function. If conductant pathway (bundle branch) tis
tracts with less force, and conduction abnormalities
sue located primarily at the septum is damaged, ar
may alter the mechanics of the contraction. If an area
rhythmias result. In addition, papillary muscles that
of the heart is infarcted, the affected myocardium
assist in closing valves can be infarcted. The result of
does not contract, thus affecting overall cardiac out
improper valve function is decreased cardiac output.
put. Another type of heart failure not directly related
Besides these two critical tissues, if significant full
to ischemia and infarction is congestive heart failure
thickness damage occurs to the myocardial wall car
(CHF) (see Congestive Heart Failure, p.
000).
diac function is compromised. HeaIt waJJ damage can
Immediately post-MI, cardiac output is reduced
result in venlricular aneurysms or ventricular wall
significantly. However, the compensatory response is
rupture. Ventricular aneurysm or bulging of the weak
to increase sympathetic innervation, resulting in in
ened ventricular wall oecurs in transmural (full wall
creased heart rate and myocardial contractility. The
thickness) infarcts. Ventricular wal I rupture, which
result of this compensation is a cardiac output that
can occur acutely following transmural infarction, but
may approach normal resting values. However, if the
more often occurs in the first to second week post-MI
damage has been great, the kidneys compensate by
following an aneurysm is usually fatal. Therefore fol
retaining sodium and water in an attempt to improve
lowing a n MI, it is critical to determine i f an
circulatory volume and venous return. Depending on
aneurysm has occurred in the myocardium so that ap
the amount of myocardial tissue death, the individual
propriate surgical intervention can be performed.
may survive with resulting chronic congestive heart
Treatment. The treatment for a complicated MI is
failure through persistent fluid retention and hypoten
initiaJly like the uncomplicated MI, where the patient
40% of the left ventricle is in
is cared for in the coronary care unit. The medical
farcted, the result is usually cardiogenic shock fol
treatment once again is designed to decrease myocar
sion. If grcater than
lowed by death of the individual.
dial work and oxygen demand. Patients are on oxy
Thrombosis. Another complication is increased inci
gen and administered vasodilators (nitroglycerin) to
dence of thrombosis from deep leg veins and from
increase myocardial blood flow and analgesics to
the damaged heart itself. Thrombosis from deep leg
help further reduce ischemic pain. Myocardium cal
veins occurs from lower limb inactivity and circula
cium channel blockers or beta-blockers are adminis
tory stasis. This is a complication that can be ob
tered to reduce contractility. Finally, antiarrhythmia
served for all surgical patients. Emboli from deep leg
medication are prescribed if an aberrant cardiac
vein thrombus usually result in pulmonary complica
rhythm is present.
tions. If the emboli are large or numerous the result
Individuals with a complicated MI have a much
can be pulmonary tissue infarction and potentially
longer stay in the coronary care unit, and their total
death. The incidence of pulmonary emboli has grown
hospital stay time is greatly increased when com
less since early ambulation is now the rule rather than
pared with the uncomplicated MI patient (Topol,
the exception. However, a pulmonary embolj must be
1988). The time in coronary care and total hospital
stay are dependent on the complications that occur
93
of pressure and resistance the heart must overcome to
following the MI. Individuals with heart failure,
eject blood into the systemic circulation (afterload);
thrombolytic events, or structural damage requiring
and myocardial contractility, which is the amount of
surgery may be in the coronary care unit for more
force the left ventricle can apply to the blood within
than 2 weeks. Total hospital stay time for compli
the chamber. If any of these three variables are nega
cated MI patients may exceed 2 to 3 weeks (Topol,
tively affected then cardiac output is reduced. The
1988). However, treatment following ICU discharge
cause of heart failure is often decreased contractility.
is similar to that of the uncomplicated MI patient

with the goal of increasing physical activity and in
Acute heart failure
educating the patient and family in risk factor reduc
If an individual has a significant myocardial infarc
tion. The major difference in Phase I cardiac rehabili
tion, the contractility and pumping ability of the heart
tation for the complicated versus the uncomplicated
is immediately reduced. The initial result is decreased
MI patient is the initial workload intensity, duration,
cardiac output and damming of blood in the veins.
and frequency (i.e., much lower workload for compli
The result is increased systemic venous pressure.
cated MI patient) (Rowe, 1989). Progression is also
This acute phase, which may reduce cardiac output to
usually a bit more conservative, since the probability
40% of normal resting values is short-lived lasting
for a recurrent MI event is much greater in the com
only a few seconds before the sympathetic nervous
plicated MI patient (Rowe, 1989).
system is stimulated, and the parasympathetics be

come reciprocally inhibited. Sympathetic innervation
Prognosis post-myocardial infarction
causes an increase in contractility of viable myocar
Prognosis following MI is dependent on many fac
dial tissue, and the increase in cardiac output may be
tors. Usually cardiovascular peliormance is reduced,
100%. In addition, sympathetic innervation also in
unless the structural damage to the ventricle is minor
creases venous return, since the tone of blood vessels
(as in the case of many uncomplicated MI patients).
is increased. The result is increased systemic filling
The most important factor is extent of ventricular
pressure, and thus increased preload. The sympa
damage. However, with early detection of transmural
thetic reflex following MI becomes maximally opera
infarction and improvement in surgical intervention
tional within 30 seconds; therefore, besides some
and coronary care, acute post-MI deaths have been
pain and fainting, an individual with a mild MI may
reduced (Wenger, 1984). Other critical factors in
not know they just suffered a heart attack! The sym
clude remaining cardiac capacity and status of CAD.
pathetic response can continue with cardiac output
Even though CAD mortality has declined in the
maintained at an adequate level for quiet rest. How
United States, the disease remains the top cause of
ever, the individual may still have persistent ischemic
sudden death in adults.
pain that should be assessed as quickly as possible.
Chronic heart failure

Cong.estive Heart Failure
Following a MI several physiological responses
CHF is characterized by the inability of the heart to
occur besides sympathetic reflex compensation. The
maintain adequate cardiac output. The etiologic fac
kidney begins to retain fluid almost immediately fol
tors of heart failure is usually from ischemia and MI
lowing an MI. The reasons appear to be related to de
secondary to CAD. For the heart to maintain an ap
creased glomerular pressure secondary to decreased
propriate amount of blood flow to the pulmonary and
cardiac output. In addition, there is an increase in
systemic circulation, heart rate and stroke volume
renin output and therefore an increase in angiotensin
must be adequate. Usually, stroke volume is the criti
production. Angiotensin promotes reabsorption of
cal factor to maintain adequate cardiac output. Stroke
water and salt from the renal tubules. The effect of
volume is a function of the amount of blood in the left
moderate fluid retention is an increase in blood vol
ventricle at the end of diastole (preload); the amount
ume and an increase in venous return. This once
94
PART I
again increases preload and thus cardiac output.
result can be deterioration of the myocardium. As the
However, if the MI was severe, the result can be ex
heart weakens, not only is systemic blood flow com
cess fluid retention. This results in detrimental effects
promised, but so is the coronary system. The area
of edema and overstretching of the heart, since blood
most affected is the suhendocardial region. As these

cells become infarcted, the heart weakens further
volume and venous return is too great.

In addition to increased kidney retention of fluid, a
until other regions of the heart also become ischemic
second process that is activated immediately follow
and infarcted. The entire process described from the
ing an MI is recovery of the myocardium. New col
acute to chronic stages is congestive heart failure.
lateral arteries are formed to supply the peripheral

portions of the infarcted region. This revasculariza
Prognosis
tion can assist cells that were marginally active to be
The result without pharmaceutical or surgical inter
come fully functional again. In addition, the unaf
vention (heart transplantation) is death. Pharmaceuti
fected myocardial cells hypertrophy. The result in a
cal intervention to halt or to delay heart failure is
mild to moderate MI is a great improvement in car
with diuretics to reduce fluid levels and cardiac gly
diac function that takes 6 weeks to several months,
cosides such as digitalis to improve myocardial con
depending on extent of injury.
tractility. This pharmacological treatment is com
Compensated and decompensated heart failure
bined with modification of salt and fluid intake.

Finally, in cases when the heart has not compensated
The final state following acute and chronic physio
well and the myocardium has sufficiently weakened
logical changes is called compensated heart failure.
so that cardiac output is minimal, then heart trans
In this state, the heart is able to pump blood effec
plant is the only recourse. Since organ donors are not
tively, but at a reduced cardiac output compared with
readily available, the number of individuals who need
the pre-MI condition. The individuals cardiac reserve
new hearts far outnumber the donor organs. As de
has been greatly reduced. The cardiac reserve can be
scribed previously, once the heart has had enough tis
defined as the difference between the maximum car
sue damage to greatly reduce the cardiac reserve, the
diac output attainable minus the resting cardiac out
prognosIs IS poor.
put. When an individual exercises or is active at a

heavy load, they experience the same symptoms of
acute heart failure, because the heart is unable to sup
ply the cardiac output required of the activity. The
SUMMARY
The first portion of the chapter has described the es
symptoms include rapid heart rate, pallor, and di
sential pathophysiological features of obstructive and
aphoresis. Decompensated failure occurs when the
restrictive lung diseases. Obstructive disorders are
heart is so severely damaged or weakened that nor
characterized by a decreased rate of airflow during
mal cardiac output can not be attained. The result is
expiration (as a result of increased airway resistance).
that cardiac output is not high enough to allow for
Restrictive disorders are conditions in which the in
normal renal function. Fluid continues to be accumu
spiratory capacity of the lungs is restricted to less
lated and the heart is stretched more and weakened
than the predicted normal.
further so that only moderate-to-Iow quantities of
A knowledge of the pathophysiology of pulmonary
blood can be pumped. With unilateral left ventricle
dysfunction assists the practitioner in relating the
heart failure the left ventricle fails, while the right
pathophysiology to the clinical signs and symptoms,
ventricle continues to pump vigorously. The result
and the appropriate treatment goals and interventions.
can be increased blood volume and pulmonary capil
The second portion of this chapter has described
lary pressure in the lungs. If this occurs, fluid begins
the essential pathophysiological features of CAD.
to filter into the interstitial spaces of the alveoli re
CAD results from atherosclerosis. The clinical syn
sulting in pulmonary edema and suffocation. Even if
dromes associated with CAD are angina, MI, and
the heart does not have a unilateral dysfunction the
heart failure.
95
A knowledge of the pathophysiology of CAD en
Caplan, A. (1953). Certain unusual radiological appearanccs in
ables the clinical practitioner to relate the etiologic
chest of coal miners suffering from rheumatoid arthritis. Tho
factors and pathophysiology to the clinical signs and

symptoms exhibited by this patient population, and
prescribes treatment.
rax
8, 29-37.
Claypool, W., Rogers, R.,
&
Matuschak, G. (1984). Update on the
clinical diagnosis, management and pathogenesis of pulmonary

alveolar proteinosis (Phospholipidosis). Chesl 85,550-558.
Cosio, M. (1978). The relations between structural changes in
small airways and pulmonary function tests. New England
REVIEW QUESTIONS
Journal of Medicine 298: 1277-1281.
I. What are the two broad categories of lung disease?

2. What is the major characteristic of obstructive
C rofton,
J.,
et al (1952). Pulmonary eosinophilia. Thorax 7, 1-35.
Crystal, R., et al (1981). Interstitial lung disease: current concepts

of pathogenesis, staging and therapy. American Journal of
Medicine 70, 542-558.
lung disease?
3. H o w does emphysema differ f r o m chronic
bronchitis?
Currie, D., et al (1987). Impaired tracheobronchial clearance in

bronchiectasis. Thorax
DeClerk,
4. How does asthma differ from emphysema?

5. What is the major characteristic of restrictive
lung disease?
c.,
42, 126-130.
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lung disease in scleroderma. A long-term follow-up study.

Arlhritis Rheumalism
30: 643-650.
DeRemee, R. (1977). The present status of treatment of sarcoido
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managed?
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RespiralOry Diseases 3, I.
CHAPTER
Cardiopulmonary Manifestations
of Systemic Conditions
Elizabeth Dean
KEY TERMS
Connective tissue dysfunction
Malnutrition
Endocrine dysfunction
Musculoskeletal dysfunction
Gastrointestinal dysfunction
Neurological dysfunction
Hematologic dysfunction
Obesity
Hepatic dysfunction
Renal dysfunction
Immunological dysfunction
Systemic disease
INTRODUCTION
lowing: musculoskeletal, connective tissue, neurolog
This chapter describes the cardiopulmonary conse
ical, gastrointestinal (GJ), hepatic, renal, hematologi
quences of systemic diseases. Systemic diseases can
cal, endocrine, and immunological systems. Finally,
significantly affect oxygen transport either directly or
the cardiopulmonary manifestations of nutritional
in combination with primary cardiopulmonary dys
d i s o r de r s , s pecifically o b e sity a n d s t a r v a t i o n
function. Although these effects can be as cata
(anorexia nervosa) are presented.
strophic as those resulting from primary cardiopul
Physical therapists (PTs) need to be able to predict
monary dysfunction, their presentation is often subtle
the impact of systemic disease on oxygen transport
and may elude detection until significant impairment
for a given patient to maximize the efficacy of their
is apparent. The pulmonary and pleural complications
treatment prescriptions. Compl ications of systemic
of cardiac disease and the cardiac complications of
disease appear to be increasingly prevalent. This may
pulmonary disease are described first. Then the car
reflect both the aging of the population and improved
diopulmonary complications of conditions involving
survival and prognosis of patients with multisystem
the following systems are described including the fol-
disease. Furthermore, PTs are treating an increasing

99
100
PART 1
number of patients without refelTal, and thus may not
whether treatment should be modified to avert an in
be alerted by a referring practitioner to the presence
cident, or whether treatment is contraindicated all to
and significance of underlying systemic disease.
gether, is essential.
Lastly, physical therapy by definition physiologically
Oxygen transport can be significantly affected by
stresses the patient, therefore, the PTs must be able to
dysfunction in the major organ systems of the body
identify all factors that compromise or threaten oxy
(see box below). The pulmonary and pleural compli
gen transport so that treatment can be prescribed
cations of heart disease and the cardiac complications
most effectively with minimal risk.
of pulmonary disease are usually predictable and
A comprehensive understanding of all factors that
therefore most readily detected clinically. The car
affect or threaten oxygen transport is essential particu
diopulmonary complications of conditions affecting
larly in those patients who are not obviously at risk,
other organ systems, however, can be more subtle, if
that is, those without overt cardiopulmonary disease.
not more devastating.
The PT must be able to "red flag" a patient with an un

derlying problem for which physical therapy may be
contraindicated or an untoward treatment response an
CARDIAC CONDITIONS
ticipated. Alternatively, treatment may need to be
The pulmonary complications of heart disease and the
modified or treatment responses monitored more often.
cardiac complications of pulmonary disease are well
Specific diagnosis of those factors that contribute
known (Scharf and Cassidy, 1989). The mechanically
to or threaten cardiopulmonary and cardiovascular
inefficient heart disrupts the normal forward propul
dysfunction is, therefore, tantamount to efficacious
sion of deoxygenated and oxygenated blood to and
treatment across all physical therapy specialties. The
from the lungs. Because the right and left sides of the
capacity of the oxygen transport system needs to be
healt are in series, a problem on one side inevitably
established to ensure that it can adequately respond to
has some effect, that can lead to a problem on the
changes in metabolic demand, including those im
other side, thus the healt and lung should be thought
posed by physical therapy treatment. Even though
of as a single functioning unit. Disruption of the car
cardiopulmonary dysfunction may not be the primary
diopulmonary circuit leads to backlogging of blood
problem, identifying whether cardiopulmonary dys
and an increased volume of blood in the capacitance
function can limit a patient's response to treatment,
vessels, or the veins. Right heart failure contributes to

increased central venous pressure (i.e., right atrial
pressure) and if sufficiently severe, leads to peripheral
edema in the dependent body parts. Because blood is
not being forwarded to the lungs adequately, hypox
Systems and Systemic Conditions That Affect the

Cardiopulmonary System and Oxygen Transport
emia can result. In turn, hypoxic vasoconstriction of

the pulmonary circulation leads to increased pul
monary vascular resistance, and hence, illcreased right
Cardiopulmonary system
Musculoskeletal system
Connective tissue conditions
Collagen vascular conditions
ventricular afterload and work. Left heart failure can

result in inadequate forward movement of blood
through the left heart, resulting in backlogging in the
Neurological system
pulmonary circulation
Gastrointestinal system
edema. Pulmonary edema alters lung mechanics and
Hepatic system
Renal system
Hematological system
nd cardiogenic pulmonary
lymphatic drainage, and in turn, these effects con

tribute to an increased risk of infection secondary to
Endocrine system
impaired macrophage function and bacterial growth.
Immunological system
Excess pulmonary fluid arollnd the alveolar capillary
Nutritional disorders
membrane creates a diffusion defect. If fluid accumu

lation is extreme, backlogging may be transmitted to
Cardiopulmonary Manifestations of Systemic Conditions
101
the right side of the heart and to the periphery. Com
the circulation, fluid balance in the lung is dependent
parable to excess fluid in the lungs, backup of fluid in
on Starling'S forces, that is, hydrostatic and oncotic
the peripheral circulation can impair tissue perfusion.
pressures. In health, several liters of fluid are ab
Other cardiovascular conditions such as systemic hy
sorbed from the pleural space, thus when the balance
peltension increases systemic afterload, which in turn
of these forces is disrupted in disease, considerable
increases the work of the heart thereby reducing its
fluid can accumulate in the pleural space. Impaired
mechanical efficiency.
alveolar expansion from pleural effusions is of clini
Pulmonary function can be significantly altered in
cal concern. There is some evidence, however, to
cardiac disease (Bates, 1989). Left heart failure, for
support that small effusions displace rather than com
example, is associated with accumulation of fluid in
press the lung (Anthonisen and Martin, 1977).
the pulmonary interstitium. This leads to reduced cal

iber of the airways and early airway closure, air trap
ping and increased residual volume. The fluid can
PULMONARY CONDITIONS
produce reflex constriction of bronchial smooth mus
Lung disease can contribute to cardiac dysfunction in
cle leading to the syndrome of cardiac asthma. The
several ways. First, lung disease invariably threatens
combination of airway collapse and bronchoconstric
oxygen transport by its effects on respiratory me
tion decreases total lung capacity, flow rates and
chanics, and ventilation and peliusion matching. To
forced expiratory volumes. Ventilation and peliusion
compensate, the heart attempts to increase cardiac
abnormalities are also associated with cardiac dis
output which produces a corresponding increase in
ease. Ventilation of underperfused lung zones con
cardiac work. Overall, ventilation and oxygen trans
tributes to increased ventilatory dead space, and per
port is less efficient. Hypoxemia secondary to inade
fusion of underventilated lung zones leads to a right
quate ventilation and perfusion matching may predis
to left shunt. In left heart failure, airway resistance
pose the patient to cardiac dysrhythmias.
contributes to inhomogeneous ventilation and perfu
Pleural complications can arise from either heart
sion. The normal pattern of increased ventilation to
or lung disease. Both heart and lung function can be
the bases is reversed in left heart failure, that is, the
compromised by altered fluid balance of the pleurae.
apices of the lungs are better ventilated (James,
Fluid balance in the pleural space is comparable in
Cooper, White, and Wagner, 1971).
terms of its regulation to that in the alveolar space.
With progression of the pulmonary edema, the alve
Both are determined by Starling forces. Specifically,
oli become flooded resulting in reduced ventilation, and
hydrostatic pressure pushes fluid into these space
significant ventilation and perfusion mismatching. The
while oncotic pressure counters the effect of the hy
alveolar-arterial gradient (A-ao2 gradient) is then in
drostatic forces. The net effect of these filtration and
creased, diffusing capacity decreased, and arterial par
absorption forces is a minimal net filtration pressure.
tial pressure of oxygen (Pao2) decreased. Lung compli
When the balance of these forces is disrupted, heart
ance is inversely related to pulmonary artery pressures
and lung function can be threatened. Excessive fluid
and interstitial fluid accumulation (Saxton, Rabinowitz,
floods the space usually reflecting both excessive hy
Dexter, and Haynes, 1956). The net effect of these ab
drostatic pressure and diminished oncotic pressure.
normalities is both obstructive and restrictive patho
The lymphatic vessels become overwhelmed and are
physiologic patterns of lung dysfunction, that is, re
unable to keep the pleural space dry. Pleural fluid ac
duced forced expiratory volumes and vital capacity,
cumulates and either displaces lung tissue (smaJ]-to
and an overall increase in the work of breathing.
moderate effusions) or restricts opening of adjacent
Pleural effusions can result from heart disease, in
alveolar sacs, causing atelectasis (severe effusions)
particular, congestive heart failure (CHF). Changes in
(Brown, Zamel, and Aberman, 1978), and if suffi
intravascular pressures lead to transudative pleural ef
ciently severe, may restrict cardiac filling. Pleural
fusions and cardiac injury leads to exudative effu
fluid accumulation poses a unique threat to oxygen
sions. Comparable to fluid balance in other parts of
transport as a result of its direct physical effect on the
102
PART I
lungs, heart, or both, thus it warrants special atten

tion by PTs.
Pulmonary lymphatics control fluid balance within
the lung parenchyma. Lymphatic vessels arise within
the pleurae and not within the alveolar capillary
space. They drain fluid from the interlobular septae
and subpleural areas, to the hilar vessels and the pri
mary tracheobronchial lymph nodes. Problems aris
ing within the heart or lungs can contribute to imbal
ances in the major lymphatic inflow and outflow
channels. This contributes to fluid accumulation,
stagnation, and physical compression of the my
ocardium and lungs (Guyton, 1991).
Cardiopulmonary Manifestations of
Musculoskeletal Conditions
General Manifestations
Reduced alveolar venti/atio"
Altered respiratory mechanics
Chest wall rigidity
Reduced chest wall excursion
Impaired IIlucocilary tra"sport

Airflow obstruction
Pulmonary restriction
Atelectasis
Inspissated secretions
Both heart and lung disease can produce deleteri

ous hematologic changes to compensate for hypox
emia. Increases in the number of red blood cells raise
the hematocrit and the viscosity of the blood. This
Increased work of breatllillg

Inefficient breathing pattern
Illcreased work of tile Ileart
phenomenon increases the work of the heart further.
Inefticient breatbing pattern
In addition, viscous blood increases the probability of
Constrictive pericorditis
thromboemboli. This risk is superimposed on the ex

isting risk of thromboemboli in hypoeffective hearts.
A thorough understanding of the interrelationship
of the heatt and lungs is essential for diagnosis and op
timal management. In addition, the cardiopulmonary
and cardiovascular manifestations of other primary
Reduced aerobic capacity

Manifestations in Specific Conditions
Rheumatoid arthritis
Pleuritis with or without effusion
Diffuse interstitial pneumonitis and tibrosis
Pulmonary arteritis
organ systems must be recognized and anticipated par
Bronchiolitis
ticularly in patients with multisystem disease.
Pleural effusions
Ankylosi"g spondylitis
MUSCULOSKELETAL CONDITIONS
Upper lobe fibrobullous disease
Musculoskeletal conditions impact on cardiopul
Chest wall restriction
monary function secondary to their effects on muscle,

in particular, the diaphragm, muscles of the chest wall,
oropharynx, larynx and abdomen, and on bones and
joints (e.g., althritis, ankylosing spondylitis, kyphosco
22). The cardiopulmonary manifestation of muscu
liosis, and the deformity secondary to neuromuscular
loskeletal conditions are summarized in the box above.
diseases and chronic lung diseases). Additional effects
The cardiopulmonary deficits associated with
are imposed by inactivity, (i.e., muscle wasting and in
musculoskeletal disorders of the chest wall include
creased joint rigidity). Increased joint rigidity limits
reduced lung volumes consistent with pulmonary re
the amount of physical activity a patient may pelform,
striction, reduced flow rates, reduced inspiratory and
which contributes to cardiopulmonary compromise, in
expiratory pressures, increased atelectasis, increased
addition to the local effect of increased chest wall
dynamic airway compression, ventilation and perfu
rigidity and compromised bucket-handle and pump
sion mismatching, inefficient breathing pattern, im
handle motions. The normal three-dimensional move
paired cough and gag reflexes, increased risk of aspi
ment of the chest wall and normal pulmonary circula
ration, increased risk of obstruction secondary to
tion and lymphatic function is compromised (Chapter
impaired mucociliary clearance, restricted mobility,
103
compression of mediastinal structures and heart, and
connective-tissue changes in the skin can lead to
impaired lymphatic drainage which depends on nor
chest wall restriction. The cardiopulmonary mani
mal expiratory and inspiratory cycles (Bates, 1989).
festations of connective tissue conditions are sum

marized in the box below.
CONNECTIVE TISSUE CONDITIONS

Connective tissue/virgule collagen vascular disor
NEUROLOGICAL CONDITIONS
ders (e.g., scleroderma and systemic lupus erythe
Cardiopulmonary consequences of neurological dis
matosus [SLE]), invariably affect the cardiopul
ease reflects the specific pathophysiologic mechanisms
1979).
involved (Griggs and Donohoe, 1982). There are three
Inflammation. and tissue injury can affect the air
basic patterns of pathology: (1) involvement of the
way, lung parenchyma, pulmonary vasculature,
central nervous system (CNS), (2) the peripheral ner
monary
system
(Bagg
and
Hughes,
pleurae, respiratory muscles, heart and pericardium.
vous system, and (3) the autonomic nervous system.
Shrinking lung syndrome associated with chronic
The cardiopulmonary manifestations of neurological
connective tissue changes is a feature of advanced
conditions are summarized in the box on p. 104.
disease and is characterized by a significant loss of

alveolar surface area, diffusion capacity, and lung
volumes. Fibrotic changes increase the elasticity of
Involvement of the CNS
the lung parenchyma and reduce lung compliance,
The primary centers for breathing control and control
thereby i n c r e a s i n g work of b r e a t h ing. T h e s e
of the heart emanate from the midbrain. The genera
changes are comparable t o those i n idiopathic pul
tor for breathing control produces a regular respira
monary fibrosis. Both the electrical conduction sys
tory rate through modulation of inspiratory and expi
tem of the heart and its mechanical behavior are ad
ratory inhibitory and excitatory neurons.
versely affected by systemic connective tissue
Activity of the central generator is affected by
changes (Goldman and Kotler, 1985). Furthermore,
arousal and the general alerting reaction of the reticu

lar activating system. In addition, breathing control is
influenced by the hypothalamus, the orbital cortex,
Cardiopulmonary Manifestations of Connective

Tissue/Collagen Vascular Conditions
Acute injury to the alveolar-capillary unit
Alveolar hemorrhage
forebrain, and amygdala (Hitchcock and Leece, 1967).

Insult to the CNS can result in cardiovascular re
sponses that precipitate neurogenic pulmonary
edema. Such responses include systemic hyperten
sion, pulmonary hypertension, intracranial hyperten
sion and bradycardia. The medulla is believed to me
Interstitial pneumonitis
diate the cardiovascular responses associated with
Interstitial pulmonary fibrosis
neurogenic pulmonary edema. Marked sympathetic
Pulmonary hypertension
Respiratory muscle dysfunction
Pulmonary edema
Pulmonary infection
Abnormal diffusing capacity
stimulation, catecholamine release, and vagotonia ap

pear to precipitate neurogenic pulmonary edema and
the resulting leaking of the alveolar capillary mem
brane and alveolar flooding (Col ice, 1985). However,
Chest wall restriction
the possibility of a primary pulmonary endothelial
Manifestations in Scleroderma
permeability abnormality has been suggested (Peter
Restrictive ventilatory impairment

Decreased diffusing capacity
son, Ross, and Brigham, 1983).

Cortical disturbances may have a direct effect on
Diaphragmatic dysfunction
cardiopulmonary function. Among the most common
Gastroesophageal reflux and aspiration
disturbances seen clinically are cortical infarction

and seizures. Hemispheric infarction can lead to
Cardiopulmonary Manifestations of Neurological Conditions

Impaired mucociliary transport

Reduced mobility
Cilia dyskinesia
Incrcased mucus accumulation
Reduced cough and gag reflexes
Impaired airway protection
Increased airway resistance
Increased risk of airway obstmction
Impaired glottic closure
Increased risk of aspiration
Impaired alveolar velltilation

Reduced lung volumes and capacities, as well as now rates
Weakness of pharyngeal and laryngeal structures
Respiratory muscle weakness
Reduced respiratory muscle endurance
Illcreased work of breathing

Reduced aerobic capacity and decollditiollillg
Manifestations in Specific Conditions
M"ltiple sclerosis
Impaired ventilation secondary to spasm
Increased oxygen consumption secondary to spasm
Increased oxygen consumplion secondary to impaired posture and gait
Impaired gag and cough reflexes
Ineffective cough
Cerebral palsy
Increased oxygen consumption secondary to increased muscle tone
Significantly reduced mobility and activity
Impaired movement economy
Impaired swallowing
Impaircd saliva control
Reduced gag and cough reflexes
Impaired coordination of thoracic and abdominal motion dUling respiration
Ineffective cough and airway clearance mechanisms
Stroke
Reduced movement economy
Spasticity and increased oxygen demands
Flaccidity of respiratory muscles
Impaired respiratory muscle strength
Impaired pulmonary function
Asymmetric chest wall
Weak and ineffective cough
Parkillsoll's disease
Increased oxygen consumption secondary to increased muscle tone
Reduced movement economy
Chest wall restriction and impaired pulmonary function
Ineffective cough
104
contralateral weakness of the diaphragm and other
105
creased muscle tone, which correspondingly increases
respiratory musc les. E pi l e ptic seizures disrupt
basal and exercise oxygen consumption, resulting in
breathing, which causes hypoxemia, respiratory aci
increased oxygen demands. Even though the demands
dosis, and a metabolic acidosis secondary to extreme
are increased in this condition, oxygen delivery is
muscle contraction and lactate accumulation. The as
compromised. For example, thoracic deformity and
sociated increase in sympathetic stimulation can pre
spasm of the muscles of the chest wall and abdomen
cipitate cardiac dysrhythmias and pulmonary edema.
impair breathing pattern and its efficiency (Fullford
Demyelinating diseases such as multiple sclerosis
and Brown, 1976). The airways of patients with cere
result in progressive deterioration of neuromuscular
bral palsy are vulnerable because of poor gag, cough,
function. The muscles of respiration become increas
and swallowing reflexes. In addition, these patients
ingly involved, resulting in respiratory insufficiency
often have poor saliva control, which increases the
(Cooper, Trend, and Wiles, 1985). In addition, with
risk of aspiration further. Mental retardation (Bates,
increasing debility cardiopulmonary conditioning is
1989) often complicates the presentation of cerebral
reduced. Weakness of the pharyngeal musculature
palsy and prevents these patients from responding ad
contributes to loss of airway protection in addition to
equately to their hydration needs or being able to co
the loss of cough and gag reflexes. Aspiration is prob
operate with life-preserving treatments. These patients
lematic for these patients as the disease advances.
harbor numerous microorganisms, which adds further
Stroke patients may have central involvement that
to their general risk of infection.
affects cardiopulmonary regulation and function, in
Patients with Parkinson's disease also exhibit sig
cluding reduced electrical activity of the respiratory
nificant cardiopulmonary deficits (Mehta, Wright,
muscles, or peripheral involvement such that weak
and Kirby, 1978). Oxygen demand is increased com
ness, spasticity, impaired biomechanics, and gait di
mensurate with increased muscle tone.
rectly affect respiratory muscle function and chest
to the patients described above, patients with Parkin
waJl excursion (DeTroyer, De Beyl, and Thirion,
son's also have reduced cardiopulmonary condition
Comparable
1981). Abdominal muscle weakness contributes to
ing levels as a result of compromised agility and abil
impaired cough effectiveness. Pharyngeal weakness
ity to be independently mobile in many cases. These
contributes to sleep apnea in these patients. The com
patients also have a restrictive pattern of lung disease
mon clinical presentation of unilateral involvement
with most lung volumes and capacities being re
leads to a posture listing to the affected side when re
duced. Chest wall rigidity impairs the normal pump
cumbent, sitting and during ambulation. This posture
handle and bucket-handle movements, thus it reduces
impairs ventilation and chest wall expansion on the
breathing efficiency. The energy cost of breathing is
affected side. Abdominal muscle involvement di
correspondingly increased. Respiratory insufficiency
rectly affects intraabdominal pressure and the effi
of Parkinson's disease likely reflects an increase in
ciency of diaphragmatic descent during contraction,
tone of the respiratory muscles, chest wall rigidity, as
that is, should the abdominal muscles become flaccid
well as increased parasympathetic tone and resulting
the efficiency of diaphragmatic contraction is signifi
airway obstruction.
cantly reduced. Lung volumes and flow rates are re
Patients with a history of poliomyelitis with or
duced proportionately giving a restrictive pattern of
without cardiopulmonary complications at onset, may
lung function. Reduced activity and exercise around
exhibit pulmonary limitation several decades later
the time of the stroke contributes to reduced car
(Dean, Ross, Road, Courtenay, and Madill, 1991;
diopulmonary conditioning and capacity of the oxy
Steljes, Kryger, Kirk, and Millar, 1990). These indi
gen transport system. Finally, a high proportion of
viduals are at risk for developing respiratory insuffi
patients with strokes are hypertensive and older, a
ciency as a result of respiratory muscle weakness,
population with a higher prevalence of heart disease
chest wall deformity, minor infection and periods of
and atherosclerosis (Chimowitz and Mancini, 1991).
relative immobility, or secondary to medical inter
Cerebral palsy is associated with significantly in
ventions, (e.g., anesthesia, sedation).
106
PART I
Diseases and lesions involving the brainstem can
the larynx, pharynx, and tongue can lead to upper
lead to various abnormal breathing patterns. Some
airway obstruction and increased airway resistance,
common breathing aberrations are Cheyne-Stokes res
and interfere with maintaining a clear airway. Aspi
piration, central neurogenic hyperventilation, ap
ration is a common and serious problem associated
neustic breathing, and ataxic breathing. Cerebellar and
with impaired motor control of the larynx, pharynx,
basal ganglia lesions may produce respiratory muscle
and tongue.
discoordination and dyspnea (Hormia, 1957; Neu,

Connolly, Schwertley, Ladwig, and Brody, 1967).
Spinal cord lesions have a variable effect on car
Involvement of the Autonomic Nervous System
diopulmonary function depending on the level of the
Cardiopulmonary consequences of disorders of the
lesion. Cervical lesions result in a high mortality rate
autonomic nervous system have been documented. Of
as a result of cardiopulmonary complications. All
those diseases with an autonomic component, auto
lung volumes are diminished with the exception of
nomic neuropathies, diabetes, and alcoholism have
total lung capacity (TLC), which over time returns to
been the most studied. MUltiple system atrophy ac
normal; tidal volume (TV), which is usually pre
companies autonomic failure affecting multiple sys
served (10% of TLC); and residual volume (RV),
tems. Because of the anatomic proximity of the auto
which is significantly increased (Estenne and De
nomic, respiratory and hypnogenic neurons and the
Troyer, 1987; Fugl-Meyer, 1971). Quadriplegic pa
degeneration of these structures in this condition, dys
tients tend to have a greater diaphragmatic contribu
function of the respiratory control mechanisms paral
tion to tidal ventilation compared with healthy people
lels autonomic and somatic dysfunction. The respira
(Estenne and DeTroyer, 1985). In addition, these pa
tory dysrhythmias that are seen in multiple system
tients have impaired cough as a result of loss of in
atrophy include central, upper airway obstruction, ir
nervation and paresis of the diaphragm in some cases,
regular rate, rhythm, and amplitude of respiration with
and abdominal and intercostal muscles. The contribu
or without oxygen desaturation, transient uncoupling
tion of accessory muscle activity to ventilation varies
of the intercostal and diaphragmatic muscle activity,
considerably (McKinley, Auchincloss, Gilbert, and
prolonged periods of apnea, Cheyne-Stokes respira
Nicholas, 1969). In quadriplegia, with only the acces
tion, inspiratory gasps, and transient sudden respira
sory muscles and diaphragm spared, platypnea (in
tory arrest (Bannister, 1989).
creased dyspnea when upright) may occur (Dantzker,
Patients with diabetes and autonomic neuropathies
1991). In the upright position, the diaphragm is flat
exhibit variable effects on cardiopulmonary status.
tened and less efficient when moved downward by
Postural hypotension is a complication of diabetic au
reduced abdominal pressures.
tonomic neuropathy and efferent sympathetic vaso
Thoracic lesions tend to have less effect on pul
motor denervation. Norepinephrine levels are gener
monary function (vital capacity and forced expiratory
ally reduced in these patients. The splanchnic and
volumes in particular) than cervical lesions, and the
peripheral circulations fail to constrict in response to
significance of this effect is reduced as the level of
standing, thus cardiac output falls. The postural effect
the lesion is reduced. Lumbar lesions may have mini
is exacerbated by reduced cardiac acceleration in pa
mal or no effect on pulmonary function; however, in
tients with diabetes. Insulin has been associated with
volvement of the abdominal muscles may limit cough
cardiovascular effects, including reduced plasma vol
effectiveness.
ume, increased peripheral blood flow secondary to va

sodilatation, and increased heart rate. In the presence
Involvement of the Peripheral Nervous System
of autonomic neuropathies, insulin can induce pos

tural hypotension. Diabetic diarrhea secondary to ab
Disorders of the peripheral nervous system include
normal gut motility can contribute to fluid loss and its
those of the motor neuron, peripheral nerve, neuromus
sequelae. Cardiopulmonary changes associated with
cular junction and muscle. Neuromuscular disorders of
autonomic neuropathy secondary to diabetes include
107
altered ventilatory responses to hypoxia and hyper
been associated with inflammatory bowel disease;
capnia, altered respiratory pattern and apneic episodes
however, their occurrence is not related to the activity
during sleep, altered bronchial reactivity and impaired
or therapy. Biopsy specimens have shown basement
cough (Bannister, 1989; Montserrat et aI., 1985).
membrane thickening, thickening of the epithelium,

and infiltration of the underlying connective tissue
with inflammatory cells (Higenbottom, et aI., 1980).
GASTROINTESTINAL CONDITIONS
The pulmonary manifestations of pancreatitis are
The cardiopulmonary manifestations of GI dysfunc
among the most important sequelae of this disease.
tion are summarized in the box below. Inflammatory
Of the deaths that occur in the first week of hospital
bowel disease and pancreatitis are principal exam
ization, 60% are associated with respiratory failure
ples of GI dysfunction that affects on cardiopul
(Renner, Savage, Pantoja, and Renner, 1985). Prob
monary function. Aspiration is a significant cause of
lems include elevated hemidiaphragms particularly
morbidity and mortality in patients with GI dysfunc
on the right side, basal atelectasis, diffuse pulmonary
tion, thus it should be prevented or detected early.
infiltrates appearing more often on the right side than
The pathophysiology, management, and outcome de
the left side, pleural effusions on the left side more
pend on the nature of the aspirate. Several predispos
than the right side, and pneumonitis. These findings
ing factors produce aspiration pneumonia including a
are not specific for pancreatitis and are probably sec
decreased level of consciousness, disorders of pha
ondary to localized peritonitis, subphrenic collec
ryngeal and esophageal motility, altered anatomy,
tions, ascitis, pain, and abdominal distension. In
disorders of gastric and intestinal motility, and iatro
chronic pancreatitis, abdominal symptoms may be re
genic factors such as surgery, nasogastric (NG) intu
duced and thoracic symptoms such as dyspnea, chest
bation, and general anesthesia.
pain, and cough may predominate. Chronic effusions
Inflammatory bowel disease can lead to the fol
may result in pleural thickening.
lowing cardiopulmonary pathologies: vasculitis, fi

brosis, granulomatous disease, and pulmonary throm
boembolism. Bronchitis and bronchiectasis have also
LIVER CONDITIONS
Both acute and chronic liver conditions can predis
pose a patient to cardiopulmonary and cardiovascular
complications (see the box, on p. 108, at left). Hepatic
failure can lead to hypoxemia secondary to intrapul
of GI Conditions
monary vascular dilatation and noncardiogenic pul

monary edema. Hepatopulmonary syndrome, hall
Risk of aspiration
marked by intrapulmonary vascular dilatation,
Gastroesophageal reflux
produces both diffusion and perfusion defects in the
Increased airway resistance
Bronchospasm
Reduced lung volumes
Elevated hemidiaphragms
Compression atelectasis
Arterial hypoxemia
Alveolar capillary leak and V/Q mismatch
Alveolar hemolThagc and consolidation worsen

shunt
Increased pulmonary vascular resistance
lungs and is the principal reason for severe hypoxemia

(Sherlock, 1988). The origin of pulmonary edema is
secondary to hepatic encephalopathy and cerebral
edema (Trewby, et aI., 1978).
With respect to chronic liver conditions, car
diopulmonary manifestations have been associated
with cirrhosis of the liver and hepatitis. The most
common pulmonary abnormalities associated with
these conditions are intrapulmonary vascular dilata
tion with and without shunt, pulmonary hypertension,
airflow obstruction, chest wall deformity, pleural ef
fusions, pancinar emphysema, pleuritis, bronchitis,
108
PART I
of Liver COllditions
of Rellal Conditions
Intra pulmonary vascular dilatation
Alveo lar hemorrhage
Pulmonary hype11ension
Airway ohstruction
Expiratory airflow obstruction
Reduced lung volumes
Chest wall deformity
Reduced diffusing capacity
Pleural effusions
Panacinar emphysema
Pleuritis
of these patients, physical therapy warrants being es
Bronchitis
Bronchiectasis
pecially aggressive given the course of the pul
Impaired hypoxic vasoconstriction
monary-renal syndromes and the potential for re
Interstitial pneumonitis
lapses and irreversible organ damage.
Pulmonary fibrosis
HEMATOLOGIC CONDITIONS
bronchiectasis, hypoxic vasoconstriction, and intersti
Hematologic disorders that can manifest cardiopul
tial pneumonitis, fibrosis. Hypoxemia results from
monary symptoms include abnormalities of the fluid
shunting, ventilation and perfusion mismatching and
and cellular components of the blood, and coagu
diffusion abnormalities.
lopathies (Bromberg and Ross, 1988). Cardiopul
Pleural effusions and ascites interfere with di
monary manifestations of hematologic conditions are
aphragm function and present unique problems in the
summarized in (the box on p. 109). The primary un
patient with Ii ver disease. Rich lymphatic connec
derlying mechanisms by which these conditions dis
tions exist between the abdominal and thoracic cavi
rupt gas exchange include hemorrhage, infection,
ties. Because of the rich lymphatic supply of the
edema, anemia, fibrosis, and malignancies.
pleural space, ascitic fluid can flow into the pleural
Abnormalities related to red blood cells and their
space. This effect is enhanced during inspiration
ability to transport hemoglobin and oxygen may pro
when the intraabdominal pressure is relatively posi
duce signs resembling pulmonary pathology, (e.g.,
tive and the intrapleural space is negative (Crofts,
tachypnea, dyspnea, and cyanosis). Abnormalities of
1954).
the deformability of red blood cells alter blood viscos

ity and pulmonary blood flow. The interstitium can be
disrupted by such factors as hemorrhage and malig
RENAL CONDITIONS
nancies. Coagulopathies disrupt the normal hemosta
Cardiopulmonary complications can result from renal
sis and clotting mechanisms of the blood. Pulmonary
disease and the category of disorders referred to as pul
hemorrhage and hemoptysis are common sequelae.
monary-renal syndromes (see the box above, at right).
The most common causes of pulmonary hemolThage
(Rankin and Matthay, 1982; Matthay, Bromberg, and
include vitamin-K deficiency, hemophilia, hepatic
Putman, 1980). The pathophysiologic characteristics
failure, and disseminated intravascular coagulation.
of these disorders include alveolar hemorrhage, inter
Pharmacologic agents such as platelet inhibitors and
stitial and alveolar inflammation, and involvement of
anticoagulants can also result in pulmonary hemor
the pulmonary vasculature. Pulmonary function testing
rhage. Pulmonary thromboemboli are common events
may detect both obstructive and restrictive abnormali
with symptoms including pleuritic chest pain, dysp
ties as a result of bronchial complications, and inflam
nea, and hemoptysis.

Of the erythrocyte disorders sickle cell anemia is
mation and hemorrhage respectively.

In systemic illness, pathology of the lungs and
probably the most common. Acute chest infection
kidneys often coexist. Like the medical management
and thrombosis leading to pulmonary infarction may
109
pending on the amount of plasma protein, particularly
of Hematologic Conditions
albumin, fluid is retained or lost from the circulation.

With reduced protein and oncotic pressure within the
vasculature, more fluid is filtered out of the circula
General Cardiopulmonary Manifestations
tion into the interstitium. In catabolic states in which
Hemorrhage
protein is broken down in the body, more protein
Edema
leaks through the capillaries taking water with it, thus
Polycythemia
leading to edema.
Anemia
Infection
AbnonnaJities of the Fluid Portion of the Blood
ENDOCRINE CONDITIONS
Abnormal blood volume

Abnormal tluid balance
Endocrine and metabolic disorders can be associated
(water excesses and
with cardiopulmonary complications (see the box on
deficits)
p. 110). (Civetta, Taylor, and Kirby, 1989; Guyton,
Abnormal electrolytes
Abnormal plasma proteins
1991). Disorders of the thyroid gland, pancreas (dia
Abnormal procoagulants and anticoagulants
betes mellitus [DM]) and adrenal glands are such disor
Abnormal clotting times
ders that are often seen clinically. Thyroid hormone in
Abnormalities of the Cellular Portion
fluences the central drive to breathe and surfactant
of the Blood
Abnormal red blood cell
synthesis. Hypothyroidism can lead to sleep apnea,

pleural effusions secondary to altered capillary perme
COllnt
Abnormal red blood cells
ability, and pericardial effusions. Decreases in vital ca
Abnormal deformability of the red blood cells
pacity have also been reported secondary to muscle
Abnormal hemoglobin
Abnormal oxyhemoglobin dissociation
weakness. Hypelthyroidism increases cellular oxidative
(e.g., carbon
monoxide poisoning)
metabolism (the metabolic rate) leading to an increase
Abnormal white blood cells and antibodies
in oxygen consumption and CO2 production, and an
Blood dyscmsias
overall increase in minute ventilation. Vital capacity,

lung compliance, and diffusion capacity can be reduced.
In addition, maximal inspiratory and expiratory pres
sures can be reduced secondary to muscle weakness.
Patients with diabetes are prone to aspiration and
occur with clinical symptoms such as fever, pleuritic
respiratory infections. Late complications of diabetic
chest pain, cough, and pulmonary infiltrates. The pul
neuropathy include renal failure, which may be accom
monary function of patients with sickle cell anemia is
panied by pleural effusions and pulmonary edema. Au
abnormal with reduced TLC, vital capacity, diffusing
tonomic neuropathy may affect vagal activity and air
capacity, arterial oxygen tensions, and reduced exer
way tone. Ischemic heart disease and cardiomyopathies
cise capacity (Femi-Pearse, Gazioglu, and Yu, 1970).
are common in patients with diabetes and may cause
The hematologic malignancy disorders that can af
CHF and cardiogenic pulmonary edema. Patients with
fect pulmonary function include the leukemias and
diabetes have been reported to have reduced sensitivity
Hodgkin's disease. The three primary mechanisms by
to inspiratory loading (O'Donnell, Friedman, Russo
which these disorders can affect pulmonary function
manno, and Rose, 1988), which may impair their sub
include direct infiltration, increased risk of oppor
jective responses to exercise.
tunistic infection and secondary effects of treatment,

such as interstitial pneumonitis and fibrosis.
Adrenal insuffiCiency can also compromise oxy

gen transport (Civetta, Taylor, and Kirby, 1989). Re
Disorders of plasma proteins can have significant
duced aerobic capacity results from symptoms of
effects on the Starling'S forces maintaining normal
weakness, fatigue, and associated muscle and joint
fluid balance within the tissue vascular beds. De
complaints. Orthostatic intolerance primarily reflects
110
PART I
Cardiopulmonary Manifestations of Endocrine

Conditions
Thyroid DisOI'ders
reduced inotrophic capacity of the heart and reduced

systemic vascular resistance.
IMMUNOLOGICAL CONDITIONS
Hypothyroidism
H ypornetabolic
Congenital and acquired defects in the immunologi
Fatigue and excessive sleep
cal status of the lung lead to cardiopulmonary dys
Reduced conditioning
function, including infection and inflammation. In
Decreased vital capacity econdary to muscle

weakness
addition, patients who are immunodeficient have an

increased risk of pulmonary malignancies (Shackle
Slecp apnea
ford and McAlister, (975).
Decreased heart rate

Decreased cardiac output
Acquired immunodeficiency syndrome (AIDS),
Decreased blood volume
an example of a primary disorder of cell-mediated
Pleural effusions
immunity, has reached epidemic proportions over
Pericardial effusions
the past 20 years. This syndrome leads to lympho
Hyperthyroidism
cyte death. The most serious pulmonary infections
Hypermetabolic
associated with AIDS is Pneul110cystis carinii pneu
Decreased vital capacity and diffusing capacity

Fluid loss (diarrhea)
monia (Murray, Felton, and Garay, 1984). The fact

that the patient with the human immunodeficiency
virus (HIV) is more likely to have recurrent pneu
Fatigue and inability to sleep
monia suggests that the infecting organisms persist
Reduced conditioning
in the lung despite treatment (Shelhamer, et aI.,
Pancreatic Disorders (Diabetes)
1984). The clinical presentation includes diffuse
Pulmonary endothelial thickening
pulmonary infiltrates, cough, dyspnea, and hemopt
Reduced TLC
ysis. These patients can also have symptoms of
Reduced vital capacity and forced expiratory
upper airway obstruction.
volumes
Reduced airway vagal tone
Increased risk of aspiration
NUTRITIONAL DISORDERS
Possible reduced elastic recoil

Impaired hypoxic and hypercapnic responses
Impaired ventilatory response to exercise
The two most common nutritional disorders seen
Defective neutrophil production
Western countries are obesity, and anorexia nervosa,
Colonization with gram-negative hacilli
which is akin to starvation. Obesity contributes in sev
Pleural effusions and pulmonary edema with
eral ways to impaired oxygen transport (Alexander,
diabetic nephropathy
Reduced sensitivity to increases in inspiratory
resistive loading
Accelerated atherosclerotic vascular and cardiac
changes
Increased ischemic heart disease
of the increased weight of adipose tissue over the tho

are increased. In addition, large abdomens, and abdom
inal contents impinge on diaphragmatic motion, and
Increased risk of infection
can restrict diaphragmatic descent. This can lead to
Adrenal Insufficiency
compression of the dependent lung fields. Recumbency
Orthostatic symptoms
Reduced aerobic capacity secondary to anorexia.
weakness and fatigue

Impaired breathing mechanics secondary to GI
symptoms
1985; Bates, (989). These include alveolar hypoventi

lation and impaired Pao2 and gas exchange as a result
racic cavity. Systemic and pulmonary blood pressures
Cardiomyopathy
Tendency to retain fluid
111
can induce respiratory insufficiency, that is positional

respiratory failure. Obese individuals have a higher in
cidence of snoring and obstructive sleep apnea sec
ondary to weakness, and increased compliance of the
postpharyngeal structures. In addition, these patients
often have weak ineffectual coughs resulting from expi
Cardiopulmon ary Manifestations of Systemic Conditions
ratory muscle weakness and mechanical inefficiency of

these muscles. Work of breathing is markedly in
111
SUMMARY
This chapter described the cardiopulmonary conse
creased. Furthermore, in chronic cases, reactive pul
quences of systemic diseases. Oxygen transport, the
monary vasoconstriction in response to chronic hypox
purpose of the cardiopulmonary system, can be sig
emia contributes to right ventricular insufficiency and
nificantly affected by dysfunction in virtually all
increased work of the heart and cardiomegaly.
organ systems of the body. The pathophysiological
The major cardiopulmonary manifestations of
consequences of diseases of the following systems on
anorexia nervosa relate to generalized weakness and
oxygen transport were presented: cardiac, pulmonary,
reduced endurance of all muscles, including the res
musculoskeletal, connective tissue/collagen vascular,
piratory muscles. Cough effectively is correspond
neurological, gastrointestinal, hepatic, renal, hemato
ingly compromised. Oxygen transport reserve is min
logic, endocrine, and immunological systems. In ad
imal. Because of poor nutrition and fluid intake, the
dition, the cardiopulmonary manifestations of nutri
patient is at significant risk of anemia, fluid and elec
tional disorders, i ncl ud ing obesi ty and anorex i a
trolyte imbalances, and cardiac dysrhythmias (Wil
nervosa, were described.
son, et ai, 1991). Common manifestations of nutri

tional disorders are summarized in the box below.
A knowledge of these effects is essential to the

practice of physical therapy across all specialties in
that the prevalence of systemic disease appears to
be increasing. The p r esentation of cardiopul
monary consequences of systemic disease is often
of Nutritional Disorders
subtle or obscured, and is associated with a poor
Obesity
management is essential.
prog nosis, thus early detection and appropriate

PTs need to be able to distinguish diagnostically
Al v eolar hypov entilat io n
cardiopulmonary manifestations of systemic dis
Obstructive sleep apnea

Reduced outward recoil of the chest wall
eases to appropriately identify indications for physi
Increased abdominal contents
cal therapy, contraindications, side effects, and un
Increased llIass of the abdominal wall
usual treatment responses. In addition, detailed
Reduced functional re sidua l capacity

Reduced expiratory
reserve vol
assessment of the patient's problems ensures that
ume
Marked reductions lung volumes, arterial oxygen

tension (Pao2) and saturation
(Sao2) in
recumbency
Basal airway closure and resul t ing decrease in Pao2

Marked pulmonary abnormalities during sleep
problems amenable to physical therapy are appro

priately treated, and those that are not are referred
back to a physician.
Reduced ventilatory responses to CO2

Cardiomegaly
Rotation and horizontal position of the heart
Axis deviation
Reduced myocardial pumping efficiency
Reduced aerobic conditioning and oxygen transport
reserve capacity
REVIEW QUESTION
Describe the cardiopulmonary manifestions of:
1. Musculoskeletal dysfunction
2. Connective tissue dysfunction
3. Neurological dysfunction
Starvation or Anorexia Nervosa
4. Hepatic dysfunction
Generalized weakness, debility, and l os s of
S.
cardiopulmonary co nd itioning
Impaired mucociliary transport
Ineffective cough
Fluid and elect rolyte dis turbance s
Cardiac dysrhythmias
Renal dysfunction
6. Hematologic dysfunction
7. Endocrine dysfunction
8. Obesity
9. Malnutrition (e.g. anorexia nervosa)
Respiratory musc le weak ness
112
PART I
Griggs, R.C., & Donohoe, K.M. (1982). Recognition and manage
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(1991). Harri
PART
II
Cardiopulmonary
Assessment
Measurement and Documentation
Claire Peel
KEY TERMS
Documentation
Reliability
Measurement
Subjective assessment
Objective assessment
Validity
INTRODUCTION
surements that relate to the cardiovascular and pul
Measurement and documentation are critical com
monary systems is essential for quality patient care.
ponents of the process of providing patient care.
Documentation of the results of measurements,
Measurements form the basis for deciding treat
the interpretation of the results and the patient care
ment strategies and therefore influence patients' re
plan is important not only for reimbursement but
sponses to therapeutic interventions. Measurements
also to assure communication among health care
are also used during treatment sessions to deter
team members. Timely and appropriate sharing of
mine rate of progression and appropriateness of ex
information on physiological responses to activity is
ercise prescriptions. Typically, therapists make a
often critical for optimal medical management. Doc
series of measurements and in combination with the
umentation needs to be written clearly and concisely,
results of measurements made by other health care
and to include objective findings that will facilitate
professionals, form an impression of the client. The
efficient and continuous care from all members of
impression includes both physical and psychosocial
the health care team.
aspects. If parts of the impression are incorrect be
This chapter provides a discussion of types and
cause of inaccurate measurements, then the course
characteristics of measurements that are common to
of treatment may be misdirected. The result could
cardiopulmonary physical therapy, followed by a dis
be treatment that is either not effective or unsafe.
cussion of the process of selecting, performing, and
Consequently, knowledgc of the qualities of mea-
interpreting measurements. A discussion of the pur

117
118
PART II
Cardiopulmonary Assessment
poses and types of documentation follows, including
function into those with obstructive lung disease, re
suggestions for providing objective and outcome-ori
strictive lung disease, or a combination of both types
ented information.
of dysfunction. The categories are mutually exclusive,

that is, all patients fit into one and only one category.
The categories of a nominal measurement scale
CHARACTERISTICS OF MEASUREMENTS
are defined Llsing objective indicators that are univer
The purpose of performing a measurement is to as
sally understood. For example, the classification of
sess or evaluate a characteristic or attribute of an in
patients with heart failure could be based on the pri
dividual. The characteristic to be measured first must
mary cause for the development of the condition (see
be defined, and the purpose of performing each mea
the box below, at left). In each case, the cause could
surement must be clear. Therapists then can select the
be determined by diagnostic testing such as angiogra
most appropriate method of measurement given the
phy or echocardiography. Clear descriptions of the
available resources and their clinical skills.
criteria for inclusion in each category facilitate clini

cians' agreement on the assignment of patients to cat
egories. A high percentage of agreement indicates
levels or Types of Measurements
high interrater reliability.
Measurements can be described according to their

type or level of measurement. There are four levels of
Ordinal
measurements which are nominal, ordinal, interval
Ordinal measurements are similar to nominal measure
1993). Recognizing
ments with the exception that the categories are or
the level of measurement aids in the understanding
dered or ranked. The categories in an ordinal scale in
and ratio (Rothstein, Echternach,

and interpretation of the result.
dicate more or less of an attribute. The scale for rating

angina is an example of an ordinal scale (Pollock,
Nominal
Willmore, and Fox,
Objects or people are often placed in categories ac
1978) (see the box below, at right).
Each category is defined and a rating of grade I angina
cording to specific characteristics. If the categories
is less than a rating of grade 4. In an ordinal scale, the
have no rank or order, then the measurement is consid
differences between consecutive ratings are not neces-
ered nominal. An example of a nominal measurement

is the classification of patients with pulmonary dys-
Allgina Scale
Grade I:
Commoll Causes for the Developmellt

of Heart Failure
Light-The discomfort that is

cstablished, but j ust established
Grade 2:
Light moderate---Discom forl from

-
which one can be distracted by a
Myoca rd ial infarction (Mf) or ischemia
noncataclysmic evcnt; it can be "pain"
Cardiac arrhythmias
but usually is not
Renal insufficiency
Grade 3:
Cardiomyopathy
Moderate-sever
Discomfort or pain
that prevents distraction by a beautiful
Heart valve abnormalities

Pericardial effusion or myocarditis
woman. handsome man. television
Pulmonary embolism or pulmonary hypertension
show, or other consuming interest;
Spinal cord injury
o nl y a tornado, earthq uake or

expl osio n can distract one from a grade
3 discomfort or pain
Congenital abnormalities
Aging
Grade 4:
From Cahalin, L. P. (1994). Cardiac muscle dysfunction. In Hille
gass, E.
A., &
Sadowsky,
H.
of cardiopul
WB Saunders.
S. (Eds.). Essentials
monary pulmonary physicaltiJerapy. Philadelphia:
Severe---Discomfort that is the most

excruciating pain experienced or
imaginable
119
sarily equal. The difference between grade 1 angina
sured using either an interval or a ratio scale. The
and grade 2 is not necessarily the same as between
Fahrenheit temperature scale assigns the zero point to
grade 3 and grade 4 angina. Consequently, if num
the temperature at which water freezes, whereas the
bers are assigned to categories, they can be used to
Kelvin scale assigns the zero point to an absence of
represent rank, but cannot be subjected to mathemati
heat. The Fahrenheit scale is an example of an inter
cal operations. Averaging angina scores is incorrect
val level of measurement, and the Kelvin scale is a
because by averaging, it is assumed that there are
ratio level of measurement.

Measuring force production using an isokinetic dy
equal intervals between categories.

Categorical measurements are considered ordinal
namometer is an example of an interval measurement
if being assigned to a specific category is considered
commonly used in physical therapy. Patients may be
"better than" or "worse than" another category. For
able to generate muscle tension and move an extrem
example, patients with angina could be classified as
ity, but register a score of zero because they cannot
having either stable or unstable angina. This mea
move as fast as the dynamometer. Interval measure
surement would be considered ordinal, because stable
ments can have negative values, and can be subjected
angina usually is considered a better condition to
to some arithmetic operations. Adding and subtracting
have compared with unstable angina (Hurst, 1990).
values is logical. A patient who generates 10 ft-lbs at

one session and 20 ft-Ibs at the following session in
Ratio
creased their torque production by 10 ft-Ibs. Interval
Ratio measurements have scales with units that are
values cannot be subjected to division or multiplica
equal in size, and have a zero point that indicates ab
tion. It cannot be stated that the patient generated
sence of the attribute that is being measured. Exam
twice as much torque on the second session compared
ples of ratio measurements that are used in cardiopul
with the first session because it cannot be assumed
monary physical therapy include vital capacity,
that a reading of zero indicated no torque production.
cardiac output, and oxygen consumption. Ratio mea

surements are always positive values, and can be sub
jected to all arithmetic operations. For example, an
Reliability
aerobic capacity of 4 Llmin is twice as great as an
Reliability is defined as the consistency or repro
aerobic capacity of 2 Llmin.
ducibility of a measurement. Ideally, if attempting to
When deciding if a measurement is ratio level or.

not, the attribute that is being measured is defined.
measure a specific attribute, the value of the measure

ment should change only when the attlibute changes.
If the zero point indicates absence of the attribute,
However, all measurements have some element of
then the scale would be considered ratio. For exam
error that contributes to the variability of the measure
ple, cardiac output can be defined as the amount of
ment. When the error is relatively high, the value of
blood in liters ejected from the left ventricle over a
the measurement can change, even though the attribute
I -minute period. A measurement of zero cardiac
has not changed. Believing that a change occurred
output would be absence of the characteristic, or no
when it did not could result in an inaccurate clinical
blood ejected from the left ventricle.
decision related to treatment planning or progression.

Many factors contribute to variability in the results
Interval
of measurements. The characteristic being measured
Measurements that are at interval level have units on
may demonstrate a certain degree of variability. Both
a scale with equal distance between consecutive mea
blood pressure and heart rate vary depending on both
surements. Interval measurements are differentiated
mental and physical factors such as body position,
from ratio measurements, because the zero point is
hydration level, anxiety and time of day. For these at
arbitrary rather than absolute. An arbitrary zero point
tributes, multiple measurements often are used to
is one that does not mean an absence of the character
provide the best estimate of the patient's true heart
istic that is being measured. Temperature can be mea
rate and blood pressure.
120
PART II
Another factor that contributes to the variability of a
ment must possess a certain degree of validity. Mea
measurement is changes in the testing instrument.
surements can be reliable but not valid. For example,
Testing instruments may vary in their readings because
measurements made using bioelectrical impedance
of changes in environmental conditions or malfunction
analyses have been shown to be valid for the estima
of parts of the instrument. Instruments should be cali
tion of total body water, but uncertainty exists as to the
brated, that is, compared with a known standard, on a
validity of estimates of percent body fat made with this
regular basis to assure accuracy of the readings. Some
device (Kusher and Schoeller,
instruments are relatively easy to calibrate. For exam
1986).
There are various types of validity. Of importance
ple, values obtained using aneroid blood pressure de
in clinical practice are concurTent, predictive, and pre
vices can easily be compared with values obtained
scriptive validity. Concurrent validity is when a mea
using mercury manometers. Values obtained using ei
surement accurately reflects measurements made with
ther palpation or a heart rate monitor can be compared
an accepted standard. Comparing bioelectrical imped
with values obtained from BCG recordings. The mer
ance measurements for estimating percent body fat
cury manometer and the electrocardiograph (BCG)
with estimates made from hydrostatic weighing is an
would be considered the standard method of measure
example of determ.ining conCUITent validity. In this ex
ment. Other devices, such as cycle ergometers, are
ample, hydrostatic weighing would be considered the
more difficult to calibrate, and the usual approach is to
"gold" or accepted standard. Measurements with pre
rely on the manufacturer's specifications as to the ac
dictive validity can be used to estimate the probability
curacy of the work rate readings.
of occurrence of a future event. Screening tests often
A third factor contributing to measurement vari
involve measurements that are used to predict future
ability is differences in the methods that therapists
events. For example, by identifying people with risk
use to make measurements. If a result is consistent
factors for coronary artery disease (CAD),
when one therapist repeats a measurement, then the
is made that the likelihood of developing CAD is
prediction
measurement is said to have high intrarater reliabil
higher than normal. Measurements with prescriptive
ity. Measurements that are consistent when multiple
validity provide a guide to the direction of treatment.
therapists perform the measurement under the same
The categorical measurement of determining a per
conditions are said to have high interrater reliability.
son's risk for a future coronary event is a measurement
Often, measurements have high interrater reliability,
that would need to have predictive validity. By classi
but lower intrarater reliability because therapists vary
fying patients into high vs. low risk categories based
in the specific methods of making the measurement.
on the results of a diagnostic exercise test, the inten
For example, a slight variation in the anatomical site
sity, and rate of progression of treatment is determined.
used for measuring skinfold thickness can produce
The accuracy of various types of exercise tests
relatively large differences in percent fat estimates
often is described by reporting sensitivity and speci
1971). Interrater relia
ficity. Sensitivity is the ability of a test to identify in
(Ruiz, Colley, and Hamilton,
bility is important in clinical settings where a patient
dividuals who are "positive," or who have the charac
may be evaluated and treated by more than one thera
teristic that is being measured. Specificity is the
pist. If the interrater reliability of a measurement is
ability of a test to identify individuals who are "nega
low, then changes in the patient over time may not be
tive," or who do not have the characteristic. If a test
accurately reflected.
produces a high number of "false positive" results,

then the sensitivity will be low. A false positive result
means that the test result was positive but the charac
Validity
teristic was absent. Young women often have posi
Valid measurements are those that provide meaningful
tive stress test results but do not have CAD. The con
information and that accurately reflect the characteris
sequence of a false positive test result could be
tic for which the measurement is intended. For a mea
unnecessary treatment. A high number of "false neg
surement to be useful in a clinical setting, the measure
ative" results would produce a low specificity. A
121
false negative result would be a negative test result,
measurement, subjective measurements usually have
even though the disease or characteristic is present.
lower interrater reliability compared to objective mea
The consequence of a false negative test result is not
surements (Rothstein and Echtemach, 1993).

Objective measurements are not affected by the per
receiving treatment when it is indicated.
son performing the measurement, that is, these mea

surements do not involve judgement of the measurer.
Objective and Subjective Measurements
Heart rate measured by a computerized ECG system is
Measurements vary in degree of subjectivity vs. objec
an example of an objective measurement. Other exam
tivity. Subjective measurements are those that are af
ples include measurement of blood pressure using an
fected in some way by the person taking the measure
intraarterial catheter or oxygen consumption using a
ment, that is, the measurer must make a judgment as to
metabolic system. Objective measurements are not nec
the value assigned. The assessment of a patient's
essarily accurate, but usually have high intelTater relia
breath sounds is influenced by many factors including
bility (Rothstein, and Echtemach, 1993).
the therapist's choice of terminology for describing the
Most measurements cannot be classified as either
findings, their perception of normal breath sounds, and
objective or subjective. The quality of a measurement
their hearing acuity. The grading of functional skills
can be placed on a continuum based on the degree of
may be influenced by the therapist's interpretation of
reliability, as shown in Figure 6-\. The attribute or
what constitutes minimal vs. moderate assistance. Be
characteristic that is being measured also can be
cause of the influence of the person performing the
viewed as a subjective o r objective phenomena
Quality of the Measurement
Subjective
Objective
100
00
Phenomena Being
Measured
Objective
SO
Reliability Continuum
Subjective
o
100
SS
OS
FIGURE 6-1
Illustration of the relationship between the quality of a measurement as being subjective or

objective, and the phenomenon being measured. The scales indicate that the objectivity of a
measurement, or reliability, lies along a continuum. For example, a subjective phenomenon may be
measured subjectively (subjective sign [SS]) or objectively (objective sign [OS]). (From Rothstein
1M: On defining subjective and objective measurements. Phys Ther 69:577-579, 1989.)
122
PART II
(Rothstein, 1989). A subjective attribute such as pain
stage post-MI could provide information to formulate
can be measured in either a subjective manner with a
an exercise prescription. However, the risks of per
low degree of reliability, or in an objective manner
forming this procedure at this time in the recovery
with a high degree of reliability.
period may outweigh the benefits.
SELECTING MEASUREMENTS
PERFORMING MEASUREMENTS
At the initial session with a client, how do therapists
When performing mcasurements, care must be
decide on the measurements to be performed? And
taken to use procedures that can be replicated for
what additional measurements need to be peltormed
future comparisons. Time must be taken to ensure
during the course of treatment and at follow-up evalu
that conditions are optimal and that the patient is
ations? Many factors influence the choice of the thera
informed of his or her part in the activity. For ex
pist, including information obtained from the medical
ample, measuring blood pressure in a noisy treat
record and the patient interview, and knowledge of
ment area immediately when the patient arrives for
available treatment options. Therapists also must
an appointment may not provide an accurate mea
strive for efficiency and not repeat tests that have been
surement of resting or baseline bJood pressure.
performed by other health care professionals. Charac
Documenting the conditions in which a measure
teristics or qualities of measurements, such as reliabil
ment was made also is important. Conditions may
ity and validity also influence the therapist's decision.
include, but are not limited to, time of day, room
Medical and personal information about the client

will be a plimary factor guiding the selection of mea
temperature, recent activities performed by the pa

tient, and type of measuring device.
surements. For example, appropriate measurements
Measurements should be made with an objective
differ for a patient with an acute MI vs. a patient who
and open mind, that is, without anticipating the result of
is 3 weeks post-MI. Other factors to consider include
the measurement. A measurement that is approached
the size of the infarction and associated complications
with a preconceived idea of the outcome may be af
such as an-hythmias, heart failure, or angina. Informa
fected by the therapist's expectations. Having confi
tion collected during the patient interview also may
dence in the results of one's measurements is impor
guide the selection. For example, for patients who dis
tant, and is developed as clinical skills are developed.
play anxiety when walking on a treadmill is discussed,
In clinics where more than one therapist is likely
another mode of exercise may be more appropriate.
to evaluate or treat a patient, written procedures for
Measurements need to be selected that are appropriate
performing measurements are needed. Therapists also
to the specific pathology, the severity of the condition,
need to review the written procedures on a regular
and other characteristics unique to the patient.
basis and practice performing the measurements as a
Another important factor to consider in selecting
group. Practicing together is especially important for
measurements is the application of the information.
therapists who are new to the clinic. The interrater re
Every measurement should contribute to the deci
liability for commonly used measurements then can
sions made by the therapist on the course and pro
be determined. If the reliability is low, the written
gression of treatment. Measurements that do not con
procedures may need to be revised to assure optimal
tribute to the assessment of the patient result in an
consistency of measurement.
inefficient use of the therapist's time and add unnec

essary costs to medical care.
Another factor that i nf! uences the selection of
INTERPRETING MEASUREMENTS
measurements is the risk-benefit ratio. How do risks
Interpreting the results of measurements often is a
of conducting a test or measurement relate to the
difficult task. Usually patients' problems are under
value of the information gained? Subjecting a patient
stood not by reviewing the results of a single mea
to a symptom-limited exercise test during the acute
surement, but by viewing the relationships between
the results of several measurements. For example,
123
and viewed in the context of the patient's personal
the finding that blood pressure does not increase
goals. Therapists develop a picture of the severity of the
with activity by itself may not be considered abnor
cardiopulmonary condition, the stage of recovery, and
mal, if the activity level is low and the patient is tak
the presence of coexisting conditions. A treatment plan
ing a beta receptor antagonist medication. The find
is developed based on the composite of findings. The
ing of no increase in blood pressure with signs and
plan is implemented and is continuously checked for
symptoms of exercise intolerance during moderate
appropriate direction by measurements made during
level activity in another patient may be indicative of
treatment sessions. Because of the progressive nature of

many of the conditions that affect the cardiovascular
inadequate cardiac output.

A knowledge of what is "normal" is important to
be able to interpret the results of tests. For some mea
and pulmonary systems, each treatment session can be

viewed as a reassessment.
surements, normal values are well-defined. Measure

ments of resting blood pressure, cholesterol, and
blood glucose have defined categories of normal,
PURPOSES OF DOCUMENTATION
borderline, and elevated. For other measurements,
To be useful, measurements need to be recorded or
population normative standards are not well-defined.
documented in a concise and organized manner.
For example, what is the normal increase in heart rate
Measurements that remain in the mind of the evalua
when walking at 3.5 mph on a level surt'ace? Values
tor often are forgotten or not remembered accurately.
for individuals differ, depending on age, medications,
Documentation is becoming more important to assist
fitness level, and walking efficiency. Results need to
and to maximize reimbursement, as well as to facili
be interpreted by considering these factors and patho
tate efficiency of care through communication be
logical conditions if present. Each individual has
tween health care professionals.
their own "normal" or usual response, and variations
Documentation includes information about evalua

tive findings, the assessment of the patient's condi
from this value could be considered abnormal.

Interpreting the results of tests is similar to putting
the pieces of a puzzle together to create a picture of
the patient and their limitations. Information is col
tion, and the plan for future care. Reasons for docu
mentation include the following:
I. To provide information for other therapists, as
lected from several sources, including the medical
sistants, or aides who may evaluate and/or treat
record, patient interview and physical therapy evalua
the client.
tion. Measurements performed and interpreted by

other health care professionals can be obtained from
2. To provide data for comparison for follow-up
visits.
the medical record and include chest x-ray, blood
3. To provide data to determine treatment effec
analyses, and echocardiography. During an interview,
tiveness and efficiency through collection of in
the patient reports information about his cunent and
formation on the results or outcomes of various
past medical problems. It is important to be sensitive

to the patient's feelings about his condition, noting
types of care.
4. To assist therapists in organizing findings to fa
his stage of emotional recovery. Detecting attitudes
cilitate logical decisions on the treatment ap
related to changing lifestyle habits also is important.
proach and overall care plan.
After the interview, the therapist should have a sense

of the patient as a person and begin to plan a strategy
for optimizing his or her physical function.
Measurements made during the physical examina
TYPES OF DOCUMENTATION
Systems for documenting information vary between
tion may include physiological responses to activity,
facilities. In acute care hospitals, physical therapy
breathing patterns, ventilatory capacity, and breath
notes may be included as a part of the patient's
sounds. The results of these measurements are inte
comprehensive medical record. In other facilities
grated with results collected during the chart review
such as private practice clinics the patient's record
124
PART II
may consist of physical therapy notes and medical
ambulation," and "abnormal tone." Written definitions
information that is relative to the physical therapy
of commonly used terms that include examples of
care plan. Whatever the system, notes can be classi
characteristics that illustrate the definition can help to
fied according to the timing and purpose of the doc
decrease confusion.
umentation, using the following categories:
Notes also need to clearly demonstrate the need
I. Initial evaluation, assessment, and plan
for professional skills if a physical therapist is per
2. Interim or progress notes
forming the evaluation and/or treatment. Activities
3. Discharge notes
that can be performed by physical therapists assis
4. Follow-up or reevaluation notes
tants, aides, nursing personnel or family members
The initial note usually is the longest, containing in
need to be delegated to the appropriate individual. In
formation on the reason for referral, other medical
addition, patients can be instructed in those activities
conditions and information that could affect physical
in which they can pelform independently.
therapy management, data collected during the pa
Another time in which documentation is essential
tient interview and physical examination, an assess
is when an unusual or adverse event occurs. For ex
ment or interpretation of the findings and the care
ample, abnormal responses to activity that may ap
plan. Interim or progress notes record short-term
pear relatively benign are important to record. Abnor
changes in the patient's status, and typically are writ
mal responses may include dizziness, anginal or
ten on a daily or weekly basis. The discharge note
musculoskeletal pain, or arrhythmias. An unusually
records the specific outcomes of treatment, the plan
high or low heart rate or blood pressure response also
for discharge, including home program, and the plan
should be noted. Combined with findings noted by
for follow-up. At follow-up visits, a note is written to
the patient or other health care professionals, these
assess changes since the time of discharge and plans
results may indicate significant changes in the pa
for additional treatment.
tient's cardiopulmonary status.

The organization of documentation varies be
tween facilities. Many facilities use the SOAP (sub
GENERAL GUIDELINES FOR CONTENT
jective, objective, assessment, plan) format (Ketten
AND ORGANIZATION
bach, 1990). Other facilities have modified this
Writing notes in a clear and concise format is impor
format, with the same information organized in a dif
tant so that information is conveyed accurately. Exam
ferent w a y . The following section presents an
ples of unclear notes are ones in which the handwriting
overview of relevant subjective and objective infor
is illegible, or that contain vague statements that could
mation, and a description of items to include in the
be interpreted in more than one way. Concise notes are
assessment and plan.
more likely to be read by other health care profession

als. In most clinicians' schedules, time is not available
to read through extensive information about a patient
Subjective Information
that may not be relevant. A concise note only includes
Subjective information contains a degree of judge
essential infOImation in a writing style that is clear and
ment or interpretation by the person reporting the in
does not include unnecessary phrases. Another impor
formation. The patient and family's perceptions of
tant rule is to use only standard or accepted abbrevia
their cardiac or pulmonary condition are considered
tions. Facilities have lists of approved abbreviations
subjective information. In the initial note, descrip
for that facility. The list should be available to those
tions of pain or discomfort that may be associated
who write, read, and review records. Within a physical
with either a cardiac event or a pulmonary complica
therapy department, common terms need to be clearly
tion are important to include. Some of the informa
defined and used in a consistent manner by all staff.
tion reported by the patient may be objective, such as
Terms that often generate confusion and carry multiple
blood cholesterol levels, resting blood pressure val
meanings include "minimally assisted," "functional
ues or number of cigarettes smoked per day.
125
In the interim note, it is impoltant to record the pa
The description of the evaluation and treatment
tient's responses to treatment including feelings of
results needs to include specific information on the
angina, dyspnea, or fatigue. Whether a prescribed home
activity, or exercise stress, and on the physiological
or ward activity program is performed and the patient's
responses. Components of the activity description in
subjective responses to the program also are important
clude the following:
to note. Any reported changes in the ability to function

either at home or in the community are important to
record. The most impoltant subjective finding to report
in the discharge note is whether the patient believes
I. Mode of activity (corridor or track walking,
lower extremity cycling)

2. Work level or rate (mph, percent grade, esti
mated resting metabolic rate level)

3. Duration of activity at each work level
personal treatment goals were achieved.
The description of the activities should be written

clearly so that the workload can be reproduced. The
Objective Information
responses to activity include changes in heart rate and
Measurable or observable information that is col
rhythm, blood pressure, respiratory rate, oxygen satu
lected during the interview, evaluation, and treat
ration levels, and heart and breath sounds as com
ment is considered objective. Information from the
pared with from preactivity to either during or imme
medical record may be included if it is relevant to
diately after activity. Signs of exercise intolerance,
the patient's current condition. To be relevant, the
such as changes in skin color, incoordination, and
information should have potential impact on the di
sweating, also need to be documented. Whether the
rection of the evaluation and treatment of the patient,
patient used oxygen during treatment, or required
such as current medications and results of diagnostic
physical assistance also should be noted. By objec
tests. Results uJ" tests and measurements conducted
tively recording the activity prescription and the
as a part of the initial evaluation are objective infor
physiological responses, therapists can estimate the
mation. A description of the treatment that is pro
patient's activity tolerance.
vided, and the patient's physiological responses to

treatment also are considered objective information.
When recording information collected during the
Assessment
evaluation, the results of various tests can be cate
The purpose of the assessment part of a note is to list
gorized as impairments or as functional limitations.
the client's major problem(s), identify treatment goals
An impairment is an abnormality of physiological
or outcomes, and provide an interpretation of the sub
function or anatomical structure at the tissue, organ
jective and objective findings. The problem list is lim
or body system level (Jette, 1994). Examples of im
ited to problems that can be addressed by physical
pairments include decreases in muscle strength or
therapy. Problems can be listed in order of priority
range of motion, or abnormal heart rate and blood
and stated in functional terms. For example, stating
pressure values. A functional limitation is a restric
"patient unable to c1imb stairs because of abnormal
tion in performance at the level of the whole person
ECG responses and dizziness," rather than stating
(Jette, 1994). Functional Ii mi tations can be attrib
"abnormal ECG response during activity."
uted to physical, social, cognitive, or emotional fac
Goals are the outcomes to be achieved by paltici
tors. Examples of functional limitations include the
pating in a physical therapy program and are generated
inability to dress, transfer, ambul ate, or climb
by the therapist and patient in consultation. Goals are
stairs. Improvements in functional status usually
stated in functional terms as to what the patient will be
are of primary interest to patients and families and
able to do at discharge. The following is an example:
to those who reimburse for health care. Measure

ments of impairments arc important, because they
Patient will be able to carry one 25-lb. bag a distance of 50
assist therapists in deciphering the causes or rea
feet with appropriate heart rate and rhythm responses,
sons for limitations in function.
within 2 weeks.
126
PART II
To be able to detennine if a goal has been met, the ther
mation from records can be organized into sections
apist must be able to observe or to measure the activity.
describing subjective and objective information, as
Therapists also estimate the time that it will take to
sessment or interpretation of the findings, and the
achieve the outcome. In the discharge note, whether
care plan. Subjective and objective information is
each goal has been met is stated. If a goal has not been
collected during an interview, medical record review,
achieved, then a reason or explanation is provided.
and evaluation and/or treatment session. The assess
The assessment also includes a brief interpretation
ment provides an interpretation of the subjective and
of the subjective and objective findings. Therapists
objective findings, and states the desired treatment
can use this section to state their "clinical hypothe
outcomes. A specific plan to achieve the outcomes
sis," or explanation of the primary problem that pro
then is described. Documentation can be viewed as a
duces the objective and subjective findings. The ini
way to assist therapists to organize their findings, re
t i a l n o t e m a y i n c l u d e statemen t s
flect on the significance of the findings, and generate
about the
individual's potential t o succeed i n a rehabilitation
an efficient and comprehensive care plan.
program, or reasons for not performing tests that

would typically be performed with individuals with
similar diagnoses. Whether the patient needs to be re
ferred to other health care professionals or to commu
REVIEW QUESTIONS
l. Describe and give examples of nominal, ordinal,
nity services also can be included.
ratio and interval measurements.

2. Identify three factors that contribute to the vari
ability of measurements.
Plan
3. Define sensitivity and specificity of tests.
The plan provides a description of the approach that
4. Differentiate between objective and subjective
will be taken to assist the patient in achieving the

stated goals. The plan may include a description of
measurements.
S. Identify four purposes for documenting the re
treatment that can be provided, education for the pa
sults of evaluation and treatment sessions.
tient and/or family, and referrals to other services.

Descriptions of home or ward programs should be in
cluded in the plan. At discharge from an inpatient
unit, the plan includes where the patient will be resid
ing and plans for follow-up. At discharge from an
outpatient facility, the plan contains recommenda
tions for follow-up care.
References
Hurst, J.W.
(J 990). The recognition and treatment of four types of
angina pectoris and angina equivalents. In Hurst, J.W., Schlant,

R.C., Rackley, C.E., Sonnonblick, E.H.,
& Wenger, N.K.
(Eds.). The hean Oth ed.). New York: McGraw-HilI.

Jelle, A . M. (1994). Physical disablement concepts for physical
therapy research and practice. Physical Therapy
74, 380-386.
Keuenbach, G. (J990). Writing S.O.A.P. notes. Philadelphia: FA Davis.
SUMMARY
Kusher, R.F.
Measurement and documentation are important com

ponents of the process of providing patient care.
Therapists select measurements because they reveal
information about patient characteristics that is
needed to determine appropriate directions for treat
ment. Performing measurements in a consistent way
allows comparison of patient characteristics at varied
points in time. The recording, or documentation, of
the results of measurements and other information
about the patient serves as a legal record. Although
& Schoeller, D.A. (J986). Estimation of total body
water by bioelecu'ical impedance analysis. American Journal of

Clinical Nutrition.
44, 417-424.
& Fox, S.M. (1978).
Pollock, M.L., Wilmore, J.H.,
Health and it
f
ness through physical activity. New York: John Wiley and Sons.
1.M. (J989). On defining subjective and objective mea

69, 577-579.
Rothstein, J .M .. & Echternach, J. L. (1993). Primer on measure
Rothstein,
surements. Physical Therapy
ment: An introductory guide to measuremelll issues. Alexan
V A: American Physical Therapy Association.

& Colley, J.R.T. & Hamilton, P.J.S. (1971). Measurement of
triceps skin fold thickness: An investigation of sources of variation.
British Joul11al of Preventive and Social Medicine 25, 165-167.
dria,
Ruiz, L.,
documentation formats vary between facilities, infor
History
Willy E. Hammon
KEY TERMS
Cough
History
Dyspnea
Pain
INTRODUCTION
words and pace (Hurst, et ai,
1990). If the therapist ap
The value of the history depends in large part on the
pears hurried, distracted, preoccupied, irritated, or un
skill of the interviewer. When eliciting the history
caring; is often interrupted; or fails to be an attentive lis
from a patient, therapists must be alert to recognize
tener, the patient-therapist relationship will likely suffer.
the symptoms that are indicative of cardiac and pul
The interviewer must be careful not to allow per
monary disease. This information is then used in the
sonal feelings about the patient's grooming, appear
decision-making process to select the most appropri
ance, demeanor, and behavior during the interview to
ate intervention for the individual.
unduly question the validity of the chief complaints

(Birdwell,
1993). By the time the patient is referred
for physical therapy, he or she may have seen one or
THE INTERVIEW
more physicians, have been subjected to a number of
Obtaining a thorough and accurate patient history is
noninvasive or invasive studies, or have been pre
truly an art. One imponant goal of histOlY taking is to
scribed oral or inhaled medications with variable or
establish a good patient-therapist rapport. The patient
unsatisfactory alleviation of symptoms. The patient is
must be allowed to explain the history in his or her own
likely to manifest a degree of anxiety and frustration.

127
128
PART n
Therefore the therapist's approach, history-taking and
2. Whether the treatment order is narrow or
interviewing style is important for gaining the pa

tient's confidence and cooperation.
broad in scope.
3. The acuteness of the patient's illness, level of
The patient history interview can be divided into
consciousness, and his ability to provide ac
the data-gathering and interpretative sections (Snider,
curate information.
1994). The data-gathering segment begins with ask
This chapter presents a comprehensive approach to
ing why the patient has sought medical attention and
history taking. Therapists may find part or all of this
has been referred for physical therapy services. In
information applicable, depending on their particular
other words, what is the patient's chief complaint
circumstances.
the symptom that caused the patient to seek help?

Each chief complaint should be carefully ex
plored. Supplementary questions should be nonlead
QUESTIONNAIRES
ing, using words the patient can easily understand.
Printed symptom or medical questionnaires can be ben
This allows the interviewer to determine the signifi
eficial or detrimental to the patient-therapist relation
cance of the complaint. An in-depth knowledge of
ship, depending on how they are used. Questionnaires
cardiopulmonary pathophysiology allows the thera
can expedite the data-gathering portion of the initial
pist to almost simultaneously gather data about the
visit by allowing the patient to note in advance, all
patient's symptoms and to interpret the likely type of
symptoms, medical conditions, surgeries, occupalions,
cardiopulmonary dysfunction that exists. This in turn
medications, and other factors that may influence phys
serves as a basis for the therapist to begin to select
ical therapy intervention. They can reduce the amount
the appropriate assessment and treatment modalities
of nontreatment time therapists may otherwise spend
for the individual.
inquiring about irrelevant symptoms and conditions.
It is important to remember that patient satisfaction
Pri nted questionnaires also allow patients sufficient
is greatest if the patient is allowed to fully express
time to recall relevant informalion and respond more
major concerns without interrupting. In addition, the
accurately than they often do in an interview selting
risk of missing what is really of greatest concern to the
(Miller, 1980). Used in this way, a printed question
patient is reduced if the patient is allowed sufficient
naire can be a valuable tool for expediting a compre
time to describe it in his or her own words. Studies
hensive evaluation of cardiopulmonary patients.
have shown this usually only takes from I to 3 minutes.
However, if questionnaires are used improperly,
The patient's view of what is the problem and his or
they can depersonalize the history-taking portion of
her suggestions for addressing the problem should be in
the initial visit (Hurst, et ai, 1990). If the therapist al
cluded in the interview. Patient satisfaction is improved
lows the printed form to become a substitute for in
by his or her involvement in the interview as well as
teraction with the patient, patient satisfaction will be
later in the establishment of short- and long-term goals.
low and the patient-therapist relationship will suffer.
The depth of the history taken by the physical ther

apist (PT) can vary according to the following factors:
1. Whether the individual is an inpatient or an
DYSPNEA
out patient. Many inpatients have detailed
Dyspnea, breathlessness or shortness of breath, can be
medical records available for the therapist to re
defined as the sensation of difficullY in breathing
view. This significantly reduces the amount of
(George, 1990). It is one of the most common reasons
information the therapist needs to obtain from
that patients seek medical attention. Dyspnea is difficult
the patient during an interview. If the informa
to quantitate, because it is subjective and at times is
tion in the chart is scant, or if the individual is
normal (i.e., at high altitudes, and during or following
an outpatient with only a treatment referral and
vigorous exercise). Dyspnea is a symptom of cardiac
little or no medical records available, the thera
and pulmonary diseases, as well as other conditions.
pist should obtain a more detailed history.
When a patient complains of shortness of breath or
MITOCHONDRIA
MUSCULOSKELETAL
CARDIOVASCULAR
History
RESPIRATORY
129
AIR
FIGURE 7-1
Schematic illustration of the oxygen transport system, which involves the interaction between the
respiratory, cardiovascular, and musculoskeletal systems. (Reprinted with permission from Mahler
D: Dyspnea: diagnosis and management. Clirz Chest Med 8 [2),215-230,1987.)
breathlessness, it should be noted that this complaint
in the work of breathing, and (3) an abnormality in the
is often unrelated to the patient's arterial oxygen
ventilatory system itself (George, 1990).
level (Pao2). Many times, it appears that altered me
An increased awareness of normal breathing is
chanical factors during breathing contribute to the
usually related to anxiety (Miller, 1980). The patient
sensation of breathlessness (Mahler, 1987). Numer
commonly complains of "not getting a deep enough
ous receptors that have a role in sensing dyspnea
breath," a feeling of "smothering," or "not getting air
have been identified and include vagal receptors
down in the right places" (Szidan and Fishman,
(e.g., irritant, stretch, and J-receptors), chemorecep
1988). These sensations have been designated as psy
tors, proprioceptive receptors (tendon organs, muscle
chogenic dyspnea. The patient's breathing pattern is
spindles, joint and/or skin receptors), and upper air
irregular, with frequent sighs. When severe, it is asso
way receptors (Snider, 1994).
ciated with tingling of the hands and feet, circumoral
Analyzing the oxygen transpOit system (Figure 7-1)
numbness, and lightheadedness. Coaching the patient
can help the therapist deterrrune the likely cause of each
to hyperventilate and to reproduce the symptoms may
patient's dyspnea and the most appropriate physical
help the patient better understand the cause of these
therapy intervention. The delivery of oxygen from am
symptoms and how to control them (Miller, 1980).
bient air to the mitochondrion within the cell depends
The hyperventilation syndrome is properly diagnosed
on the intact interaction of the respiratory, cardiovascu
only after organic causes have been excluded and
lar, and muscular systems. Also, carbOn dioxide (C02)
pulmonary function tests indicate normal respiratory
is eliminated in the opposite direction. Dyspnea can be
mechanics and Pao2.

The second cause of dyspnea is an increase in the
caused by dysfunction in any of the systems.

Dyspnea commonly occurs when the body's re
work of breathing. Greater inspiratory pressures must
quirement for breathing (ventilation) exceeds the
be generated by the respiratory muscles to move air in
body's capacity to provide (Snider, 1994). In other
and out of the lungs when the mechanical properties
words, the symptom varies directly with the body's
of the lungs have changed. This may be related to an
demand for ventilation and inversely with ventila
increase in lung water resulting from cardiac disease
tory capacity.
or the high cardiac output of anemia. A loss of com
There are three basic causes of dyspnea: (I) an in
pliance (increased lung stiffness) because of diffuse
creased awareness of normal breathing, (2) an increase
inflammatory or fibrotic lung disease often causes
130
PART II
shortness of breath. Small or large airways obstruction
I. Are you short of breath at rest? If the answer
as a result of bronchoconstriction, sputum, inflamma
is yes, it suggests a severe physiological dys
tion, and other effects commonly produces dyspnea.
function. The patient likely needs prompt eval
The third cause of dyspnea is an abnormality in
uation by a physician if this is of recent onset
the ventilatory apparatus or pump. The ventilatory

apparatus consists of the thoracic cage, respiratory
and has not had a medical workup.
2. Do you have chest pain'? If so what part of
muscles, and nerves. Any of these may become dys
your chest? Unilateral localized chest pain
functional. Thoracic cage abnormalities include
raises the possibility of spontaneous pneumoth
kyphoscoliosis, extreme obesity, and large pleural ef
orax, pulmonary embolism, or chest trauma.
fusions. Diseases of the respiratory muscles include
3. What were you doing immediately before or
polymyositis and muscular dystrophy. Neurologic ab
at the time of onset of shortness of breath?
normalities include spinal cord injuries, phrenic nerve
Approximately 75% of spontaneous pneumotho
injuries, brachial plexus neuropathy, ascending
races occur during sedentary activity, 20% dur
polyneuritis (GuiJlain-Barre syndrome), myasthenia
ing some strenuous activity, and 5% are related
gravis, amyotrophic lateral sclerosis, poliomyelitis,
to coughing or sneezing. A history of immobi
neurotoxins, and exposure to paralytic agents.
lization of a lower extremity, recent surgery, bed
The time course of the appearance and progression
rest, travel requiring prolonged sitting, obesity,
of dyspnea should be identified (Sharf, 1989). Acute
CHF, venous disease of the lower extremities,
dyspnea is common in pulmonary embolism, pneu
are all risk factors for pulmonary embolism. If
mothorax, acute asthma, pulmonary congestion related
the patient's symptoms are related to chest
to congestive heart failure (CHF), pneumonia, and
trauma, the fact that a fall, a blow, or an accident

occurred can usually be quickly established.
upper airways obstruction. Most of these conditions re

quire immediate physician evaluation of the acute
4. Do you have any major medical or surgical
problem before physical therapy inlervention. Suba
conditions? Cystic fibrosis, chronic obstructive
cute or chronic progression of dyspnea generally pre
pulmonary disease (COPD), interstitial lung
sents as increasingly severe dyspnea with exertion over
disease, and malignancies are important causes
time. It occurs with emphysema, restrictive lung disor
of secondary spontaneous pneumothorax.
ders such as pulmonary fibrosis, chest wall deformi
If the therapist strongly suspects pneumothorax or
ties, respiratory muscle dysfunction, occupational lung
pulmonary emboli because of the history and physi
diseases, chronic CHF, or large pleural effusions.
cal assessment, the patient should be referred for im
Dyspnea may also be related to body position.
mediate medical evaluation.
Therefore when evaluating dyspnea, the patient

should be asked if he or she has difficulty breathing
when reclining horizontally. Is it necessary to be
Dyspnea on Exertion
propped up on several pillows to sleep at night (or
Dyspnea on exertion is a common complaint of pa
thopnea)? Does she have more difficulty breathing
tients with cardiopulmonary dysfunction. Dyspnea
when reclining on one side (trepopnea)? Does he ever
during exercise or exertion usually precedes dyspnea
wake up at night short of breath, and need to sit up or
at rest (Wasserman, 1982). It most often is a result of
walk around the room to "catch his breath" (paroxys
chronic pulmonary disease or CHF. Some causes of

dyspnea during exertion or exercise are listed in
mal nocturnal dyspnea)?
Table 7-1.
It is important to establish the amount of activity re
Acute Dyspnea
quired to produce dyspnea. Various scales (Borg, 1982;
The patient that has acute dyspnea requires a rapid and
Mahler and Harver, 1990) have been developed to cate
thorough history and physical assessment. The thera
gorize the level of dyspnea and impairment present in
pist should ask several important questions to address
patients (Figures 7-2, 7-3 and Table 7-2). The patient
the possible causes of acute dyspnea (Mahler, 1987):
should be asked about daily activity, and what activities
History
131
TABLE 7-1
Disorders Limiting Exercise Performance, Pathophysiology, and Discriminating Measurements*
DISORDERS
PATHOPHYSIOLOG Y
MEASUREMENTS THAT
DEVIATE FROM NORMAL
Mechanical limitation to ventilation
VE maxlMVV, expiratory flow pattern, VDNT;
Pulmonary
Airflow limitation
mismatching of VA/Q, hypoxic
V02 max, VEiVo2 VE response to hyperoxia,
stimulation to breathing
(A-a)po2
Restrictive
Mismatching V A/Q, hypoxic stimulation
Chest wall
Mechanical limitation to ventilation
VE max/MVV, Paco2 V02 max
Pulmonary circulation
Rise in physiological dead space as
Vo/VT, work-rate-related hypoxemia V02 max,
to breathing
VENo2, (a-ET)pco2, Orpulse
fraction of VT, exercise hypoxemia
Cardiac
Coronary
Electrocardiogram (ECG), V02 max, anaerobic
Coronary insufficiency
threshold O2, VENo2 Orpulse, blood

pressure (BP) (systolic, diastolic, pulse)
Valvular
Cardiac output limitation (decreased
Myocardial
Cardiac output limitation (decreased
Anemia
Reduced O2 carrying capacity
02-pulse, anaerobic threshold Vo2, V02 max,
Inadequate O2 flow to metabolically
Anaerobic threshold V02, V02 max
Obesity
Increased work to move body;
effective stroke volume)

ejection fraction and stroke volume)
VEiVo2
active muscle
V02-work rate relationship, Pao2, Paco2,
Vo2max
if severe, respiratory restriction and

pulmonary insufficiency
Psychogenic
Hyperventilation with precisely regular
Breathing pattern, PC02
respiratory rate
Breathing pattern, PC02
Hyperventilation and hypoventilation
Malingering
with irregular respiratory rate

Deconditioning
02-pulse, anaerobic threshold Vo2, V02 max
Inactivity or prolonged bedrest; loss of

capability for effective redistribution of
systemic blood flow
*VA-alveolar ventilation; Q---pulmonary blood flow; MVV-max-imum voluntary ventilation; VoIV.-physiologic dead space/tidal
volume ratio;
Or- oxygen: V02-02
consumption; (A-a)P02-alveolar-arterial P02 difference; (a-ET)pco2-anerial-end tidal Peo2
difference. (Reprinted with permission from Wasserman
1982
K:
Dyspnea on exertion:
Is
it the heart or lungs?
lAMA 248: 2039-2043, 1982.
American Medical Association.)
produce breathlessness (Constant,
1993). Does the pa
cent onset of dyspnea is more characteristic of heart
tient become short of breath climbing a flight of stairs
failure than chronic lung disease, which has a longer,
or walking uphill? Is the patient able to walk and talk
insidious onset. Acute pulmonary problems such as
simultaneously? Does walking slower affect the indi
pneumothorax, atelectasis, pneumonia, and other

conditions superimposed on chronic lung disease can
vidual's dyspnea?
In addition, when the patient began to notice an in
crease in shortness of breath should be noted. A re
also explain a recent increase in symptoms.

Is wheezing present with the dyspnea on exertion?
132
PART II
TABLE 7-2
American Thoracic Society Dyspnea Scale
GRADE
I
2
DEGREE
None
Not troubled with breathlessness except with strenuous exercise
Slight
Troubled by shortness of breath when hurrying on the level or walking up a slight hill
Moderate
Walks slower than people of the same age on the level because of breathlessness or has to
Severe
Stops for breath after walking about
Very severe
Too breathless to leave the house or breathless when dressing or undressing
stop for breath when walking at own pace on the level
100 yards or after a few minutes on the level
Reprinted with permission from Brooks SM (Chairman): Task group on surveillance for respiratory hazards in the occupational setting.
Survei Ilance for respiratory hazards,
ATS News 12-16, 1982.
o
0.5
GREATEST BREATHLESSNESS
Nothing at all
Very, very slight (just noticeable)
Very slight
Slight
Moderate
Somewhat severe
Severe
6
7
Very severe
8
9
NO BREATHLESSNESS
10
Maximal
FIGURE 7-3
FIGURE 7-2
The visual analogue scale is a vertical line of
Very, very severe (almost maximal)
100 mm in
length. The patient is asked to make a mark along this line
The Borg category scale for rating breathlessness.

(Reprinted with permission from Borg G: Psychophysical
that represents his level of breathlessness. The distance of
bases of perceived exertion, Med Sci Sports Exerc 14,
the patient's mark above zero represents the measurement
377-381,1982.)
of dyspnea. (Reprinted with permission from Mahler D:

Dyspnea: diagnosis and management, Clin Chest Med
[2],215-230,1987.)
History
133
Has there been an associated weight gain? Does the
volume, the patient develops a rapid heart rate and a
patient have a positive smoking history and sputum
wide arteriovenous O2 difference (decreased capillary
production? If a positive response is received, these
P02) at an inappropriately low work rate. Therefore
suggest that COPD is the primary cause of symptoms
the exercising muscles (both skeletal and myocardial)
(Constant, 1993).
have increased difficulty getting an adequate oxygen
The basic defect that cardiac diseases produce dur
supply to perform the necessary work, which results
ing exertion is a limited cardiac output, primarily
in dyspnea, fatigue or pain. The lactic acidosis that
caused by a reduced stroke volume (Wasserman,
results from the low oxygen delivery to the muscles
1982). To compensate for the relatively low stroke
can be measured by either invasive or noninvasive
Functional and Therapeutic Classification of Patients with Heart Disease

Functional Classification
Class I
Patients with cardiac disease but without resulting limitations of physical activity; ordinary physical activity does not
l:ause undue fatigue, palpitation, dyspnea, or anginal pain.
Class II
Patients with cardial: disease resulting in slight limitation of physical activity; they are comfortable at res. Ordinary
physical activity results ill fatigue. palpitation, dyspnea, or anginal pain.
Class III
Patients with cardiac disease resulting in marked limitation of physical activity; they are comfortable at rest. Less
than ordinary physical activity causes fatigue, palpitation, dyspnea. or anginal pain.
Class IV
Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort; symptoms of
cardiac insufticiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken,
discomfort increases.
Therapeutic Classification
Class A
Patients with cardiac disease whose physical activity need not be restricted in any way.
Class B
Patients with cardiac disease whose ordinary physical activity need not be restricted but who should be advised
against severe or competitive efforts.
Class C
Patients with cardiac disease whose ordinary activities should be moderately restricted and whose more strenuous
efforts should be discontinued.
Class D
Patients with l:ardiac disease whose ordinary activity should be markedly restricted.
Class E
Patients with cardiac disease who should be at complete rest, confined to bed or chair.
Reprinted with permission from the New York Heart Association (1964). Diseases of the heart and blood vessels; Nomenclature alld crite'
ria for diagnosis. (6th ed.). Boston: Little, Brown.
134
PART II
gas-exchange methods during exercise testing. The
stenosis, it is probably related to an inadequate car
functional and therapeutic capacity of the patient with
diac output during exercise. Patients with tetralogy of
hean disease can be estimated based on the history
Fallot and other forms of cyanotic heart disease, ex
and symptoms (see box on p. 133).
perience both dyspnea and fatigue during exercise
Dyspnea in cardiac patients is usually related to

metabolic acidosis-induced hydrogen ion stimulus.
when the aJterial oxyhemoglobin saturation has fallen

appreciatively below the resting level.
Also, increased pressure in the right side of the heart

and pulmonary circulation during exertion may stim
ulate mechanoreceptors that increase ventilation and
induce dyspnea.
Orthopnea
Orthopnea is dyspnea brought on in the recumbent
Diseases that involve the lungs or thoracic cage
position (Hurst, 1990). The patient may state the need
generally prevent external respiration (ventilation)
for two or three pillows under the head to rest at
from keeping pace with internal respiration (in the
night. This symptom is commonly associated with
cells) (Wasserman, 1982). In other words, patients
CHF but may also be associated with severe chronic
outwalk or outrun their lungs during activities or ex
pulmonary disease.
ertion. The primary symptom that limits exercise in

pulmonary patients is dyspnea because of the diffi
culty they have eliminating CO2 produced by metab
Paroxysmal Nocturnal Dyspnea
olism. Some individuals such as those with pul
Paroxysmal nocturnal dyspnea (PND) is an impor
monary fibrosis and some with COPD do experience
tant type of shortness of breath. This symptom has
a decrease in P02 with exercise. Hence, dyspnea on
strong predictive value as a sign of CHF (Hurst, et
exertion in pulmonary patients is usually related to
ai, 1990). The patient usually falls asleep in the re
hypoxic or hypercapnic stimuli.
cumbent position, and 1 or 2 hours later, awakens

from sleep with acute shortness of breath. The pa
tient sits upright on the side of the bed or goes to an
Dyspnea in Cardiac Patients
open window to breathe "fresh air" to get relief from
The cause of dyspnea in cardiac patients depends on
shortness of breath.
whether an associated stiffness of the lungs (fall in
The mechanism of PND is the transfer of fluid
compliance) is also present (Szidan and Fishman,
from extravascular tissues into the bloodstream (or
1988). Dyspnea is the primary symptom of a decom
intravascularly) during sleep (Constant, 1993). The
pensating left ventricle (Marriott, 1993). As the ven
intravascular volume of fluid gradually increAses
tricle fails to eject the normal volume of blood, it pro
until the compromised left ventricle can no longer
duces chronic pulmonary venous hypertension,
manage it. The left atrial pressure rises when the rate
congestion, and pulmonary edema, resulting in stiff or
of lymphatic drainage from the lungs is unable to
less compliant lungs. This, along with modest hypox
keep up with the increased volume of tluid. The in
emia that augments the respiratory drive, increases
creased atrial pressure leads to a sufficiently elevated
ventilation and the work of breathing. Tachypnea is
pulmonary capillary pressure to produce interstitial
often seen at rest. Exercise exaggerates the pulmonary
edema. Patients who are light sleepers awaken early
congestion and edema, promotes arterial and mixed
with dyspnea. Deep sleepers may not awaken until
venous hypoxemia, which also increases the amount
they develop alveolar edema.
of dyspnea and tachypnea manifested. Fatigue, result
Classic PND cannot usually be eliminated by only
ing from low cardiac output, also affects the respira
elevating the trunk without lowering the legs. The pa
tory muscles, further increasing the sensation of
tient must pool blood in the extravascular tissues of
breathlessness.
the legs to get adequate relief, which usually takes at
Dyspnea in cardiac patients without stiff lungs is

primarily seen during exertion or exercise (Szidan,
least 30 minutes. This is why the patient must sit up

or stand up, and ambulate.
and Fishman, 1988). In uncomplicated pulmonic
The patient should be asked about the amount of
History
135
40, is
1990). When
exercise or work performed during the day before an
symptom, if first reported in patients over age
attack on PND. A true left ventricular failure episode
often related to heart failure (Hurst, et aI,
of PND is more likely to occur after a day of unusual
confilmed that the wheezing is because of heart dis
exertion, which has caused an increased amount of
ease, the patient is said to have cardiac asthma.
extravascular fluid to accumulate in the legs. If the
Wheezing in cardiac patients is a manifestation of nar
patient is participating in an exercise or rehabilitation
rowed airways and thickened bronchial walls as a re
program, the level of exercise may need to be re
sult of pulmonary edema (Szidan, and Fishman,
duced to prevent PND.
1988). However, if patients have a history of episodes

of wheezing and dyspnea since childhood, COPD, or
asthma is the likely cause. Other pulmonary condi
Platypnea
tions such as eosinophilic pneumonia, bronchopul
Platypnea is the onset of dyspnea when assuming the
monary aspergillosis, allergic granulomatosis, etc.,
sitting position from the supine position (Sharf,
can cause wheezing (Miller,
1989). This unusual phenomenon is often found in
differentiated from stridor, which is commonly caused
1980). Wheezing must be
patients with basilar pulmonary fibrosis or basilar ar
by laryngotracheal narrowing due to tracheostomy
teriovenous malformation. It can be related to the re
scar, trauma of intubation, laryngeal paralysis,
distribution of blood flow to the lung bases in the sit
epiglottitis, or tumors. Chronic pulmonary patients
ting position with resultant ventilation-perfusion
may also develop heart conditions, so it is good to re
mismatching and hypoxemia.
member patients that complain of wheezing may have

both cardiac and pulmonary disease.
Trepopnea
Trepopnea refers to dyspnea in one lateral position
COUGH
1994). It is often produced
Cough is a common symptom of pulmonary disease.
by unilateral respiratory system pathology such as
The cough mechanism consists of three phases:
lung disease, pleural effusion, or airway obstruction.
(1) an inspiratory phase, (2) a compressive phase, and

(3) an expiratory phase (Irwin, 1977).
but not the other (Snider,
It also is commonly seen in patients with mitral
1993). Occasionally it may be the
There are numerous cough irritant receptors lo
result of a fall in blood pressure in the left lateral de
cated on the mucosa of the larynx, trachea, bronchi,
cubitus position. If the patient has ischemic heart dis
pleura, and external auditory canal. These receptors
stenosis (Constant,
ease, the reduction in coronary perfusion can cause
are most sensitive at the glottis and carina, and di
either angina or dyspnea.
minish rapidly beyond the fourth generation bronchi.

A cough follows stimulation of these mucosal recep
tors by any of a number of factors including inflam
Functional Dyspnea
mation, sputum, foreign bodies, noxious gases or
Functional dyspnea is defined as shOltness of breath at
odors, chemical substances, endobronchial tumors,
1989). It is most
and extrabronchial pressure on the trachea or bronchi
rest but not during exertion (Shmf,
commonly seen in young women who complain of the
(Sharf,
1989).
need to take a deep breath or to sigh and interpret this
A productive cough is beneficial for clearing the
sensation as shortness of breath. The physical exami
airways of sputum and foreign material, and gener
nation and pulmonary function tests are negative. Re
ally should not be inhibited. However, a dry, hacking
assurance is usually all that is necessary.
cough is usually of no value and can have a self

perpetuating irritant effect on the respiratory mucosa.
A dry cough may be the initial symptom of certain
WHEEZING
interstitial lung diseases such as allergic alveoli tis,
Patients that complain of wheezing associated with
sarcoidosis, and pulmonary fibrosis. Some causes and
dyspnea may have pulmonary or cardiac disease. This
characteristics of coughs are listed in Table
7-3.
136
PART II
TABLE 7-3
Some Causes and Chnracteristics of Coughs
CAUSE
CHARACTERISTICS
Acute infection of lungs

Tracheobronchitis
Cough associated with sore throat, running nose, and eyes
Lobar pneumonia
Cough often preceded by symptoms of upper respiratory infection; cough dry,
Bronchopneumonia
Usually begins as acute bronchitis; dry or productive cough
Mycoplasma and viral pneumonia
Paroxysmal cough, productive of mucoid or blood-stained sputum associated
Exacerbation of chronic bronchitis
Cough productive of mucoid sputum becomes purulent
painful at first; later becomes productive
with influenza-like syndrome
Chronic infections of lungs

Bronchitis
Cough productive of sputum on most days for more than 3 consecutive months
and for more than 2 successive years; sputum mucoid until acute exacerbation,
when it becomes mucopurulent
Bronchiectasis
Cough copious, foul, purulent, often since childhood; forms layer on standing
Tuberculosis or fungus
Persistent cough for weeks to months often with blood-tingling of sputum
Parenchymal inflammatory processes
J nterstitial fibrosis and infiltrations
Cough nonproductive, persistent, depends on etiologic factors
Smoking
Cough usually associated with injected pharynx; persistent, most marked

in morning, usually only slightly productive unless succeeded by chronic
bronchitis
Tumors
Bronchogenic carcinoma
Nonproductive to productive cough for weeks to months; recurrent small
Alveolar cell carcinoma
Cough similar to bronchogenic carcinoma, except in occasional instance when
Benign tumors in airways
Cough nonproductive, occasionally hemoptysis
Mediastinal tumors
Cough, often with breathlessness, caused by compression of trachea and bronchi
Aortic aneurysm
Brassy cough
hemoptysis common
large quantities of watery, mucoid sputum are produced
Foreign body
Immediate, while still in upper airway
Cough associated with progressive evidence of asphyxiation
Later, when lodged in lower airway
Nonproductive cough, persistent, associated with localizing wheeze
Cardiovascular
Left venuicular failure
Cough intensifies while supine along with aggravation of dyspnea
Pulmonary infarction
Cough associated with hemoptysis, usually with pleural effusion
Reprinted with permission from Szidon J, Fishman A: Approach to the pulmonary patient with respiratory signs and symptoms. In Fishman
A, editor: Pulmol1{//y diseases alld disorders. New York, 1988, McGraw-Hill.
History
137
Cough may be the only presenting symptom of
deep breathing suggests asthma or interstitial lung
asthma. In asthmatics, cough is precipitated by inhal
disease. Allergens or irritant fumes at home or at
ing cold air or exercise, and is dry. Cough can precip
work may be a cause of cough. Postviral cough may
itate an asthma attack in sensitive patients and is
be present for weeks following a viral illness.
known as cough-induced bronchospasm.
Some medications can elicit coughing. Beta
It is important to determine the length of time
blockers prescribed to treat hypertension, migraine
cough has been present (Sharf, 1989). The most com
headaches, cardiovascular disease (CVD), or glau
mon cause of an acute cough is a viral respiratory in
coma may precipitate asthma. Many drugs, including
fection, which generally resolves within a few days
chemotherapeutic agents, can cause interstitial lung
or 2 to 3 weeks. Exposure to noxious gases also pre
disease and coughing.
cipitates acute coughing.
Cough and wheezing may result from COPD,
A cough that has persisted for more than 3 weeks
asthma, or early left heart failure. Early left heart fail
can be termed chronic (Snider, 1994). The most com
ure predisposes the patient to respiratory infections
mon cause of chronic cough is chronic bronchitis,
and may be responsible for chronic bronchitis.
and is present in up to 30% of cigarette smokers. The

next most common cause is the postnasal discharge
syndrome. Patients describe a sensation of secretions
Cough Complications
dripping from the back of the nose into the throat,
One of the more common complications of cough is
prompting throat clearing or coughing.
syncope. Tussive or cough-induced syncope, which is
Various cardiac conditions may stimulate receptors
more common in men than women, can be recognized
in the bronchi and provoke coughing (Goldberger,
through accurate history taking (Miller, 1980). It is
1990). Because the bronchial veins empty into the
typically reported by middle-age men who "smoke
pulmonary veins (leading to the left side of the heart),
hard, eat hard, drink hard, and cough hard." They ex
systemic veins, and the superior vena cava (leading to
perience fainting or near-fainting following cough
the right side of the heart), venous congestion and
paroxysms. The cause is obscure but may be related to
coughing may occur with either right- or left-side
vagal-induced cardiac slowing or vasodilatation, or
CHF. It is more common, however, with left-sided
high intrathoracic pressures that impair venous return,
CHF. The onset of a cough in a patient with paroxys
decrease cardiac output, increase intracranial pressure,
mal tachycardia or acute myocardial infarction (MI) is
and result in a reduced cerebral blood flow. Cough
often an early symptom of acute left-side heart failure.
syncope is often resolved by smoking cessation.
Coughing may be caused by other cardiovascular
Complications of cough include headache, back
conditions such as a large left atrium displacing the
pain, muscular tears, hematomas, rib fractures (along
left main-stem bronchus upward, aortic aneurysms
the posterior axillary line), occasionally vertebral
placing pressure on the bronchi, or a double aortic
compression fractures (in osteopenic patients), urinary
arch compressing the trachea.
incontinence (UI) (in women), and inguinal hernias
A specific diagnosis can be made in 80% of cases
(in men) may occur (Braman and Corrao, 1987).
of chronic cough by an appropriate history alone

(Stulberg, j 985). Determining the precipitating
causes or the time of onset points the clinician to a
CHEST PAIN
probable diagnosis. For example, does the patient
Taking an accurate history is crucial to the proper
cough primarily at night? If so, it points to heart fail
evaluation of chest pain (Snider, j 994). Although the
ure, esophageal problems, bronchiectasis or asthma
definitive cause of chest pain cannot be fully estab
as the potential cause. An early morning cough is
lished without diagnostic medical tests, it is usually
more common in bronchitis and individuals with
possible to determine whether the pain originates in
postnasal drip. Cough following meals suggests
the pleura, chest wall, or thoracic organs by means of
esophageal disease. Cough precipitated by exertion or
careful history taking.
138
PART II
Chest pain can be divided into two basic types:
palpated at the wrist. If a patient opens and
chest wall pain and visceral pain (George, 1990). The
closes a fist, pain will gradually appear and es
first arises from involved thoracic cage structures and
calate in the forearm. The causal mechanism of
tends to be superficial and well-localized. The latter
this pain is the same as that of myocardial pain:
arises from the heart, pericardium, aorta, medi
continuing muscular contraction in the absence
astinum, bronchi, or esophagus. It is described as
of an adequate oxygen supply. This type of

pain requires several contractions of the my
deep and difficult to localize.
ocardium to reach its maximal intensity. In

other words, there is a characteristic buildup or
Pleuritic
escalation of angina pain.
Pleuritic chest pain originates from the parietal pleura
2. Can you point to the area of pain with one
or endothoracic fascia, but not the visceral pleura,
finger? Anginal pain is characteristically
which has no pain receptors. The patient can usually
demonstrated by patients using their entire
identify it as being close to the thoracic cage (Szidan,
hand or closed fist against the anterior chest
Fishman, 1988). Pleuritic chest pain worsens sharply
wall. It is described as a sign of angina, because
with inspiration as the inflamed parietal pleura is
it is so typical (Marriott, 1993). By contrast,
stretched with chest wall motion. Deep breathing,
any pain that can be localized by pointing with

a fingertip is unlikely to be angina.
coughing, or laughing are extremely painful, requir

ing the patient to apply pressure over the involved
3. Is the pain deep inside your chest or does it

seem as though it is close to the surface?
area to control the pain.

Pleuritic chest pain is ordinarily found in patients
Anginal pain is visceral pain that may be re
that have other signs of respiratory illness, such as
ferred superficially but always has a deep inter

nal component to it.
cough, fever, chills, malaise. Inflammation of the di

aphragmatic pleura produces ipsilateral shoulder pain
by way of the phrenic nerve (Miller, 1980).
Myocardial ischemia may be completely painless

(silent ischemia). Angina may in fact not be painful
The onset of pleuritic chest pain varies according
but rather described as discomfort, pressure, squeez
to its cause (Snider, 1994). Sudden severe pleuritic
ing, a tight band, heaviness, burning, indigestion. It
chest pain suggest a spontaneous pneumothorax, pul
usually is located substernally and radiates into one
monary embolism, or infarct. Pulmonary embolism is
or both arms, neck, jaw, or back.
usually accompanied by sudden dyspnea, hemoptysis,
Angina is not limited only to patients with CAD
tachycardia, cyanosis, hypotension, anxiety, and agi
(Marriott, 1993). Individuals that have normal coro
tation (Marriott, 1993).
nary arteries but an insufficient oxygen supply for a

given cardiac workload can also experience angina.
These include individuals with anemia, hypertension,
Cardiac
tachycardia, and thyrotoxicosis. Hypertrophic and di
There are three cardinal features that are characteris
lated cardiomyopathy can produce typical angina
tic of cardiac chest pain. The patient should be asked
pain, although the latter tends to be intermittent, usu
the following questions (Marriott, 1993):
ally occurring with episodes of CHF. Aortic valve
I. Does the pain have maximal intensity from
the onset or does it build up for several sec
disease can cause angina as a result of impairment of

adequate coronary artery blood tlow.
on ds? Ischemic cardiac pain or angina is
Angina is usually precipitated by exertion such as
caused by the myocardium contracting in the
walking uphill, against the wind, or in cold weather
absence of an adequate oxygen supply. The
(Marriott, 1993). It also is more likely to be brought
same type of pain can be produced by placing a
on after a meal or by emotional stress. The rapid
blood pressure cuff around the upper arm and
resolution of chest pain by rest
inflating it until the brachial pulse is no longer
glycerin strongly suggests a cardiac origin. The pain
or
sublingual nitro
History
139
produced by MI is longer, persisting more than 20
suggest an esophageal origin (Snider, 1994). Also,
minutes; occurs at rest; and is accompanied by nau
diffuse esophageal spasm is often associated with

pain on swallowing (odynophagia), dysphagia, and
sea, diaphoresis, hypotension, and dyspnea.
regurgitation of stomach contents. Swallowing hot or

cold liquids, or emotional stress tend to precipitate
Pulmonary Hypertension
this type of chest pain.
Chest pain related to pulmonary hypertension may

mimic angina pectoris. It is usually found in patients
with mitral stenosis or Eisenmenger's syndrome (pul
Chest Wall
monary hypertension related to an interventricular
Chest wall pain is the most common type of chest
septal defect, patent ductus arteriosus, or atrial septal
pain. Clues in the patient's history to this type of pain
defect). This type of chest pain is usually absent at
include intermittent occurrence, variable intensity,
rest, occurs during exertion, and is invariably associ
and local tenderness (Miller, 1980). Because it is
ated with dyspnea (Hurst, et ai, 1990). It is believed
often located on the anterior chest wall, many pa
to be because of dilation of the pulmonary artery or
tients believe it is heart pain. However, an important
right ventricular ischemia. The pain is not relieved by
differentiation from cardiac pain is that it does not
nitrates. Primary pulmonary hypertension may be ac
occur during but rather following exertion. It may
companied by syncope and Raynaud's phenomenon
worsen with inspiration, but its association with trunk
(Sharf, 1989).
motions (flexion, extension, rotation) distinguish it

from pleuritic chest pain.
Localized anterior chest pain as a result of costo
Pericardial
chondritis of the second to fourth costosternal articu
Pericardial chest pain is also midline, but because of its
lations (Tietze's syndrome) is described as tender to
anatomical relationship with the mediastinal pleura, it
touch (George, 1990). A complaint of rib tenderness,
has features that suggest pleural involvement (Snider,
together with a history of trauma, fall, long-term
1994). Deep breathing, coughing, swallowing, move
steroid use, coughing, or upper extremity exertion,
ment and lying down may make it worse. If the central
suggests rib fracture.
tendon of the diaphragm is involved, the pain may be
Degenerative disk disease and arthritis of the cervi
referred to the left shoulder or scapular area (Marriott,
cal or thoracic spine, thoracic outlet syndrome,
1993). The patient may report that each hemibeat af
spondylitis, fibromyalgia, kyphoscoliosis, and herpes
fects the pain. Sitting up and leaning forward, or lying
zoster can all produce chest wall pain (Epstein, Ger
on the right side often relieves the pain.
ber, and Borer, 1979; Miller, 1980; Pellegrino, 1990;

Snider, 1994; Wise, Semble, and Dalton, 1992). Pri
mary lung cancer that invades the adjoining chest
Esophageal
wall, ribs, or spine produces severe persistent local
Diffuse esophageal spasm or esophageal colic is a
ized pain (Snider, 1994). Pancoast's syndrome (supe
common cause of chest pain. It is often confused with
rior sulcus tumor), in which a primary lung tumor lo
cardiac pain because it is located substernally, has a
cated in the extreme apex of the lung invades the
squeezing or aching quality, and may radiate into one
brachial plexus and produces pain in the shoulder,
or both arms (George, 1990). Furthermore, diffuse
scapular region, or medial aspect of the arm and hand.
esophageal spasm may be relieved by sublingual ni
Chest wall pain may rarely be caused by thrombo
troglycerin as a result of its generalized function as a
sis of a superficial vein on the chest wall (Mondor's

disease). It is a self-limiting condition of unknown
smooth muscle relaxant.

Pain that radiates through the chest to the back,
origin and can last several weeks (Snider, 1994). The
pain that decreases by a change in position from
only physical finding is a subcutaneous cord that can
supine to upright, or relief by ingesting antacids, all
be palpated along the lateral chest wall.
140
PART II
FATIGUE AND WEAKNESS
HEMOPTYSIS
is defined as coughing up blood. It can
vary in amount from blood-streaked sputum to convirtually all blood. The
site may be
anywhere in the upper or lower respiratory tract.

The timing and frequency of
as deter
mined in the history, can offer clues about its cause.

since blood
A history of nosebleeds is
may be aspirated duling
and expecto
rated the following morning. Intermittent bouts of he

is more characteristic of resoiratorv infec
tions such as bronchiectasis,
or broncholithiasis (Miller,
blood-streaked
basis is highly
of
hrr;,nf"hAfT"n
The lung receives its blood supply in two ways: the

pulmonary arteries (a low pressure
and the
bronchial arteries (a high pressure
off of the
may
aorta (Shalf, 1989). The appearance of

vary according to which blood
is involved. If the
bronchial vessels are the source, there tends to be large

or massive amounts of bright red blood. This is often
PEDAL EDEMA
the site of bleeding in bronchiectasis, since bronchial ar
CHF is a common cause of bilateral pedal edema
teries undergo enlargement and extensive anastomosis
(Marriott, 1993). Ifowever, several pounds of fluid
with the pulmonary artery system.

where there is increased
in mitral steno-
(10 to 20 Ibs.) generally accumulate in the body be

fore foot and ankle swell
I-IUJJJJ'-'JJ<ll
tance, hemoptysis arises from
is evident. Therefore
weight gain is an even earlier indication of fluid re

tention due to CHF. Occasionally, patients may only
mucosal bronchial veins

Hemoptysis from the
complain about an increase in abdominal
artery system tends to occur in small amounts and is
ascites virtually
of dark or clotted venous blood

It may arise from the
occurs after
present If the amount of ascites is
as in the case of the
vascular
found in the walls of
abscesses. These abscesses
tissue
that of
constrictive
restrictive CardlOmyopatny or
should be a consideration.
It is important to determine whether the
may be caused by infections such as

or chronic irrita
anaerobic bacteria,
result
CHF. the onset of
ing from ascites. When caused
had dyspnea on exertion before the onset of lower-ex
tion from a fungus ball in an abscess cavity. If a
tremity edema. If the edema is a result of a
blood vessel ruptures in an abscess
functioning left
rhage tends to be massive, even
monale, it usually follows

and
aortic aneurysm are also associated with hemoptysis

(Hurst, et aI, 1990). Pink frothy
with acute pulmonary edema.
fully evaluate
of
or cor pul
on exertion.
Patients with CHF and altered renal function
Cardiovascular conditions such as mitral

pulmonary infarction,
mitral
commonly report edema of the ankle and lower legs

while upright during the
but indicate a de
is often found
crease during the night (Hurst, et ai, 1990). This is
should care
a result of local hydrostatic factors related to the
and be certain
of its cause before cautiousIv conducting treatment.
upright position.
Edema may be Dresent in nephrosis or starvation
when the total blood protein falls below 5 gmllOO ml

(hypoproteinemia). Other causes of pedal edema in
clude liver disease, kidney disease, and anemia.
Edema of one leg is ordinarily because of local fac
tors such as thrombophlebitis or varicose veins.
HOARSENESS
Hoarseness, abnormal vocal cord motion during

phonation, is a symptom of laryngeal dysfunction
(Miller, 1980). It is usually associated with upper res
piratory tract infections or allergies, and resolves in 1
to 2 weeks (Sharf, 1989). Trauma following intuba
tion, laryngeal polyps, or tumors are other common
causes of hoarseness. However, this symptom is also
related to cardiopulmonary conditions. Because the
recurrent laryngeal nerves pass through the upper
thorax, intrathoracic pathology that involves one of
these nerves can cause unilateral vocal cord paralysis,
resulting in hoarseness (Shalf, 1989). These include
lung or mediastinal tumors, granulomatous disease,
enlarged mediastinal lymph nodes, and pericardial or
mediastinal adhesions.
Several cardiovascular conditions can produce
hoarseness, because the left recurrent laryngeal nerve
loops under the arch of the aorta and above the pul
monary artery as it returns to the neck (Hurst, et ai,
1990). Therefore an aneurysm of the arch of the
aorta, a dilated pulmonary artery or atrium resulting
from an atrial septal defect, or mitral stenosis can
cause hoarseness (Goldberger, 1990).
Hence, if patients manifest hoarseness, it is neces
sary to inquire about the length of time it has been
present, the patient's smoking history, and any his
tory of cardiac or pulmonary diseases.
OCCUPATIONAL HISTORY
Taking an occupational history is particularly impor

tant for pulmonary patients who arrive for physical
therapy with little or no accompanying medical infor
mation. The internal surface of the lung measures 50 to
100 m] and is in constant contact with the environment
(Miller, 1980). Jobs that involve exposure to silica or
silicates (e.g., miners, sandblasters, foundry workers,
stone cutters, brick layers, or quarry workers) or other
inorganic substances place workers at risk for combi
History
141
nations of obstmctive and restrictive lung disease (e.g.,

silicosis). Constmction workers, shipyard workers,
pipefitters, and other industJial workers exposed to as
bestos are at increased risk for developing a restrictive
lung disease such as asbestosis (Varkey, 1983). Benign
pleural plaques may be found on the diaphragmatic
pleura and bilaterally between the sixth and tenth ribs
on the anterolateral or posterolateral chest wall. Pro
gressive pleural thickening rarely occurs. These indi
viduals have an increased incidence of malignant neo
plastic diseases such as bronchogenic carcinoma and
malignant mesothelioma.
Coal workers are exposed to coal mine dust.
About 10% have simple pneumoconiosis, whereas a
smaller proportion develop the complicated form
progressive massive pulmonary fibrosis (Brandstetter
and Sprince, 1982).
A history of paroxysmal coughing, chest tightness,
or dyspnea that is worse during the week but remits
on weekends strongly suggests occupational asthma
(Brandstetter, and Sprince, 1982). This condition is
difficult to diagnose because symptoms often occur
several hours after exposure to the provoking agent.
Causal agents include grain dusts, wood dusts, forma
lin, enzyme detergents, ethanolamines (in spray
paints and soldering flux), nickel and hard metals
(tungsten carbide). Workers exposed to cotton flax
and hemp dusts may develop byssinosis, an obstmc
tive lung disease. In the early stages, it is reversible,
but long-term exposure over a number of years
causes chronic irreversible obstructive lung disease.
A history of fever, cough, shortness of breath,
and recurrent pneumonias in farmers in the north
ern United States suggests farmer's lung (Brand
stetter, and Sprince, 1982). This is the most com
m o n h y p e r s e n s i t i v e pneumonitis, c a u s e d b y
inhaling fungal agents such a s thermophilic actino
mycetes. Long-term exposure can lead to pul
monary fibrosis. There are numerous occupations
that expose workers to etiologic factors that cause
hypersensitive pneumonitis.
SMOKING HISTORY
The patient should be asked their tobacco-smoking

history (Snider, 1994). The number of pack-years of
cigarettes smoked may be calculated (average number
142
PART II
of packs/day
number of years smoked) as a relative
risk of lung cancer and COPD. Regular smoking of

marijuana is more damaging to the lungs than ciga
rette smoking.
REVIEW QUESTIONS
1. What are the basic causes of dyspnea?
2. What questions can be asked of a patient with
dyspnea to determine the likely cause?

3. What scales have been developed to quantitate
FAMILY HISTORY
dyspnea?
The family history is useful in evaluating the possi
4. What are the principal features of chest pain that
originate from the pleurae? The chest wall? The
bility of hereditary p ulmonary diseases such a s

alphaj-antitrypsin deficiency, cystic fibrosis, allergic
asthma, hereditary hemorrhagic telangiectasia, and
others (Miller, 1980; Szidan, and Fishman, 1988). A
family history of diabetes, hypertension, CAD, or
thoracic organs?
5. What are the cardinal features of cardiac chest
pain?
6. What occupations can place workers at rish for

respiratory disease?
rheumatic fever raises the possibility of these condi

tions existing in the patient as well (Marriott, 1993).
References
PRIOR TREATMENT
Herbers, J., & Kroenke, K. (1 993). Eva lua ting chest

s dia g
n o s ti c a p p r oach . Arch ives of In/ernal Med i c ine, 153,
Birdwell, B.,
It is important to deterrnine what treatment(s) the pa

tient has received for his or her condition. Specifically,
has the patient ever received physical therapy for this
or any other condition? What type of treatments were
done? Were they helpful in improving or resolving the
condition? In this way we determine what treatment
modalities have been used, which of these the patient
believes may have merit, and those with which the pa
tient finds objectionable or lacks confidence, thus
avoiding alienating the patient by not repeating what
he or she believes to be ineffective therapy is avoided.
pain: the patient's presen tation style alte rs the phy si c ia n
'
1991-1995.
Borg, G. (1982).
Psyc ho physic al bases
of perce i ve d exertion. Merl
icine and Science in SPOrlS and t:rercise, 1 4,
Braman, S., Corrao,
W. (1 987) .
377-381.
Cough: differen/ial diagnosis and
8(2), 1 77-188.
N. (1982). Occ u p at i on al lun g disease.
June, 56-63.
/realinel1l. Clinical Ches/ Medicine
Brandsteller, R .. Sp rince,
Medical Times,
Constant,
J.
(1993). The evolving checklist in history-taking. In
Bedside cardiology. Bo st on : Linle. Brown.

Epstei n S., Gerber, L., & B o re r, J. (1979). Chest wall syndrome: a
common cause of unexplained cardiac pai n . Journal of /he
American Medical Associa/ion, 241, 2793-2797.
Constant
J.
George, R. (1990). History an d physical examination. In Geo rge
SUMMARY
ai/ical care medicine. Baltimore:
Obtaining an accurate and thorough history is the

cornerstone of the physical t herapy e v a luation
process. The probable cause and severity of many
cardiopulmonary symptoms can be determined by
careful history taking. This information enables ther
apists to select the most appropriate evaluation and
treatment techniques. When properly performed, ac
curate h istory taking gains the patient's confidence
and cooperation, and provides the basis for a good
patient-therapist relationship.
R., et al (Eds.), Chest medicine: Essen/ials of pulmonary and
G o l dbe rger, E.
Wi l l ia ms and Wilkins.
(1990). Symptoms referable to the cardiovascular
E. Essentials of clinical cardiology.

Phi la delp hi a: JB Lippincott.
Irwin, R., Rosen, M., & Braman, S. (1977). Cough: a comprehen
system. In Goldberger,
sive review. Arch h7lem Medicine 137,1186-1191.

Hurst, 1., et al. (1990). The
h ist ory: past events and symptoms re

J. (Ed.). The heall.
lated to cardiovascular disease. In Hurst,
N ew York: McGraw-Hili.
Clin ics ill
Ches/ Medicine. 8(2), 215-230.
Mahler, D., & Harvel', A. (1990). Clinical measureme nt s of dysp
nea. In Mah l e r, D. (Ed.). Dysp/1ea. Mount Kisco, NY: Futura.
Marriol!, H. (1993). Taking the history. In Marriol!, H. Bedside
cardiac diagnosis. Ph i ladelphia: JB Lippincott.
Mahler, D. (1987). Dyspnea: diagnosis and management.
History
143
Miller, D. (1980). The medical history. [n Sackner, M. (Ed.).
Szidan, P., & Fishman, A. (1988). Approach to the pulmonary pa
Diagnostic techniques in pulmonary disease. New York:
tient with respiratory signs and symptoms. [n Fishman, A.
(Ed.). Pulmonary diseases and disorders. (2nd ed.). New York:
Marcel Dekker.
Pellegrino, M. ( 1990). Atypical chest pain as an initial presentation
of primary fibromyalgia. Archives of Physical Medicine and
Rehabilitation
71, 526-528.
McGraw-HilI.
Varkey, B., (1983). Asbestos exposure: An update on pleuropul
monary hazards. Postgraduate Medicine, 74(4),93-103.
Sharf, S. (1989). History and physical examination. [n Baum, G.,
Wasserman, K., (1982). Dyspnea on exertion: is it the heart or the
& Wolinski, E. (Eds.). Textbook of pulmonary diseases. (4th
lungs? Journal of the American Medical Association, 248,
ed.). Boston: Lillie, Brown.
2039-2043.
Snider, G. (1994). History and physical examination. [n Baum, G.,
Wise, C., Semble, E., & Dalton, C. (1992). Musculoskeletal
& Wolinski, E. (Eds.), Textbook of pulmonary diseases. (5th
chest wall syndromes in patients with noncardiac chest pain:

A study of 100 patients. Archives of Physical Medicine and
ed.). Little, Brown.

SlUlberg, M. (1985). Evaluating and treating intractable cough
R eha bilitation,
Medical Staff Conference, University of California, San Fran

cisco. West 1 Med, 143,223-228.
73, 147-149.
Pulmonary Function Tests
Donna Frownfelter
KEY TERMS
Expiratory reserve volume
Dead space
Inspiratory reserve volume
Lung capacities
Residual volume
Tidal volume
Inspiratory capacity
Total lung capacity
Obstructive component
Vital capacity
Predicted values
Restrictive component
Lung volume
sis of pulmonary disease or dysfunction and improve
INTRODUCTION
ment with treatment win be evaluated as a result of in
Pulmonary function tests (PFfs) help in the evaluation
terpreting a patient's pulmonary function tests.
of the mechanical function of the lungs. (Cherniak,

Crapo, and Youtsey, (992). They are based on re
searched norms taking into account sex, height, and
DEAD SPACE
age. For example, there are predicted values for a
The most important function of the lungs is to supply
male, age 65 who is 6 feet tall. (Morris, Koski, and
the body with oxygen and to remove carbon dioxide
Johnson, (971). When the patient performs the test ac
(C02) produced as a waste product of metabolism.
tual results (observed) will be compared with the pre
As this continuous gas exchange takes place suffi
dicted value expected of a person of gender, height,
cient ventilation is needed to move the gases to the
and age to see if he falls within the "nonnal" range, or
alveoli. There is a series of conducting airways in the
has a restrictive or obstructive component based on the
lungs from the trachea down to the terminal bronchi,
tests. If the patient is not within the nonnal range, a
which do not participate in respiration but only move
bronchodilator is given, and the test will be repeated to
the gases to the alveoli. This is the volume known as
see if there is significant improvement with medica
anatomic dead space. Generally, the anatomic dead
tion. Basically, the pulmonary function tests are cate
space i s app r opria tely equal to the adult body
gorized as volume, flow, or diffusion studies. Diagno-
weight. For example, in a ISO-lb. person, there is an

145
146
PART II
approximately I SO mL anat(}mic dead space. A nor
functioning alveoli. This causes increased work of
mal tidal volume (TV), the breath normally taken,
breathing and may result in patient fatigue. Neurolog
needs to be large enough to reach the alveoli well
ical and neuromuscular weakness may result in an in
past the anatomic dead space. In a normal adult, the
ability to take a normal TV. Similarly, surgical proce
TV is generally 450 to 600 mL. The anatomic dead
dures
space would thus represent about one third TV vol
compromise a patient's ability to take a breath. As
or
p a i n f r o m fractured
r i b s c a n also
ume. The rest of the breath would reach the alveoli
the TV drops a large percentage of the breath is
and be considered "alveolar ventilation." With many
anatomic dead space. This results in increased work
neurologically impaired patients who have a limited
of breathing for the patient and may ultimately result
TV, it is important to note that little alveolar ventila
in respiratory failure if the patient is unable to pro
tion may be taking place when the patient is breath
vide alveolar ventilation.
ing in a rapid and shallow pattern. For example, if a

p a t i e nt's TV w a s 200 mL,
IS O
mL w o u l d be
anatomic dead space and only SO mL of each breath
lUNG VOLUMES
The lung has four volumes, TV, inspiratory reserve
would be alveolar ventilation.

There are many diseases or conditions that can alter
volume (IRV), expiratory reserve volume (ERV), and
8-1).
the volume of dead space that needs to be ventilated. In
residual volume (RV) (Figure
some cases the dead space decreases, such as in a pneu
TV is the normal breath.
monectomy, where it is physically removed, or in
IRV is the maximal amount of air that can be in

haled from the end of a normal inspiration.
asthma, where bronchospasm may narrow the airways.

In other conditions such as pulmonary embolus, dead
be perfused. The alveoli continue to receive fresh gas,

but there is no blood available for gas exchange. This
type of dead space is known as physiologic dead space.
ERV is the maximal amount of air that can be ex

pired after a normal exhalation.
space increases when ventilated areas of lung cease to
RV is the volume of gas that remains in the lungs

at the end of a maximum expiration.
Changes in RV can help in the diagnosis of certain
When dead space is increased, a larger percentage
medical conditions. An increase in RV means that
of the tidal volume is ventilating the dead space,
even with maximum effort, the patient cannot exhale
leaving a smaller percentage for alveolar ventilation.
excess air from the lungs. This results in hyperin
The patient must work harder to get enough air to the
flated lungs and indicates that certain changes have
---I
\tj
( C,\.'-'- '--
FIGURE 8-1
A
spirogram (pulmonary function testing).
147
occurred in the pulmonary tissue, which in time may
FRC is the volume of air remaining in the lungs at
cause mechanical changes in the chest wall (e.g., in
the resting expiratory level. It contains the ERV and
creased AP diameter, flattened diaphragms). These
the RV.
changes may be reversible in patients with partial
The FRC prevents large fluctuations in Pa02 with
bronchial obstruction, such as young asthmatics, or
each breath. An increase in FRC represents hyperin
irreversible, as in patients with advanced emphy
flation of the lungs. It causes the thorax to be larger
sema. Restrictive lung disease can cause a decrease in
than normal, which results in muscular inefficiency
residual volume, as can cancer of the lung, microat
and some mechanical disadvantage. Patients on me
electasis, or musculoskeletal impairment. (Smith and
chanical ventilators may increase their FRC with pos
Dickson, 1994).
itive pressure and by additional modes such as posi

tive end expiratory (PEEP), or BiPap. Spontaneously
breathing patients can also be on continuous positive
LUNG CAPACITIES
airway pressure (CPAP), which keeps the lungs at a
A lung capacity is two or more volumes added to
positive airway pressure to improve oxygenation.
gether (Figure 8-1). The capacities include total lung

capacity (TLC), vital capacity (VC), inspiratory ca
pacity (IC) and functional residual capacity (FRC).
TLC is the amount of gas the lung contains at the
AIR FLOW MEASUREMENTS

Forced Expiration
end of a maximum inspiration. It is made up of all four
When patients peIform a VC maneuver, it can either
lung volumes. An increased TLC is seen with hyperin
be slow or fast. During exhalation, the amount of air
flation such as emphysema. A decrease in TLC may be
exhaled over time can be measured. In a slow VC a
seen in restlictive lung disease such as pulmonary fi
patient with emphysema can take a great deal of time
brosis, atelectasis, neoplasms, pleural effusions, and
to empty his lungs. In a forced VC a normal individ
hemothorax, as well as in restrictive musculoskeletal
ual can exhale 75% of the VC in the first second of
problems such as spinal cord injury, kyphoscoliosis, or
exhalation (FEV I). Patients with emphysema often
as secondary to morbid obesity or pregnancy.
have greatly decreased VCs, only 40% of which are
VC is the maximum amount of gas that can be ex
predicted.
pelled from the lungs by forceful effort following a

maximum inspiration. It contains the IRV, TV, ERV.
A decrease in VC can occur as a result of absolute re
Flow Volume Curve
duction in distensible lung tissue. This is seen in
The flow volume curve is helpful in diagnosing lung
pneumonectomy, atelectasis, pneumonia, pulmonary
disease, since it is independent of effort. The curve in
congestion, occlusion of a major bronchus by a tumor
Figure 8-2 demonstrates that flow rises to a high
or foreign object, or restrictive lung disease.
value and then declines over most of expiration
A decrease in VC may also be seen without pri
(Rahn, et ai, 1946). In restrictive lung disease, the
mary lung disease or airway obstruction. In neuro
maximum flow rate is reduced, as is the total volume
muscular or musculoskeletal dysfunction, VC can be
exhaled. In obstructive lung disease, the flow rate is
compromised (Guillain-Barre, spinal cord injury,
low in relation to lung volume, and a scooped-out ap
drug overdose, motor vehicle accident with fractured
pearance is often seen (see Figure 8-2).
ribs, severe scoliosis, and kyphoscoliosis). Restrictive
Another diagnostic test that uses forced expiration
contributing factors such as morbid obesity, preg
is the flow volume loop. It is a graphic analysis of the
nancy, enlarged heart, and pulmonary effusion may
flow generated during a forced expiratory volume
involve the limitation of expansion of the lungs.
maneuver followed by a forced inspiratory volume
IC is the maximal amount of air that can be in
maneuver (Figure 8-3). This graph offers a pictorial
spired from the resting expiratory level. It contains
representation of data from many individual tests
the IRV and the TV.
(e.g., peak inspiratory and expiratory flow rates,
148
PART II
FLOW
VOLUME CURVES
NORMAL
Z
o
wi=
a:a..
:> X
U
Q)
II)
'
:;>o w -.J
o
-.J<..9
u...Z
0::
OBSTRUCTIVE
=:J
o
oI
10
r' ,.,.,.,.,.,.,.,\. """''"""'T

8
.... .
/
4
",
. . ..' 'j' xx;,i
",.",., ' '
LUNG VOLUME (Liters)
FlliURE 8-2
Comparison of tlow volume curves in the normal patient and in the patient with obstructive and
restrictive lung disease.
+5
-r---- /\,.----;;;50%
/
PFexp
EXPIRATION
U
Q)
II)
,
i 01
Ie
o
-.J
u...
-5
F;
\
INSPIRATION
PF insp
OBSTRUCTION
__
VOLUME (Liters)
FIGURE 8-3
Compatison of flow volume loops in the normal patient and in the patient with obstructive
lung disease.
FVC, and FEV). The shape of the graph may also be

helpful in diagnosing disease, again seeing a more
scooped-out appearance with obstructive disease.
CLOSING VOLUME AND AIRWAY CLOSURE

The assessment of closing volume is used to help di
agnose small airway disease. A test called the single
breath nitrogen (N2) washout is used for assessing
closing volume and closing capacity of the small air
ways. In this test, the patient takes a single VC breath
of 100% oxygen. During complete exhalation, the N2
concentration can be measured. The characteristic
tracing of N2 concentration can be measured. The
characteristic tracing of N2 concentration vs. lung vol
ume reflects sequential emptying of differentially ven
tilated lung units, resulting in different expiratory N2
concentrations. Four phases can be identified (Figure
8-4). Phase I contains pure dead space and virtually
none of the potential N2 from the RV. Phase Il is asso
ciated with an increasing N2 concentration of a mix
ture of gas from the dead space and alveoli. The
plateau in N2 concentration observed in Phase III re
flects pure alveolar gas emanating from the bases and
middle lung zones. Phase IV occurs toward the end of
expiration and is characterized by an abrupt increase
in N2 concentration. This high N2 concentration re

flects closure of airways at the base of the lungs and
expiration of gas from the upper lung zones, because
in the single breath of 100% oxygen, less oxygen was
initially directed to this area.
Closing volume is the lung volume at which the
inflection of Phase IV, the marked increase in N2
concentration after the plateau, is observed. Closing
capacity refers to closing volume and RV. The same
characteristic tracing of the single breath nitrogen
washout test can be obtained with an inhalation of a
bolus of tracer gas (e.g., argon, helium, xenon-133).
The closing volume is 10% of the vital capacity in
young, healthy individuals. It increases with age and
is 40% of the vital capacity at age 65. Closing vol
ume is used as an aid in the diagnosis of small airway
disease and as a means of evaluating treatment or
drug response.
MAXIMAL VOLUNTARY VENTILATION

Maximal voluntary ventilation measures the maximal
breathing capacity of the patient. It reflects strengths
and endurance of the respiratory muscles. The patient
is asked to pant for 15 seconds into the spirometer tub
ing. This is often examined preoperatively with the
CLOSING VOLUA1E and CLOSING CAPACITY
z
o
(f)f
(9
0:::
f-f
o:::Z
WW
ZU
-z
o
U
I
I
I
I
I
I
I
I
DEPENDENT AIRWAY BEGIN

TO CLOSE ------,
TLC
149
VOLUME (Liters)
RV
Closing
Vol.
HCVl----!
FIGURE 8-4
The single breath nitrogen washout test to assess airway closure.
150
PART II
other results to determine a patient's prognosis for suc
ration). An obstructive component generally relates to
cess after surgery, such as his or her ability to cough,
problems in exhalation air flows and characteristic
to take deep breaths, and to enhance airway clearance.
patterns of obstruction, such as in the first second of

expiration FEY I measurement). Patients do not often
have only one primary disease process but many times
DIAGNOSIS OF RESTRICTIVE
AND OBSTRUCTIVE LUNG DISEASE
have overlapping lung conditions (Clausen, 1984). A
Physicians use the results of pulmonary function tests
emphysema with bronchospastic component; good re
diagnosis may read: PFTs consistent with moderate
to diagnose lung disease or characteristic components
sponse to bronchodilators. A patient with an abnormal
of lung disease, such as bronchospasm. A restrictive
PFr is given a bronchodilator and retested. If there is
component describes conditions that limit the amount
a 15% to 20% increase in the PFr after bronchodila
of volume coming into the lungs (restriction to inspi
tors are administered, they will be a recommended
NORMAL
RESTRICTIVE
OBSTRUCTIVE
IRV
IC
VC
IRV
TLC
TV
VC
IC
C
TV
TI C
ERV
ERV
FRC
FRC
RV
RV
FIGURE 8-5
Examples of proportional changes of lung volumes and capacities characteristic of
obstructive and restrictive lung diseases.
151
part of the patients' medications. However, some pa
a loss of intrapleural negative pressure. In older indi
tients are given a trial of bronchodilators, even if there
viduals, therefore, airway closure occurs at higher lung

volumes. For example, closure has been reported to
is not such a dramatic response on PFfs).

A pictorial demonstration of the differences in ob
occur at the age of 65 in the upright lung during nor
structive and restrictive lung disease is shown in Fig
mal breathing. In the supine position, where FRC is re
ure 8-5. Disease has a marked effect on pulmonary
duced, closure occurs at a significantly younger age
function, yet TV usually remains 10% of total lung
(about age 44). In addition to the often compounding
capacity until the disease is relatively severe. Physio
effect of age, the lung volume at which airway closure
logic pulmonary reserves in both disease processes
occurs increases with chronic smoking and lung dis
are limited and generally affect a patient's response
ease, and is changed with the alterations in body posi
to exercise. Exercise will be limited by the ventila
tion (Ben)" Pai, and Fairshter, 1990; Zadai, 1985).
tory status ratlier than by a cardiac end point. As ob

structive lung disease progresses, TLC, FRC, and RV
are markedly increased. In severe COPD, the in
creased FRC can compromise the Vc. More energy
SUMMARY
Pulmonary functions change as a patient's condition
is expended to breathe compared with that expended
gets better or worse (Emery et ai, 1991; Emerson,
by a normal individual. This effect can be dispropor
Lukens, Effron, 1994). There are normal declines in
tionally increased with minimal amounts of activity.
volumes and flows with aging as well as disease
In restrictive lung disease, restriction of the chest
processes. Basic bedside spirometry is often done to as
wall or lung tissue can produce a decrease in TLC. A
sess the patient's breathing mechanical ability. For ex
VC of 80% or less of predicted values for a patient is
ample, in a patient with Guillain Ban'e, as breathing be
considered a diagnostic feature. A residual decline in
comes labored, the VC is monitored to determine

whether a ventilator is needed. On the other hand, a pa
FRC potentiates airway closure.

The phenomenon of closing volume in the lungs is
tient with obstructed airways, such as the patient with
particularly significant to physical therapists (PTs)
cystic fibrosis, the pulmonary function tests will im
who prescribe breathing exercises and body position
prove (Versteegh, et ai, 1986). In patients with spinal
ing, and can thereby alter pulmonary mechanics and
cord injury or neuromuscular weakness, as their
gas exchange. These treatment interventions may
strength improves, their vital capacity increases. How
have a pronounced effect on the lung volumes and
ever, because of the lack of abdominal muscles, the
airway closure (Dean, 1985). At low lung volumes
flows may be reduced.
(e.g., breathing at FRC, Trendelenberg position, and

in lung disease) intrapleural pressures are generally
less negative and the pressure of dependent lung re
REVIEW QUESTIONS
gions may equal or exceed atmospheric pressure. In
1. What effect will an obstructive component have on
trapleural pressure is less negative because the lungs
exercise performance? What effect will a restric
are less expanded and elastic recoil is decreased. As a
tive component have on excercise peliormance?
result, airway closure is potentiated. In young indi
2. Why is it important to compare the patient's pre
viduals, closure is evident at RV; however, in older
dicted values with the actual observed values in a
individuals, closure is observed at higher lung vol

umes, such as at FRC. Premature closure of the small
airways results in uneven ventilation and impaired
gas exchange with a given lung unit. Airway closure
occurs more readily in chronic smokers and in pa
pulmonary function test?

3.
What response should you see to determine if

bronchodilators have a positive effect on pul
monary function?
4. How can pulmonary function tests be used to as

sess patient improvement or decline?
tients with lung disease.

Aging has a significant effect on airway closure.
With aging, a loss of pulmonary elastic recoil results in
5. How valuable are pulmonary function tests if pa

tients do not give maximal effort?
152
PART II
References
Berry, R., Paj,
Rahn,
U. &
in !low rates and airway conductance after a deep breath, Jour
nal of Applied Physiology. 68, 635-{543.

Cherniak, R,M,
and
function in health
Pulmonary function tcstlng; guidelines and
Physical Therapy 65, 613-{5 J 8,
CL.,
in acute exacerbation of COPD, Chest, 105(6),
1709-1712,
c.E.,
J"
et a!. (1991). Psychological outcome of a pulmonary
Koski, A"
sis of
spine in patients who have idiopathic scoliosis.
76
BOI1<'
(I), I
Ven;tcegh, F.G,A., et a!. (1986), Relationship between pulmonary

brosis. Advanced Cmdiology,
cations,
Is
p"
lSI-ISS, 1986,
el aL (1992), Predicting postoperative compli
it a real problem
Archives
of /l1Icrnal Medicine,
Youtsey, J.W. (1990).

Scanlon,
CL,
Basic
Spearman,
pulmonary function measurement In
CB., &
Sheldan, R.L. (Ed,.). Egan's
fundamentals of respiratory care. (5th ed.). SL Louis: Mosby.
Johnson,
L (1971),
Zadai,
Prediction nomograms
(BTPS) spirometric values in normal males and females. Am e r
ican Review of Respiratory
C (1985)
Pulmonary physiology of
The role of re
habilitation, Topics in CeriO/ric Rehabililation, 1,49-56,
rehab program. Ches/, 100 (3), 613-{517,

Morris,
Dickson, R,A. (1994), Changes in residual volume
152 (6), 1209-12l3,
Lukens, T.W., Effron, D, (1994), Physician estima
&
Williams-Russe,
Dean, E. (1985). The effect of body position on pulmonary fUlle
tion of FEV
of the thorax
J 61.
function, O2 saturation during sleep and exercise with cystic
Pulmonary function testing, New England
Joumal of Medicine, 331 (I),
Emerson,
Smith, R.M.,
and Join! Surgo)'
controversies, London: Grune and Stratton,

Crapo, R.O, (1
et aL (1946), The prcS'urcvolume
relative to vital capacity and total lung capacity after arthrode
(! 992J, Evaluation of respiratory

Dis Man,
(7),505-76,
J.L. (1984).
Clausen,
H"
lung, American Journal of Physiology, 146,
Fairshter, R, (1990). Effect of age on changes
Diseases, 163, 57-{57.
Arterial Blood Gases
Donna Frownfelter
KEY TERMS
Acid/base balance
Hypoxemia
Alveolar ventilation
Oxygen saturation
Arterial blood gas
Partial pressure of gases
INTRODUCTION
metabolites must be kept from accumulating in high
Arterial blood gases are assessment tools to help the
amounts, because the body's cardiovascular and ner
physical therapist (PT) understand the patient's
vous systems operate in a relatively narrow free H+
acid/base balance, alveolar ventilation and oxygena
ion range (narrow pH). Free H+ ion concentration is
tion status (Cherniak, 1992). They are valuable re
discussed as pH (-log [H+]). Maintenance of body
sources of information, from respiratory monitoring
systems requires an appropriate acid/base balance
in the intensive care unit to following outpatients to
(Shapiro, 1994).
Approximately 98% of normal metabolites are in
evaluate the therapy and progress of their diseases.

The purpose of this chapter is to help the clinician
evaluate and interpret arterial blood gases more effec
the form of carbon dioxide (C02)' Carbon dioxide re

acts readily with water to form carbonic acid:
tively and to integrate the information into treatment
CO2 + H20
planning and progression of the patient.
H2C03
Carbonic acid can exist either as a liquid or a gas. Be

cause carbonic acid can change to CO2, much of the
ACID/BASE BALANCE
acid content can be excreted through the lungs during
Normal body metabolism consists of consumption of

nutrients and excretion of acid metabolites. Acid
respiration.
The Henderson-Hasselbach equation demonstrates
153
154
PART II
how the H+ ion concentration results from the disso
acidemia o r alkalemia. Acidosis i s a n abnormal
ciation of carbonic acid and the interrclationship of
acid/base balance where the acids dominate. Alka

lemia is an abnormal acid/base balance where the
the blood acids, bases, and buffers:

H2 0 + CO2
H2C03 H+ + HC03
bases dominate. When there is a decrease in the
Heo3-, it is seen in a negative base excess and referred

to as a base deficit, which is usually seen as a negative
Renal Buffering Mechanisms
number on the blood gas report, that is, -3.
The kidneys are the mai n route of excretion for the
termine whether the patient's condition is acute or
normal metabolic acids. Hydrogen ions are excreted
chronic. Another method is to examine whether the
When interpreting a blood gas, it is helpful to de
in the urine and also resorbed by bicarbonate into
situation is uncompensated, partially compensated or
the blood. In this manner, the kidneys can respond
completely compensated. The pH is the key to mak
when there is an acid/base imbalance to return to
ing this determination. If the pH is not in the normal
normal homeostasis.
7.35 to 7.45 range, then the patient will be in an acute

state. As it progresses back toward normal, it may be
pa11ially compensated. When a normal pH exists, it is
Normal Blood Gas Values
compensated or chronic.
Acid/base is denoted by the pH. The pH values are
For example, in a patient who is retaining a CO2 of
normally 7.35 to 7.45. If the pH is below 7.35, the
55 mm Hg, the pH may read 7.25; this would be con
patient is considered to be in an acidotic state (more
sidered acute. As the body retains base, the pH will
acid). If the pH is above 7.45, the patient is consid
rise back toward the normal numbers. If the pH was
ered to be in an alkalotic state (more basic).
7.32 with a Peo2 of 55 and + 3 base excess, the read
Alveolar ventilation is reflected in the partial pres
ing would be partially compensated. When the pH is
sure of carbon dioxide (Peo2). Normal Peo2 values
within normal limits with the Peo2 of 55 and a pH of
are 35 mmHg to 45 mmHg. If the PC02 is below 35
7.35, the reading would be compensated or chronic.
mmHg the patient is said to be hyperventilating (in

creased ventilation, blowing off more C02 than nor
mal). If the Peo2 is above 45 mmHg the patient is hy
PARTIAL PRESSURE Of GASES
p o v e nt i l a t i n g , or not h a v i n g e n o u g h a l v e o l a r
To better understand blood gases, it is important to
ventilation o r not blowing off enough CO2 t o main
remember the properties of gases. The earth's surface
tain normal alveolar ventilation.
consists of gas molecules that have mass and are at
Arterial oxygen is measured as Po2, the partial pres
tracted to the earth's center of gravity. At the surface,
sure of oxygen. Normal values are 80 to 100 mm Hg. If
this atmospheric weight exerts a pressure that can
the P02 is below 80 mmHg in someone less than 60
support a column of mercury 760 mm high.

Dalton'S law states that in a mixture of gases, the
years old, the patient is hypoxemic. A value of 60 to 80
total pressure is equaJ to the sum of the partial pres
mmHg
would be considered moderate hypoxemia, and less
sures of the separate gases. Oxygen is 20.9% of the at
than 40 mmHg is severe hypoxemja (Chemiak, 1992).
mosphere, so it has a partial pressure of 159 (760 x
20.9%
159). Nitrogen is 79% of the atmosphere, so

600).
Other gases make up 0.1% of the atmosphere.
=
it has a partial pressure of 600 (760 x 79%
Base Excess/Base Deficit
The blood normally has a capacity to buffer acid
Diffusion of gases across semipermeable mem
metabolites. The normal level of base Heo3 in the
branes show gradients from higher concentrations to
blood is 22 to 26 milimoles per liter (mmollL). This
lower concentrations. Each gas moves independently
buffering capacity diminishes in the presence o f
from the others.
During respiration, oxygen and CO2 exchange
155
with no circulation, a dead unit is credited. Figure
across the alveolar capillary membrane. Special situa
9-1 demonstrates the regional differences seen In
tions may affect the normal progress of respiration
respiratory units.
and gas exchange.

Normally, alveolar units ventilate and capillary
Hemoglobin
units bring oxygenated blood to the tissues, excret

i n g C02 b a c k i nto t h e alveoli to be removed
Hemoglobin (Hgb) is the main component of the red
through the lungs. However, some abnormal situa
blood cell. It is crucial for oxygen transport. The nor
tions may occur, such as shunts and dead space
mal Hgb is 12 to 16 gmllOO mL blood. In patients that
units. In a shunt unit, the alveoli has collapsed, but
have lost blood through surgical procedures or dis
blood flow continues and is unable to pick up oxy
ease, the decreased hemoglobin can account for their
gen. An example of this is atelectasis, where a lung
extreme weakness as a result of decreased oxygen
segment or part of a segment has retai ned secre
transport capacity. In addition, patients with advanced
tions and lung tissue distal to the mucous plug col
chronic obstructive pulmonary disease (COPD) can at
lapses. Circulation continues but oxygenation does
times desaturate with exercise when their Po2s are
not occur and the POl decreases. On the other hand,
low; during exercise, they use increased oxygen.
a dead space unit can have ventilation but not per
Cyanosis, a bluish color to the skin, mucous mem
fusion. This occurs with pulmonary embolism,
branes, and nail beds, is indicative of an abnormal
blood clot obstructs the circulation. The
amount of reduced Hgb concentration, usually greater
oxygen is available in the ventilated alveoli, but
than 5 gm of reduced Hgb. The presence of cyanosis
where
B
A
FIGURE 9-1
A, Normal alveolus. B, Dead space. C, Shunt.
156
PART II
suggests a high probability of hypoxemia; however, it
can occur without cyanosis. Two examples may be

cited, one in which an anemic patient with hypox
For every 20 mm Hg increase in Peo2, the pH de

creases by 0.10.
emia can have little cyanosis, and the other in which
For every 10 mm Hg decrease in PC02, the pH in

creases by 0.10.
There is also a relationship between the Peo2 and
a patient with polycythemia can have cyanosis with
the plasma bicarbonate:
minimal hypoxemia.
There is a predictable relationship between the arter
sented in the oxyhemoglobin dissociation curve as fol
For every increase of 10 mm Hg in the Peo2, there

is a decrease of I mmollL plasma bicarbonate
ial oxygen saturation of the Hgb and the POz. It is repre
For every 10 mm Hg Peo2, there is a decrease in

plasma bicarbonate of 2 mmollL.
lows. When oxygen saturation is monitored during

exercise, saturation is kept at or above 90%. As the
Knowing these guidelines, it can be determined if
curve denotes at a level of approximately 60 mm Hg,
the changes in the arterial blood gases are in line with
the saturation is about 90%. As the P02 drops at the
respiratory problems vs. metabolic problems such as
sharp part of the curve, for every mm Hg POz, there is a
acidosis from diabetic ketoacidosis, where the base
marked decrease in oxygen saturation (Guyton, 1986).
deficit can be very low, the pH can be low (acidemic),

but the Peo2 can be within normal limits (Shapiro,
1994; Shapiro, Peruzzi, and Templin, 1994).
Chemoreceptor Response to Hypoxemia

The peripheral chemoreceptors, the carotid, and the
aortic bodies, are located at the bifurcation of the in
ternal and external carotid arteries and the arch of the
RESPIRATORY FAILURE
Respiratory failure is defined as the failure of the pul
aorta. These receptors are nervous tissue that have a
monary system to meet the metabolic demands of the
high metabolic rate and an abundant oxygen supply.
body, that is, ventilation and oxygenation (Shapiro,
When tissue P02 decreases, their response to the brain
Peruzzi, and Templin, 1994). The blood gases usually
is to increase ventilation and cardiac output. When
have a pH below 7.30 and a Peo2 above 50. Generally
this is not sufficient to effect a normal POz, supple
the patient is also hypoxemic.
mental oxygen or increased mechanical assistance
During the acute phase, the kidneys have not
such as continuous positive airway pressure (CPAP)
started to compensate and the base HCO,- is within
is given (Tarpy, 1994).
normal limits. Later, a base excess can be noted as

the kidneys try to compensate for the acidotic pH.
Chronic respiratory failure can be noted by an in
BLOOD GAS INTERPRETATION
creased Peo2 with a pH within normal limits.
The norms for the pH, Peo2, Po2, and base have pre
In assessing the Po2, the following ranges are
viously been given and should first be considered. Is
used: mild hypoxemia less than 80 mm Hg, moderate
the value normal or not? Is the patient acute, that is,
hypoxemia 60 to 80 mm Hg, and severe hypoxemia
uncompensated, partially compensated, or fully com
below 40 mm Hg.
Positional changes can affect the oxygenation sta
pensated (chronic)? There are also "acceptable"

ranges to consider, as in the following:
tus. For example, unilateral right lower lobe atelecta
pH 7.30 to 7.50
sis with the patient lying on the right side causes in
Pe02 30 to 50 mm Hg
cre a s e d blood fl o w to the right lung, which i s
pH 7.45 alkalemia
collapsed. This causes increased shunting and a de
pH 7.35 acidemia
crease in oxygenation lying on the right side (differ
Pae02 45 respiratory acidosis (hypercapnia)
ential shunting). If the patient lies on the left side, the
Pae02 35 respiratory alkalosis (hypocapnea)
oxygenation will improve. Lying supine, a mixed P02
A relationship between the pH and the PC02 also
can be observed.
When hypoxemia is noted, treatment consists of
exists. There is a predictable change caused by varia

tion in carbonic acid:
oxygen therapy and alleviation of the cause of hypox
157
emia, if possible. This may be airway clearance tech
duced less O2 is available. This is particularly impor
niques or medication, in addition to the oxygen ther
tant if a patient already has a decreased P02 and is
apy. Oxygen therapy treats the hypoxemia, decreases
traveling to an area with lower barometric pressure.
the patient's work of breathing, and decreases my
Patients on oxygen will need an oxygen prescription
ocardial work.
based on the area in which they are living.

Barometric pressure increases, such as a hyper
baric oxygen chamber with higher barometric pres
FACTORS AFFECTING ARTERIAL BLOOD GASES
sure, can be helpful in delivering increased oxygen
There are many normal causes that have an affect on
for many patients. Wound-healing needs and carbon
arterial blood gases, such as extremes of age-neonatal
monoxide poisoning are two .such indications.
to geriatrics. The neonate has many changes going on
Increased temperatures (febrile state) can increase
in the initial life process; fetal circulation changes
metabolism and therefore increase oxygen consump
dramatically in the first hours and days of life. In the
tion. Decreased temperatures can decrease the oxy
geriatric patient, decreases in cardiac output (CO),
gen consumption, as seen in patients involved in cold
residual volume (R V) of the lungs, and maximal
water near drowning, where they survived several
breathing capacity gradually decrease P02 over the
minutes under the water, and were resuscitated and
life cycle. It is estimated that after 60 years of age,
resumed normal lives.
the P
It is important to note on the arterial blood gas
decreases by I mm Hg per year of age from
60 to 90 years.
report the status of the patient when the blood gas
Exercise or any increase in activity from rest may
was drawn. Usually patients are at rest when the

is low at rest (60 mm
result in increased oxygen consumption for patients
blood gas is drawn. If the P
with cardiopulmonary dysfunction. In the normal
Hg) it is close to the sharp part of the oxyhemoglo
population, the human body compensate by increas
bin dissociation curve and the patient may desatu
ing oxygen consumption to meet the workload. Usu
rate with exercise.

If the patient was on supplemental oxygen and the
ally, a plateau is reached and a constant oxygen con

sumption for that activity is achieved. In patients with
cardiopulmonary dysfunction, oxygen consumption
with additional 02 (Carpenter, 1991). Similarly, if a
continues to increase even at the same workload in
patient is on mechanical ventilation, the blood gases
untrained patients. It is important to monitor oxygen
should be within or near normal limits.
was only 55 mm Hg, the P02 is still inadequate
saturation to prevent desaturation of these patients

(Guyton, 1986). During pregnancy, hormonal and
mechanical factors have a negative effect on car
diopulmonary function. During the last trimester,
SUMMARY
This cha pter discussed the normal arterial blood
women often observe shortness of breath and diffi
gases and what their values mean to the therapist.
culty taking a deep breath secondary to diaphrag
Relationships between pH and Pe02, Pe02 and He03-,
matic encroachment.
and O2 saturation and POz have been examined. We
During sleep, there is a decrease in minute ventila
saw predictable changes that are caused by respira
tion and a decreased responsiveness to CO2 and hy
tory changes were described. In addition we noted
poxemia. Many patients with spinal cord injury and
that metabolic changes can have marked effects on
COPD have been noted to have hypoxemia during
blood gases. Oxygen therapy and airway clearance
sleep studies. This should be considered in any tired
techniques can improve hypoxemia, and position
or groggy patient.
changes can be detrimental, causing differential
Low barometric pressure associated with high alti

tude significantly decreases the amount of oxygen
shunting
or
i m p r o v i ng
the
P02
by
better
ventilatiOn/perfusion matching.
available to the individual. As noted before, the par
As PTs, it is necessary to be acutely aware of the
tial pressure 20% of oxygen is dependent on the total
respiratory monitors that can assess and progress pa
atmospheric pressure. When the total pressure is re
tients safely to their optimal rehabilitation potential.
158
PART II Cardiopulmonary Assessment
References
REVIEW QUESTIONS
1. Which factors affect arterial blood gases?
2. How can exercise have a deleterious effect on
blood
3. What predictable
occur between pH and
and oxygen saturation?

4. What two theraDeutic t echniques can improve
K.D. (199]). Oxygen transport in the blood.

!J (9), 2033,
Chernlak, R.M. (1992). Evaluation
r<:'spiratory function in health
and disease. Dis MOrl.
(7),505-576.
Guyton, A. (1986). Textbook of medical physiology (7th ed,),
Shapiro, B.A. (1994), Evaluation
blood gas monitors: pelfor-
Carpenter,
Care Nurse,
mance criteria, clinical impact, and cosrlbenefit (editorial com
5. What affect can body position have on blood

gases?
ment). Crilical Care Medicine, 22 (4), 546-548,

Shapiro,
B,A" Peruai. W., & Templin, R, Clinical applicalion of
blood gases, (5th
St. Louis: Mosby,
& Farber. H,W, (1994), Chronic lung

prescnbe home oxygen, Ceriatrics, 49 (2), 27-28,3
Tarpy, S,P"
Principles of Chest X-Ray

Interpretation
Michael Ries
Thomas Johnson
KEY
TERMS
Air bronchogram
Hyperlucency
Air fluid levels
Mass formations
Atelectasis
Pneumonia
Densities
Radiograph
Diffuse patterns
Silouette sign
There are three general categories of radiographic
One of the first things to check before interpreting
studies of the chest-fixed-position studies, sus
the film is the quality of the film. An optimal PA
pended motion studies, and motion studies. The rou
chest film is one in which the dim outline of the ver
tine posteroanterior (PA) and lateral chest film is a
tebral bodies is seen through the mediastinum. Films
fixed-position, suspended motion study. The patient
may be overpenetrated (of increased density) or un
is positioned with chest against the x-ray film holder
derpenetrated (of decreased density) and still be ade
and is asked to hold his breath in deep inspiration.
quate for interpretation. Suboptimal films may also
The radiograph (x-ray) is named from the source
hide pathology and cause misinterpretation.
of the x-rays to the film. Thus a PA chest film is po
The purpose of a radiograph is to see inside the
sitioned so that the source of the x-rays is 72 in. be
otherwise opaque body by shifting the spectrum of
hind the patient and the film is in front. An antero
light to above the high ranges of the visible spectrum,
posterior (AP) chest film is the reverse, with the
thus converting the body structures into densities
back of the patient against the film. During interpre
rather than colors. The densities recorded on the x
tation, the conventional position of the fi 1m on the
ray film range in shades of gray to black depending
view box is as if the physical therapist (PT) were
on the amount of x-ray energy the structures of the
facing the patient.
body absorb as the x-ray passes through them.

159
160
PART II
FIGURE 10-1
(A and C) transform into two-dimensional

(B and D). The pictures (A and C) also show a box of cherry tomatoes and a
jar of bird seed (millet seed) and their x-rays. B, is the radiograph of A, and D, is the radiograph of
C. Changes in position of the same objects from A to C illustrate the changes of shape in the
corresponding x-rays. B to D, and emphasize the need for PA and lateral x-rays for evaluating
Familiar fruits such as an apple, orange, pear and banana
objects when x-rayed
three-dimensional structures.
There are five basic densities, varying from very

radiolucent to very radiopaque. The darkest or most
third dimension, which is used to interpret the inter

nal problems of a patient.
radiolucent density is gas or air. Fat is moderately ra
The routine examination of the chest should in
diolucent. An intermediate or water density is seen
clude a PA and lateral chest film on maximum inspi
reflecting the connective tissues, blood, muscle, skin,
ration at least for the first examination. Without the
and other structures. Bone and deposited calcium are
lateral film, disease processes behind the heart and
moderately radiopaque. Metal is the most opaque
posterior in the thorax may be missed. Very ill pa
(white or clear). The structures of the body absorb
tients who cannot be transported to the radiology de
most of the x-rays as they pass through the body, and
partment must often be evaluated at the bedside from
the remainder of the rays expose the film.
a single PA or AP view (taken with the portable x-ray
An example of an x-ray is the familiar fruits or
unit). The size of the patient introduces mechanical
objects that have been converted into a two-dimen
limitations to the performance of a lateral chest film.
sional reproduction of densities in Figure
10-1.
These three-dimensional structures are reduced to

two dimensions and only the edges or structures tan
Portable x-ray units are not as powerful as the sta

tionary departmental machines.
Additional radiographic views may be ordered to
gential to the beam of the x-rays are recorded. Thus
verify
two views, taken at 90 from each other (PA and lat
(I) oblique views, (2) apical lordotic views, (3) de

cubitus views, (4) iaminograms, (5) inspiration and
eral), are required for a mental reconstruction of the
or e l u c i d a t e f i n d i n g s.
These i n clud e
10
Principles of Chest X-Ray Interpretation
161
FIGURE 10-2
These A, PA and B, lateral x-rays anatomically localize the basic structures that must be reviewed
during chest x-ray evaluation. Some of the structures are seen in both views and others are seen in
only one view. During evaluation, one should identify and see the foJlowing basic anatomical
structures.
Soft /issues and ex/ralhoracic s/rucltlres: soft tissues (ST), breast shadows (BS), diaphragm (D).
(L). and fundus of stomach (F).
Bony /homx: ribs (RI), vertebrae (V), scapulae (5, seen best on PAl, clavicles (CL. seen best on
PAl and sternum (SN. seen best on lateral).
Medias/ina! s/rucll/res: mediastinum (M), trachea (T), carina (CA). aortic knob (AK). heart (H).
anterior clear .'pace (ACS. seen on lateral) and hilus of lungs (HI).
LUlIgjields: hilus of lungs (HI). pulmon;Jry vessels (arise from hilus and branch outward).
costophrcnic angles (CPA) and lung apices (LA. seen best on PAl.
liver
There arc many other structures that must be evaluated in addition to these basic ones, and
pathologics must be identified.
ex.piration films,
since other pathologies may be present. All the
trast materials,
(6) special studies requinng con

(7) physiologic mOlion evaluation
with the fluoroscopc, (8) computed tomography (CT
scan), and (9) magnetic resonance imaging (MRI).
anatomical structures on the film should be exam

bones and soft tissues (including the abdomen), the
ined. A body system approach is recommended:
Film interpretation requires a solid knowledge of
mediastinum from larynx to abdomen, the cardiovas
gross anatomy and gross pathology. The PT is liter
cular system, the hila, and finally, the lungs (Figure
ally examining the internal structures of the body
10-2).
without an autopsy or surgical intervention. The

structures of the body are thus converted into the den
sities of air, fat, water, calcium, and metal. The PT
The tools of radiographic interpretation include

the following:
1. The principle of bilateral symmetry ( when
should ex.amine the entire film, not just one area, and
structures are paired, then in general one should
should not get "tunnel vision." Once an abnormality
look like the other).
is found, the PT should continue to evaluate the re
2. The presence or absence of air fluid levels
mainder of the film and should not stop at that point,
(there are almost no straight lines in the chest).
162
PART II
If a line appears to be straight, then it must be
Bronchi are not usually seen unless they are sur

rounded by fluid or have a disease causing thickening
explained.
3. The silhouette sign. When densities are next to
of the walls. The vascular pattern may be distorted,
each other, they obliterate normal margins and
blurred, increased, or decrcased by pulmonary dis
show no separation (normal silhouette of a
ease. Air space or alveolar disease is manifested by
structure is obliterated). When densities or
opacification (white appearance) of air-filled struc
structures are in front or in back of other densi
tures of the l ung. Thus pneumonia may appear as
ties or structures, then a margin is seen.
patchy coalescent areas of acini, or segmental and/or
4. An a i r b r o n c h o g r a m is seen w h e n t h e air
lobar consolidation. An air bronchogram is seen
around a bronchus is pathologically filled with
when the air-filled lung tissuc about the bronchus is
fluid or other material.
filled with fluid or other material and the bronchus is
5. Lobar and s e g mental collapse follows the
filled with air (Figure 10-3).

Certain lung diseases cause a decrease (increase in
anatomy of the lung.
6. Pleural changes may be manifested by gas in a
translucency) , such as emphysema (generalized) or bUl
pneumothorax, fluid in a pleural effusion, cal
lae (localized). Interstitial pulmonary disease is mani
cium or soft tissue from scarring or mesothe
fested by distoltion or increase in volume of tissues sur
home. A hydropneumothorax demonstrates an
rounding the air spaces. An enormous number of
air fluid level.
diseases can produce interstitial roentgenographic
7. The presence or absence of mass formation as
changes. Sometimes a diagnosis is strongly suggested
in tumors, nodular changes or miliary changes.
by the roentgenographic appearance, but in most, a his
The conventional terminology depends on the
tologic evaluation is required for diagnosis. Enlarge
size of the abnormality.
ment of the bronchi may result in bronchiectasis (Fig
8. Air-containing spaces such as bullae or cysts.
ure 10-4). Bronchiectasis is characterized by tubular
FIGURE 10-3
A, There is total pneumonic consolidation of right upper lobe with complete alveolar and bronchial
filling. B, Approximately 24 to 36 hours later, the consolidation has cleared markedly with patchy
coalescent residual. A few air bronchograms are seen in the perihilar region.
10
FIGURE 10-4
A, Fibrosis and saccular bronchiectatic changes are present in the left lower lobe. A few cystic
"circular" changes are present in the right upper lobe but are best seen on the bronchogram. B,
The bronchogram demonstrates the dilated abnOImal bronchi of cystic and saccular
bronchiectasis in the left lower I.obe with fibrosis around them. The right upper lobe reveals a
few cystic changes.
FIGURE 10-5
A, The PA chest film demonstrates the water density of a pneumonic consolidation in the right
lower lobe. The diaphragm is blurred. B, The lateral film shows obliteration of the posterior right
diaphragm and the costophrenic angle by the pneumonic consolidation.
163
164
PART II
shadows that are double-line paraliel shadows follow

ing the bronchovascular distribution. The shadows may
branch similar to the bronchial tree.
P n eu m on ias are u s u ally classified by their
causative agents of anatomical distribution. A lobar
pneumonia is one that involves the entire lobe, and a
segmental pneumonia involves the anatomical seg
ment of a lobe. Generalized pneumonic processes
occur with aspiration of vascular spread of an infec
tious agent (Figure 10-5). The roentgenographic find
ings of bronchopneumonia are varied. The earliest
manifestation may consist only of peribronchial cuff
ing. The disease, however, spreads rapidly to the
alveoli. More often, however, bronchopneumonia is
manifested by multiple, ill-defined nodular densities
(acinar nodules) that are patchy. As these acinar nod
ules become confluent, airspace consolidation devel
FIGURE 10-6
ops. As the disease progresses, segmental and lobar
A 5-cm cavitary ahscess is seen on the le ft with an air fluid
pneumonias can be seen.
level and a relatively smooth wall. This patient was
Pulmonary abscesses and cavities may occur sec

ondary to pneumonia. An abscess occurs when there
is a breakdown of the tissues of the lung, with the
area replaced by infectious materials (of water den
probably recumbent and lying slightly on the left side to

aspirate materials to this area, which was first a pneumonic
process in the superior segment of the left lower lobe and
progressed to an abscess cavily.
sity). When the infectious materials empty into the

bronchus and air communicates with the abscess, a
cavity develops in that area of the lung. Lung ab
scesses often result from aspiration and they are
catheters may result in a traumatic pneumothorax.
often found in the area s dependent at the time of the
The appearance is fairly characteristic, and there may
aspiration. Thus abscesses occur in the area that is
be an associated air fluid level with a hydropneu
downward by gravity, depending on the upright or
mothorax (secondary to minor bleeding from the
reclining position of thc individual (Figure 10-6). If
punctured lung). Pleural effwiions, or the accumula
the pleura is penetrated by the abscess, an empyema
tion of fluid between the lung and chest wall, can be
develops; and if a cavity communicates with the
seen in increased hydmstatic pressure (congestive
pleura, a pneumothorax de velops with a br on
heart failure [CHFJ), diseases of the pleurae (malig
chopleural fistula.
A pneumothorax
nancies) or diseases of the lung (emphysema sec

or
gas in the pleural space devel
ondary to pneumonia).
ops when the pleural .'pace communicates air through
Ale/ectasis is thc term used for incomplete expan
ei ther a defect in the chest wall or a defect in the
sion of a portion or all of the lung. A loss of air in the
pleural surface of the lung. As the air accumulates be
alveoli in the atelectatic area occurs. Atelectasis is a
tween the chest wall and the lung, the lung becomes
sign of disease, since it is always secondary to an
compressed and moves away from the chest wall
other lesion, such as (I) obstruction of a bronchus;
(separated by air) (Figure 10-7). Chronic interstitial
(2) loss of ability for pulmonary expansion as a result
disease and emphysema are often complicated by a
of pleural disease, diaphragmatic disease, and masses
spontaneous pneumothorax. Traumatic causes such
in the thorax; or (3) volume loss from local or gener
as automobile accidents or inseltion of central venous
alized pulmonary fibrosis. Atelectasis is a loss of vol
10
165
ume in the area involved and results in a decrease in

size or a change in position of the surrounding struc
tures (Figure 10-8).
Congestive heart failure, uremia and pulmonary
edema may be manifested by a "diffuse" pattern on
the chest film (Figure 10-9). In CHF, there is a pro
gression of roentgenographic changes as the disease
evolves into pulmonary edema. The first manifesta
tion is an increase in the antigravity vasculature of
the lungs (redistribution of blood flow to the upper
lobe vessels). The next stage is manifested by a loss
of the distinct margins of the vessels. This is fol
lowed by accumulation of fluid in the interstitial
spaces (around the alveoli). Pulmonary edema is pre
sent when the fluid seeps from the interstitium and
makes the alveoli opaque. Pulmonary edema is radi
ographically indistinguishable from diffuse pneumo
nia. CHF usually is associated with cardiomegaly
FIGURE 10-7
The chest x-ray reveals separation of the visceral from the
(enlargement of cardiac silhouette) and may be asso
parietal pleural line and absence of vessels laterally. A
ciated with pleural effusions and/or pericardial effu
"straight line" is seen at the rIght base, indicating a gas
sions (Figure 10-10).
fluid level in a hydropneumothorax. Fibrotic and irregular

pulmonary changes in the lungs indicate underlying
interstitial disease, which was a pneumoconiosis (silicosis).
Pulmonary malignancies may be both primary and

metastatic. Mass formation is characteristic, and there
may be atelectasis when the mass o b s tructs a
FIGURE 10-8
A, The PA film demonstrates loss of the right heart border and the downward shift of the minor
fissure, with atelectasis of the right middle lobe secondary to a radiolucent foreign body in the right
middle lobe bronchus. No air remains in the middle lobe, thus it is dense. B, The
arrow
on the
lateral view points to the residual tissue density of the right middle lobe, which is atelectatic.
166
PART II
FIGURE 10-9
FIGURE 10-10
The central lung fields reveal increased density and there is
The chest film reveals cardiomegaly (enlargement of the
sparing of the peripheral areas in "butterfly" pulmonary
cardiopericardial silhouette) and bilateral pleural effusions
edema. The patient has had a thoracotomy, and chest tubes
are more marked on the right than on the left. Vascular
are in place.
structures are blurred with interstitial edema.
FIGURE 10-11
A, A mass is present in the left hilar area obstructing the left upper lobe bronchus. There is
atelectasis of the left upper lobe and lingula secondary to the malignancy. B, The lateral view
reveals an S-shaped curve of tumor mass and atelectasis.
10
167
articulating facets in rheumatoid arthritis of the spine.

An obese individual may have severe difficulty with
respiration, not only because of the excess fat and
added weight on the thorax, but also because of the
increased load on the cardiovasculature system. This
increased load and hypoxemia may result in CHF.
REVIEW QUESTIONS
1. What are the three categories of radiographic
studies of the chest?
2. How may the quality of the film impact interpre
tation?
3. What are the five basic densities seen on a radi
FIGURE 10-12
ograph?
This chest x-ray of a kyphoscoliotic patient reveals a

markedly abnormal, reverse S-shaped curve of the thoracic
spine deforming the mediastinal structures and ribs. This
4. What principles are used consistently to interpret

radiographs?
5. How can lung disease cause a change in translu
patient is breathing primarily with the diaphragms.
cency of the Xray?

6. How can mediastinal deviation diagnose pneu
mothorax or atelectasis?
bronchus (Figure 10-11). Secondary findings such as

widening of the mediastinum, rib metastasis, pleural
masses or pleural fluid, and encasement of vascula
Bibliography
ture with hyperlucency beyond the tumor may be
Felson, B. (1973). Fundamentals of chest roentgenology (2nd ed.).
seen. Alveolar cell carcinoma may appear like a
Fraser, R.G. & Pare, J.A. (I 988). Diagnosis of diseases of the chest
(3rd ed.). Philadelphia: WB Saunders.
pneumonia. Involvement of the phrenic nerve may

result in paralysis of the diaphragm with elevation.
Thoracic deformities such as kyphoscoliosis may
severely impair the respiration of an individual (Fig
ure 10-12). The abnormal shape and direction of the
spine interfere with the leverage necessary for move
ment of the ribs with respiration. Severe impairment
of respiration may occur when there is fusion of the
Freundlich, I.M. & Bragg, D.G. (I 992). A radiographic approach

to diseases of the chest Baltimore: Williams and Wilkins.
Meschan, I. (1976). Synopsis of analysis of roentgen signs in gen
eral radiology Philadelphia: WB Saunders.
Murray, J.F. & Jade, J.A. (1994). Textbook of respiratory medicine

Paul, L.W. & Julll, J.H. The essentials of roentgen interpretation
(3rd ed.). New York: Paul B Hober, 1972.
Electrocardiogram Identification
Gary Brooks
KEY TERMS
Arrhythmia
Electrocardiogram (ECG)
Artifact
Syncytium
Bradycardia
Supraventricular
Depolarization
Tachycardia
INTRODUCTION
The ECG is an essential tool in the physician's di
The heart is a vital link in the oxygen transport sys
agnosis and medical treatment of cardiac disease. In
tem, pumping blood to the pulmonary and peripheral
formation provided by the ECG may also assist the
circulation systems to supply oxygen and other nutri
physical therapist (PT) in the assessment of a pa
ents required for metabolism in all tissues. The beat
tient's readiness for and response to physical activity.
ing heart generates rhythmic, electrical impulses that
PTs in many different practice environments have ac
cause mechanical contraction, or the pumping action,
cess to information afforded by the ECG. For exam
of cardiac muscle. Some of the electrical current pro
ple, in an acute care or rehabilitation setting, a pa
duced by these rhythmic impulses is detectable by
tient's baseline ECG, with an interpretation, may be
electrodes that may be placed on the surface of the
available within the medical record. Documentation
skin. Current flow during the cardiac cycle is then
accompanying a referral for outpatient physical ther
recorded as the characteristic waveforms of the elec
apy may include a reference to the patient's ECG. In
trocardiogram (ECG). Mechanical events such as con
other settings such as an intensive care unit or cardiac
traction and relaxation of the myocardium are infelTed
rehabilitation program, ongoing monitoring of a pa
from the waveforms produced by the ECG.
tient's ECG may be performed during evaluation and

169
170
PART II
treatment procedures. It is therefore crucial that all
polarization, during which a stimulus of greater than
PTs have a basic understanding of the uses and limi
normal intensity is necessary to depolarize the cell
tations of the ECG in their practices.
again. The refractory period of atrial cells is signifi
This chapter briefly reviews the basic anatomy
cantly shorter than that of ventricular cells allowing a
and physiology of the myocardial conduction sys
more rapid intrinsic atrial rhythm than intrinsic ven
tem as it relates to the ECG. The configuration of
tricular rhythm. Therefore atrial rhythms pace the
the normal ECG is presented and discussed along
heart, including the ventricles, given intact atrioven
with several methods of quickly determining heart
tricular (AV) conduction.
rate a n d rhythm from an electro c a r d i o g r a p h i c
Closure of the slow Ca++ channels at onset of repo
record or "strip." Some o f the more common dys
larization is accompanied by opening of K+ channels,
rhythmias are examined, as are some other patho
causing a rapid outflow of K+, which restores resting
logic features. Throughout the chapter, the uses and
negative membrane potential. During the cell's resting
limitations of the ECG in physical therapy practice
phase, Na+ and Ca++ are actively pumped out of the
are highlighted.
cell, and K+ is pumped into the cell, restoring ionic

gradients needed for repolarization (Shih, 1994; Guy
ton, 1991; Smith and Kampine, 1990).
PHYSIOLOGY AND ANATOMY
It is the electrical current produced by ionic
OF THE CONDUCTION SYSTEM
flow that is transmitted through the conductive tis
Generation of the Action Potential
sues surrounding the heart. This current is de
The action potential, or cardiac impulse, is generated
tectable by surface electrodes, enabling the record
by ionic flow across myocardial cell membranes. In
ing of the ECG.
the cell's resting state, a negative membrane potential

exists, based on the relative concentrations of sodium
(Na+), Calcium (Ca++), and Potassium (K+) in the in
The Conduction System
ternal and external cellular environments. Membrane
Because myocardial cells are arranged as a syn
potential changes rapidly at the onset of depolariza
cytium, an impulse propagates, or spreads to adjacent
tion, with the opening of Na+ and Ca++ channels, al
cells, causing them to make contact also. This
lowing these ions to cross the membrane and enter the
arrangement alone does not pellllit the heart to func
cell. Calcium then becomes available for contraction
tion as an effective pump. It is the conduction system
of cardiac muscle myofibrils. During depolarization,
that initiates and rapidly transmits impulses to other
the membrane's potential becomes positive and the
locations within the myocardium, allowing for effec
cell contracts. As in skeletal muscle, the Na+ channels
tive, coordinated myocardial contraction and pump
are fast-opening and fast-closing mechanisms, allow
ing. The conduction system is comprised of special
ing Na+ to rapidly enter the myocardial cell on depo
ized cardiac muscle that contracts minimally, because
larization. Unlike skeletal muscle, however, cardiac
it contains few contractile myofibrils.
muscle has a prolonged depolarization phase as a re
Any portion of the conduction system is capable
sult of the slower and extended opening of the Ca++
of self-excitation and may act as a pacemaker, gener
channels. During depolarization, there is also a de
ating action potentials. However, because of the in
crease in membrane permeability to K+, for which
trinsically more rapid rate of spontaneous depolariza
there is an outward gradient. A plateau phase of the
tion of the sinoatrial (SA) node, it normally acts as
action potential exists, during which outward flow of
the heart's pacemaker. The rate of depolarization of
K+ ions is inhibited. This prolongs depolarization and
the SA node determines the heart rate. In the absence
delays return to the resting membrane potential.
of an impulse from the SA node, the atrioventricular
Each cell has an absolute refractory period during
(AV) node depolarizes spontaneously, taking over as
depolarization, meaning that an additional stimulus
pacemaker, with the important difference that the rate
will not cause an additional depolarization. A brief,
of depolarization is lower than that of the SA node.
but significant, relative refractory period follows de-
The pathway of a normal cardiac impulse may be
11
171
R
R-R
I
I
I
I
I
FIGURE 11-1
Relationship of ECG complex to conduction pathway. (From Brown, K.R., & Jacobson. (1988).
MCI.I'lering dysrhYlhmias: A problem-soLving guide. Philadelphia: FA Davis.)
followed, highlighting its relationship to the cardiac
suiti ng in a dela y i n g of the impulse b ef o r e i t
cycle. Figure I I-I displays the association of the con
reaches t h e ventricular conduction system. This
duction system and its components with the ECG.
pause in impulse propagation allows the atria to
Atrial depolarization is initiated by a spontaneously
contract and fill the ventricles with blood_ The P-R
generated impulse that originates in the SA node. The
interval of the ECG represents this period between
impulse is then transmitted throughout the atrial mus
onset of atrial depolarization and the onset of ven
cle resulting in atrial contraction. This event is
tricular depolarization. Normally the P-R interval
recorded as the P-wave of the ECG. The impulse is
lasts between
also transmitted, via rapidly conducting internodal
Jacobson, 1988).
12 and
W seconds
(Brown and
pathways, to the A V node. Atrial repolarization is not
Following passage through the AV node, the im
recorded by the ECG, because it occurs during and is
pulse continues to the Purkinje's fibers, which trans
hidden by ventricular depolarization.
mit the impulse rapidly to the ventricular endo
Impulse conduction within the A V node and the
cardium. This initiates ventricular depolarization,
AV bundle (bundle of His) slows considerably, re
which is represented in the ECG by the QRS complex.
172
PART II
The depolarization wave propagates relatively slowly
U-wave may be seen. The U-wave was considered
throughout the ventricular myocardium. The span of
to have little physiologic or pathologic significance
1990).
However, U-wave in
time elapsing during ventricular depolarization is re
(Smith and Kampine,
flected by the
version may now be considered to correlate with
between
1988;
0.06
RS interval, which normally ranges
and
0.11
secon s
Smith and Kampine,
1990).
n an
Jacobson,
myocardial ischemia (American College of Sports

Medicine,
Ventricular depo
1991).
Note that the ventricles remain in
larization originates in the interventricular septum,
a state of contraction until slightly after repolariza
creating the Q-wave, which is normally small or ab
tion. This period of contraction corresponds to the
sent. The depolarization wave next spreads to the apex
Q-T interval on the ECG. Diastole, therefore, begins
and then to the right and left ventricles, causing the R
subsequent to the end of the T-wave and continues
and S-waves. Depolarization also propagates in an en
until the next ventricular depolarization. Note also
docardial to epicardial direction within the ventricles
that atrial depolarization and contraction occur dur
(Lilly,
J993;
Guyton,
1991).
ing diastole.
The T-wave of the ECG represents ventricular re

polarization. It is preceded by the S-T segment, dur
THE ELECTROCARDIOGRAM
ing which depolarization has been completed and
Recording the Electrocardiogram
repolarization is yet to begin. The configuration of

the S-T segment is an important marker of myocar
Before examining the timing of the wave forms and
dial ischemia or infarction. Following the T-wave, a

----
the rhythms of the ECG, a basic understanding of the
I I n-- ilr-fi-r-.VR 1 IT '-l- I Tl vl

I I'
i - 1-
ITl-I-H-j 1 I I '
I
, I I
I
I
,!
!
I
! I I
'"
'
I
'
I
1
1 . ,
-R
rD . V1 '
JJ ,
1 = _t-bD7iTI--1- ' i. T
-r- I I I
'
I !
I
I -, I !. .J +! l I
U0.--'-.l.-b.L_L_;'.J.0
io.,
! I ,
I '!
-'
,L',.
1 r
;-t-.
"r-;
:
.
"IA.....
t-LLLL
LiII.,LLLL
Iffi1
rl- f I+H i ! ;ffft-TmTfFI' r: i}Tiii H {if
ttl-mUll I I 111 1 ! i II ! 1I11I1II1I CB-8 i j LU i..Ult LI I I ttr
I, ! !
:.
.! .
____
K+
m.J
, " , ." . ",,=g
;;.: . l,w,ll- IIII, .,mOOJ.
"
. ,
t ru!8fffi
t-+TH--r-H+-:-:+.Lf+H+H-+-!--H-:- =-1._!'I-l-l-H-l.-
....
FIGURE 11-2
A normal 12-lead ECG tracing.
]1
173
-------
principles of
is needed. A stan
A VR. A VL, and A VF are derived from the electrical
12-lead
and
sum of the three standard limb leads. The transverse
medical management of cardiac conditions. An ex
plane leads are referred to as the precordial leads.
11
Imagine that each of the 12 leads "views" the heart
ample of a normal 12-1ead ECG is seen in

2. Six leads record the electrical
in the frontal
from a different angle, therefore
plane, and six leads record signals in the transverse
different locations of the heart
plane.
The frontal plane leads include three standard limb
II, and III. Three augmented limb leads,
(downward) when current travels away from a lead.
V6
V5
I-- V6
I- V5
,.i
Vl
V2
-'\.
VA
V3
FIGURE 11-3
leads.
174
PART II
indicates appropriate conduction of impulses from
Other lead configurations may be used for exercise
testing (American College of Sports Medicine, 1991).
atria to ventricles.
Single-lead monitoring is commonly used during ex
What is the P-R interval? A P-R interval of greater

than
ercise training or in acute care settings.
0.20
seconds indicates delay in conduction
from atria to ventricles.
Evaluating the ECG Strip
Is the QRS complex of normal duration and mor

phology (shape)? A QRS complex greater than
The evaluation of an ECG should be approached in a
0.12
systematic fashion. The following questions are use
within a ventricle or was conducted abnormally

through the ventricular conduction system.
ful to appreciate the information that is relevant to

current clinical practice (Cummins,
seconds indicates either that an impulse arose
1994).
By answering each of these questions, the tendency
What is the rate and pattern (regularity) of the
to "eyeball" the rhythm and make a quick but inaccu
rhythm? If the R-R interval, that is, the distance
rate assessment is avoided.
between successive R-waves, is inconsistent, is the
Determination of Heart Rate
pattern irregular?
Does a P-wave precede every QRS complex? This

indicates appropriate atrial activity.
Several quick methods estimate heart rate. Most
Is there a QRS complex after every P-wave? This
printed and displayed ECG recordings indicate a heart
J I
m =l-rIlIl_
L-J- -+ -- +-+--r-t-i R !-t- lr-r 0.2second
4s , .oo n +-+- -r1
L-+-t-t
r1
rt lIlr
segment
I--H--+--t---t-I' t
PR
-.l
I-+-
-r-rI,
j
Ll"
!.i
'
I!
segment I-++-t -nrmmnml 50.5mmmv. -+I

I '
I!
-'
',
111 i
0.1mv
,
!
interval I ITi1
I 1 1 , aRS-.lInterva
' ..l
PR
1.--+-++
- -
ST
ll
,
"
''
I
I
.:.. interla,
a. T
1-'
1 1
FIGURE 11-4
A normal ECG showing characteristic waves, intervals, and segments, and some of the features of
the traci ng paper.
11
175
rate. This must be interpreted with caution, however.
the rate would be estimated as falling between 100
The presence of artifact (extraneous deflections of the
and 75, or close to 80 beats per minute (BPM).
waveform caused by movement or electrical intelfer
In many clinics, rulers are available that are cali
ence) may render inaccurate the displayed or printed
brated so that heart rate may be estimated quickly by
heart rate. This is a common problem dUling activity
aligning markings on the ruler with features of the
or exercise, the circumstances during which many PTs
ECG strip. For example, after the arrow on the ruler
monitor patients. It is possible to calculate or to esti
is placed on an R-wave, count two R-waves to the
mate a heart rate from a printed ECG strip because, by
left and read the number at that position on the ruler.
convention, the recording paper is divided into I mm
In Figure 11-6, this method approximates the heart
squares and larger 5 mm squares, which are defined
rate as 74 BPM.
by heavier lines (Figure 11-4). Also by convention,
It is important to note that the preceding two
the standard paper speed for an ECG recording is a
methods are useful only if the rhythm of the ECG
rate of 25 mm/second. Each millimeter of length then
strip is regular, that is the R-waves are equally
represents 1125th, or 0.04 seconds, and each 5 mm
spaced, occurring at consistent intervals. Should the
block represents one fifth, or 0.20 seconds. Some
rhythm be irregular, with R-waves appearing at vary
monitor systems place a mark on the recording paper
ing intervals, another method must be employed to
at 25 mm, or I-second intervals.
estimate the heart rate.
There are several methods of estimating heart rate
Recall that the ECG graph paper is divided into
from a printed ECG strip. On a printed ECG strip,
boxes, with the horizontal spacing representing time
find an R-wave located on or near a heavy vertical
intervals of 0.04 seconds for each small (I mm) box
line. Proceeding to the left of that R wave, for each
and 0.20 seconds for each larger (5 mm) box. It fol
subsequent heavy vertical line, assign the following
lows that I second in time is represented by five
numbers: 300 for the first heavy line encountered,
larger boxes. A mark may be placed at 1- or 3-second
150 for the next followed by 100, 75, 60, 50, and 42
intervals, enabling quicker appraisal of heart rate
(Figure 11-5). Stop at the first heavy vertical line fol
based on a 6-second strip. The procedure is as fol
lowing the next R wave that is encountered. The
lows. Obtain a printed strip of sufficient length, cov
heart rate may be estimated as falling between the
ering more than 6 seconds. If l-second marks are not
two most recently assigned values. In Figure 11-5,
present, it may be convenient to place a mark at every
FIGURE 11-5
"Count-off" method of estimating heart rate.
176
PART II
, ' , f' f'z',
,J
+b
'
V2
.. ...
IfPL_, t. l
1 -.1
;:It"
-I '
- '
.
tH-
'
I'
..
. ....
+
I t
r.-- 'f' T ' 'r '4rf'
1.. ....11
t'.. ,.
II .
..; . t 't "

,.. .r......
..
"
.--
. ..,
.. 1..
;..
?r t_" 1"
, '""' '/,j
._
'''lift'
111111111 nil ] II r 1 1 II
"
'''t-,
fj7r'
.
-F
'
I I
"
1.
I "
1', :;-rt
"
Heart rate (two cycles from reference arrow) chart rate (25 mm/ sec)
,".
.r
.!..
t
"I
FIGURE 11-6
Using a rate-ruler to confirm heart rate.
FIGURE 11-7
Heart rale estimation in an irregular rhythm (atrial fibrillation).
fifth large block. Next, select a I-second mark or a

heavy vertical line on the left side of the strip, and
Evaluation of Rhythms
Electrocardiographic monitoring is an impOitant evalu
proceed to the right for a length corresponding to 6
ation tool during the treatment of individuals with his
seconds. If I-second marks are counted, do not count
tory of or potential for acute myocardial infarction (MI)
the starting mark or there will be only as-second
or myocardial ischemia. Most cardiac deaths are a re
strip. Count the number of R-waves within the 6-sec
sult of lethal arrhythmias, for which there is increased
ond recording, and multiply by lO. That is estimated
risk in the presence of infarction or ischemia. Rapid
heart rate. Several 6-second strips may be analyzed to
recognition of lethal anhythmias, or arrhythmias that
document a heart rate range of an irregular rhythm
may deteriorate into lethal a.rrhythmias, is essential for
11-7). The rate of this irregular rhythm is es

timated at 70 BPM.
all health professionals involved in the care of individu
(Figure
als with cardiac disease. The arrhythmias described in
11
177
FIGURE 11-8
Normal sinus rhythm.
this chapter are those that must be recognized by

providers of Advanced Cardiac Life Support as deter
mined by the American Heart Association (Emergency
Cardiac Care Committee and Subcommittees, 1992).
Normally, a cardiac impulse is generated by the
SA node, causing atrial depolarization. This is fol
lowed by a slight delay in the A V node, after which
the impulse is conducted to the ventricles causing
ventricular depolarization. These events are seen in
their normal spatial and temporal sequence in normal
sinus rhythm (Figure 1 1-8). A P-wave precedes every
QRS complex and every P-wave is, in turn, suc
ceeded by a QRS complex. This occurs within an in
terval of 0.20 seconds (one large box), as determined
by the P-R interval. The QRS complexes occur
within a range of 0.04 to 0.11 seconds, indicating that
ventricular impulse conduction and depolarization is
occurring in a normal interval. The positively de
flected T-wave indicates normal ventricular repolar
ization. Because the SA node spontaneously depolar
izes at a rate of between 60 and 100 BPM, the rate of
normal sinus rhythm must fall within these limits.
The identification of arrhythmias affects clinical
decision making, particularly with regards to a pa
tient's readiness for and/or response to activity. Clini
cal significance of arrhythmias range from benign to
lethal. The clinical significance of a given arrhythmia
is determined by a number of considerations. Some
of these considerations include the following: Is there
evidence of hemodynamic compromise? Is the ar
rhythmia a new or unusual finding? Might the ar
rhythmia be a precursor to a more serious or perhaps

lethal arrhythmia? Is this an acute occurrence or a
chronic arrhythmia pattern? The clinical response to a
patient with an arrhythmia depends on the answers to
these questions and the treatment setting.
ARRHYTHMIA IDENTIFICATION
Supraventricular Arrhythmias
Supraventricular arrhythmias arise from an abnormal

ity of impulse generation or conduction "above" the
level of the ventricles. The abnormality may occur in
the atria or at the level of the A V junction. Supraven
tricular arrhythmias may be categorized as sinus,
atrial, or junctional alThythmias.
A cardiac rhythm may be a sinus rhythm, but with
an irregular or abnormally rapid or slow rate. Sinus ar
rhythmia is an in'egular sinus rhythm with varying R-R
intervals (Figure Il-9). This is a normal variant that is
associated with the individual's respiratory pattern.
Sinus bradycardia is a sinus rhythm occumng at a rate
of less than 60 BPM (Figure 11-10). This rhythm may
significantly reduce cardiac output, causing hemody
namic compromise, manifested by hypotension or
symptoms such as dizziness, lightheadedness, or syn
cope. On the other hand, individuals taking beta-block
ers, medication that slows the heart, may exhibit this as
their normal rhythm, as may individuals who achieve a
high level of physical conditioning. Sinus tachycardia
is a sinus rhythm OCCUlTing at a rate of greater than 100
BPM (Figure 11- 1 1). Sinus tachycardia, or any other
178
PART II
ft' 'trr.
" ''
-,
'
+t-;
. ,.. , '.
_",-,-::C' .
,.
.4
:
'
"
fr"
,t" " ,., '
L
'
'
:
.
,.
i' "
..
...:.1._ t
FIGURE 11-9
Sinus arrhythmia.
tt
"
.... . ..
"
: '!.'" L
FIGURE 11-10
Sinus bradycardia.
l , of
fl
I I (}t L,
l'"r
L..1-L r
t::
. "
I,
. .J.:... L
1"1
FIGURE 11-11
Sinus tachycardia.
' L t
'
.1' I
11
179
FIGURE 11-12
Premature atrial complex.
form of tachycardia, increases myocardial oxygen de
abruptly and spontaneously reconverting to the previ
mand, or the workload on the heart. This may initiate
ous rhythm within seconds or minutes. The P-wave is
or exacerbate ischemia in the presence of coronary
often not visible, making assessment of atrial or junc
artery disease (CAD).
tional origin difficult, but the duration of the QRS
A common form of arrhythmia is a "premature"
complexes occurs within an appropriate interval. The
complex, that is, a beat that occurs sooner than ex
R-R interval, however, is markedly shortened. Figure
pected given the established rhythm. A premature
11-13 demonstrates supraventricular tachycardia at a
atrial complex, or PAC, is an early beat of atrial origin
rate of [90 BPM. Other related forms of SVT include
(Figure [1-12). An R-wave appears closer to its pre
paroxysmal atrial tachycardia (PAT) and multifocal
ceding R-wave than the other R-waves in the estab
atrial tachycardia (MAT). Clinically, patients with
[ished rhythm. Closer inspection reveals the presence
SVT may perceive a "racing" heart rate, which may
of a P-wave associated with the QRS complex, mean
be quite distressing. At very rapid heart rates, for ex
ing that the impulse first depolarized the atria before
ample, greater than 170 BPM, diastolic ventricular
being conducted to the ventricles. Sometimes the AV
filling time is markedly reduced, which may cause
junction may initiate an early beat, causing a premature
hemodynamic compromise. Symptoms associated
junctional complex or PJc. When this occurs, the R
with inadequate cardiac output, such as dizziness,
wave appears earlier; however, there may be no associ
lightheadedness, and syncope may ensue. Some indi
ated P-wave, or there may be an unusual P-wave, one
viduals with SVT remain asymptomatic; the rhythm
that is inverted or following the QRS complex. An in
being detected incidentally, for example, during rou
verted or late P-wave indicates that the impulse was
tine pulse or telemetry monitoring.
conducted in retrograde (backward) fashion. Clinically,
Atrial fibrillation is the most common, clinically
a premature atrial or junctional complex may be pal
encountered arrhythmia, seen in more than 5% of pa
pated as a "skipped" or early beat during pulse taking,
tients over age 69. (National Heart, Lung and Blood
or the patient may perceive a palpitation or skipped
Institute, Working group on atrial fibrillation, 1993)
beat. Otherwise, these arrhythmias are usually of little
Atrial fibrillation is characterized by inconsistent, ir
clinical significance (Brown and Jacobson, [988).
regular R-R intervals with an absence of true P-waves.
A more serious supraventricular arrhythmia is
P-waves may be replaced by multiple, fibrillatory F
supraventricular tachycardia, or SVT. In this arrhyth
waves of varying configuration. This arrhythmia signi
mia, the healt rate is rapid, exceeding 150 BPM. The
fies that there is no established sinus or atrial pace
tachycardia may be sustained, lasting hours or even
maker, rather that many impulses are simultaneous[y
days, or may be "paroxysmal" (PSVT), appearing
generated from multiple locations within the atria. The
180
PART II
FIGURE 11-13
Supraventricular tachycardia.
atria, therefore, are not pumping effectively which, in
(Figure 11-15), the QRS complex is not preceded by
turn, may impair ventricular contraction. This is be
a P-wave. The AV node may generate an isolated
cause of the loss of the additional ventricular filling
"escape" beat, or it may take over as the heart's pace
supplied by atrial contraction. Impulses do conduct
maker. Sustained nodal
through the AV junction to the ventricles; however,
ally between 40 and 60 BPM, corresponding with the
this occurs inconsistently resulting in the irregular R-R
inherent rate of spontaneous AV node depolarization.
or
junctional rhythm is usu
interval. The ventricular response to atrial fiblillation

is important. A rapid ventricular response, resulting in
tachycardia, may cause hemodynamic compromise
with associated symptoms or poor activity tolerance.
Ventricular Arrhythmias
Ventricular arrhythmias result from spontaneous de
Of additional clinical significance is the association
polarization of a region within ventricular my
between atrial fibrillation and embolic cerebrovascular
ocardium; a region outside the normal pathway for
accidents. Figure 11-7 illustrates atlial fibrillation with
impulse generation. For this reason, the site of im
a "controlled," that is, less than 100 BPM, ventricular
pulse generation is called an ectopic focus. Ventricu
response. Pulse monitoring of an individual in atrial
lar arrhythmias may be distinguished from supraven
fibrillation reveals an irregularly irregular pattern.

Another arrhythmia that is characterized by abnor
tricular arrhythmias, in that the QRS duration of a

ventricular arrhythmia is longer than normal 0.12
mal atrial activity is atrial flutter, seen in Figure 11-
seconds. The appearance of ventricular arrhythmias
14. In this rhythm, P-waves are replaced by F-waves
may be characterized as being "wide and weird." It is
that have a distinctive morphology often referred to
important to point out that not all rhythms with a
as a "saw tooth" or "picket fence" appearance. Of
QRS duration greater than 0.11 seconds represent ec
clinical importance is the ratio of atrial to ventricular
topic ventricular beats; some widened QRS rhythms
conduction and whether or not the patient is hemody
result from d isturbances of impulse conduction
namically stable (Brown and Jacobson, 1988).
within the ventricles, rather than from impulse gener
Because the intrinsic rate of spontaneous depolar
ation within the ventricles.
ization of the AV node is less than that of the SA
The reason for the widening of the QRS complex
node, spontaneous AV node depolarization is nor
resulting from ventricular impulse conduction distur
mally prevented. However, in the absence of an atrial
bance or impulse generation is apparent when one con
impulse the AV node depolarizes spontaneously and
siders the normal conduction of a sinus impulse within
generates an impulse that then is conducted to the
the ventricles. An impulse normally is rapidly con
ventricles. Thus in junctional rhythm or nodal rhythm
ducted to ventricular myocardium via the Purkinje's
11
FIGURE 11-14
ff--
TI
"fir rtJ
181
hi:. f ,1t;f
TT1 _n_1
,_
Atrial fluller.
FIGURE 11-15
Junctional rhythm.
11-16).
fibers. This assures that the impulse reaches all regions
during an ectopic beat (Figure
of ventricular myocardium in a timely fashion, with
rhythm (bottom) is recorded simultaneously with the
An ECG
subsequent coordinated depolarization and contraction.
record of arterial blood pressure monitoring (top).
Within ventricular myocardium itself, however, propa
The appearance of the "wide and weird" complex re
gation of the depolarization wave proceeds more
sults in significant diminution of the corresponding
slowly, as a result of the syncytial anangement of my
arterial pressure wave.
ocm'dial cells.
The most common form of ventricular arrhythmia
An impulse generated within the ventricles, out
is a premature ventricular complex, or PVc. In Fig
11-16 the wide and weird QRS complex appears
side the normal conduction pathways, initially depo
ure
larizes surrounding local myocardium. The depolar
early, interrupting the established rhythm. A pause
ization wave then spreads outward from that focus,
often follows a PVC, after which the established
but is propagated at a slower velocity. Ventricular
rhythm resumes. Clinically, a PVC may be perceived
contraction, in this case, is not coordinated; some re
by a patient as a "skipped" beat or a palpitation. If
gions contract well b e fo re the depolarization wave
pulse monitoring occurs during a PVC, the examiner
reaches regions remote from the ectopic focus. It fol
will likely sense a "skipped" or irregular beat.
lows that the ventricular ejection of blood is reduced
PVCs sometimes happen in patterns, occurring at
182
PART II
l.L
I
.... '
t' SPEEIJ)
If
j
25
+
l
L
Uti
1_-,-
.J.:.
I.
f
t1 t-r
"
MM/SECOND
I
1"""'j
LL
+- t
.:]
FIGURE 11-16
Diminished arterial pressure wave following a PVc.
FIGURE 11-17
Ventricul ar bigeminy.
m!EulittIOOIOO,
t1 '
IOOlfirkifmlffE[fffil
Tl-tffhtm flffimf!r.::17YrnCTftlTmrT];T1T Hfflt
regular i n t e rvals. A pye o ccurs in ventricular

big eminy on every second b e a t, i n ventricular
trigeminy on every third beat, and in ventricular
quadrigeminy on every fourth beat. Figure 11-17 il
lustrates ventricular bigeminy. With these rhythms, a
regularly irregular pattern may be noted during pulse
monitoring. pyes may also occur twice in succession
as a ventricular couplet. seen in Figure 11-18.
pyes that originate from more than one ectopic
rnl%'I@I#tllff#tmlL'.r, gMtmIff1F atffi lmmm..
focus are termed multifocal pyes. In this circum

stance, the waveforms will have different morphol
FIGURE 11-18
ogy according to the locations of the ectopic foci. Re
Ventricular couplet.
member that the positive or negative deflection of the
11
183
FIGURE 11-19
Multifocal PVCs.
FIGURE 11-20
Ventricular tachycardia.
waveforms depends on the direction of depolariza
to most arrhythmias is beyond the scope of this chap
tion, as viewed by the lead used for monitoring. In
ter; however, some arrhythmias demand an immedi
Figure 11-19 the first pve seen has an initial positive
ate response if observed.
deflection, whereas the second pve seen has an ini
Ventricular tachycardia (V -tach, or VT) (Figure
tial negative deflection. Each of these pves comes
11-20) is defined as three or more consecutive pves

at a rate greater than 100 BPM (Akhtar, 1990). This
from a different ectopic focus.

The physical therapists's (PT's) decision-making
is a serious and potentially lethal arrhythmia that may
process in response to observation of ventricular ec
require emergency measures be undertaken. During
topic beats is complex and may not be easily grasped
v-tach all complexes are ventricular in origin. V-tach
by the entry-level practitioner. Factors such as pres
sometimes occurs in "runs" of three or more ectopic
ence or absence of symptoms, the acuity of the pa
complexes followed by reversion to the baseline
tient, and whether the rhythm is a new finding all in
rhythm, or it may be sustained. Effective circulation
fluence a clinical response. The presence of a pattern
may be preserved, or it may be seriously compro
such as bigeminy, couplets, or multifocality is also
mised or absent in sustained v-tach. A patient may be
considered. Further elucidation of clinical responses
asymptomatic, particularly if only a brief run of
184
PART II
. ::;
. : ;,' -r-l
t-f.,r.-f+-r"*,
-'-!
+O-O
L& 'I
'--o-rl-.-...-,b-4';""'-"-+. '
. J
n
J /.
. ,. ,. 1
'
1\ ,
1 _tl_, ,..,t
. .
.
+-
' .
:- ..!r....
FIGURE 11-21
Ventricular fibrillation degenerating into asystole.
v-tach was experienced. If VT is sustained, the pa
ment artifact. Unwary therapists have hastily sum
tient may be asymptomatic, symptomatic, or uncon
moned help on observing v-fib or asystole, only to
scious and pulseless. The PT's response depends on
feel foolish when a lead is reattached to the patient.
the rhythm, regardless of whether it is sustained, and
These arrhythmias are always accompanied by loss of
the patient is symptomatic or conscious. Clinical re
consciousness and pulse; a clinician should assess the
sponses range from cessation of activity, ongoing pa
patient before taking action. Similarly, during activity
tient observation and immediate notification of a
or exercise, movement artifact may easily be mistaken

for v-tach. By assessing the patient and asking him or
physician to a full code.

Ventricular fibrillation (V-fib, VF) is a lethal ar
her to "hold still," the issue may be quickly resolved.
rhythmia accompanied by immediate loss of con

sciousness and loss of circulation, that is, cardiac ar
rest. It is characterized by disorganized, simultaneous
Conduction Blocks
firing of multiple, ectopic ventricular foci; there is no
Conduction blocks are another type of ECG abnor
organized rhythm (Figure 11-21). Effective ventricular
mality with which PTs should be familiar. The propa
contraction ceases and cardiopulmonary resuscitation
gation of a cardiac impulse may be inhibited or termi
is indicated until defibrillation is available. Death fol
nated along the conduction pathway. Blockage can
lows unless defibrillation successfully restores an ef
occur at the sinus node, between the atria and ventri
fective rhythm. Conditions that render the myocardium
cles, Or within the ventricular conduction system.
vulnerable to ventricular fibrillation include v-tach,
Sinus block occurs if the impulse cannot propagate
myocardial ischemia or infarction, dilatation of the
beyond the sinus node. In this case, the AV junction
heart, hyperkalemia, or electric shock (Guyton, 1991).
usually takes over as the pacemaker, and a junctional
If not successfully treated, v-fib may further de
rhythm is seen with the absence of P-waves.
generate into asystole, which indicates complete ab
More common are the AV blocks. They are ranked
sence of ventricular electrical activity (Figure 11-21).
as first-, secondo, or third-degree, depending on the
Asystole may also occur as a primary event. This is
extent of delay or obstruction of the cardiac impulse
known colloquially as "flat line" rhythm. Like ven
between the atria and ventricles. First-degree AV
tricular fibrillation, asystole requires that cardiopul
block is characterized by a prolongation of the P-R in
monary resuscitation begin immediately to save the
terval beyond its normal 0.2 seconds (Figure I 1-22).
patient's life.
Remember that the P-R interval is measured from the
Care must be taken to distinguish an apparent
beginning of the P-wave to the beginning of the QRS
lethal arrhythmia from lead disconnection or move
complex_ Each impulse is delayed between the atria
11
185
FIGURE 11-22
First degree A V block.
-,:.1 l fW'
.,
.j.
',
-I--r
!t+t'
' -1 +*'-'+
FIGURE 11-23
Second degree A V block, Mobitz type I.
and ventricles but each eventually reaches the ventric
P-wave. The conduction ratio in Figure 11-24 is 3: I,
ular conduction system resulting in a normal QRS
or three P-waves for each QRS complex. Both first
complex. Thus for each P wave, there is a QRS com
and second-degree A V blocks are considered to be
plex; therefore the conduction ratio is 1: 1.
incomplete heart blocks.
Second-degree A V block takes two forms, al
Third degree A V block or complete heart block
though in each form, there are some sinus impulses
is also known as A V dissociation. In this rhythm
that are not conducted to the ventricles. In second
(Figure 11-25), P-waves are present, but there is no
degree block Mobitz type I, also known as Wencke
relationship between P-waves or QRS complexes.
bach, the P-R interval lengthens progressively uotil a
P-waves may be superimposed on QRS complexes,
P-wave fails to conduct to the ventricles (Figure 11-
but none of the sinus impulses are conducted to the
23). Notice how the first three P-R intervals lengthen
ventricles; the atria and ventricles are contracting
until, after the fourth P-wave, a QRS complex fails
independently of each other. In the absence of clini
to appear. The cycle then repeats itself. Second
cal intervention such as artificial pacing, ventricular
degree block Mobitz type 2 (Figure 11-24) is charac
depolarization is initiated by a junctional or ventric
terized by a fixed P-R interval with a "dropped"
ular pacemaker.
QRS f o llowing every seco nd, t h i r d, or f o u r t h
Clioically, A V blocks range in severity from benign,
186
PART II
'j.,1
,. i'
'
; : .
L1Ji;! i
" . fi
l..r-
t t 1L ?
M , +.::;,
.
..
: "
"
:;
......
.:
rr
"ti
....
+-....
FIGURE 11-24
Second degree A V block, Mobitz type 2,
. ,;;Y
t1ft
'
:
I. t
I
'
FIGURE 11-25
Third degree A V block with ventricular pacing,
as is usually the case with first degree AV block, to po
often treat patients with coronary hearl disease, infor
tentially lethal. Whether hemodynamic compromise oc
mation regarding MI or myocardial ischemia is also
curs depends on the extent of impairment of cardiac
of interest. Although PTs do not medically diagnose
output caused by too slow of a rate of ventricular con
myocardial ischemia or MI, they should have a work
traction (Brown and Jacobson, 1988), Slow rates of
ing knowledge of its electrocardiographic evidence.
ventricular contraction may cause lightheadedness or
During myocardial ischemia, blood flow to a portion
syncope. In most cases of third degree block, treatment
of myocardium is compromised, resulting in alter
now includes implantation of an artificial pacemaker.
ation of myocardial metabolism. In MI, a portion of
In Figure 11-25, the needlelike spikes indicate that an
myocardium has died, but an adjacent zone of is
artificial pacemaker is depolarizing the ventricles at a
chemic myocardial cells endures. These ischemic
rate of 60 BPM.
cells may remain "leaky," and be unable to repolar

ize. The persistent current flow from the "leaky" re
MYOCARDIAL ISCHEMIA OR INFARCTION
gion results in a current of injury, which is seen as a

shifting of the S-T segment above or below the iso
The EeG provides much more information, beyond
electric line (Guyton, 1991; Lilly, 1993). S-T seg
that gleaned from arrhythmia analysis. Since PTs
ment shift has significant diagnostic value. For exam
11
FIGURE 11-26
S-T segment elevation during myocardial infarction.
pIe, S-T segment elevation (Figure 11-26) is associ

ated with transmural Ml. whereas S-T segment de
pression is associated with nOn transmural or suben
docardial MI. Also, the O n s e t of S-T s e g m e n t
depression during activity i s often considered diag
nostic of myocardial ischemia. Figure 11-27 is an ex
ample of exercise-induced S-T segment depression
observed in one lead during exercise.
The following is a brief discussion on other abnor
malities of the ECG observed in coronary artery disease
(CAD). A prominent, pathological Q-wave is indicative
of a t.ransmural MI (Lilly, 1993). Indeed, "non-Q" is syn
FIGURE 11-27
S-T segment depression during exercise.
onymous with nontransmural concerning MI. The pres

ence of a prominent Q-wave (Figure 11-28) does not,
however, distinguish between an old or an acute event.
The T-wave may also undergo changes during
myocardial ischemia or MI. During ischemia, for
example, the T-wave may invert as a result of pro
longation of repolarization (Guyton, 1991). Simi
l a r ly, d uring MI, c h a n g e s in the T - w a v e m a y
"evolve" with the infarct, a t first becoming indistin
guishable within an elevated S-T segment, then in
verting, then perhaps reverting to original configu
ration following the passage of time.
CONCLUSION
Understanding the changes in the ECG during is
chemia or MI may help PTs integrate all available in
FIGURE 11-28
formation to optimize patienl evaluation. This knowl
Significant Q wave.
edge, combined with astute arrhythmia recognition
187
188
PART II
and symptom assessment, provide entry-level PTs
7. What is the possible clinical significance of S-T
with important tools for management of patients at
segment depression, of S-T segment elevation?
risk for cardiopulmonary dysfunction.
What symptoms might be anticipated in the pres

ence of those conditions?
REVIEW QUESTIONS
1. How may the following dysrhythmias be per
ceived by a clinician without benefit of ECG
monitoring? How may they be perceived by a
atrial fibrillation
supraventricular tachycardia
premature ventricular contractions
third degree A V block
ventricular fibrillation
Cummins,
4. Does an impulse originating within ventricular

myocardium generate an effective myocardial
contraction? If not, why not?
ocardial infarction?
6. What event is represented by each of the following:
T wave
U wave
R.O.
(Ed.). (1994). Tex/book of advanced cardiac I'fe
Emergency Cardiac Care Committee and Subcommittees. (1992).

Guidelines for cardiopulmonary resuscitation and emergency
of/he American Medical Associa/ion,
Guyton, A.C. (199
I).
268,
2199-224 I.
Tex/book oj medical physiology. Philadel
phia: WB Saunders.
Lilly, L.S. (1993). POIhophysiology oj hear! disease. Philadelphia:
Lea and Febiger.
National Heart Lung and Blood Institute Working group on atrial
fibrillation. (1993). Atrial fibrillation: Current understandings
5. Why is ECG monitoring indicated following my
Jacobson. S. (19 88). Mas/ering dysrhy/hmias: A
cardiac care, Ill: Adult advanced cardiac life support. Journal
tions of the conduction system act as pacemakers?
&
SUppOrl. Dallas: American Heart Association.
the heart? Under what conditions do other por
QRS complex
1561-1573.
problem solving guide. Philadelphia: FA Davis.
3. What propelty of the SA node allows it to pace
82,
Febiger.
Brown, K . R . ,
arrhythmia?
P wave
Cireula/ioll,
cise /es/il1g and prescrip/ion. (4th ed.). Philadelphia: Lea and
2. What determines the clinical significance of an
Akhtar, M. (1990). Clinical spectrum of ventricular tachycardia.

American College of Sports Medicine. (1991). Guidelinesfor exer
patient?
References
and research imperatiws. Journal of AmericanCollege nfCar
diologis/s, 22,
1830-1834.
Shih, H.T. (1994). Anatomy of the action potential in the heart.
Texas J-iear/lns/i/u/e lournal, 21, 30-41.

& Kampine, J.P. (1990). Circula/OI)'
Smith, J.1.,
essentials. Baltimore: Williams and Wilkins.
physiology-/he
C HAP T E R
1 2
Multisystem Assessment and

Laboratory Investigations
Elizabeth Dean
KEY TERMS
Blood
Liver
Endocrine function
Lungs
Heart
Multisystem assessment
Immune function
Peripheral vascular circulation
Kidneys
INTRODUCTION
fected by virtually every organ system in the body.
The purpose of this chapter is to describe the ratio
The signs and symptoms of systemic disease can
nale for multisystem assessment in the patient man
mimic other conditions, including cardiopulmonary
aged for cardiopulmonary dysfunction and some
dysfunction treated by physical therapists. Therefore
common laboratory tests related to multisystem as
the physical therapist must be able to differentiate
sessment. The bases of tests to assess the function of
these presentations to determine what treatment, if
the following organ systems are presented: blood,
any, is indicated, and what treatments may be con
pulmonary, cardiac, peripheral vascular, renal, en
traindicated. Knowledge of multisystem function
docrine, liver, and immune systems. The information
helps confirm a diagnosis, as well as predict a pa
in this chapter is supplemental to the elements of car
tient's response to treatment and his or her recovery
diopulmonary and cardiovascular assessment and re
and prognosis. In addition, this information is crucial
lated laboratory investigations described in Part 2.
in refining and modifying treatment prescription.
The cardiopulmonary system affects and is af-
These abilities are particularly important in this era of
189
190
PART II
professional accountability and with the advent of di
response, recovery, and prognosis. The CBC includes
rect patient access.
the red blood cell count (RBC), a variety of red blood

cell indices, white blood cell count (WBe), hematocrit
RATIONALE FOR MULTISYSTEM ASSESSMENT
(Hct), hemoglobin (Hgb), and platelet count.

Tests of coagulation and hemostasis reflect bleeding
The cardiopulmonary system supports cellular respi
pathology, which often involves injury of blood vessels
ration and life. Thus every system and every cell in
and cells. Damage to the blood vessel wall leads to con
the body is affected by the adequacy of oxygen trans
striction, a primary mechanism of hemostasis. Circulat
port, which is dependent on cardiopulmonary and
ing platelets adhere to exposed subendothelial tissues,
cardiovascular function. In addition, these systems
which can predispose thrombus formation.
are affected by virtually every other system in the
The fluidity of the blood is regulated by the facili
body. The cardiopulmonary physical therapist (PT)
tation and the inhibition of thrombin formation.
therefore needs thorough knowledge of multisystem
When these two processes are in balance, the blood
function and the interdependence of the organ sys
has an optimal consistency; it is neither too thick nor
tems, an ability to assess multisystem function and to
too thin. This allows blood to flow optimally through
integrate this information into a comprehensive and
the circulation. Blood vessel injury can disrupt this
progressive treatment plan.
balance and can promote coagulation.
The lungs and heart are anatomically and physio
Disseminated intravascular coagulation (DIC) re
logically interconnected, and function as a unit to
sults from an imbalance between the formation and
transport oxygen via the peripheral circulation to per
deposition of fibrin, which leads to the formation of
fuse and nourish tissues. Tissue homeostasis is de
thrombi. The continuous production of thrombin
pendent on the adequacy of the anatomy and physiol
causes depletion of the coagulation factors and bleed
o g y of t h e b l o o d . T h e a d e q u a c y of p e r i p h e r a l
ing results. Tests used to assess bleeding capacity in
perfusion determines the adequacy o f the function of
clude thrombin time and fibrin clotting time (partial
all organ systems in the body. Therefore a knowledge
thromboplastin time [PTT]).
of the failure of the various organ systems can reflect
Proteins (amino acids) serve as regulators of me
impaired oxygen transport or may identify a threat to
tabolism. Much clinical information is obtained by
oxygen transport.
examining and measuring proteins, because proteins
The elements of laboratory evaluation and testing,
regulate many impoltant physiologic functions in the
as well as normal values, have been compiled from
body. Plasma proteins serve as a source of nutrition
Bauer (1982), Dean (1987), Fishbach (1988), Guyton
for the body tissues and function as buffers when
(1991 ), Jacobs et al. (1984), Le Fever Kee (1990),
combined with hemoglobin.
Pagan a and Pagana ( I 992), Siest et al. (1985), and

Wallach (1986).
Albumin, a protein formed in the liver, maintains

normal water distribution in the body (colloid os
motic pressure). It transports blood constituents such
ELEMENTS OF MULTISYSTEM ASSESSMENT

Blood
as ions, pigments, bilirubin, hormones, fatty acids,

enzymes, and certain drugs. Approximately 55% of
total protein is albumin. The remainder is globulin,
Some common blood tests are summarized in Table
which functions in antibody formation, and other
12-1 along with their normal values.
plasma proteins (fibrinogen and prothrombin) in
The average blood volume consists of 5 L of blood:
volved with coagulation.
3 L of plasma and 2 L of cells. Plasma is the medium
Lactic acid, a product of carbohydrate metabolism, is
which suspends and transpOIts blood cells. The com
produced when cells receive inadequate oxygen in rela
plete blood count (CBC) is one of the most commonly
tion to oxygen demand (anaerobic metabolism). When
ordered laboratory procedures. This basic screening
the production of lactic acid exceeds its removal from the
test helps to establish the patient's diagnosis, treatment
blood by the liver, lactic acid accumulates in the blood.
12
Multisystem Assessment and Laboratory Im'estigations
191
TABLE 12-1
Common Test'! of Multisystem Function and Their Normal Values: Blood Tests
NORMAL VALUES (SI UNITS)
TEST
Red blood cell count (RBC)
Hemoglobin (Hgb)
Hematocrit (Hcr)
Men
2.09-2.71 nmolfL
Women
1.86-2.48 nmolfL
Men
8.7-11.2 nmolfL
Women
7.4-9.9 nmolfL
Men
40% to 54%
Women
37% t047%
150.000-350.000/mm3
Platelet count
Prothrombin time (PT)
10-14 seconds
Partial thromboplastin time (PTT)
60-85 seconds
White blood cell count (WBCC)
5-10
103/iJl
(Differential WBCC includes counts of neutrophils,

eosinophils. basophils, lymphocytes. and monocytes)
Erythrocyte sedimentation rate (ESR)
Men
0-15111m/hr
Women
0-20 mm/hr
Proteins
Albumin
38-50 gm/L
Globulin
23-35 gm/L
Fibrinogen
2.0-4.0 gm/L
Lactate
Venous
0.5-2.2 mmolfL
Arterial
0.5-\.6 mmollL
Electrolytes (blood)
Sodium (Na+)
135-148 mmollL
Potassium (K+)
3.5-5.0 mmol/L
Calcium (Ca++)
TOTAL
4.5-5.3 mmolfL
IONIZED
2. 1-2.6 mmolfL
Chloride (Cl-)
98-106 mmolfL
Cholesterol
Creatine kinase
:-;OTI,:
3.63-6.48 mmollL
Men
0.42-1.5 I mmol/sfL
Women
0.17-1.18 mmol/sfL
Normal values may vary depending on the laboratory performing the measurement. Within subject variation occurs from age, and
variations in the pre-test sLandardization procedures.
Cholesterol is used in the production of steroid hor

mones, bile acids, and cell membr::mes. Cholesterol is
of cholesterol are associated with atherosclerosis and

increased risk of coronary artery disease (CAD).
found in muscles, red blood cells, and cell membranes.
Electrolyte assessment is based on the electrolyte
Low-density and high-density lipoproteins (LDLs and
constituents of a b lood or urine sample. Although
HDLs) transport cholesterol in the blood. High levels
present in minute quantities, electrolytes are essential
192
PART II
in mainlaining normal cellular function and home
inspection of the integrity of the peripheral circulation
oslasis. The electrolytes that are routinely studied are
particularly to the eXlremities, palpation to assess pe
sodium, potassium, chloride, calcium, phosphorus,
ripheral pulses, and auscultation, which can be helpful
and magnesium.
in detecting bruits or areas of turbulent blood flow as

sociated with arterial stenoses.
Some common tests of peripheral vascular func
Pulmonary Function
tion are summarized in Table 12-2 along with their
See Chapters 8 and 14 for a detailed description of the
normal values.
assessment of the pulmonary system and its function.
Kidney Function
Cardiac Function
Urine consists of the end products of cellular metabo
A detailed description of the assessment of the car
lism and is produced as large volumes of blood (ap
diac system and its function appears in Chapters 11
proximately 25% of the cardiac output [CO]) flow
and 14.
through the kidneys. When the kidneys are compro

mised, death can ensue within a few days. Although
fluid is lost through several routes, the kidneys are
Peripheral Vascular Function
primarily responsible for processing and regulating
Assessment of the peripheral vascular circulation is

essential to provide information regarding central and
fluid balance in the body.

Urea, the major nonprotein nitrogenous end product
of protein catabolism, is measured in the blood as blood
peripheral hemodynam.ic
tissue perfusion. This assessment is essential to estab
urea nitrogen (BUN). The urea is then carried to the
lish the integrity of the patient's hemodynamic status
kidneys by the blood to be excreted in the urine.
at rest and during physical and exercise stress which is
Creatinine is a byproduct in the breakdown of
associated with most physical therapy treatments.
muscle creatine phosphate resulting from energy me
Laboratory tests include segmental blood pressure
tabolism. Production of creatinine is constant as long
studies, skin temperature studies, pulse wave analysis,
as muscle mass is constant. Kidney dysfunction re
Doppler venous studies, and arteriography. The physi
duces excretion of creatinine resulling in increased
cal examination corroborates the results of the labora
levels of blood creatinine. Analysis of urine for crea
tory investigations and includes the patient's history,
tinine provides an index of kidney function.
TABLE 12-2
Common Tests of Multisystem Function and
TABLE 12-3
Their Normal Values: Tests of Peripheral

Vascular Function
TEST
NORMAL VALUES
Skin temperature
Ranges from ambient

temperature to 30DC
Ankle systolic pressures
97% of brachial pressure
Peri phera/ pu Ises
Apex heart rate
Capillary filling
Instantaneous filling
following quick pressure
over the nai I bed
Their Normal Values: Tests of Renalf'ullctioll

NORMAL VALUES
TEST
(SI UNITS)
Blood urea nitrogen (BUN)
3.6-7.1 mmollL
Creatinine
7.6-30.5 IlmollL
NO'll::
Normal values Jllay vary depending on the laboratory
performing the measureJllent. Within subject variation occurs from

age, and variations in the pretest standardiz.ation procedures.
12
Multisystem Assessment and Laboratory Investigations
Increased osmolality stimulates the secretion of
193
marized in Table 12-4 along with their normal values.
anti-diuretic hormone (ADH) that acts on renal
Pancreatic function and insulin production
tubules. This results in the reabsorption of water,

more concentrated urine, and less concentrated serum.
Insulin, a hormone produced in the pancreas by the beta
Some common tests of renal function are summa
cells of the islets of Langerhans, regulates the metabo
rized in Table 12-3 along with their normal values.
lism of carbohydrates along with liver, adipose tissue,

muscle, and other target cells and is responsible for
maintaining a constant level of blood glucose. The rate
Endocrine Function
of insulin secretion is determined primarily by the level
Endocrine glands are responsible for producing those
of blood glucose perfusing the pancreas and is also af
substances and neuromediators responsible for main
fected by hormonal status, the autonomic nervous sys
taining homeostasis and enabling the body to adapt
tem, nutritional status, smoking, restricted mobility,
when physically and psychologically challenged or
physical stress such as traumatic insult to the body dur
perturbed from a resting state. The key endocrine
ing illness and injury, and pharmacologic agents.
glands are the pancre as, thyroid gland, and the
Amylase is an enzyme produced in the salivary
adrenal glands. Endocrine glands regulate metabo
glands, pancreas, and liver, and c onverts starch to
lism and are responsible for increasing blood flow
sug ar. Inflammation of the pancreas or salivary
and pressure, and reducing vascular resistance when
glands results in more of the enzyme entering the
metabolic demands increase.
blood. The amylase test is used to diagnose and mon
Some common tests of endocrine function are sum-
itor treatment of acute pancreatitis.
TABLE 12-4
Common Tests of Multisystem Function and Their Normal Values: Tests of Endocrine Function
NORMAL VALUES
(SI UNITS)
TEST
Thyroid Function
Total thyroxine (T4)
65-155 nmol/L
Total triiodothyronine (T3)
1.77-2.93 nmollL
Adrenal Function
0.0-81.9 nmoll24 hr
Epinephrine
Norepinephrine
0.0-591 nmol/24 hr
Cortisol
Morning
138-635 nmollL
Evening
82-413 nmollL
Pancreatic Function
At I hl' glucose
Glucose tolerance test
1.1-2.75 mmollL
At 2 hl' glucose
0.2-0.88 mmol/L
Insulin
12 hr fasting
35-145 pmollL
Amylase
Blood level
25-125 UnitslL
N<Y,E:
Normal values may
vary
depending on the laboraLory peli'orming the measurement. Within subject variation occurs from age, and
variations in the pretest standarLiization procedures.
194
PART II
Thyroid
TABLE 12-5
The function of the thyroid gland is to take iodine
from the circulating blood, combine it with amino
Their Normal Values: Tests of Liver Function
acid tyrosine, and convert it to the thyroid hormones

thyroxine (T4), and triiodothyronine (T3). Thyroid
hormones have a profound effect on metabolic rate.
Increased metabolism causes more rapid use of oxy
gen than normal and causes greater quantities of
Alkaline phosphatase
Bilirubin (total)
metabolic end products to be released from the tis

sues. These effects cause vasodilatation in most of
the body tissues, thus increasing blood flow. Increase
in the thyroid hormones increases cardiac output,
NORMAL VALUES
(SI UNITS)
TEST
NOTl'.:
0.18-0.40 nmol/slL
5.1-I 7.1 fJmollL
Normal values may vary depending on the laboratory
performing the measurement. Within subject variation occurs from

age and variations in the pretest standardization procedures.
heart rate, force of cardiac contraction, blood volume,

arterial blood pressure, oxygen consumption, and car
TABLE 12-6
bon dioxide (C02) production, hence an increase in

the rate and depth of breathing, increased appetite,
Common Tests of Multisystem FUllction
food intake and gastrointestinal motility. The thyroid
and Their Normal Values: Tests
gland also stores T3 and T4 until they are released
of Immunological Function
into the blood stream under the influence of thyroid

stimulating hormone (TSH) from the pituitary gland.
Differential White Blood Cell Count
Adrenal function
Catecholamines, epinephrine and norepinephrine, are
Neutrophils
produced by the adrenal medulla of the adrenal
Lymphocytes
glands. Urine samples are used to test for these im

portant vasoactive neurotransmitters in the investiga
tion of various disorders. In addition to their vasoac
MOllocytes
Eosinophils
Basophils
ABSOLUTE VALUE
(No/uL)
RELATIVE VALUE
(by Percent)
3,000-7,000
1,000-4,000
100-600
50-400
25-100
60-70
20-40
2-6
J-4
0.5-1
tive properties, the catecholamines are essential in

stimulating the sympathetic response in the fight or
with tests of liver enzymes such as amylase and al
flight mechanism.
Cortisol is produced by the adrenal cortex of the
kaline phosphatase.
adrenal glands and is involved with metabolism of
Some common tests of hepatic function are sum
carbohydrate, protein, and fat. In addition, it inhibits
marized in Table 12-5 along with their normal values.
the action of insulin and thus the uptake of glucose

by the cells. The normal secretion of cortisol varies
diurnally, that is, high in the morning and low in the
Immunological Function
Immunological function is dependent on the ade
evening.
quacy of the function of several tissues and organs,

namely bone marrow, the thymus gland, lymph
liver Function
nodes, and vessels of the lymphatic system, spleen,
Liver function is especially important in that dys
tonsils, and intestinal lymphoid tissue. Immunologi
function of this organ can be life threatening. The
cal function can break down if insufficient protective
liver has a primary role in carbohydrate and protein
immune factors are produced, or the system is over
metabolism, it produces bile, and is responsible for
whelmed by an invading organism for which the
detoxification of the blood. Its function is assessed
body has inappropriate or insufficient resistance.
Multisystem Assessment and Laboratory Investigations
12
Some common tests of immunological function are

summarized in Table 12-6 along with their normal
values. Specific detailed accounts of immmunodiag
nostic studies and tests for autoimmune deficiencies
are beyond the scope of this chapter but can be re
viewed in Fischbach (1988) and Le Fever Kee (1990).
SUMMARY
This chapter described the rationale for multisystem
195
REVIEW QUESTIONS
I.
Describe common tests of blood composition.
2. Describe pulmonary function tests.

3.
Describe tests of heart function.
4. Describe tests of peripheral vascular function.

5. Desacribe tests of renal function.
6.
Describe tests of endocrine function.
7.
Describe tests of liver function.
8. Describe tests of immune function.
assessment in the patient being managed for car

diopulmonary dysfunction and some common tests of
multisystem function. The cardiopulmonary system
affects and is affected by virtually every organ system
in the body. Thus primary cardiopulmonary dysfunc
tion can lead to multiorgan system complications, and
dysfunction of other organ systems can have car
diopulmonary manifestations. In addition, the signs
and symptoms of systemic disease can mimic other
conditions treated by physical therapists. Therefore
the PT must be able to differentiate these presenta
tions to determine whether a pathology will respond
to physical therapy management, what treatment is
not indicated and what treatments may be contraindi
cated. Multisystem monitoring provides fundamental
information needed to refine and progress the treat
ment prescription. These abilities are essential in this
era of increased professional responsibility and with
the advent of direct patient access.
References
Bauer, J.D.
(1982).
Clinic allaboratOlY melhods (9th ed.). St.
Louis: Mosby.
Dean,
E. (1987).
Assessment of the peripheral circulation: An up
date for practitioners. The Australian Journal of Physiotherapy,
33,
164-171.
(1988).
Fischbach, F.
A manual of laboratory diagnostic tests
(3rd
ed.). Philadelphia: J.B. Lippincott.
(1991).
Guyton, A.c.
Textbook of mediad physiology (6th ed.)
Philadelphia: W. B. Saunders.
Jacobs, D.S., Kasten, B.L.,
(1984).
Le Fever Kee, J.
tests
Demott,
W.R.,
&
Wolfson, W.L.
Laboratory test handbook. Stow: Lexi-Comp, Inc.
lVilh
(1990).
Handbook oflaboratOlY and diagnostic
nursing implications. Norwalk: Appleton and Lange.
Pagana, K.D.,
&
Pagana,
TJ. (1992). Mosbys
diagno.Slic
and lab
ora/Ory leSI reference. St. Louis: Mosby.

Siest, G., Henny, J., Schiele, F.,
&
Yonge, D.S.
(1985).
Inlerpretalion
ofclinical laboratory lests. Foster City: Biomedical Publications.

Wallach, J.
(1986).
Interpretation of diagnostic tests. A synopsis of
laboratory medicine. Boston: Little, Brown.
Special Tests
Gail M. Huber
KEY TERMS
Echocardiography
Stunned myocardium
Ejection fraction
Thallium-201 scan
Hibernating myocardium
Ventilation-perfusion scan
Positron emission scans
INTRODUCTION
lungs, as well as determining cardiac anatomy, and
In assessing the cardiopulmonary patient, the physi
direct volume and pressure measures, it is without
cian uses many tools. The patient interview, physical
equal. Transesophageal echocardiography is another
examination, chest x-ray, and electrocardiogram
invasive test. Following the initial assessment of the
(ECG) provide information to make a diagnosis.
problem, these same special tests may be lIsed to as
When more information is needed, a variety of inva
sist in the determination of appropriate therapy and
sive and noninvasive tests can be pelformed. Nuclear
evaluate prognosis and response to treatment. The
medicine offers a variety of tools for evaluation of
noninvasive tests are most important in determining
cardiac and pulmonary function. EChocardiography is
ongoing surgical, interventional, or medical therapy.
a noninvasive method that offers information about
Physical therapists (PTs) need to understand these
the cardiovascular system, including valve function,
invasive and noninvasive tests for several reasons. It
ventricular performance, and estimation of filling
is useful to understand how the information is used
pressures. It is particularly useful with children.
to make a differential diagnosis and determine treat
At some point in a patient's workup, the physi
ment. These tests have helped to clarify our under
cian may need to use an invasive test. Pulmonary
standing of the physiology and pathophysiology of
and cardiac angiography is not without risk; how
the system. Therapists need to understand the patho
ever, for evaluating blood flow in the heart and
physiological basis f o r a p a t i e n t ' s m o v e m e n t

197
198
PART II
dysfunctions to select the most appropriate treat
moved from time to time for patient use (Kim, 1987).
ment strategies. Many special tests can and are
A generator system produces short-lived radionu
being used in research to evaluate treatment inter
clides (lskandrian, 1987).
ventions. For example, radiolabeled aerosols are
These elements are often attached to other sub
used to evaluate mucociliary clearance, providing a
strates for transport in the body to the particular tis
method to evaluate the effectiveness of pulmonary
sue of interest. The elements have differing character
hygiene techniques (Miller and O'Doherty, 1992).
istics such as energy output and half-life. Because of
C linically, PTs need to use information from the
their vaIied distribution in the body tissues, they pro
tests to develop a framework for predicting how the
vide different information.
patient may respond to a physical therapy interven
Detection of the radioactive energy emitted by a
tion. For example, nuclear imaging can provide in
specific radiopharmaceutical requires a camera.
formation about left ventricular ejection fraction.
When certain materials are struck by ionizing radia
This information helps the PT determine if the pa
tion, light is emitted. A scintillation detector detects
tient should be stratified into high-risk or low-risk
this light. A gamma camera is a scintillation detector
categories. Monitoring of an exercise session may
able to detect photons exiting the body. It uses a
depend on the risk level, and interpretation of the
large, collimated crystal monitored by an array of
patient's response to treatment may be effected.
photomultiplier tubes (Kim, 1987). A collimator is a

device that allows only those photons traveling in an
appropriate direction to reach the crystal. There are
NUCLEAR IMAGING SYSTEMS
several types of collimators: parallel-hole collima
AN 0 RAD I 0 PHARMACEUTI CALS
tors, pinhole collimators, and converging and diverg
A general view of how nuclear imaging systems work
ing collimators. The photomultiplier tube records the
should help the PT understand some of the differences
amount of light from the crystal and converts it into a
between the wide variety of tests used today. This
voltage, that is proportional to the intensity of the
area of medicine is experiencing rapid growth and
light (Kim, 1987).
change as technology changes the equipment used to
The camera system is connected to a computer
perform the test, the radiopharmaceuticals available,
that stores the light images. The computer is able to
and the computer's increasing ability to analyze data.
derive two dimensional images from the data. The
Radionuclide imaging allows for the noninvasive

acquisition of images from a variety of body tissues.
computer can also quantify the data and perform a

variety of data analyses (Iskandrian, 1987).
An imaging system requires three basic parts. The

first requirement is a radiopharmaceutical that emits
gamma radiation and is taken up by the body tissue
Planar Imaging
of interest. Next, a radiation detector or camera is
A single crystal camera (Anger) produces a two dimen
needed. FinalIy, computers are required to collect and
sional or planar image. Multicrystal cameras (Blau and
analyze the data.
Blender) also produce planar images but are able to per
Radionuclides are elements that are unstable; they
form fast dynamic imaging used in first pass and gated
gain stability by emitting particles or photons. This is
studies. Planar imaging may be the only option available
called radioactive decay, and gamma radiation is re
to obese patients who do not "fit" the single photon
leased. Radionuclides are either cyclotron- or genera
emission computed tomography (SPECT) camera.
tor-produced. The cyclotron accelerates alpha-parti

cles, deuterons, and protons to energies suitable for
the production of the required radionuclide (Kim,
1987). A radionuclide generator is a system of parent
Tomographic Imaging
If a gamma camera is rotated about the patient and
and daughter radionuclides in equilibrium. The sys
mUltiple projections obtained, a three-dimensional
tem is constructed so that the daughter can be re
distribution of tracer is acquired. This is the basis for
13
Special Tests
SPECT (Kim, 1987). The s ame gamma-emitting
TESTS OF THE CARDIOVASCULAR SYSTEM
pharmaceuticals are used. Regular gamma cameras or
Radionuclide Imaging
specially designed systems can be used (Iskandrian,
1987). SPECT imaging produces higher spatial reso

lution (Schwaiger, 1994), and increased sensitivity
for coronary artery disease (CAD) over planar images
(Beller, 1994). However, attenuation artifacts (ab
sorption of the radioactive energy by other body tis
sues such that the camera does not detect it) are
greater than with planar images, particularly those
images involving the inferior wall of the heart in men
and the anterior wall in women, and may produce
false-positive scans (Schwaiger, 1994). Quality of the
images are dependent on the use of stringent quality
control measures and experience of the staff. Image
quality is also patient-dependent. Patients must be
able to lie perfectly still for 15 to 20 minutes, with
their hands over their heads, while data are collected.
PTs can identify patients who would have diffi
culty with arm movements or with remaining still.
For these patients, other imaging modalities such as
echocardiography may be appropriate.
P o s itron e m i s s i o n t o m o g r a p h y (PET) u s e s
positron-emitting radionuclides. The images ob
tained by PET can provide information regarding
metabolism in lung tissue and cardiac muscle, my
ocardial perfusion, and myocardial receptor density
(Maddahi, 1994). PET is valuable in delineating my
ocardial areas with reversible and irreversible injury
199
Gated/ungated first pass scan

In an ungated first pass study, data are collected on a
radiolabeled bolus of blood as it passes through the car
diac chambers. This allows for clear identification of
the four cardiac chambers. During gated first pass stud
ies, data are collected at specific periods in the cardiac
cycle. Each R-wave of the EKG triggers the acquisition
of data, thus the average cycle observed is the compila
tion of several cycles. Gated equilibrium studies or
multiple uptake gated acquisition (MUGA) scans aver
age several hundred cardiac cycles. The quality of the
image is best when the patient has a stable sinus
rhythm. Patients with irregular heart rates, such as atrial
fibrillation have images of poorer quality.
Exercise stress studies

Many of the tests pert'ormed using radionuclides are
coupled with an exercise test. A treadmill exercise
test is pelformed, and at the peak of exercise, a tracer
is injected. Shortly afterward, depending on the
tracer, images are acquired. Exercise imaging en
hances the identification of ischemic areas. These
tests are then often compared with rest studies.
Rest/stress or stress/rest protocols can be used.
Pharmacologic stress studies
and in assessing the feasibility of surgical revascu
Many patients are unable to exercise to an intensity
larization, coronary angioplasty, or thrombolysis
sufficient to produce stress on the cardiovascular sys
with respect t o potentially s a l v a g e a b le t i s s u e
tem. When patients are unable to exercise, pharmaco
(Niemeyer, 1992). Many o f the radionuclides used in
logic agents can be used to dilate the coronary arteries
PET scans require a cyclotron for generation and a
or incr e a s e t h e metab olic demand of the heart.
specialized detection system. PET images offer s u
Dipryridimole (Persantine) and adenosine are often
perior resolution compared with SPECT images
used. Pharmacologic stress tests can be coupled with
(Schwaiger, 1994). PET also allows greater correc
SPECT and PET nuclear imaging techniques or with
tion for attenuation artifact (Schwaiger, 1994). PET
echocardiography to determine regions of ischemic
imaging is a newer technology that offers improve
myocardium suggesting functionally significant block
ment in sensitivity and specificity when compared
age in the coronary artery supplying that territory.
with SPECT (Mullani, 1992).

PET studies use short scanning times. Protocols
Nuclear-derived measurements
can last about I hour. The studies can be done at rest
Data derived from radionuclide images provide infor
or with a pharmacologic stress agent (Schwaiger,
mation about perfusion and function. Radionuclides
1994). Cost may prohibit the widespread use of this
taken up by the myocardium provide a picture of the
technology.
heart that includes wall thickness and an outline of
200
PART II
the chamber. In radionuclide angiography, which in

cludes first pass and gated studies, the blood is high
lighted as it passes through the chambers. Qualitative
and quantitative measurements can be taken. The
most important of these measurements, the ejection
fraction (right and left ventricle) is a measure of my
ocardial function. It is derived from quantitative
counts of the ventricular area during diastole and sys
tole (lskandrian, 1987):
(End-diastolic counts - End-systolic counts) x 100
End-diastolic counts
Left ventricu lar ejection fraction (L VEF) has been
shown in several studies (Cass study and the Multi
center Postinfarction Research Group Database) to be
highly predictive of 1 year survival (Port, 1994; Mad
dahi, 1994). Right ventricu lar ejection fracti o n
(RVEF) has been found t o have a wide range o f nor
mal values (35% to 75%) (Kinch, J 994) but is not
that predictive of function without data about wall
motion abnormalities. The strongest radionuclide pre
dictor of outcome is the exercise LVEF. When pre
dicting outcome, multivariate analysis of clinical
data, catheterization data and radionuclide measure
ments have shown that the radionuclide results (exer
cise LVEF, resting end-diastolic volume, and change
in heart rate [HR)) have the same prognostic power
as the catheterization data (Port, 1994).
Another important measurement is wall motion.
Quantitative and qualitative evaluation of the move
ment of the myocardium can be made. Wall thick
ness, and movement are compared with systole and
diastole. Assessments are made about akinesia,
global or regional hypokinesia, and dyskinesia.
Global left ventricular function is a strong predictor
of survival. It can help clinicians differentiate a weak
heal1 from one that is stiff, allowing the appropriate
treatment. Regional wall function when correlated
with knowledge of coronary artery anatomy allows
for the identification of potential blockages or areas
of infarct. Assessing wall thickness can provide in
formation about hypertrophy or aneurysm but is done
more reliably by echocardiography.
Anatomical measurements can be made of cham
ber size. From these data, chamber volume can be
calculated, as well as stroke volume and cardiac out
put (Table 13-1).
Tests to Evaluate Myocardial Perfusion

Perfusion of the myocardium is a vital factor in the via
bility and function of the heart. Information about my
ocardial perfusion is used for diagnostic decisions,
treatment decisions and prognosis. Peliusion of the my
ocardium under rest and exercise conditions is impor
tant in the diagnosis of CAD. Efficacy of reperfusion
strategies, such as angioplasty and thrombolytic therapy
must be evaluated. Identifying tissue that is viable but
still at risk is one of the newer applications of myocar
dial peliusion tests. Information gained from combined
perfusion and metabolic studies has helped to increase
the understanding of ischemic myocardium. Two types
of contractile dysfunction have been delineated. Hiber
nating myocardium is the result of prolonged ischemia.
The contractility of the muscle fiber is effected so that
there may appear to be regional wall motion abnonnali
ties. The tissue is alive but not contracting. It is theo
rized that this is a measure to reduce energy expendi
ture and ensure myocyte survival. The second
condition, myocardial stunning, occurs under condi
tions of acute ischemia. In this case, there is contractile
dysfunction during the acutc ischemic episode that per
sists for some time after perfusion has returned to nor
mal. Both conditions are reversible. Patients demon
strating hibernating myocardium may benefit from
revascularization procedures. Patients with stunned my
ocardium may only require supportive care until con
tractile function returns. (SchelbeI1, 1994).
Thallium-201
Thallium-20l is the radioactive isotope most often
u sed in myocardial perfusion studies (Wacker,
1994). It is a cyclotron-produced isotope that emits
low-energy radiation (69 to 83 kiloelectron volt
[keY)). Administered intravenously, its distribution
throughout the body depends on blood flow. Thal
lium concentrations in the myocardium depend on
four processes. First, there is a linear relationship
between thallium concentration and coronary blood
flow. Second, extraction-transport across the cell
membrane depends on active and passive transport
mechanisms. Thallium is thought to be transported
across the cell membrane through the sodium-potas
sium ATPase pump (Maddahi, 1994). The third
process is washout, also called redistribution. Thal
13
Special Tests
201
TABLE 13-1
Summary of Special Tests of the Cardiopulmonary System
SPECIAL TESTS
CLINICAL FINDINGS
Cardiac Scans
Planar, SPEeT, MUGA, First pass

Thallium-20I
Evaluates myocrdial perfusion, used in exercise stress studies and to assess
Technitium-99M-sestamibi
reversibility of defects. Quantitatively can be used to determine: EF, SV,
Technitium teboroxime
CO, regional function, ventricular volumes, intra-cardiac shunt, valvular

regurgitation.
PET Scans
IS-FOG
Assesses myocardial viability by evaluating glucose metabolism. Can
II C acetate
Assesses myocardial viability by evaluating oxidative metabolism. Can
identify areas that improve with reperfusiol1.

identify areas that will improve with reperfusion.
Illfarct avid scans

Technetium-99M-pyrophosphate
Indium I II antimyosin
Identifies areas of infarction by binding with elements released by the death

of myocardial tissue.
Pulmonary Scans
Perfusion scan
MAB
Identifies regions of decreased pulmonary perfusion, used to identify

pulmonary embolism.
Velltilation scall
99mTc OTPA
I33-Xe
Gallium scan
Identifies regions of decreased ventilation. Used in conjunction with

perfusion scan to identify patients with pulmonary embolism.
Identification of neoplastic or inflammatory pulmonary lesions
Echocardiography
M-mode
Evaluates myocardial structure. 2- 0 used in exercise stress studies.
2 D
Quantitatively measures: chamber size, wall thickness, valve structure
TEE
and function, pressure and flow through valve, valve area, EF.
Doppler
Angiography
Quantitative measures of pressure, resistance, flow, O2 consumption,

arteriovenous oxygen difference EF, CO
Abbreviations: EF=ejection fracl.ion, CO=cardiac output, SV=stroke volume
lium enters the cell initially and then is redistributed
titatively evaluated. Normally perfused myocardium
until an equilibrium is attained based on a net bal
demonstrates uniform uptake of the tracer. Uniform
ance between Thallium-201 input through recircula
uptake can occur as long as blockages are less than
tion and intrinsic Thallium washout (Beller, 1994).
50% of the artery. Ischemic but viable myocardium
Finally, concentrations arc decay-related, dictated
initially appears as areas of decreased uptake, these
by the half-life of the isotope (Brown, 1994; lskan
areas fill in over time, a function of redistribution. Be
drian, 1987).
cause blood flow is decreased, clearance of Thallium
Thallium-201 images can be qualitatively and quan
201 from the defect region is slower (Maddahi, 1994).
202
PART II
In infarcted areas, these defects remain unchanged
in acutc situations. A patient with an acutc myocardial
over time. Qualitative evaluation requires visual in
infarction (MI) can be injcctcd with tracer, given
spection of the images. Quantitative evaluation is per
thrombolytics, stabilizcd, and scanned 4 hours later.
formed by computer. The computer analyzes the
The scan results show myocardial pert'usion at the time
amount of radioactivity taken up in a palticuJar region
of injection when the myocardium was ischemic. Later
of interest. It then quantifies this count so that regions
scans demonstrate the new perfusion situation.
can be compared with each other and with normalized

data. In this way, unperfused or hypoperfused areas
Technetium-99M-teboroxime
Another newer isotope is Technetium (Tc)-99M
can be identified.
Thallium-201 is used to acquire planar and tomo
teboroxime. I t i s not yet widely accepted because of
graphic images (SPECT) for rest studies, exercise stress
its rapid washout and visualization problems related
studies, and pharmacologic stress studies. The tradi
to hepatic uptake (Berman et aI., 1991; Go, j 992).
tional Thallium-201 stress study calls for injection of
The half-life for teboroxime is 5 to 6 minutes (John
the tracer at the peak of exercise with collection of the
son, 1994). It has a myocardial extraction fraction
stress data shortly after. The redistribution study is com
higher than either sestamibi or thallium (Johnson,
pleted 4 hours later. Newer study protocols include rein
1994). Tc-99M-teboroxime uptake parallels myocar
jection of thallium before the 4-hour redistribution study
dial blood flow under both ischemic and nonischemic
(Go, 1992) and use in dual-isotope studies (Berman,
conditions (Johnson, 1994) and does not appear to
1994). Reinjection of thallium and repeat imaging 24
rely on active cellular processes.
hours after initial study can help identify severely is
Because of the short half-life, rapid acquisition
chemic (greater than 90% blockage) areas, which may
imaging systems are required so that the images do
take much longer to demonstrate redistribution.
not reflect washout. SPECT and first pass studies can

be performed but Tc-99M-teboroxime does not per
Technetium-99M-sestamibi
mit gated SPECT acquisition (Berman, 1991). Proto
New isotopes were approved by the FDA for perfusion
cols using this isotope are designed to take advantage
imaging in 1990. Technetium (Tc)-99M-sestamibi was
of the rapid uptake and washout. When used with
developed because of the number of advantages it has
pharmacologic stress studies, a rest-stress study can
over thallium imaging. Sestamibi provides improved
be completed within minutes (Johnson, (994). This
SPECT image quality as a result of higher count rates
may have future application in studying reperfusion
and higher energy, in the 140 keY range. Tc-99M-ses
following balloon angioplasty or reperfusion therapy
tamibi is generator-produced. The isotope has a 6-hour
with thrombolytic agents (Johnson, 1994). PET trac
half-life (Berman et aI, 1994). Because of the short
ers are also used to evaluate perfusion and will be
half-life, higher doses can be injected, and although the
discussed below. They include, 13-N ammonia, 82
percentage of extraction is lower, sestamibi uptake in
Rb rubidium, or 15-0 water.
relation to flow is similar to that of thallium. These fac

tors result in higher count rates, which thus allow the
use of gated images and first pass acquisition studies.
Tests to Evaluate Myocardial Viability
Higher count rates are preferred when evaluating obese
Identification of the size of an infarct has traditionally
patients. One of the greatest limitations of Tc-99M-ses
been helpful in determining prognosis. Infarct avid trac
tamibi is that it does not readily redistribute; therefore
ers were used. The tracers bind with elements released
reversibility of defects cannot be ascertained as well as
by necrotic myocardial tissue.
with thallium. This factor is one reason thallium is
With the development of reperfusion strategies,
much more popular. Two-day protocols or dual isotope
angioplasty, bypass grafting, and thrombolytic ther
protocols can be used to overcome this limitation
apy it was noted that areas that appeared to be non
(Berman, 1994). Lack of redistribution has been ex
functional on perfusion scans regained function once
ploited in evaluating the impact of thrombolytic therapy
the area regained adequate blood supply, Tests were
13
developed that were able to distinguish these areas of

stunned or hibernating myocardium. These tests of
myocardial viability often look at metabolism.
According to Maddahi, four different PET ap
Special Tests
203
revascularization (Scheiber!, 1994).
11-C-Acetate
Another way to evaluate myocardial viability is to
proaches have been used for assessment of myocar
use an isotope that is incorporated into the meta
(I) perfusion-FOG metabolism imag
bolic pathways related to myocardial oxygen con
ing, (2) determination of oXidative metabolism with
sumption. II-C-acetate in its activated form, acetyl
dial viability:
(3) uptake and retention of 82-Rb and
CoA, represents the entry point for all metabolic
(4) the water perfusable tissue index (Maddahi, 1994).
pathways into the tricarboxylic acid cycle, which is
II-C-acetate,
tightly coupled to oxidated metabolism. It's advan
1BF-fluoro deoxyglucose
tage over 18-FOG, is that it does not rely on sub
18F-f1uoro-deoxyglucose (FOG) is a glucose ana
strate use (i.e., glucose vs. fat metabolism). It accu
logue that crosses the capillary and sarcolemmal
r a t ely r ef l e c t s o x i d a t i v e m e t a b o l i sm a n d c a n
membrane at a rate proportional to that of glucose. It
distinguish viable from nonviable myocardium in
becomes trapped in the myocardium, because it is not
b o t h a c u t e a n d c h r o ni c i s che m i c c o nd i t i o n s
a useful substrate in metabolic pathways. FOG distri
(Bergman, 1994.)
bution is relative to uptake of unlabeled glucose

(Maddahi, 1994).
Technetium-99M-pyrophosphate
Identification of areas with normal metabolism,
Technetium-99M-pyrophosphate (TcPyp) identifies
altered metabolism or no metabolism is based on the
areas of myocardial infarction by forming a complex
use of glucose as an energy substrate. Normally,
with calcium, which is released when myocardial
perfused myocardial cells use fatty acids for adeno
cells die. TcPyp scans have the best results when ob
sine triphosphate (ATP) production when in a fast
tained 24 to 48 hours postinfarction. This time frame
ing state and use glucose as the primary energy
is obviously after reperfusion strategies would have
sour ce in the postprandial state. Ischemic m y
been employed. Sensitivity of this scan is high, but
ocardium uses glucose in the fasting state and the
specificity is low, since a number of other processes
postprandial state. Infarcted areas show no meta
can result in a positive scan (e.g., myocardial trauma,
bolic activity. Therefore increased uptake of FOG in
ventricular aneurysm, and uptake in skeletal struc
the postprandial state occurs in both hibernating and
tures) (Niemeyer, 1992).
normal myocardium, but in the fasting state, it oc

curs only in the hibernating myocardium. Clinical
Indium-111-antimyosin
studies in infarct patients showed that area with per
Indium III antimyosin is a radiolabled monoclonoal
sistent thallium-20 I perfusion defects have evidence
antibody that identifies infarcted myocardial tissue. It
of remaining metabolic activity in 47% of regions
binds with myocardial myosin, which is released when
when studied with a PET scan, indicating overesti
the muscle cell dies. It can be used in conjunction with
mation of irreversible injury. Usc of reinjection and
thallium-20I to distinguish infarcted tissue from per
late redistribution imaging has significantly lowered
fused viable tissue. It is most reliable when performed
this number (Hendel, 1994). The implication de
48 hours after infarction (Niemeyer, 1992).
rived from this finding is that in areas with perfu

sion defects, if glucose activity remains, the region
is viable (mismatch pattern); conversely, if such ac
Echocardiography
tivity is absent, the area is likely to be infarcted or
Another noninvasive method of evaluating the heart
necrotic (match pattern) (Niemeyer, 1992). Viewed
uses the physical properties of sound. Echocardiogra
in functional terms, mismatch simply implies the
phy provides information about blood flow, structure,
potential for improvement; rnatch implies no poten
and function of the heart. Motion mode (M-mode)
tial for improvement in contractility after successful
and two-dimensional (2-0) images are highly reliable
204
PART II
methods of evaluation. Recent developments of tech
with indication of flow direction in real time (Wag
nique and technology include color flow Doppler
goner, 1990). Color is matched based on the direction
echo, transesophageal echo, and intravascular
of flow, and shading is indicative of intensity based
echocardiography. These techniques, when used in
on the mean velocity flow estimates (Waggoner and
combination can provide much of the information
Perez, 1990). It is primarily used to assess the extent
previously available only by cardiac catheterization
of regurgitant jets across "leaky valves," as well as to
(Hartnell, 1994).
indicate areas of abnormal shunts such as atrial septal

defects. Turbulence created by narrowed valves cre
Physics of echocardiography
ates wide color shading.
Imaging systems that use ultrasound require a source
Measurements derived from echocardiography
for generation of the sound wave, a transducer, and a

receiver to pick up the reflected sound waves. Sound
Echocardiographic results can be viewed qualita
is absorbed or reflected differentially by specific tis
tively and quantitatively. An experienced viewer can
sues. Therefore the sound wave reflected from mus
analyze the anatomical relationships and structure of
cle differs from that reflected from vascular space,
the heart, wall motion, valve movement and configu
or valvular structures. Returning signals are con
ration, and chamber size.
verted into electrical signals that generate an image.
Quanti tati ve measures are calculated from the
This is the basis for M-mode and 2-D echo. In M
Doppler frequency shifts. Velocity measures can be
mode echocardiography, the transducer transmits a
used in other equations to estimate pressure and valve
single sound wave through the chest wall. A thin
area. The modified Bernoulli equation is used to cal
slice of the heart, an "ice pick" view, directly under
culate pressure changes around the valve:
the sound wave, reflects the wave back to the trans

L'1 P (mm Hg)
ducer. M-mode, though useful, is rarely used; 2-D is
4 X VIllax2 (m/second),
the primary diagnostic mode. In 2-D echocardiogra
where P is the pressure gradient across the valve and
phy, the transducer is able to pick up a wedge sec
V is the velocity of blood flow through the valve.
tion of the heart. In 2-D the transducer acts as the

transmitter and receiver. A "real time" two-dimen
These measurements allow calculation of stenotic
sional picture of the heart is recorded on videotape.
valve gradients and right-sided filling pressures,
The heart can be viewed in motion, and wall motion
valve regurgitation, and ventricular septal defects
can be evaluated.
(Waggoner and Perez, 1990). Valve regurgitation and
Doppler echocardiography relies on the Doppler

effect to determine velocity. W hen a sound wave is
shunt calculations are more complicated than the

Bernoulli equation alone.
aimed at moving objects such as red blood cells,
Another important quantitative measure is the
the known transmitted frequency and the reflected
estimated area of the valve. The continuity equation
frequency differ, a phenomenon, known as a fre
is used to estimate valve area. It is based on the
q u e n c y s h i f t . The g r e a t e r the frequency s h i f t
principle of conservation of mass; that is, in a nor
the greater the speed o f the targeted object (Wag
mal heart, the volume of blood that enters the right
goner and Perez, 1990). The velocity of flow is
atrium should be conserved as it passes through the
the terminology used to express Doppler frequency
other chambers. Flow. volume at different sites is
shifts. Both continuous wave and pulsed wave
related to the flow velocity and the cross sectional
Doppler are used.
area of the site. Therefore AI x VI
A2 X V2,
Color flow Doppler echocardiography was intro
where VI is the velocity of flow at one side of the
duced in the mid-1980s. It is usually superimposed
valve and V2 is the flow velocity at the other side
on a two-dimensional image in real time but can be
of the valve, and A is the cross-sectional area
used with M-mode. It is a method that displays
(W aggoner and Perez, 1990) (Wilson, Va cek,
anatomic and spatial blood flow velocity estimates
1990).
13
Transesophageal echocardiography (TEE)
Special Tests
205
saturation can be obtained. When selective coronary
Because of consistent technical difficulties with
arteriography is performed, radiopaque contrast mate
transthoracic echocardiography, the technique of trans
rial is injected into the left main or right coronary
esophageal echo was developed to improve spatial res
artery. Cine recordings are made after the injection,
olution. The technique can obtain M-mode, 2-D, and
and injections are repeated until the entire coronary
color flow Doppler images by using a small probe
tree is visualized.
mounted on the tip of a modified gastroscope. The
Cardiac ventriculography is when dye is injected
probe is advanced into the esophagus and positioned so
into the ventricle and the entire chamber becomes
that multiple views of the heart are available (Kerber,
outlined. Several cardiac cycles are recorded on cine.
1988). Initially, the technique was performed intraoper
It provides valuable information about global and
atively on anesthetized patients and on intubated pa
segmental wall motion, valve motion, and the pres
tients in the intensive care unit. It is now used on awake
ence of abnormal anatomy (Grossman, 1986).
patients who are mildly sedated (Schneider, 1993). The

semiinvasive nature of this test has slowed its adoption.
It is most useful in ruling out thrombus or heart valve
TESTS OF THE RESPIRATORY SYSTEM
vegetation as a cause of transient ischemic attack (TIA)
Unlike the cardiovascular system, special tests of the
or stroke. Especially excellent views of the left atrium
respiratory system are less commonly used in the initial
and atrial appendage are seen. The atrial appendages
diagnosis and treatment of disease. This is the result of
cannot be visualized by traditional transthoracic echo. It
the generally high quality information obtained from
is also a good assessment of prosthetic valve function.
standard x-ray examination when combined with the

patient's respiratory symptoms and the results of the
physical examination (Lillington, 1987). When further
Cardiac Angiography
information is needed to refine the diagnosis or treat
The standard with which many of the noninvasive tests
ment decision several tests are available to clinicians.
are compared is that of cardiac catheterization. It is an
Radionuclide imaging of the chest is useful in the non
invasive test, with a small but serious risk to the pa
invasive evaluation of pulmonary embolism, whereas
tient. Complications include death, stroke, myocardial
pulmonary angiography is the invasive but definitive
infarction (MI), bleeding, arterial trauma or thrombus,
test. A computed tomography (CT) scan of the chest
renal dysfunction, and aIThythmias (Reagan, Boxt, and
also has a variety of applications (Webb, 1994). Al
Katz, 1994). The test is indicated in patients with a
though magnetic resonance imaging (MRI) provides
high risk of atherosclerotic heart disease whose stress
improved tissue contrast in comparison to a CT scan,
perfusion scans are positive. Patient's with diagnosed
imaging applications in pulmonary disease continue to
CAD with angina, unresponsive to medical therapy,
suffer from technical limitations (Mayo, 1994).
may also need catheterization.
Bronchoscopy
Test Procedure
Bronchoscopy is often used as both a diagnostic and
The cardiac catheterization laboratory requires an x
therapeutic treatment modality (Mars and Ciesla,
ray generator tube and image intensifier/cine camera.
1993). It allows direct visualization of the trachea and
Data are stored using 35mm file (Reagan, Boxt, and
its major subdivisions. Fiberoptic bronchoscopy has
Katz, 1994).
virtually replaced bronchography (Lillington, 1987).
The procedure for cardiac catheterization of the
In fiberoptic bronchoscopy, a flexible tube is inserted
left side of the heart requires the threading of a
into the trachea of mildly sedated patients. This tude
catheter, guided by fluoroscopy, through the femoral
is able to enter small brochial subdivisions. Secre
artery or brachial artcry 10 thc aorta. Direct measure
tions can be removed for evalutation or as a treat
ments of chamber pressures, blood flow, and oxygen
ment. It is also possible to obtain biopsy samples
206
PART II
using tiny forcepts or cell brushings. Bronchoscopy is
standard against which ventilation/perfusion scans
particularly important in the diagmosis of bron
are compared (Juni, 1992). Contrast dye is injected
chogenic carcinoma (Price and Wilson, 1986).
into the pulmonary circulation through the pulmonary

artery. Additional techniques such as balloon occlu
sion, segmental injections, or increased magnification
RADIONUCLIDE IMAGING
improve the sensitivity of the test (Lillington, 1987).
Ventilation-Perfusion lung Scan
Interobserver reliability studies pelformed on the in
The ventilation-perfusion lung scan is a combination of
terpretation of pulmonary angiograms are 83% to
two separate imaging procedures. It is primarily used in
86% (Juni, 1992).
the diagnosis of pulmonary embolism, with limited use

for other clinical problems (Lillington, 1987). The per
fusion portion requires the injection of radioacti ve
Gallium SCintigraphy
tracer. Technetium-99M-macroaggregated albumin is
Gallium-67-citrate concentrates in neoplastic and in
(almost universally accepted as) the perfusion tracer of
flammatory lesions of the lung (Lillington, 1987).
choice (Juni and Alavi, 1991). The ventilation scan re
Gallium is more sensitive than normal chest x-ray in
quires the inhalation of radioactive gas, usually 133-XE
identifying infectious and noninfectious inflamma
gas or Tc-99M-diethylene triamine penta-acetic acid
tory processes. This is particularly important in iden
(DTPA) aerosol. Other isotopes can be used for ventila
tifying opportunistic infections in the immunocom
tion scanning (e.g. Kr-8IM, Xenon-I27) but they are
promised patient. In patients with acquired immune
more difficult to obtain.
deficiency syndrome (AIDS) the sensitivity of gal
A normal perfusion scan essentially rules out re
lium scanning for pneumocystis carinii pneumonia
cent pulmonary embolus. If the perfusion scan is ab
approaches 94% to 96% (Kramer and Divgi, 1991).
normal, it is compared with the ventilation scan for
The radioisotope is injected but it takes 48 to 72
match or mismatch of defects. An interpretation
hours before imaging can be pelformed (Miller and
scheme is used, such as Biello or Pioped, which clas
O'Doherty, 1992).
sifies the probability of pulmonary embolism into
Gallium is commonly used in the evaluation of pa
normal, low, intermediate (indeterminate), or high
tients with interstitial lung disease; this includes sar
(Juni, J 991; MiJJer and O'Doherty, 1992). Patients
coidosis, amiodarone toxicity, and following cyto
with high probability scans should begin anticoagula
toxic therapy with bleiomycin, as well as many other
tion therapy (Juni, 1991). Patients with intennediate
entities (Miller and O'Doherty, 1992). In conjunction
(indeterminate) scans may need to have a pulmonary
with neoplasms, the scan's use is limited to assessing
angiogram before beginning treatment (Miller and
tumor extent (Kramer and Divgi, 1991).
O'Doherty, 1992).
Miller and O'Doherty (1992) note other applica
tions of ventilation/perfusion scanning to include
monitoring of response to radiotherapy and assess
Computed Tomography
A computed tomography (CT) scan of the chest pro
ment of resectability of bullae. The scan is used to
vides a series of cross-sectional x-ray images. Com
predict whether someone can tolerate a pneumonec
pared with the standard x-ray, it is not commonly
tomy based on percent flow to the opposite lung and
used in the initial diagnQsis of pulmonary disease. CT
extent of disease present.
scan has been found to be a useful first-line diagnos

tic tool in the evaluation of mediastinal disease, in
cluding mediastinal masses, staging of mediastinal
Pulmonary Angiography
cancers, and identification of cysts (Lillington, 1987).
The diagnosis of pulmonary embolism is the primary
High-resolution computed tomography (HRCT)
indication for pulmonary angiography. It is the gold
has improved the documentation of morphologic
13
associated with chronic airflow obstruction.

Webb's (
review of the application of this new

identified the utility of this test in a vari
ety of obstructive diseases. HRCT is sensitive in the

although
of
such as
used
Many tests are available t o
mines which tests are appropriate for the

medical condition. When the tests are
results are
HRCT demon
In the diagnosis of
to the selection of exercise and
It is the procedure of choice

work loads the PT
tween the three different
PT reaches a certain
of abnormal bronchi
seen in bronchiectasis (cylindrical,
Until a
for the
level, as well as a
level of understanding and application of the test
but again there is l ittle clinical
treatment, it is
results to
1994). It can be used to differentiate
encouraged
that the PT discuss the test and results with the pa
spread of cancer versus heart failure when un
tient's physician. These discussions are excellent

for learning both for the PT and to
clear clinically. HRCT also can be used to evaluate

of
wiH apply to
function and response to exercise. This Ull
after plain chest X-rays. HRCT can discriminate be
(Webb,
and an evaluation of
the results are documented. PTs need to understand

the results of the tests and how
well as waH thickness.

strates a high
card
monary dysfunction. The attending physician deter
10 m m i n diameter, as
207
SUMMARY
HRCT is a b l e t o
demonstrate cysts less than
Special Tests
the
Overall, HRCT has

but the clinical
understand what physical ther
apy has to offer the
with
function is less clear.
REVIEW QUESTIONS
Magnetic Resonance Imaging
Why is the
sure of
mea
function?
2. What i s the difference between
stunned my
ocardium and
3.
embolism?
4, Which tests can be used to evaluate myocardial

vjability?
5. Why is
a good choice for eval

cardiac defects?
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medicine. Clinics ill Chesl Medicine 12:1. 55-75.
doppler. Cardiology Clinics, 12, 385-389.
Lillington, G. (1987). A diagnos tic approach to chest disease. Bal
Webb, W.R. (1994). High-resolution computed tomography of ob

structive lung disease. Radiologic Clinics of North A merica,
timore: Williams and Wilkins.

Maddahi, 1., Schelbert, H., Brunken, R., & DiCarli, M. (1994).
Role of Thallium-201 and PET imaging in evaluation of my
32, 745-757.
Wilson, D., & Vacek, J. (1990). Echocardiography. Postgraduate
ocardial viability and management of patients with coronary
Medicine. 87. 191-202.
Clinical Assessment of the
Cardiopulmonary System
Susan M. Butler
KEY TERMS
Barrel-chest
Hyperresonant
Crackles
Resonant
Cyanosis
Wheeze
Dyspnea
Whispered pectoriloquy
Egophany
INTRODUCTION
the inpatient setting, a chart review is the first point
To develop an effective treatment program for the pa
of contact, whereas in the outpatient population, the
tient with a cardiopulmonary problem, it is essential
information may be only what is obtainable from the
that a thorough evaluation be peliormed by the physi
patient. Time management is an ever-present issue in
cal therapist (PT). This provides "baseline" data for
today's era of cost containment and health care re
comparison with subsequent reassessments that occur
form. Thus a medical chart review should be con
on a daily basis. Any progress or deterioration in sta
ducted in an organized fashion. Most PTs develop
tus can then be easily identified with appropriate ad
their own method.
justments made in the treatment plan.
One strategy to chart review is the following se

quence:
1. Read the history and physical and admission
CHART REVIEW/PATIENT INTERVIEW
medical note (i.e., preadmission symptoms).
The first patient contact can be indirect, through the
2.
medical chart, or direct, through patient interview. In
3. Scan remainder of chart.
Read the last medical note.
209
210
PART II
4. Read any reports from medical specialists, con

sultants, i.e., pulmonologist, neurologist, oncologist.
5. Review any pertinent lab tests. EXAMPI.ES: chest
and respiratory systems. These questions could in

clude the following: What is the smoking history?
Does the patient have a family history of premature
x-ray, arterial blood gases (ABG's), complete blood
coronary artery disease (i.e., a parent or sibling who
count (CBC).
had a myocardial infarction)? Can the symptoms pre
6.
Review medications, in particular, pulmonary
and cardiac drugs.
sented also be signs of a cardiovascular or pulmonary

illness? Does the patient have an active versus a
7. Review the psychosocial information (i.e., fam
sedentary lifestyle? What activities precipitate symp
ily, architectural barriers).
toms? Do these symptoms include breathlessness?
This last step is crucial in this time of shortened hos
The patient should be seen as a human being with
pital stays. Any detail of the patient's background
multiple organ systems. The patient's prob.lem,
that would affect discharge planning is crucial to
whether oI1hopedic or cardiopulmonary, should not be
know even on the first day of treatment. Additional
viewed in isolation. An example is the outpatient with
information to review that may be helpful and falls
a physical therapy diagnosis of low back pain. When
into the cate gory of "as time allows" is the documen
questioned about limiting symptoms, the patient might
tation of other allied health professionals (i.e., nurs
describe cramping leg pain more suggestive of periph
ing, occupational therapy, speech pathology). Finally,
eral vascular disease (PYD).
when the initial chart review is finished, a mental pic

ture of the patient should exist, even before the PT
steps into the patient's hospital room.
PHYSICAL EXAMINATION
Details regarding the patient interview have been
The traditional components of a chest assessment are
covered in chapter 7. However, there are questions

that should be posed to any patient regardless of
visual inspection, auscultation, percussion, and

pal pation. The information provided by each of
whether their primary condition is cardiopulmonary.
these techniques, when integrated with the patient's
The patient whose referring problem is musculoskele
history and chal1 contents, allows the PT to piece to
tal or neurologic still must have operational cardiac
gether the pieces of the puzzle. For instance, to aus

cultate breath sounds without observing the symme
try of the chest wall fails to provide the needed clues
Anatomic Structures
to the total patient picture; thereby the development
Suprasternal /lotch-A depression palpable at the

tip of the sternum
Sternomanubrial angll'-A bony bump where the
manubrium meets the body of the sternum; about 5
cm distal to suprasternal notch; also known as
angle of Louis; palpating hlle.ral to this junction,
of an appropriate plan of care for the patient is maqe

more difficult.
Before each individual component of the assess
ment is discussed, a review of the pertinent anatomical
landmarks and topographical lines is to be discLlssed.
the .l'econd ribs is found and thus a reference point
Knowledge of the superficial anatomy arid its relation
for identifying intercostal spaces and successive
ship to the Llnderlying heart and lungs aids the therapist
ribs; also, a superficial marking for where the

underlying trachea divides into right and left
mainstem bronchi.
in decision making. The topographical lines allow for

more accurate description of the physical findings.
Costal angle-The angle formed by the joining of

the costal margins with the sternum; normally, no
greater than 90 degrees.
Vertebra prominens-The spinous process of the
seventh ccrvical vertebra (C7); allows numbering
of thoracic vertebra
TOPOGRAPHICAL ANATOMIC LANDMARKS

Key anatomical structures include the following:
Sternum
Clavicles
14
Clinical Assessment of the Cardiopulmonary System
211
-------
Suprasternal notch
Sternomanubrial angle (angle of Louis)
(MAL), and posterior axillary (PAL)-Like the
Costal angle
MCLs, these lines are also bilateral.
Vertebra prominens
The posterior chest has the following three lines:
See the box on p. 210 and Figures 14-1 and 14-2 for
thorax. Imaginary topographical lines are used to

more clearly describe any physical findings (e.g., lo
cation of surgical incisions, abnormal breath sounds,
etc.) (Figure 14-3).
The anterior view of the thorax has three vertical
runs through the
Mid-scapular lines (MSL)-lie parallel to the

mid-spinal lines; bisect inferior angles of scapulae.
VISUAL INSPECTION
Inspection is the foremost element of a chest assess
ment. Not only should the features of the patient be
lines. These are the following:

Mid-sternal line (MSL)-a vertical line bisecting
. the sternum
Vertebral or mid-spinal line
spinous processes of the vertebrae.
specific definitions and anterior and lateral views of
Anterior axillary line (AAL), mid-axillary line
observed, but also the equipment and any aspect of

the patient's surroundings that would contribute to
Mid-clavicular fine (MCL)-lies parallel to the
delineating the true picture of that patient. Remem
MSL, bisects each clavicle; the lower lung borders
ber, the PT has speculated a preliminary picture of
cross the sixth rib at the MCL.
the patient based on chart review. Now, the ultimate
Laterally there are three vertical lines, originating
test: how realistic was this initial impression? What
in their respective axillary folds:
are the outward clinical signs that the therapist should
Clavicle
-----1n Manubrium
ManubriostemaI junction
(Angle of Louis)
Nipple
Costal angle
FIGURE 14-1
Topographical landmarks of the chest. (Adapted with permission from Seidel HM et al: Mosby's
guide to physical examination, ed 3, Boston, 1995, Mosby.)
212
PART II
Suprasternal notch
Clavicle
'j,\
.1
'_=:,. c/:.Ay".J
,
Manubrium
Costal cartilages
Ribs
Xiphoid process
)
FIGURE 14-2
Anterior view of the thorax. (With permission from Swartz MH: TeXfbook
ofphysical diagnoses
hi story and examination, ed 2, Philadelphia, 1994, WB Saunders.)
look for? It will be broken down into categories for
patient's build-stocky, thin or cachectic? Is the pa
clarity.
tient's mobility limited? Can the patient sit unsup

ported? Should the assessment be performed in stages
such
General Appearance
as
supine or alternate sidelying? Is there any extra
equipment in the patient's surroundings? Is the patient
Does the patient appear comfortable? Is there any facial
wearing supplemental oxygen? Is the oxygen delivered
grimacing? Is the patient awake and alert or disori
through a nasal cannula or a mask? What is the fraction
ented? Is there any nasal flaring or pursed-lip breath
of inspired oxygen (Fi02)? Are there any monitoring
ing? These are signs of respiratory distress. Nasal flar
lines and where are they located. For instance, if an ar
ing can be defined as the outward movement of the
terial line is present, is it placed in the radial or femoral
1994).
Are the accessory
artery? Are there electrocardiogram (ECG) leads? Is it a
muscles of respiration (i.e, sternocleidomastoid, trapez
"hard line" (directly connected to monitor) vs. teleme
ius) hypertrophied? How is the patient positioned? Is
try (through radio transmitter)? Are there intravenous
the patient resting comfortably or leaning forward over
(IV) sites? Are these peripheral (antecubital) or central
the bedside table and struggling for breath? What is the
(subclavian or jugular)? Is there a urinary catheter?
nares with inspiration (Swartz,
System
Clinical Assessment of the
14
L----j::::- SuprasternaJ notch

t---t----"1- SlernomanubriaJ angle
t---;---/---'r--- Midsternal line
r--+--t-..4f.1\\--::::---\--- Midclavicular lioe
1
A
/1
6"///
,"--4i
If
--
Spinous process of C7
Anterior axillary liM --t----I
Midaxillary li ne ----+
+-_1
___
1--.....,..-+1-+---+----::>--+- Scapula line
dJ
pi
Posterior
line
---r----t-+--j
J/I F'
II---+--/!--":--- Midspinalline
FIGURE 143
lines. A, Anterior view. 8, Lateral view.
Posterior view. (Adapted with
and examination, ed 2,
permission from Swartz MH: Textbook

Philadelphia, 1994, WB Saunders.)
213
214
PART II
Skin
desaturation has been noted, but this is not an exclu
Does the skin have a pink, healthy color versus a pal
sive phenomenon. Clubbing has been o bserved in
lor? Is cyanosis present? Cyanosis is a bluish tinge
non pulmonary diseases such as hepatic fibrosis and
that can be seen centrally or peripherally. Central
Crohn's disease. (George, Light, Matthay, and
cyanosis is a result of insufficient gas exchange
Matthay, 1990; Seidel, Ball, Dains, and Benedict,
within the lungs and is not usually seen unless oxy
1995; and Swartz, 1994).
gen saturation is less than 80%. A bluish tint may be

seen at the mucous membranes (e.g., tongue, lips).
Peripheral cyanosis, on the other hand, occurs when
Neck
oxygen extraction at the periphery is excessive. This
Are the accessory muscles of respirations being re
type is also more associated with low cardiac output
cruited for a resting breathing pattern? Do the stern
states. Areas to observe for peripheral cyanosis might
ocleidomastoid or trapezius muscles appear promi
be fingertips, toes, nose, or nail beds. A differentiat
nent? This is an early sign of obstructive lung disease
ing feature between central and peripheral cyanosis is
(Swam, (994).
that peripheral cyanosis occurs, usually in the cooler

body parts such as nail beds and vanishes, usually
when the part is warmed. In contrast, central cyanosis
does not disappear when the area is warmed.
Jugular venous distension

The jugular veins empty into the superior vena cava
Are any scars, bruises or ecchymoses observed?
and reflect right-sided heart function. Right atrial
Are there reddened areas suggestive of prolonged
pressure (RAP) is evident based on the extent to
pressure anywhere? Do the bony landmarks appear
which the jugular venous pulse (JVP) can be visual
more prominent than usual? Are there any signs of
ized. The more superficial external jugular veins may
trauma to the thorax or any other body parts? Does
be seen superior to the clavicles; the internal jugular
the skin appear edematous? Does this edema appear
veins, though larger, lie deep beneath the sternoclei
to limit joint motion? Are there any surgical inci
domastoids and are less visible. Jugular venous dis
sions, new and old? Do these incisions appear to be
tention (JVD) can be best seen when the patient lies
healed or seem reddened and swollen? Is there evi
with the head and neck at an optimal angle of 45 de
dence of clubbing of the digits? Clubbing can be de
grees (Figure 14-5). Symmetry of JVD should be
fined as the loss of angle between the nail bed and the
noted. The veins are distended bilaterally if there is a
distal interphalangeal joint (Figure 14-4). The cause
cardiac cause such as congestive heart failure (CHF).
of clubbing has a variety of theories, including in
A unilateral distention is an indication of a localized
creased perfusion. Its association with arterial oxygen
problem. (Seidel, Ball, Dains, and Benedict, (995).
CHEST WALL CONFIGURATION

The normal thoracic cage is elliptically shaped when
free of disease. The anteroposterior (AP) to lateral di
ameter is 1:2 or 5:7. The angle of the ribs is less than
90 degrees. The ribs articulate with the vertebra, pos
teriorly, at a 45-degree angle. The thorax should be
FIGURE 14-4
A, Clubbing of the fingers is best assessed by detemtining the
ratio of the diameter at the base of the nail B, to the diameter at
observed both anteriorly and p osteriorly. With

chronic obstructive pulmonary disease (COPD), the
the distal interphalangeal joint. This ratio is n ormally less than
ribs become more horizontal and the A-P diameter
I. (Reprinted with permission from George RB et al: Chest
increases, thus the term barrel chest is used. In in
medicine, ed 2, Baltimore, 1990, Williams and Wilkins.)
fants, the chest is round with the anteroposterior and
14
215
Carotid mCfY
Internal jugular vein
Horiz nlal line

FIGURE 14-5
Proper positioning to observe jugular venous distention. (Reprinted with permission from Seidel
HM et al: Mosby's guide to physical examination, ed 3, Boston, 1995, Mosby.)
transverse or lateral diameters of about equal dimen
pathology. Again, any asymmetry should be observed
sions. As the child grows to adulthood, the chest be
from both anterior and posterior views.
comes more elliptical. Again, with the aging process,
Structural defects of the anterior chest may in
the chest returns to a more rounded appearance. The
clude the following: pectus excavatum, or funnel
increased anteroposterior diameter, in this population,
chest-a depressed lower sternum that usually causes
is a result of the multiple factors of decreasing lung
restriction only when severe; pectus carinatum, or pi
compliance, decreased strength of the thoracic and di
geon chest-a prominent upper sternum which does
aphragmatic muscles and skeletal changes of the tho
not restrict chest wall movement; and flail chest-the
racic spine. The sym metry of the thoracic cage
chest wall moves inward with inspiration, such as
should also be noted. Asymmetry can be the result of
with multiple rib fractures.
structural defects or an underlying intrathoracic
Other structural defects are spinal deformities.
216
.-
PART H
t \
.JPI4/1h
./
" /
./
\ 'I
(j>";-.
(";" \,\"'\\
Jilii/
\{
/'
"',r-
\
.
/(
Kyphosis
"Barrel chest"
:Jil!
..:,:.-
Normal
} -\,
.
Pectus excavatum
Pectus carinatum
FIGURE 14-6
Chest walJ configurations. (Reprinted with permission from Swartz MH: Textbook o/physical
diagnoses-his/ol)! and examination, ed 2, Philadelphia, 1994, WB Saunders.)
These are best viewed posteriorly. Kyphoscoliosis is
Dyspnea describes the sensation of breathlessness
one example of how a posterior and lateral spinal devi
or shortness of breath and is seen in cardiopulmonary
ation can limit chest wall and lung expansion. Another
disorders. The level of dyspnea worsens as the sever
example is a patient with COPD, who usually has a
ity of the disease increases. An easy method to docu
forward head and thoracic kyphosis (Figure
14-6).
ment the level of dyspnea is to count the numbers of

words that the patient is able to speak per breath. For
instance, six-word dyspnea is not as significant as
BREATHING PATTERN
one-word dyspnea. The type of activities that elicit
Respiratory rate normally ranges between 12 and 20
shortness of breath should also be ascertained. For
breaths per minute (bpm). Eupnea is the term used to
example, is breathlessness precipitated by stair climb
describe a normal breathing cycle. Apnea is a tempo
ing, taking a shower, etc? The "normal" ratio of in
rary halt in breathing. Tachypnea is a rapid, shallow
spiratory time to expiratory time is j :2. As the respi
breathing pattern; this is an indicator of respiratory
ratory rate increases this ratio decreases to j: I. This
distress.
is seen in respiratory distress, as the patient struggles
Bradypnea exists when respiration is slowed, less
to breathe in, the expiratory phase is shortened, and a
than 12 bpm. Causes could be neurologic or metabolic.
vicious cycle continues. With pursed lip breathing,
Kussmaul's breathing is an increased rate and depth of
the idea is to prolong the expiratory phase and slow
respirations and is associated with metabolic acidosis.
the breathing pattern.
14
AUSCULTATION
Auscultation is the art of listening to sounds pro

duced by the body. Lung and heart sounds are the
focus of this chapter. Skill in auscultation is depen
dent on the following four factors:
I. A functional stethoscope
2. Proper technique
3. Knowledge of the different categories of lung
sounds: normal, abnormal, and adventitious
breath sounds and voice sounds
4. Knowledge of the different categories of heart
sounds and murmurs
Stethoscope
A stethoscope need not be fancy to be effective. A

PT, skilled in auscultation, can use any basic stetho
scope and be able to identify lung sounds. The stetho
scope functions more as a filter to the extraneous
noises than as an amplifier. A basic stethoscope con-
Tubing
FIGURE 14-7
217
sists of ear pieces, tubing, and a chestpiece. The bell

portion of the chestpiece assesses low-pitched
sounds, that is, heart sounds. The diaphragm portion
discerns high pitched sounds (Figure 1 4-7). The tub
ing should not be so long that sound transmission is
not dampened. Length of tubing should be between
about 30 cm (12 in) to 55 cm (21 to 22 in). The ear
pieces should fit the PT's ears comfortably and allow
tuning out of external sounds. Other considerations
would be to position the ear pieces anteriorly or for
ward toward the ear canals. Finally, an aside gained
from the author's clinical experience: warming the
diaphragm with the hands before placing it on the pa
tient's skin is a first step in developing good patient
rapport.
Technique
Environment is another element in the correct pedor

mance of auscultation. The room or cubicle should be
as quiet as possible. Television and radio should be
turned down or off. Any extraneous noises should be
minimized or eliminated. This is especially important
when auscultation is a new technique for the thera
pist. The patient should be positioned sitting, if possi
ble, for lung sounds. The anterior, lateral, and poste
rior aspects of the chest should be auscultated both
craniocaudally (apices to bases) and side to side (Fig
ure 14-8). The PT places the diaphragm on the pa
tient's skin so that it lies flat. The patient is instructed
to breath in and out through the mouth. A slightly
deeper breath than tidal breathing is suggested. A
minimum of one breath per bronchopulmonary seg
ment allows for a comparison of the intensity, pitch,
and quality of the breath sounds. Movement of the di
aphragm from one side to the other side while, at the
same time, moving it craniocaudally, enables the PT
to compare the right to the left chest. Clothing should
be removed and/or draped so that it does not interfere
in the assessment of the breath sounds.
Chest Sounds
Stethoscope. (Replinted with permission from Wilkins RL,

Hodgkin JE, Lopez B: Lung sOllnds, St. Louis, 1988, Mosby.)
Chest sounds may be divided into these categories:
218
PART II
FIGURE 14-8
Stethoscope placement for auscultation of breath sounds. A, The chest. B, The back. (From
Buckingham EB: A
primer of clinical diagnosis,
I. Breath sounds-normal , abnormal, adventi
ed 2, New York, 1979, Harper & Row.)
piratory phase. A distinguishing feature is the pause

that exists between the inspiratory and expiratory
tious
2. Voice sounds - egophany , bronchophany,
phases (Figure 14-9). This sound is also described as

tracheal as its norma/ location is over the trachea.
whispered pectoriloquy
3. Extrapulmonary sounds-pl eural or friction
Brol1chovesicular suunds are similar in that these are
also high-pitched and have an equal inspiratory and
rubs
4. Heart sounds
expiratory cycles. However, a differentiating feature

is the lack of a pause (Figure 14-9). Brol1chovesicular
sounds are heard best wherever the bronchi or central
Breath Sounds
lung tissue is close to the surface. These include su
The terminology of breath sounds given in this chap
perior to the clavicles and suprascapular (apices), and
ter is a compilation of multiple resources and clinical
parasternal and interscapular (bronchi). The ATS
experience. Recognition of normal breath sounds is
AACP, in its 1977 recommendations for pulmonary
the key to the identification of abnormal and adventi
nomenclature, used the term bronchial to include
tious sounds by offering the listener a point of refer
both bronchial and bronchovesicular sounds. The fi
ence. Normal breath sounds can be broken down into
nite difference is minor (the pause between the inspi
bronchial, bronchovesicular, and ves icular_ The
ratory and expiratory phases). This recommendation
American Thoracic Society (ATS) and the American
is meant to provide uniformity to lung sounds tenni
College of Chest Physicians (ACCP) has attempted to
nology. Vesicular brealh suunds are heard over the
provide standardization of the nomenclature and con
remaining peripheral lung fields. These sounds have
tinues to conduct surveys of health care professionals
primarily an inspiratory component with only the ini
for use of this terminology in clinical practice.
tial one third of the expiratory phase audible. Their
Bronchial sounds can be described as high
intensity is also softer because of the dampening ef
pitched and are heard both in the inspiratory and ex
fect of the spongy lung tissue and the cumulative ef
14
BRONCHIAL
loud, high pitched; hollow quality;
heard over manubrium; louder on
expiration; distinct pause between
inspiration (I) and expiration (E)
BRONCHOVESICULAR
mixture of bronchial and vesicular; I:
E is 1: 1; heard over main-stem bronchi
-- anteriorly: ICS # 1 and 2, posteriorly:
between scapulae
/\
219
when it becomes airless-either partially or com

pletely. In a consolidation type of pneumonia, the
lung tissue is Hairless" because of the complete ob
struction of segmental or lobar bronchi by secretions.
Sound from the adjacent bronchi is enhanced and be
comes more high-pitched and the expiratory compo
nent louder and more pronounced. Compression of
lung tissue from an extrapulmonary source also pro
duces bronchial sounds. Examples include compres
sion secondary to increased pleural fluid (pleural ef
fusion) or tumor. Tubular breath sounds is a term
used synonymously to describe abnormal bronchial
VESICULAR
soft, low pitched; heard over peripheral
lung tissue; no pause between I and E;
ratio is 3: 1
FIGURE 14-9
/'
breath sounds.
Decreased or absent breath sounds occur when
sound transmission is diminished or abolished. De
creased breath sounds are when the normal vesicular
sounds are further diminished. Absent sounds are
when no sounds are audible. Decreased or absent
sounds can be caused by an internal pulmonary
Normal breath sounds.
pathology or can be secondary to an initially nonpul

monary condition. Hyperinflation caused by emphy
sema causes decreased sound transmission as a resull
of the destruction of the acinar units and increased air
as a result of loss of normal lung structure. The loss
fect of the air entry from numerous terminal bronchi
of lung compliance resulting from pulmonary fibrosis
oles. The idea that vesicular sounds reflect air entry
also may produce decreased or absent breath sounds.
in the alveoli has been disproved. Thus as the thera
Extrapulmonary causes include tumors, neuromuscu
pist auscultates from top to bottom, the breath sounds
lar weakness (i.e, muscular dystrophy), and muscu
are quieter at the bases than at the apices. Infants and
loskeletal deformities (i.e., kyphoscoliosis). Pain is a
small children have louder, harsher breath sounds.
common cause for decreased or absent breath sounds.
This is as result of the thinness of the chest wall and
When the patient attempts to take a deep breath, the
the airways being closer to its surface.
volume is limited because of the onset of pain. The

etiologic factors of the pain can be varied-from in
cisional (i.e., midsternotomy) to traumatic (fractured
Abnormal Breath Sounds
ribs). Given that no underlying pathologies are pre
Abnormal breath sounds can be described as when
sent, decreased breath sounds may also be a reflec
the sound transmission changes as a result of an un
tion of the depth of respiration and/or the thickness of
derlying pathologic process. Sound is filtered by the
the chest wall (e.g., in obesity or with the presence of
lung tissues because these organs are air-filled; thus
bandages). The skill of auscultation lies in the differ
there is dampened sound transmission over the bases
entiation b etween normal and abnormal breath
versus the apices. On the other hand, sound transmis
sounds.
sion is enhanced when a liquid or solid is the

medium. Certain lung pathologies produce abnormal
lung sounds. Abnormal sounds can be divided into
Adventitious Breath Sounds
three types: bronchial, decreased, and absent.
Adventitious breath sounds are the extraneous noises
Bronchial sounds occur in peripheral lung tissue
produced over the bronchopulmonary tree and are an
220
PART II
indication of an abnormal process or condition. These
three." Egophany is also described when there is in
sounds may be more easily identifiable than abnor
creased transmission of the vocal vibrations. In this
mal sounds. Adventitious sounds are classified as
case, the patient is asked to say "eeee." The underly
c rackles (rales), rhonchi, and wheezes. Crackles
ing process distorts the "e" sound so that an "aaa"
(rales) are described as discontinuous, low-pitched
sound is heard over the peripheral area by the exam
sounds. They occur predominantly during inspiration.
iner. Egophany co-exists with bronchophany.
The sound of rubbing hair between the fingers or vel
Whispered voice sounds also produce low-pitched
cro popping simulates crackles. Crackles usually in
vibrations over the chest that are muftled by normal
dicate a peripheral airway process. Rhonchi are low
lung parenchyma. Whispered pectoriloquy describes
pitched but continuous sounds. These occur both in
when these whispered voice sounds become distinct
inspiration and expiration. Snoring is a term used to
and clear; "one, two, three" or "ninety-nine" are used
describe its quality. Rhonchi are attributed to an ob
to evaluate this sound. Whispered pectoriloquy can
structive process in the larger, more central airways.
be present when bronchophany and egophany are ab
Wheezes are continuous but high-pitched. A hissing
sent. This sign is helpful in identifying smaller or
or whistling quality is present. Wheezes predomi
patchy areas of lung consolidation.
nantly occur during expiration and are an indication
Voice sounds are a means of confirmation of the
of bronchospasm (i.e., asthma). However, wheezes
abnormal breath sounds. If a patient with significant
can also be caused by the movement of air through
atelectasis secondary to compression of lung tissue
secretions, thus inspiratory wheezes can be described.
presents with bronchial breath sounds, then egophany

and bronchophany are also audible.
Extrapulmonary Sounds
An adventitious sound that is nonpulmonary is the
HEART SOUNDS
friction rub. It can be described as a rubbing or leath
As with lung sounds, superficial topographical land
ery sound and occurs during both inspiration and ex
marks assist the therapist in auscultation of heart
piration. The sound is produced by the visceral
sounds and murmurs. The left ventricular apex is nor
(inner) pleural lining rubbing against the parietal
mally located at the MCL in the fifth intercostal
(outer) pleura and is a sign of a primary pleural
space (rCS). The cardiac apex is also known as the
process such as inflammation or neoplasm. Pain is
point of maximum impulse (PM/). There are four ref
usually associated with a friction rub.
erence areas for cardiac auscultation; these do not

c o r r e s p o n d directly to the u n derlying cardiac
anatomy. On the other hand, these areas do relate to
Voice Sounds
the events arising at the individual cardiac valves.
Voice sounds are vibrations produced by the speak
These four areas are defined as the following:
ing voice as it travels down the tracheobronchial tree
aortic: second rcs, at right sternal border
pulmonic: second ICS, at left sternal border
The transmission of these vocal vibrations can be in
tricuspid: fourth and fifth lCS, LSB
creased or decreased in the presence of an underlying
mitral: cardiac apex fifth ICS, MCL.
and through the lung parenchyma when heard with a
(RSB)
stethoscope. These sounds, over the normal lung, are

low-pitched and have a muftled or mumbled quality.
(LSB)
pulmonary pathologic process. Bronchophany de

scribes the phenomenon of increased vocal transmis
sion. Words or letters are louder and clearer. Causes
Technique
are conditions where there is an increased lung den
An environment that is as quiet as possible is recom
sity as in consolidation from pneumonia. The patient
mended. Positions used for cardiac auscultation in
is usually asked to repeat "blue moon" or "one, two,
clude the following: supine-used for all areas; left
14
221
lateral decubitus (sidelying)-iistening to cardiac
ever, it is usually abnormal in individuals over age
apex or mitral area, bell usually used; and sitting
40. An extra effort must be made to auscultate S3; the
used for all the areas.
bell of the stethoscope should be used. The ideal po

sition to hear S3 would be left side1ying; the bell
would be placed over the cardiac apex. Causes of a
Heart Sounds
pathological S3 may include ventricular failure,
The first heart sound (Sl) signifies the closing of the
tachycardia, or mitral regurgitation. "Ken-TUCK'-y"
atrioventricular valves. Its duration is O. 10 seconds; it
is one sound that has been used to approximate the
is heard the loudest at the cardiac apex. The two com
sound sequencing of S3 in the cardiac cycle (SJ, S2,
ponents of Sl are tricuspid and mitral. Both the di
S3).
aphragm and the bell of the stethoscope can be used
The fourth heart sound (S4) signifies the rapid ven
to hear Sl. Its loudness is enhanced by any condition
tricular filling that occurs after atrial contraction.
in which the heart is closer to the chest wall (i.e., thin
When present, it is heard before Sl. S4 may be heard
chest wall) or in which there is an increased force to
in the "normal" trained individual with left ventricu
the ventricular contraction (e.g., tachycardia resulting
lar hypertrophy. Location of S4 is similar to S3' Its
from exercise).
sound can be described as dull because of the sudden
The second heart sound (S2) represents the clos
motion of stiff ventricles in response to increased
ing of the semilunar valves and the end of ventricu
atrial contraction. Pathologies eliciting an S4 may in
lar systole. Its components are aortic and pulmonic.
clude systemic hypertension, cardiomyopathies, or
During expiration, these two components are not
coarctation of the aorta. "TENN'-ess-ee" is a sound
distinct, since the time difference in the closure of
that approximates the sound sequencing when S4 is
the valves is less than 30 milliseconds. However,
present (S4, Sb Sz).
during inspiration, a splitting of S2 is audible. This

physiological split results from the increased venous
return to the right heart secondary to the decreased
Murmurs
intrathoracic pressure that occurs during inspiration.
Cardiac murmurs are the vibrations resulting from
The pulmonic valve closure is delayed as the right
turbulent blood flow. These may be described based
ventricular systolic time is lengthened. A split S2 is
on position in cardiac cycle (systole, diastole), dura
heard normally in children and young adults. The
tion, and loudness. SYSlolic murmurs occur between
diaphragm of the stethoscope shou ld be used to hear
Sl and S2; diastolic murmurs occur between Sz and
the split. The pulmonic component is the softer
SJ' A continuous murmur starts in SJ and lasts
sound and is best heard at the LSB, in the second to
through S2 for a portion or all of diastole. The loud
fourth ICS. The two components may be heard best
ness of a murmur is a factor of the velocity of blood
in the aortic and pulmonic areas, respectively. When
flow and the turbulence created through a specific
the split is heard both phases of respiration. an un
opening such as a valve. Grades I to VI are described
derlying cardiac abnormality is suspected. Causes
as folJows:
may include right bundle branch block and pul
monary hypertension. ( S w a r tz, 1994; T i lki a n ,
I: faint-requires concentrated effort to hear
II: faint-audible immediately
III: louder than II-intermediate intensity
IV: loud-intermediate intensity; associated with
V: very loud-thrill present
sound and reflects thc early (diastolic) ventricular
VI: audible wilhout stethoscope
filling that occurs after the atrioventricular valves
Murmurs that are Grade III or greater are usually as
open. S3 is normal in children and young adults; how
sociated with cardiovascular pathology.
Conover, 1993).
Gallops
palpable vibration (thrill)
The third heart sound (S3) is a faint, low frequency
222
PART II
MEDIATE PERCUSSION
Mediate or indirect percussion allows the therapist to
assess the density of the underlying organs. Striking
the chest wall produces vibrations in the underlying
structures which, in turn, gives rise to sound waves or
percussion tones. The quality of that tone depends on
the density of the tissue or organ, that is, it becomes
louder over air-filled structures. These tones are de
scribed by the following terms:
resonant: loud or high amplitude, low-pitched,

longer duration, heard over air-filled organs such
as the lungs
dull: low amplitude, medium to high-pitched,

short duration, heard over solid organs such as the
liver
flat: high-pitched, short duration, heard over

muscle mass such as the thigh
/.
FIGURE 14-10
Mediate percussion technique. (Reprinted with permission
tympanic: high-pitched, medium duration, heard
from Swartz MH:
over hollow structures such as the stomach
and examinaliol1, ed 2, Philadelphia, 1994, WB Saunders.)
Textbook of physical diagnoses-history
hyper-resonant: very low-pitched, prolonged

duration, heard over tissue with decreased density
(increased air: tissue ratio); abnormal in adults;
heard over lungs with emphysema.
to breathe deeply and hold that breath. The lowest
Technique
level of the diaphragm on maximal inspiration co
The middle finger of the nondominant hand is placed
incides with the lowest point where a resonant tone
firmly on the chest wall in an intercostal space and par
is heard. The patient is then asked to exhale, and
allel to the ribs. The top of the middle finger of the
mediate percussion is repeated. The lowest area of
dominant hand strikes the distal phalanx of the station
resonance now moves higher, as the diaphragm as
ary hand with a quick, sharp motion. The impetus of
cends with relaxation. The distance between these
the blow comes from the wrist versus the elbow and
two points is described as the diaphragmatic excur
has been likened to that of a paddle ball player (SWaItz,
sion; normal is three to five cm (Figure 14-11). Di
1994) (Figure 14-10). As with auscultation, the thera
aphragmatic movement is decreased in patients
pist must follow the sequence of apices to bases and
with COPO.
side to side so that comparisons can be made. This

technique is not usually used in infants, since percus
sion is too easily transmitted by a small chest.
PALPATION
PTs use palpation in all areas of practice. Touch is an
integral part of physical therapy. As part of the chest
Diaphragmatic Excursion
examination, palpation is used to assess: areas of ten
Assessment of diaphragmatic movement can b e
derness and/or abnormalities; chest wall excursion;
made with mediate percussion. The patient i s asked
edema; taclile fremitus; and tracheal deviation.
14
Inspiration
223
Expiration
FIGURE 14-11
Diaphragmatic excursion. (Reprinted with permission from Swartz MH: Textbook of physical
diagnoses-history and examination, ed 2, Philadelphia, 1994, WB Saunders.)
Tenderness
is a crunchy sound often associated with articular
Specific superficial or deep landmarks are identified
structures. However, when bubbles of air occur
through palpation. Determination of gross spinal
within subcutaneous tissue, a crackling sensation can
alignment can be performed by tracing the spinous
be palpated. An air leak from a chest tube site is one
processes in a cephalocaudal direction. Structures can
cause when crepitus is palpated over the chest wall.
be identified, such as the T-4 vertebra or the sternal
Crepitus can also be secondary to a pleural or friction
angle, which only augment the PTs evaluation. Areas
rub.
of tenderness can be assessed for degree of discom

fort and reproducibility. Differentiation of chest wall
discomfort of an organic nature, such as with angina,
from that of a musculoskeletal condition may b e
Edema
Palpation allows the PT to assess petipheral edema.
made through palpation. I n a patient complaining of
Dependency of body parts can cause swelling from
chest pain, angina may be ruled out if the PT can re
cardiac and noncardiac conditions. Assessment of
produce or increase the discomfort with increased
edema is performed by pressing two fingers into the
tactile pressure. However, one must also determine
particular areas for 2 to 3 seconds. If an impression is
that corroborating symptoms (e.g., diaphoresis,
left once the fingers are removed, then pitting or de
tachycardia) are not present. Angina or chest pain
pendent edema is present. The degree of edema is
secondary to myocardial ischemia usuaJly results
based on the length of time that the indentation lasts.
from exertion and may be relieved by rest. Crepitus
I + is the least; 4+ is the worst.
224
PART II
Chest Wall Excursion
of the sternal angle and meet at the midline,

slightly stretching the skin.
Evaluation of thoracic expansion allows the
4. The patient is asked to inhale.
to observe a "baseline" level by which to measure
5, The hands should be relaxed to allow for
progress or decline in a patient's condition. Chest
movement beneath,
wall movement can be restricted unilaterally as a re
6. The symmetry and extent of movement are
or a surgical incision. A
sult of lobar
assessed.
decrease in chest wall motion occurs in

withCOPO.
The hyperinflation associated withCOPO
an increase in the
diameter with a pro-
loss of
excursion. Normal
chest wall excursion is about 3.25 inches
em) in a
young adult between 20 to 30 years of age. One

method is to use a
measure at the level of the
xiphoid. However, the most common method involves

in all
direct hand contact. This technique is
planes and from top to bottom. Symmetry and extent

of movement are both noted. Procedures for this
method are described in the
or upper lobe motion
I. The PT faces the patient. The area to be

examined is
2. The PT's hands are
and
as needed.
over the anterior
chest. The heel of the hand is about the level

of the fourth rib and the fingertips reach
FIGURE 14-13
Evaluation of middle lobe and lingula motion (anterolateral
excursion), (From Cherniak RM, et al: Respiration ill health
and disease, ed 2, Philadelphia, 1972, WB Saunders.)
toward the upper
3, The thumbs Jie horizontal at about the level
FIGURE 14-12
Evaluation of upper lobe motion. (From Cherniak RM, et

al:
'
in health and disease. ed 2,
1972, WB Saunders,)
FIGURE 14-14
Evaluation of lower lobe motion (posterior
(From Cherniak RM, et al: Respiration in health and
disease. ed 2, Philadelphia, ]972, WB Saunders.)
14
225
Anterolateral or middle lobe/lingula motion

(Figure 14-13)
I. See above.
2. The PT's hands are placed with the palms
distal to the nipple line with the thumbs
meeting in the midline. The fingers lie in the
posterior auxiliary foi' d.
3. See steps 4 to 6 above.
Posterior excursion/lower lobe motion (Figure

14-14)
1. The PT stands behind the patient.
2. The area to be examined is exposed with
draping used as appropriate.
3. The PTs hands are placed flat on the
posterior chest wall at the level of the tenth
rib. The thumbs meet at the midline; fingers
reaching toward the anterior axillary fold.
FIGURE 14-15
4. See steps 4 to 6 above.
Evaluation of fremitus, method one.
Tactile Fremitus
Spoken word produces vibration over the chest wall.
aspect of the suprasternal notch. This is repeated on
Voice sounds have been previously discussed under
the opposite side. An equal distance between the
auscultation. With the PTs hands placed on the chest
clavicle and the trachea should exist bilaterally. Tra
wall, vibrations from spoken words can be felt and
cheal deviation may be caused by a pneumothorax,
are described as tactile fremitus. The presence or ab
atelectasis or a tumor among other conditions.
sence of tactile fremitus provides information on the
Whether the deviation will be ipsilateral or contralat
density of the underlying lungs and thoracic cavity
eral depends on the underlying cause. A right pneu
(Swartz, 1994).
mothorax or pleural effusion will deviate the trachea

away (toward the left); a left lower lobe atelectasis,
however, deviates the trachea toward the affected
Technique (Figures 14-15 and 14-16)
side, that is, the left.
Two methods can be used. The first technique is one

in which the therapist uses the palmar surface of one
or both hands. The second method involves the use of
the ulnar border of one hand. With both techniques,
CASE STUDIES
Case Study One
the sequence is, again, cephalocaudal and side to
A 30-year-old man with cystic fibrosis shows symp
side. In either method, the next step is to ask that the
toms of a one-week history of increased sputum pro
patient speak a predetermined phrase. The two most
duction, loss of appetite, fatigue, and 3-lb. weight
commonly used are "99" or "one, two, three." A light
loss. 'The results of the initial chest examination are
but firm touch is recommended.
as follows:
Inspection: Forward head, kyphotic posture,
increased anteroposterior diameter, appears thin
Tracheal Deviation (Figure 14-17)

The trachea's midline position can be examined ante
riorly. The PT places an index finger in the medial
and fatigued, no dyspnea observed, effective wet

cough
226
PART II
:/"1\" , i '
f!
'
"""- "'\
::--...
'.
-II . ..:--_
,
:
'
'"
1J;
FIGURE 14-17
Technique for determining the position of the trachea.
(With permission from Swartz MH: TextboQk of physical
diagnoses-history and examination. ed 2. Philadelphia,
1994, WB Saunders.)
FIGURE 14-16
Technique for evaluating tactile fremitus, method two.
(With permission from Swartz MH: Textbook of physical
diagnoses-history and examination, ed 2. Philadelphia,
1994, WB Saunders.)
14
227
Mediate percussion: dull over affected area
Auscultation: Decreased breath sounds with

scattered crackles throughout all lung fields,
Palpation: trachea midline, markedly decreased
especially over right middle and lower chest
CWE on right side
Palpation: Limited chest wall excursion (CWE),
Case Study Three
especially laterally
Mediate percussion: Dull over right middle and
A 72-year-old woman shows symptoms of persistent
lower chest, especially laterally
fevers, left chest wall discomfort, and history of fall I

week ago. CT scan shows loculated pleural effusion
Case Study Two
on the left. Left chest tube is inserted for drainage;
An ll-year-old girl is admitted to Pediatrics with a 4-
working diagnosis is empyema. Patient is nonsmoker,
day history of recurrent fevers, shortness of breath,

and lethargy. CXR showed an RML pneumonia.
Inspection: tachypnea; respiratory rate (RR) of 44;
Ratio of inspiration to expiration (I:E ratio
==
I: I;
Inspection: RR 30; l:E ratio
==
I:2; epidural
catheter for pain control

Auscultation: Absent breath sounds halfway up
left lower lateral chest wall
weak, shallow cough
Mediate percussion: flat over left lower lateral
Auscultation: bronchial over right midanterior
chest wall
chest, ego ph any also present
Palpation: trachea deviated to right, decreased
TABLE 14-1
Differentiation of Common Pulmonary Conditions
Palpation
Inspection
Emphysema
Auscultation
Increased anteroposterior
Decreased tactile
Increased resonance;
Decreased lung
diameter; use of accessory
fremitus
decreased excursion
sounds; decreased
of diaphragm
vocal fremitus
Often normal
Often normal
Early crackJes
Increased tactile
Dull
muscles, thin individual

Chronic bronchitis
Percussion
Possible cyanosis; short,

stocky individual
Pneumonia
Possible cyanosis
Late crackles;
fremitus; splinting
bronchal breath
on affected side
Pulmonary embolism
Sudden onset of dyspnea;
sounds
Usually normal
Usually normal
Usually normal
Absent fremitus;
Hyperresonant
Absent breath sounds
Dullnes s
Dullness
chest pain
Pneumothorax
Rapid onset
trachea may be
shifted to other side;
may have decreased

chest wall excursion
on affected side
Pleural effusion
May be no outward
Decreased fremitus;
clinical sign
trachea shifted to
other side; decreased

on affected side
Atelectasis
Often no outward
Decreased fremitus;
clinical sign
trachea shifted to
same side; decreased
on affected side
Adapted with permission from
Swartz, MH:
Textbook ofphysical diag/Uises-history and examirulliOI1,
ed 2.
Philadelphia,
1994, WB
Saunders.
228
PART II
eWE on left, range of motion of left shoulder joint
7. Which components of the chest physical examina

a physical therapist include in the initial
limited in flexion and abduction at about 90
tion
nP<Y,.p,,>< maximum
assessment of a geriatric
the elements of a chest
with a recent left
total hio renlacement aud a history of COPD?
See Table 14-1 for a differentiation of Ul<11411U:>C;'

examination.
References
SUMMARY
Chemiak.
As demonstrated in the case
each element of
the chest physical examination contributes to the phys

ical therapist solving the
of the individual pa
tient. It is through "putting all the
together that
au effective treatment program can be developed.
R.M., & Cherniak, L. ([983).
Respirmiorl in heailh and
disease. (3rd ed.). Philadelphia: WB Saunders.
Fraser, KG., Pare lA., Pare, P.O. Frazer,
R. S .. & Genereux, G.P.:
(1988). Diagnosis of diseases ill the chest. Philadelphia: WB

Saunders.
George,
R.B., Light, R.W. Matthay, M.A. & Matthay, RA ( l990).
Chesf medicine (2nd ed.). Baltimore: Williams and Wilkins.
Lehrer,
(1993). Understanding lung sound.," (2nd ed.). Philadel-
phia: WB Saunders.
Mikami, et
REVIEW QUESTIONS
International symposium on
sounds, Chesl
92(2):342-345, 1987.
Describe the sequence for auscultation of lung

sounds.
2. State the difference between oerioheral and cen
tral cyanosis.
3. How are normal bronchial breath sounds different

from abnomUlI bronchial breath sounds?
& Benedict, G.W. (1995).
Mosby's guide 10 physical examinatioll (3rd ed.). Boston: Mosby.
Swartz, M.H. (1994). Textbook of physical diagnoses-llIslOry and

examination (2nd ed). PhiJadeJphia: WB Saunders.
& Conover, M.D. (1993). Understanding heart

ed.). Philadelphia: WB Saunders.
Wilkins, R.I., Hodgkin, J.E., & Lopez, B. (1988). Lung sounds. Sl.
Tilkian, A.G.,
sounds and murmurs (3rd
Louis: Mosby.
4. Name two causes for a oathollOl?:lC

5. Name two causes for decreased breath sounds.
6. Formulate a plan for evaluation of a patient with

an acute Right Lower Lobe Pneumonia.
Seidel, RM., Ball, J.W., Dains, J.E.,
Wilkins, et al: Lung sound nomencla ture survey, C hest

98(4)886-889,1990.
Willerson, J.T.,
& Cohn, J.N. ([995).
New York: Churchill Livingstone.
Cardiovascular medicine.
Monitoring Systems
in the Intensive Care Unit
Elizabeth Dean
KEY TERMS
Acid base balance
Intraaortic balloon counter pulsation
ECG monitoring
Intracardiac pressures
Fluid and electrolyte status
Intracranial pressure monitoring
Hemodynamic status
INTRODUCTION
may differ among intensive care units, the principles
The primary goal of the intensive care unit (ICU)
are similar and relate either directly or indirectly to the
team is the achievement of stable cardiopulmonary
foremost goal of optimizing oxygen transport.
function and optimal oxygen transport. This chapter
Cardiopulmonary status is often jeopardized with
presents an introduction to monitoring systems used
the ICU patient by fluid and electrolyte disturbances
in the evaluation of cardiopulmonary status in the
and acid-base imbalance. Regulation of these systems
ICU and describes some related elements of car
and the clinical implications of imbalance are de
diopulmonary regulation that are relevant to assess
scribed first with special reference to the JCU patient.
ment and treatment in physical therapy.
The principles of monitoring systems used in assess
ICUs are becoming more specialized. In major hos
ing cardiopulmonary sufficiency are presented in
pital centers, units are often exclusively designed and
cluding the electrocardiogram (ECG) monitor, moni
staffed for the management of specific types of condi
tors related to left- and right-sided heart function
tions e.g., medical, surgical, trauma, bums, and coro
utilizing arterial and venous lines, and the intracranial
nary and neonatal care. Although monitoring priorities
pressure (ICP) monitor. The intraaortic counter pulsa

229
230
PART II
FIGURE 15-1
General view of a typical leU.
tion technique used to augment myocardial efficiency

is also described.
FLUIIJ AND ELECTROLYTE BALANCE

When the normal regulation of fluid intake, utilization,
Familiarity with the extensive monitoring facilities
and excretion are disrupted, fluid, electrolyte, and acid
in the lCU allays some of the apprehensions the
base imbalances result. Essentially, all medical and
(PT) may have working in a critical
surgical conditions threaten these life-dependent mech
care. On introduction to the unit, the PT is immedi
anisms to some degree. Minor imbalances may be cor
ately struck by the high technology atmosphere.
rected by modification of the patient's nutrition and
physical therapist
Quality care in this setting depends on harnessing the
fluid intake. More major imbalances can be life-threat
potential of the monitoring equipment to optimize as
ening and can necessitate prompt medical attention.
sessment, treatment selection, and effectiveness, as
Imbalances are reflected as excesses, deficits, or as

an abnormal distribution of fluids within the body
well as reduce untoward risk for the patient.

For further detail on the monitoring topics pre
(1978), Burki and

Albert (1983), Copel and Stolarik (1991), Cromwell,
Weilbell, and Pfeiffer (1980), DeGowin and De
Gowin (19 81), and W e i d e ma n n, M a t t h a y , and
Matthay (1984).
Figure 15-1 illustrates a general view of a typical
sented refer to Barrell and Abbass
(Folk-Lighty,
1984; Phipps, Long, and Woods, 1991).
Excesses result from increased intake and decreased

loss of fluid and electrolytes. Deficits result from ab
normal shifts of fluid and electrolytes among the in
travascular and extravascular fluid compartments of
the body. Excesses occur with kidney dysfunction pro
moting fluid retention and with respiratory dysfunction
lCU. A closer view of the patient at bedside indicates
promoting carbon dioxide retention. Deficits are com
to the PT the parameters that are being monitored, and
monly associated with reduced intake of fluids and nu
the types of lines, catheters, and leads in place (Figure
trition. Diaphoresis and wounds can also contIibute to
15-2). A closer view with the patient's gown removed
significant fluid loss. Diarrhea and vomiting drain the
demonstrates precisely where the various lines, leads,
gastrointestinal tract of fluid stores. Hemorrhage is al
and catheters are positioned, and identifies where cau
ways responsible for fluid and electrolyte loss. Deficits
tion must be observed. Treatments are modified ac
may be secondary to fluid entrapment and localized
cording to the types and positions of the lines and
edema within the body, making this source of fluid un
leads for each individual patient (Figure 15-3).
available for regulation of homeostasis.
15
Monitoring Systems in the Intensive Care Unit
231
FIGURE 15-2
A and B, Closer bedside views of patients in an ICU. Note that with all the equipment, the patient is
almost lost. C, Note two IV lines with flow monitors. Blood infusion is also being received.
Continued.
Moderate to severe fluid imbalance can be re
with fluid overload. Normally, the jugular pulse is
flected in the systemic blood pressure and jugular ve
not visible 2 em above the sternal angle when the in
nous pressure (CVP). Elevated blood pressure can be
dividual sits at a 45-degree angle. If the jugular pulse
indicative of fluid overload, but an intravascular fluid
is noted, this can be a sign of fluid overload.
deficit of 15% to 25% must develop before blood
Fluid replacement is based on a detailed assess
pressure drops. The jugular vein becomes distended
ment of the patient's needs. Whole blood is preferred
232
PART II
FIGURE 15-2-conl'd
D, Bedside oxygen and suction set-up. E, Close-up piped in O2 and suction units, F, Close-up IVs
and drip monitoring flow devices (IMEO). G, Note IABP, ventilator, IVs, organization of unit at
the head of the bed. ECG unit overhead, suctioning and airway care equipment at the right of the
patient and "Ambu" bag at bedside.
IS
FIGURE 153
A, Patient after open heart surgery. Note insert of Swan Ganz, CV tubing connection taped to left
chest. On ventilator with oral endotracheal tube, oral airway is in place. Note the nasogastric tube,
ECG leads, and dressing covers sternal split incision site. B, Patient after open heart surgery. Note
ECG leads. Patient is now weaned from ventilator and endouacheal tube; pacemaker wires are held
intact at upper abdomen in syringe area. Patient has a11erial Li ne in right forearm; Swan Ganz, CVP
also removed. Patient is almost ready to leave ICU; he is receiving an aerosol treatment.
233
234
PART II
to replace blood loss. Plasma, albumin, and plasma
complaints of headache, thirst, and nausea, as well as
volume expanders such as Dextran can be used to
changes in dyspnea, skin turgor, and muscle strength.
substitute for blood loss and to help reestablish blood
More objective assessment is based on fluid intake,
volume. Albumin and substances such as Dextran in
output, and body weight. Fluid balance is so critical
crease plasma volume by increasing the osmotic pres
to physical well-being and cardiopulmonary suffi
sure of the blood, hence the reabsorption of fluid
ciency that fluid input and output records are rou
from the interstitial space. Low molecular weight
tinely maintained at bedside. These records also in
Dextran has the added advantage of augmenting cap
c l u d e f l u i d v o l u m e lost in w o u n d dra inage,
illary blood flow by decreasing blood viscosity, and
gastrointestinal output, and fluids aspirated from any
is therefore particularly useful in treating shock.
body cavity (e.g., abdomen and pleural space).

A patient's weight may increase by several pounds
before edema is apparent. The dependent areas mani
Clinical Picture
fest the first signs of fluid excess. Patients on bed rest
Excesses and deficits of fluids and electrolytes can be
show sacral swelling; patients who can sit over the
determined on the basis of laboratory determinations
bed or in a chair for prolonged periods tend to show
of serum levels of the specific electrolytes. Elec
swelling of the feet and hands.
trolyte levels and hematocrit are decreased with fluid
Decreased skin turgor can indicate fluid deficit.
excess (hemodilution) and increased with fluid loss
Tenting of the skin over the anterior chest in response

to pinching may suggest fluid depletion. Wrinkled,
(hemoconcentration).
Excess fluid can be managed by controlled fluid
toneless skin is more common in younger patients.
intake, normal diuresis, and diuretic medications. Re
Weight loss may be deceptive in the patient on IV
placement of fluid and electrolyte losses can be
fluids, who can be expected to lose a pound a day.
achieved by oral intake, tube feeding, intravenous
This sign should therefore not necessarily be inter
(IV) infusion, and parenteral hyperalimentation.
preted as underhydration.
Assessment of fluid and electrolyte balance is
The cardiopulmonary assessment can reveal
based on both subjective and objective findings
changes in fluid balance. Lung sounds are valuable in
(Table 15-1). At the bedside, the PT must be alert to
identifying fluid overload. Vesicular sounds may be-
TABLE 15-1
Assessment of Fluid and Electrolyte Imbalance
FLUID EXCESSfELECTROL YTE
IMBALANCE
FLUID LOSS/ELECTROL YTE

IMBALANCE
Head and neck
Distended neck veins, facial edema
Thirst, dlY mucous membranes
Extremities
Dependent edema "pitting," discomfort from
Muscle weakness, tingling, tetany
AREA
weight of bed covers

Skin
Warm, moist, taut, cool feeling when edematous
Dry, decreased turgor
Respiration
Dyspnea, orthopnea, productive cough, moist
Changes in rate and depth of breathing
Circulation
Hypertension, jugular pulse visible at 45-degree
breath sounds
sitting angle, atrial dysrhythmias
Abdomen
Modified
from
Increased girth, fluid wave
Phipps WJ, Long
Be,
Woods
NF,
Pulse rate irregularities. dysrhythmia, postural

hypotension, sinus tachycardia
Abdominal cramps
editors: Medical-surgical nursing: concepts in clinical practice, cd
Mosby.
4, SI.
Louis.
1991,
15
235
come more bronchovesicular in quality. Crackles
and collection system is shown in Figure 15-4. The
may increase in coarseness. In the presence of fluid
removal of thick fluids such as blood and organized
retention involving the pleurae, breath sounds dimin
exudates with chest tubes is often indicated to pre
ish to the bases. Dyspnea and orthopnea may also be
vent entrapment and loculation. Chest tubes are com
symptomatic of fluid excess.
monly inserted in the sixth intercostal space in the
An early sign of congestive heart failure (CHF)
mid or posterior axillary line. Chest tubes inserted
with underlying fluid overload is an S3 gallop (Ken
into the pleural space are used to evacuate air or exu
TUCK'-y) caused by rapid ventricular filling.
date. Chest tubes can also be inserted into the medi
Vigilance by the PT is essential in all areas of

practice and not only the ICU. Fluid imbalance is
astinum after open heart surgery, for example, to

evacuate blood.
common in older people and in young children, thus
Any collection system is designed to seal the
it needs to be watched for on the ward, in the home,
drainage site from the atmosphere and offer minimal
and community.
resistance to the drainage of fluid and gas. This is ac

complished by immersing the end of the collection
tube under water (Figure 15-4). This is referred to as
CHEST TUBE DRAINAGE AND FLUID
an underwater seal system. Additional reservoirs are
COLLECTION SYSTEMS
included to decrease the resistance to fluid leaving
Chest tubes are large catheters placed in the pleural
the chest. This resistance is greater in a single reser
cavity to evacuate fluid and air, and to drain into a
voir system in which the reservoir serves both as the
graduated collection reservoir at bedside (Phipps,
collection receptacle and underwater seal. A third
Long, Woods, 1991). A typical chest tube drainage
reservoir can be added to the system that is attached
FIGURE 154
A, Chest tube drainage. B, Anterior view, Mediastinal drains.
236
PART II
to the suction and serves as a pressure regulator. The
TABLE 15-2
more elaborate drainage systems are used to precisely

measure fluid loss in patients following thoracic and
Signs and Symptoms of Common
cardiovascular surgery.
Acid Base Disturbances
The amount of exudate collected in the reservoir is

measured every several hours or more often if the pa
tient is losing considerable amounts of fluid or less
RESPIRA TORY ACIDOSIS
METABOLIC ACIDOSIS
Hypercapnia
Bicarbonate deficit
Hypoventilation
Hyperventilation
than the amount predicted. This information is incor
Headache
Headache
porated into the overall fluid balance assessment. In
Visual disturbances
Mental dullness
addition, changes in the quantity and quality of exu
Confusion
Deep respirations
date should be noted by the PT before, during, and

after changes in position and therapeutic interventions.
Drowsiness
Stupor
Coma
Coma
Depressed tendon reflexes
Hyperkalemia
Hyperkalemia
Cardia dysrhythmias
Ventricular fibrillation
ACID-BASE BALANCE
(secondary to
Control of acid-base balance in the body is achieved

by regulation of hydrogen ion concentration in the
body fluids (Guyton, 1991; Shapiro, Peruzzi, and
Kozelowski-Templin, 1994). The pH of the body is
(secondary to
hyperkalemia)
hyperkalemia)
RESPIRATORY ALKALOSIS
METABOLIC ALKALOSIS
Hypocapnia
Bicarbonate excess
Lightheadedness
Depressed respirations
normally maintained within a range of 7.35 to 7.45,
Numbness/tingling of digits
Mental confusion
or slightly alkaline. When pH of the blood drops
Tetany
Dizziness
Convulsions
Numhm:ss/tingling of
Hypokalemia
Muscle twitching
Tetany
below 7.35, a state of acidosis exists; above 7.45, a

state of alkalosis exists. Regulation of pH is vital be
cause even slight deviations from the normal range
cause marked changes in the rate of cellular chemical
digits
(secondary to hypokalemia)
Convulsions
Hypokalemia
reactions. A pH below 6.8 and above 8 are incompat
Cardia dysrhythmias
ible with life.
(secondary to
Acid-base balance is controlled by several regula
hypokalemia)
tory buffer systems; primarily carbonic acid-bicarbon

ate, phosphate, and protein buffer systems. These sys
tems act very quickly to prevent minute-to-minute
changes in pH. In compensation, pH is returned to
normal primarily by altering the component not pri
marily affected. If the primary cause is respiratory, the
ume, potassium excess (hyperkalemia) is associated
compensating mechanism is metabolic. If the primary
with both respiratory and metabolic acidosis, and
cause is metabolic, the compensating mechanism is
neuromuscular hyperexcitability is associated with
respiratory. The lungs compensate for metabolic prob
both respiratory and metabolic alkalosis.
lems over hours, whereas the kidneys compensate for

respiratory problems over days (Chapter 9).
BLOOD GASES
Analysis of the composition of arterial and mixed
Clinical Picture
venous blood provides vital information about respi
A guide to the clinical presentation of acid-base im
ratory, cardiac, and metabolic function (Ganong,
balances is shown in Table 15-2. Besides the major
1993; Snider, 1973; Thomas, Lefrak, Irwin, Fritts,
distinguishing characteristics of acid-base imbalance
and Caldwell, 1974; Marini, 1987; West, 1995) (see
described in this chapter and elsewhere in this vol-
Chapter 9). For this reason, blood gases are usually
15
analyzed daily in the ICU. In cases where the pa

tient's condition is changing for better or worse over
237
HYPOXEMIA
In health, age and body position are factors that re
a short period of time or a specific treatment re
duce arterial oxygen tension (Oakes, 1988). Arterial
sponse is of interest, blood gases may be analyzed
oxygen levels diminish with age as a result of reduc
several times daily. With an arterial line in place,
tions in alveolar surface area, pulmonary capillary
frequent blood gas analysis is feasible and not trau
blood volume and diffusing capacity. Normal PaOz
matic for the patient. Should the patient be anemic,
levels in older people should exceed 110-0.5 age. In a
however, blood loss associated with repeated arter
young adult, Paoz ranges from 90 to 100 mm Hg in
ial blood sampling can be detrimental. Thus re
the upright seated position. In supine, this range is re
quests for arterial blood gas analysis need to be par
duced to 85 to 95 mm Hg and in sleeping, to 70 to 85
ticularly stringcnt in anemic patients.
mm Hg. These values are significant in that in older
Arterial saturation (Sao2) can be readily monitored

noninvasively with a noninvasive pulse oximeter.
people, smokers, and people with pathology, these po

sitional effects are accentuated.
The ear lobe or a finger is initially warmed by rub
Hypoxemia refers to reduced oxygen tension in
bing before attachment of the oximeter. Within a cou
the blood. Some common signs and symptoms of var
ple of minutes, the Sao2 can be directly read from the
ious degrees of hypoxemia in adults appear in Table
monitor. Pulse oximetry is a useful adjunct for rou
15-3. Although the brain is protected by autoregula-
tine evaluation of the effectiveness of mechanical

ventilation, the effect of anesthesia and treatment re
sponse. Continuous estimation of Saoz is particularly
useful before, during, and after mobilization and ex
ercise, position changes, and other therapeutic inter
TABLE 15-3
Signs and Symptoms of Hypoxemia
Paoz
SIGNS AND SYMPTOMS
tients who are anemic, jaundiced, have heavily
80-100 mm Hg
Normal
pigmented skin, or have reduced cardiac output.
60-80 mm Hg
Moderate tachycardia, possible onset of
50-60 mm Hg
Malaise
ventions. The Sao2 may appear to be reduced in pa
Mixed venous oxygen saturation (SV02) provides a

useful index of oxygen supply and utilization at the tis
respirat ory distress

Lightheadedness
sue level (Copel, and Stolarik, 1991). Svoz is highly
Nausea
correlated to tissue oxygen extraction, and thus is a
Vertigo
good index of the adequacy of oxygen transport. The
Impaired judgment
Incoordination
Sv0:2 is particularly useful as a significant warning sign,
Restless
a guide to myocardial function, and has been used as a

tool to titrate positive end-expiratory pressure supp0l1.
Increased minute ventilation
35-50 mm Hg
Cardiac dysrhylhmias
NOImal values of SVD2 are 75%. SVD2 values less than

60% or a drop of 10% for several minutes are cause for
concern. Excessive Svo2 values in excess of 80% are
Marked confusion
Labored respiration
25-35 m m Hg
Cardiac an-est
Decreased renal blood flow
also cause for concern. High SV02 values may occur in
Decreased urine output
patients with left to right shunts, hyperoxia, hypother
Lactic acidosis
mia, cyanide toxicity, sepsis, anesthesia, and drug-in
Poor oxygenation
duced paralysis. Despite its general clinical usefulness,
Lethargy
Maximal minute ventilation
SV02 is a nonspecific indicator of the adequacy of oxy

gen transport, that is, of the balance between oxygen
supply and demand. Abnormal Svoz values do not indi
Loss of consciousness
<25 mm Hg
cate precisely where the problem lies; thus other hemo

dynamic variables need to be considered.
Decreased minute ventilation

(secondary to depression of
respiratory center)
238
PART II
tory mechanisms, an arterial oxygen tension of 60
of nonpulmonary tissues is little altered. In the lung,
mm Hg produces signs of marked depression of the
high concentrations of oxygen replace nitrogen in
central nervous system (NS) reflecting the extreme
poorly ventilated regions. This results in collapse of
sensitivity of cerebral tissue to hypoxia.
areas with reduced ventilation perfusion matching.
H y poxemia is compensated primarily by in
Lung compliance is diminished.
creased cardiac output, improved perfusion of vital
High concentrations of oxygen (inspired oxygen
organs, and polycythemia. Secondary mechanisms of
fractions greater than 50%) directly injure bronchial
compensation include improved unloading of oxygen
and parenchymal lung tissue. The toxic effect of oxy
as a result of tissue acidosis and anaerobic metabo
gen is both time and concentration dependent. Very
lism, that is, rightward shift to the oxyhemoglobin
high concentrations of oxygen can be tolerated for up
dissociation curve.
to 48 hours. High concentrations of oxygen in combi
The progressive physiologic deterioration ob
nation with positive pressure breathing can predis
served at decreasing arterial oxygen levels will occur
pose the patient to oxygen toxicity. At concentrations
at higher oxygen levels if any of the major compen
of inspired oxygen less than 50%, clinically de
sating mechanisms for hypoxemia is defective. Even
tectable oxygen toxicity is unusual regardless of the
a mild drop in Pao2 for example, is poorly tolerated
duration of oxygen therapy.
by the patient with reduced hemoglobin and impaired

cardiac output. Alternatively, the signs and symptoms
of hypoxemia may appear at lower arterial oxygen
HYPOCAPNIA
levels, (e.g., in patients with chronic airflow limita
Acute reductions in arterial carbon dioxide levels
tion who have adapted to reduced Pao2 levels).
(hypocapnia) results in alkalosis and diminished cere

bral blood flow secondary to cerebral vasoconstric
tion. The major consequences of abrupt lowering of
HYPEROXIA
Paco2 are altered peripheral and central nerve func
Mean tissue oxygen tensions rise less than 10 mm Hg
tion. Mechanical ventilation may initially cause an
when pure oxygen is administered to a healthy sub
abrupt decrease in arterial PC02 and lead to a Iife
ject under normal conditions. Therefore the function
threatening situation. In addition to blood gas anaJy-
FIGURE 15-5
BCG oscilloscope, printout for BCG. Note defibrillator paddles and BP cuff on shelf.
Systems in the Intensive Care Vnit
15
end tidal
measurement is useful in that it
239
mal information regarding
chest to provide
in rhythm and heart rate, and thereby ensure
provides an index of
close patient monitoring. The positive electrode is

positioned at the fourth intercostal space at the right
HYPERCAPNIA
sternal border. The
CO2, the principal end product of metabolism, is a

relative benign gas.
has a key role in ventilation
and in
in cerebral blood
pH,
tone. Acute increases in
and
electrode is
at
the first intercosta l space in the left midclavicular

electrode used to
line. The
space in the
electrical
at the first intercostal
interference is often
the
midclavicular line,
wherever conve
capnia) depress level of consciousness
ground electrode may be
the effect of acidosis on the nervous
nient. Other electrode placements may be required,
but slowly
for
increases in
relatively well-tolerated. A high
is
in alveolar and arterial
with
Some patients with se
vere chronic airflow obstruction have been
rPT,r.rtp(,\
to be able to lead relatively normal lives with
Problems with the monitor

faulty
Ie electrical interference. An erratic

often results from
oxygen to
cause of any
disease, how
because it inteli'eres with the
hypoxic drive to breathe observed in these

an increase in cardiac
and in pe
vascular resistance. These effects may help

to offset the effect of excess
ward
and movement. The

must be explained and unto
in electrical activity of the myocardium
ruled out. It is a dangerous practice for the PT to turn
enhances sympathetic stimula
Acute
and move
ment artifact. A thickened baseline can be caused
90 mm Hg if hypoxemia is countered
ever, may be
result from
electrical
with supplemental oxygen. Acute administration of

with chronic
or in pa
secured to the patient's gown.
which causes a reduction
of alveolar
in excess of
in
tients with chest burns. The electrode wires are usu
ion on the car
off the ECG alarm system during treatment.

Cardiac
can be broadly
into t a c h dy s r h y th m i a s a n d b radydysrhythmias.
Tachydysrhythmias are subdivided into
diovascular system, allowing better tolerance of flow
ular and subjunctional tachycardias. Bradydysrhyth
than with metabolic acidosis of a similar degree.
mias are subdivided into sinus bradycardia, and those
At extreme levels of hypercapnia, muscle
related to heart block and conduction abnormalities.
and seizures may be observed. Trends in Paco2 can
The subjunctional
be monitored
rhythmias are
end tidal CO2 measurements.
or ventricular dys
Ventricular
dia and ventricular fibrillation are medical emergen
MONITORING
A
ECG
The characteristic features of

are illustrated in Chapter
channel ECG monitor with an oscilloscope,

at bedside in the lCU
\5-5). The ECG can often be observed both

at bedside as well as at a central monitoring console,
where the ECGs of all patients
11. PTs
in ICU management should be thoroughly famil
strip recorder, and digital heart rate display is

cally located above the
and treatment.
immediate
cies
monitored can
be observed
iar with ECG interpretation and the implications of

the various dysrhythmias for
management.
For further elaboration of ECG application and inter

pretation refer to Andreoli, Fowkes,
lace
and Wal
( 1991), Dubin (1989), and Fisher (1981).
The ECG monitor allows for continuous surveil

lance of the
of
Low and
heart rates are determined below and above

which the alarm will be
For routine moni
in the coronary care unit, a modified chest lead

is often used. Three electrodes are positioned on the
Clinical Picture
The clinical
tivity of the heart
associated with dysrhythmic ac

on the nature of the dys
rhythmia, the age and condition of the patient, and
240
PART II
TABLE 154
Clinical Picture of Common Dysrhythmias
DYSRHYTHMIA
IN HEALTHY INDIVIDUALS WITH NO

UNDERLYING CARDIOVASCULAR
DISEASE
IN INDIVIDUALS WITH
DISEASE
No symptoms
May precipitate
I. Tachycardias
A. Supraventricular
tachycardia
Abrupt onset palpitations, light-headness

nausea, fatigue
congestive heart failure, acute

coronary insufficiency, myocardial
infarction, pulmonary edema
1. Sinus tachycardia
Awareness of the heart on exertion

or with anxiety
Secondary to some precipitating

factor, e.g., fever, electrolyte
imbalance, anemia, blood and fluid
loss, infection, persistent hypoxemia
in COPD, acute MI, congestive
heart failure, thyrotoxicosis
2. Paroxysmal atrial
tachycardia (PAT)
Prevalent, sudden onset, precipitated by

coffee, smoking, and exhaustion
Common supraventricular
tachycardia
Spontaneous onset of regular
palpitations that can last for several
hours
May be obscured by myocardial
insufficiency and CHF in older
patients
Increased anxiety and report
of fatigue
3. Atrial flutter
Rapid regular-irregular rate
Rare
May be difficult to distinguish from PAT
Suggests block at AV node
May be precipitated by alcohol, smoking,
Atrial flutter waves in jugular venous
physical and emotional strain
pulse
4. Atrial fibrillation
Rare, occasionally with alcohol excess
5. Paroxysmal atrial
Rare
Common arrhythmia seen with
Rare
Usually related to MI, pulmonary
in the young
of cardiac disorders
digitalis toxicity
tachycardia with block

B. Subjunctional
Usually secondary to a variety
embolus, severe CHF

Often unconscious, cyanotic,
ineffective pulse, blood pressure
and respiration
I. Ventricular tachycardia
2. Ventricular fibrillation
Rare
Predisposed to ventricular fibrillation
Rare
Ineffective cardiac Ol tpUt,

unconscious, dusky, cardiac
arrest threatens
II.
Bradycardias
A. Sinus bradycardia
Physiologic in very fit young adults
In older patients may suggest sinus

node and conduction system
pathology; can produce syncope or
congc:-;tive heart failure
B. Heart block
Hypotension, dizziness, Iight
Rare
headedness, syncope
In chronic block with sustained
bradycardia, congestive heart failure
may be more frequent
15
241
TABLE 15-4
Clinical Picture of Common Dysrhythmias
DYSRHYTHMIA
IN HEAL THY INDIVIDUALS WITH NO

IN INDIVIDUALS WITH
DISEASE
DISEASE
Most common dysrhythmia

iatrogenically produced with
digitalis excess
Associated with numerous cardiac
conditions; commonly in age
related degenerative disease in
conducting system, inferior and
occasionally anterior Mis
specifically the absence or presence of underlying
be measured directly from this line. A digital moni
heart disease. Distinguishing clinical features of com
tor displays systolic and diastolic blood pressures
mon atrial and ventricular dysrhythmias are outlined
above the patient at bedside. High and low blood
in Table IS-4.
pressure levels are set, above and below which the
The subjunctional or ventlicular dysrhythmias are
alarm will sound. Blood gas analysis can be per
typically associated with an extremely ill individual.
formed routinely with an intraarterial line in place
Cyanosis and duskiness of the mucosal linings and pe
without repeated puncturing of a blood vessel (Fig
riphery may be apparent. The patient is unresponsive,
ure IS-6).
the pulse if ineffective, and spontaneous respirations

are likely absent. Defibrillation is initiated to restore
an effective, more normal rhythm. The high incidence
of myocardial conduction ilTegularities warrants a de
Pulmonary Artery Balloon Flotation Catheter

(Swan Ganz Catheter)
fibrillator being present at all times in the lCU for
The pulmonary artery balloon floatation catheter or
rapid implementation of this commOn cardioversion
Swan Ganz catheter is designed to provide an accu
procedure by the medical personnel. Ventricular dys
rate and convenient means of hemodynamic assess
rhythmias may be tolerated better if ventricular rate is
ment in the lCU (Buchbinder, and Ganz, 1976; For
low, thereby improving cardiac output. Even in this
rester, Diamond, McHugh, and Swan, 1971; Swan,
circumstance, however, these dysrhythmias still pre
1975). The catheter is usually inserted into the inter
sent an emergency.
nal jugular vein, the subclavian vein, or a large pe
The ECG of a patient with a pacemaker will re
ripheral arm vein and directed by the flow of blood
flect either an imposed fixed or intermittent rhythm
into the right ventricle and pulmonary artery (see
and rate depending on whether a fixed rate or demand
Figure IS-3A (arrow), p. 233). The catheter is se
pacemaker has been inserted.
curely taped to the patient's anTI, which is splinted

with an arm board to prevent dislodging. The proce
dure is generally associated with little risk and dis
Intra-Arterial Lines
comfort. Some of the complications that have been
An arterial line is established by direct arterial punc
associated with pulmonary artery catheterization,
ture, usually of the radial artery. Blood pressure can
however, include infection, venous thrombosis, my
242
PART II
atrial pressure (LAP) and the pressure in the left

ventricle (LVP). More elaborate catheters have pac
ing wires, thermistors for cardiac output determina
tion, and sensors for arterial saturation. Figure 15-7
shows the normal cardiac pressures in each heart
chamber. Abnormal cardiopulmonary function may
vary these readings.
The PAP increases as a result of elevated pul
monary blood flow, increased pulmonary arteriolar
resistance secondary to primary pulmonary hyperten
sion or mitral stenosis, and left ventricular failure.
Measurement of PAP and PAWP in particular allows
for more prudent management of heart failure and
cardiogenic shock.
The PAP, PAWP, and end diastolic LVP are di
rectly related. Impaired left ventricular contractility
that compromises normal emptying, (e.g., left ven
tricular failure, mitral stenosis, or mitral insuffi
ciency), result in an elevated end diastolic LVP,
which in turn elevates PAWP and PAP. An end dias
tolic PAP or PAWP greater than 12 0101 Hg is consid
ered abnormal.
The PAP and PAWP are low during hypotension
secondary to hypovolemia. Infusion of normal saline,
FIGURE 15-6
whole blood, or low molecular weight Dextran ele
Intraarterial blood gas line.
vates the blood volume and blood pressure. Restora

tion of blood volume returns end diastolic PAP and
PAWP to normal.
Elevation of the end diastolic PAP secondary to
ocardial irritation, air embolism, and pulmonary is
heart failure with pulmonary edema can typically
chemia or infarct to segmental lung tissue (Puri,
be reduced with appropriate medication. The effec
Carlson, Bander, and Weil, 1980).
tiveness of a drug and its prescription parameters
Complex catheters are available for monitoring a

variety of parameters. In a two-lumen catheter, the
can be assessed by the observed changes in the end

diastolic PAP.
first lumen is used to measure pulmonary artery
Deterioration of cardiovascular status and wors
pressure (PAP) and obtain mixed venous blood sam
ening of the clinical signs and symptoms of heart
ples. The second lumen terminates in a balloon with
failure elevate end diastolic PAP and PAWP, de
a volume of less than 1 011, which is inflated and de
crease cardiac output, decrease arterial and right
flated to obtain pulmonary artery occlusion or
atrial oxygen tension, a!ld increase the oxygen dif
wedge pressure (PAOP or PA WP). The average
ference between arterial and venous blood. As the
Hg, and
heart pump continues to fail, arterial oxygen ten
normally reflects right ventricular pressure (RVP).
sion decreases suggesting abnormal lung function
Hg and
and probably elevated LAP. Pulmonary dysfunction
range of the systolic PAP is 20 to 30
mOl
The diastolic PAP ranges from 7 to 12
mOl
reflects left ventricular pressure in the absence of
at this stage includes diffusion abnormalities, redis
pulmonary disease. The average range of PA WP is
tribution of pulmonary blood flow into the less
8 to 120101 Hg and gives an estimation of mean left
well-ventilated upper lobes, and right to left shunt
15
243
Pulmonary Artery
Aorta
Left Ventricle
Right Ventricle
FIGURE 157
Normal cardiac pressures in each heart chamber.
ing. All patients with acute infarction or shock have
MEASUREMENT OF CENTRAL VENOUS PRESSURE
reduced arterial oxygen tension. Pulmonary conges
Central venous pressure (CVP) is monitored by means
tion must be cleared before the patient responds to
of a venous line or catheter inserted into the subclavian,
15-3A,
233). The catheter is advanced to the right atrium by
basilic, jugular or femoral vein (see Figure
oxygen administration.
Despite the enormous benefits of direct invasive
p.
hemodynamic monitoring to patient assessment and
way of the inferior or superior vena cava depending on
management, the benefits of basic hemodynamic as
the site of insertion. Minimal risk of phlebitis or infec
sessment are a fundamental part of the cardiopul
tion is associated with this procedure.
monary assessment regardless of whether the patient
Central venous pressure is the blood pressure mea
has an invasive line in or not (Kirby, Taylor, and
sured in the vena cavae or right atrium. Normal CVP
0 to 5 cm H20 and 5 to 10 cm H20
Civetta, 1990). Basic hemodynamic monitoring in
is approximately
cludes heart rate, ECG, blood pressure, and periph
if measured at the sternal notch and midaxillary line,

respectively. Essentially the CVP provides informa
eral tissue pelfusion.
tion about the adequacy of right-sided heart function,

including effective circulating blood volume, effec
INTRAVENOUS LINES
tiveness of the heart as a pump, vascular tone, and
IV lines are routinely established in the supelficial
venous return. Measurement of CVP is particularly
veins of patients, such as in the hand, usually before
useful in assessing fluid volume and fluid replace
admission to the ICU. These lines provide an imme
ment. If the patient has chronic airflow limitation,
diate route for fluids, electrolytes, nutrition, and med
ventricular ischemia, or infarction, the CVP will re
ications. The specific lines used depend on the pa
flect changes in pathology rather than fluid volume.
tient's individual needs determined by the history,

laboratory tests, and physical examination.
Specifically, CVP provides an index of RAP. The

relationship between RAP and end diastolic LVP is
244
PART II
unreliable; therefore end diastolic PAP and PA WP
into the femoral artery. To maintain proper placement
are used as the principal indicators of cardiopul
and good circulation, the leg must be extended. The
monary sufficiency in patients in failure and shock.
presence of an intraaortic balloon must be taken into

consideration whenever the patient is being treated
and positioned. Inflation and deflation of the balloon
INTRAAORTIC BALLOON
COUNTER PULSATION (IABP)
with helium is correlated with the ECG. The intraaor

tic balloon is deflated during venlricular systole and
Intraaortic balloon counter pulsation (Figure 15-8)
assists the emptying of the aorta. Stroke volume is
provides mechanical circulatory assistance with the
potentiated, afterload is reduced (hence, ventricular
use of an intraaortic balloon. The balloon is inserted
pressure), and myocardial oxygen delivery enhanced.
FIGURE 15-8
A, Patient near the window is receiving intraaortic balloon pump (lABP) support. B, Close-up of an IABP unit.
15
245
The balloon is inflated during diastole, thereby
neurons; progressive muscle weakness results. A con
restoring arterial pressure and coronary perfusion.
tralateral weakened hand grasp, for example, may
Counterpulsation improves cardiac output, reduces
progress to hemiparesis or hemiplegia. The Babinski
evidence of myocardial ischemia, and reduces ST
sign, hyperreflexia, and rigidity are additional motor
segment elevation. lntraaortic balloon counterpulsa
signs that provide evidence of decreasing motor func
tion is commonly used after open heart surgery, for
tion as a result of upper motor neuron involvement.
CHF, medically refractive myocardial ischemia, ven
Herniation can produce incoordinate respirations
tricular septal defects, and left main coronary stenosis
that are correlated with the level of brainstern com
in patients who have shock. The intraaortic balloon
pression. Cerebrate rigidity results from tentorial
pump provides protection for the myocardium in
herniation of the upper brainstem. This results in
many instances until surgery can be pelformed. Limb
blocking of the motor inhibitory fibers and the famil
ischemia, the most common complication, occurs in
iar extended body posture. Seizures may be present.
10% to 15% of patients.
These neuromuscular changes may further com
Left ventricular assist devices are used postopera

tively in patients following open heart surgery who
pound existing cardiopulmonary complications in

the ICU patient.
have developed cardiogenic shock and are unrespon
Clinically, increased rcp is best detected by altered
sive to conventional management. These devices take
consciousness, blood pressure, pulse, pupillary re
over the pumping action of the left ventricle and de
sponses, movement, temperature, and respiration
crease myocardial workload and oxygen consump
(Luce, 1985). The rcp monitor provides direct mea
tion. These types of assistive devices may have con
surement of ICP. A hollow screw is positioned through
siderable potential in the management of refractory
the skull into the subarachnoid space. The screw is at

tached to a Luer-Lok, which is connected to a trans
heart failure.
ducer and oscilloscope for continuous monitoring.

The prevention of further increase in rcp and a
MEASUREMENT OF INTRACRANIAL PRESSURE
corresponding reduction in cerebral perfusion pressure
rncreased intracranial pressure (ICP) resu Its from
is a treatment priority. High ICP and low cerebral per
many neurological insults including head injury, hy
fusion pressure are highly con-elated with brain injury.
poxic brain damage, or cerebral tumor, and may re
Measures to reduce venous volume are maintained
quire surgery. rn the adult, the cranial vault is rigid
until ICP has stabilized within normal range. Prudent
and noncompliant. rncreases in the volume of the cra
body positioning is used to enhance venous drainage
nial contents result in an elevated ICP and decreased
by elevating the bed 15 to 30 degrees and maintaining
cerebral perfusion pressure.
the head above heart level. Neck flexion is avoided.
Changes in consciousness are the earliest and most
Fluid intake and output are carefully monitored; the
sensitive indicators of increased rcp (Borozny, 1987;
patient may need to be fluid restricted. The Valsalva
Luce, 1985). Altered consciousness reflects herniation
maneuver is avoided, since intrathoracic pressure and
of the brainstem and compression of the midbrain.
rcp may increase correspondingly.
Compression of the oculomotor nerve and the pupillo
Normal range of ICP is 0 to \0 mm Hg for adults,
constrictor fibers results in abnormal pupillary reac
and 0 to 5 mm Hg for patients under 6 years of age.
tions associated with brain damage.
The ICP may reach 50 mm Hg in the normal brain;
The effect of rcp on blood pressure and pulse is
typically, however, this pressure returns to baseline
variable. Blood pressure may be elevated secondary
levels instantaneously. In patients with high levels of
to elevated rcp and hypoxia of the vasomotor cen
rcp and low cerebral compliance, extra care must be
ter. A reflex decrease in pulse occurs as blood pres
exercised during routine management and therapy.

An ICP elicited by turning or suctioning up to 30 mm
sure rises.
Compression of upper motor neuron pathways in
Hg may be acceptable provided the pressure drops
terrupts the transmission of impulses to lower motor
immediately following removal of the pressure
246
PART IJ
potentiating stimulus. Patients may be mechanically
bency. The selection of treatment and the assessment
hyperventilated to keep arterial PC02 at low levels,
of treatment response must be based upon quantita
since hypercapnia dilates c e rebral v e s sels and
tive evaluation of the parameters affecting oxygen
hypocapnia constricts them.
transport and cardiopulmonary function. Meticulous
To establish whether a patient will tolerate a treat
monitoring contributes substantially to more rational
ment that requires movement or body positioning, an
management of the lCU patient (i.e., the optimization
indication of cerebral compliance is needed. This can
of physical therapy efficacy, in addition to minimiz
be obtained by observing changes in ICP during rou
ing deleterious treatment outcomes).
tine nursing procedures or by titrating small degrees

of movement or position change and observe the rate
at which the ICP returns to baseline following the
REVIEW QUESTIONS
challenge. Rapid return to baseline minimizes the risk
1. Explain the determinants of fluid and electrolyte
of reduced cerebral perfusion pressure secondary to
balance, and factors that contribute to fluid ex
the increased lCP. A slow return to baseline or sus
cesses and deficits.
tained elevation of rcp is consistent with poor cere
2. Describe the basis of acid and base balance.
bral compliance and indicates treatment should be
3. Describe the physiological effects of hypoxia

and hypercapnia.
modified or possibly not performed at all depending
4. Explain the physiologic basis of ECG monitoring
on the absolute level of the lCP.
and common supraventricular and ventricular

dysrhythmias.
ELECTROENCEPHALOGRAM MONITOR
5. Explain (a) the physiologic basis of the pul
An electroencephalogram, or EEG, provides useful
monary artery balloon floatation catheter, and (b)
information about gross cerebral functioning and
what is represented by altered CYP, RAP (sys
changes in level of consciousness. A single-channel
tolic and diastolic), PAP (systolic and diastolic),
EEG monitor can be readily used in the lCU to reveal
and the PAOP.
evidence of posttraumatic epilepsy when the clinical
6. Describe the basis of intra aortic balloon counter

pulsation.
signs may be inhibited by muscle relaxants. An EEG

assessment may also be of some benefit to the PT in
7. Describe intracranial pressure monitoring, its

physiological basis and clinical implications.
assessing the effects of arousal, treatment and senso

rimotor stimulation on cerebral function.
References
SUMMARY
V. K.. Zipes. D. P .. & Wallace.
Andreoli. K. G., Fowkes.
Monitoring cardiopulmonary function and oxygen

transport is an essential component of the manage
ment of the patient in the lCU. Regulation of home
ostasis is disrupted in disease or following medical
and surgical interventions. PTs working in the unit
require a thorough understanding of homeostatic reg
ulation and monitoring of fluid and electrolyte bal
Barrdl. S.
E. &
Abbas. H. M. (1978). Monitoring during physio
therapy after open heart surgery. Physiotherapy. 64(9). 272-273.

Borozny. M. L. (1987). Intracranial hypertensi()n: Implications for
the physiotherapist. Physiotherapy Cwwdu. 39. 360-366.
Buchbinder, N. .
&
Ganz, W. (1976). Hemodynamic monitoring:
Invasive techniques. Anesthesi%

Burkj. N. K..
&
45(2). \46-\55.
Noninvasive monitoring of
tory pathophysiology. Chest. 83(4).666-670.

Copel L.
c.. &
Stolarik. A. (1991). Continuous Sv02 monitoring.
in patients requiring intensive care, using conserva
A research review.
tive, noninvasive approaches, in addition to averting
202-209.
the musculoskeletal, neuromuscular, and multisystem
gy.
R. K.'(1983).
Albert.
arterial blood gases. A report of the ACCP section on respira
ance, acid base balance, and blood gases. Physical

therapy has an essential role in res tOling homeostasis
A. G. (Eds.)
(1991). Comprehensive cardilu: care (7th ed.). Sl. Louis: Mosby.
Cromwell, L.. Wei bell.
complications associated with immobility and recum
Dimensions of Cri/ica/
F. l, &
Pfeiffer.
C a re
Nursin!i. lO,
A. (1980). Biomedical
ins/rumentarion and measuremen/s (2nd ed.). Englewood
Cliffs: Prentice-Hall.
15
DeGowin, E, L, & DeGowin, R L (1981), Bedside diagnostic ex
247
Monitoring Systems ill the Intensive Care Unit
Oakes, D, F. (1988), Clincfal practitioners pocket
10
respira
lory care. Old Town: Health Educator Publications.
aminatioll (4th cd.). New York: Macmillan.
Dubin, D, (1989). Rapid illterprelatiotl of EKGs, (4th ed,), Tampa,

Fl.: Cover.
Phipps, W. J., Long, B.
& Woods, N. F. (Eds,). (1991). Med
iced-surgical nursing: concepts and clinical practice (4th ed.).
Fisher, J, D, (1981). Role of electrophysiologic testing in the
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nosis and treatment of patients with known and suspected
Pmi, V. K, Carlson, R. W., Bander, J. J, & Wei!, M. H. (1980).
bradycardias and tachycardias. Progress in Cardiovascular
Complications of vascular catheterization in the critically ill. A

prospective study. Critical Care Medicine. 8(9),495-499.
Diseases, 24(1),25-90.
Folk-Lighty, M. (1984). Solving the puzzles of patients' lluid im

balances. Nursing, 14(2),34--41,
Shapiro, B. A., Peruzzi, W. T., & Kozelowski-Templin, R. (1994).

Clinical application of blood gases (5th
Forrester, J. S., Diamond, G., McHugh, 1'. 1. (1971), Filling pres
SL Louis: Mosby.
Snider, G. L. (1973). Interpretation of the arterial oxygen and car
sures in the right and left sides of the heart in acute myocardial
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Swan,H. J, (1975), Second annual SCCM lecture. The role of he

modynamic monitoring in the management of the critically ill.
Ganong, W. F. (1993), Review o.fmedical physiology, (16th

Los Altos: Lange :Vledical Publications
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paniol! Critical Care Immediate C once rns. Philadelphia: JB
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Journal of Medicine, 57(3), 331-348.
West, J. B, (1995), Respiralory physiology-the essentials (5th
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Luce, 1. M. (1985), Neurologic monitoring. Respiratory Care, 30,

Wiedemann, H, P , Mauhay,M. A" & Matlhay, R. A, (1984). Car
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Kirby, K R., Taylor, K W., & Civetta, J. M, (1990), Pocket Com
Marioi, J. J. (1987). Respiratory medicine and intensive
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(Part I) Chesr, 85(4), 537-549.
(2nd ed.). Baltimore: W
PART
III
Cardiopulmonary Physical
Therapy Interventions
Optimizing Treatment Prescription:

Relating Treatment to the Underlying
Pathophysiology
Elizabeth Dean
KEY TERMS
Clinical decision making
Pathophysiological factors
Extrinsic factors
Problem definition
Intrinsic factors
Problem list
Oxygen transport deficits
Restricted mobility and recumbency factors
Oxygen transport threats
Treatment prescription
INTRODUCTION
I. What is the problem?
The purpose of this chapter is to provide a basis for

clinical decision making and treatment prescription in
2. What is the treatment and why?

3. What is the course of treatment?
cardiopulmonary physical therapy (CPPT) for patients
This chapter focuses on the elements involved in
ranging from the medically unstable critically ill pa
addressing these questions when managing a patient
tient to the medically stable patient with cardiopul
with impaired to threatened oxygen transport. The
monary dysfunction living in the community. Clinical
basic principles for relating CPPT treatment to the pa
decision making and treatment prescription is based on
tient's underlying pathophysiologic problems (i.e., the
the answers to three primary clinical questions related
pathophysiological mechanisms responsible for im
to oxygen transport. With respect to a given patient,
pairment of oxygen transport and cardiopulmonary
the following must be considered:
function) are described. A physiologically based treat

251
252
PART III
Cardiopulmonary Physical Therapy Interventions
Fundamental Knowledge and Expertise
Steps in Critical Problem-Solving De.flCits
to Critically Problem-Solve Deficits in
in Oxygen Transport
Oxygen Transport
I. De t ermine what factors are specifically con

tributing to impaired oxygen transport and which
Norm al c a rd i o p u l m o n ary a n d c a r d i o v a s cul ar
steps in the pathway are affected
anatomy. as well as physiology and how these are

affected by normal conditions such as aging and
2. Determine those factors that threaten oxygen
lifestyle habits (e . g .. smoking. stress. and the
transport and the steps in the pathway that are
physical environment)
involved
Physio lo gic adaptation to hypoxia and cardiopul
3. Determine the relative magnitude of the effect of
monary impairment
each factor either impairing or threatening oxygen

transport, and prioritize the importance of each
Cardiopulmonary and cardiovascular pathophysiology

and disease processes, and how these affect nonnal
4. Distinguish those factors that arc amenable and
cardiopulmonary and cardiovascular function
those that are not amenable to CPPT in that the

latter will modify treatment and affect the moni
Multisystem and integrative pathophysiology that
toring that is needed
can have a secondary effect on cardiopulmonary

function and oxygen transport
5. Giv en the answers to I through 4. select, priori

tize, and apply specific treatments prescrip
Effects of medical. surgical, and nursing procedures
tively to address each factor that nmtributes to
on oxygen transport and gas exchange
cardiopulmonary dysfunction and is amenable
Investigative laboratory procedures and tests and
toCPPT
their effects on cardiopulmonary function

Pharmacological effects on cardiopUlmonary function
ment hierarchy is presented, with the premise that
detailed understanding of the relevant anatomy and
physiologic function, including oxygen transport, is
physiology, multisystem and integrative pathophysiol
optimal when humans are upright and moving. Apply
ogy, the impact of medical, surgical, and nursing pro
ing a systematic physiologic approach to the analysis
cedures, the effect of various laboratory tests and pro
of the patient's problems, with respect to deficits in the
cedures, and the impact of pharmacological agents on
oxygen transport pathway, leads directly to the most
cardiopulmonary function (see box above, at left).
efficacious treatments. Such an approach provides a
For a given patient, the cardiopulmonary
PT pre
basis for modifying or discontinuing treatment based
scribes treatment by extracting the relevant information
on the use of appropriate treatment outcome measures.
from the history, laboratory tests and investigative pro

cedures, and the assessment (see box above. at right).
Problems are prioritized based on the relative magni
WHAT IS THE PROBLEM?
tude of each one's effect on impairment of oxygen
Oxygen transport is determined by a multitude of fac
transport. Once the mechanisms for the cardiopul
tors which affects different steps in the oxygen trans
monary and cardiovascular dysfunction have been iden
port pathway (see Figure I-I, p.
4) (Chapter I). For
tified, specific treatments are selected and prioritized.
treatment to be directed specifically to the underlying

problems, the physical therapist
(PT) needs to consider
several levels of analysis of the deficits contributing to
The Problem list

Impaired oxygen transport
impaired or threatened oxygen transport. To be profi
PT must have a thorough
Two levels of problems need to be identified. namely,
knowledge of the multiple factors that contribute to ab
functional and physiologic deficits. The functional
normal gas exchange. This knowledge base includes a
deficits are those that affect the patient's ability to
cient in such analysis, the
16
Optimizing Treatment Prescription: Relating Treatment to the Underlying Pathophysiology
253
ExampLes of Deficits in and Threats to Steps in the Oxygen Transport Pathway

Central Control of Breathing
Altered central nervous system (CNS) afferent input and control of breathing
Impaired efferent pathways
Pharmacologic depression
Substance abuse depression
Airways
Aspiration related to lack of gastrointestinal (GI) motility

Aspiration secondary to esophageal retlux
Obstruction secondary to airway edema, bronchospasm, or mucus
Inhaled foreign bodies
Lungs
Altered breathing pattern secondary to decreased lung compliunce

Ineffective breathing pattern related to decreased diaphragmatic function and increased lung volumes, respiratory
muscle weakness, respiratory muscle fatigue, CNS dysfunction, guarding, reflex, fatigue, and re spirato ry inflam
matory process
Ineffective airway clearance related to restricted mobility, immobility, sedation, and pulmonary dysfunction sec
ondary to long smoking history, impaired mucociliary transport, absent cilia. or dyskinesia of cilia, retained secre
tions, ineffective cough and mucociliary mechanisms, infection, inability to cough efficiently, artificial airway/in
tubation and cndotracheal tube, drug-induced paralysis, and sedation
Large airway ob:,truction secondary to compliant oropharyngeal structures
Chest wall regidity and decreased compliance
Loss of normal chest wall excursion movements (pump and bucket handle motions) and capacity to move appropri
ately in all three planes of motion
Chest wall and spinal deformity
Impaired lung t1uid balance and acute lung injury
Blood
Bleeding abnormalities, altered body temperature (hypothermia, hyperthermia). fever, inflammation, hypermetabo
lism secondary to mediator systems
Altered body temperature related to integumentary disruption
Low hematocrit secondary to GI bleed (more prone to hypoxia)
Anemia
Thrombocytopenia
Dissemin ... ted intravascular coagulation
Abnorm... 1 clotting faclOrs (i,e" halance between clotting and not c1olling, sludging of blood)
Thromboelllboli
Bleeding disorders with liver disease; ...bnormal clotting factors
Continued,
254
PART III
Examples of Deficits in and Threats to Steps ill the Oxygen Transport Pathway-cont'd
Gas Exchange
Alveolar collapse, atelectasis, intrapulmonary shunting or pulmonary edema, shallow breathing and tenacious mucus,
body position, consolidation and alveolar collapse, ventilation/perfusion mismatch, airway constriction, t1uid vol
ume excess, pleural effusions. breathing at low lung volumes. abdominal distension and guarding. ineffective air
way clearance, pulmonary microvascular thrombi and altered capillary permeability secondary to circulating medi
ators. closure of small airways secondary to dynamic airway compression. decreased functional residual capacity,
and intrapulmonary shunting, increased lung surface tension
Diffusion defects
Respiratory Muscles
Upper abdominal surgery. weakness, fatigue. neuromuscular discase. ileus related to gastric distension, mechanical
dysfunction
Myocardial Perfusion
Coronary artery occlusion
Tachycardia
Potential for cardiac dysrhythmia related to reperfusion
Cardiac dysrhythmia related to myocardial hypoxia
Compression by edema or space-occupying lesions
Heart
Decreased venous return and cardiac output, secondary to volume deficit, ascites, myocardial ischemia, hemorrhage,
and coagulopathies
Conduction defects
Mechanical defects
Defects in electromechanical coupling
Abnormal distension characteristics
Abnomlal afterload
Blood Pressure
Volume deficit/bleeding
Alteration in peripheral tissue perfusion related to acute myocardial infarction. myocardial depression, maldistribu
tion of blood volume, and altered cellular metabolism
Volume excess
Tissue Perfusion
Impaired cardiac output
Impaired secondary to disseminated microvascular thrombi
Atherosclerosis and thromboembolic events, decreased circulating blood volume. decreased circulating blood vol
ume, decreased vascular integrity. and int1ammatory process
Decreased cardiac output related to reduced venous return. impaired right ventricular function, dysrhythmias, in
creased afterload, and bradycardia
Low oxygen content in the blood
Thromhoembolism. vasoconstriction secondary to toxins. sepsis, etc., blood flow alterations and hypermetabolism
secondary to mediator systems
16
255
Examples of Deficits in and Threats to Steps in the Oxygen Transport Pathway-cont'd

Fluid Volume Excess
Related to excessive intravenous administration
Related to impaired excretion
Apparent hypervolemia secondary to restricted mobility and recumbency (e.g., resulting from hemodynamic instability)
Renal failure
Water intoxication
Therapeutic volume expansion. acute myocardial infarction (MI) and acute renal failure. related to renal retention of
sodium and water and increased levels of aldosterone, renin, angiotensin II, and catecholamines
Fluid Volume Deficit
Fluid volume deficit related to volume losses during surgery and inadequate oral intake, blood loss, internal injuries
(e.g.. hematoma and third spacing phenomenon: hormonal imbalance; increased intestinal motility; vomiting; diar
rhea: tluid sequestration in tissues; nasogastric (NG) suction and diarrhea: hypovolemia; sepsis and shock; surface
capillary leak and fluid loss as in burns and excoriated wounds; tluid shifts)
Tissue Oxygenation
MultisysteJll organ failure with allered peripheral tissue perfusion and gas exchange at the cellular level
Indirect Factors That Contribute to Oxygen Transport Deficits

Infection
Pulmonary and nonpulmonaty infection increase the demands on the oxygen transport system
Cognition
Impaired neurological status and ccntral cardiopulmonary control
Alleration in mental status secondary to inadequate cerebral perfusion with hypotension and cardiogenic shock
Sleep pattern disturbance; altered blood gases and fatigue
Anxiety and agitation relatcd to powerlessness and lack of knowledge, breathlessness, pharmacological paralysis, im
paired verbal community secondary to intubation, paralysis etc.
Psychosocial Factors
Anxiety related to the condition, shllltncss of breath. hospitalization. et\:.
So\:ial isolation second.uy to impaired wl11l11unication
Fear and hopelessness
Pain response
Nutrition
Altered nutritional needs secondlllY to greater need than resting state (i.e.. increased caloric need and nutrients asso
ciated with illness, inability to ingest food, inability to absorb food)
Restricted ingestion orders of food and water
High caloric needs sen)l1dary to infectious process and protein catabolism
256
PART III
perform activities of daily living (ADLs) (e.g., re
Factors That Call Impair Oxygell Trallsport
duced activity or exercise tolerance as a result of re

duced peripheral oxygenation, reduced mobility re
I. Cardiopulmonary pathophysiology
lated to deconditioning resulting from resting in bed,
primary (acute, chronic, acute on chronic)
extremity or internal injury, anticoagulant therapy,
secondary (chronic, acute on chronic)
drug-induced paralysis, impaired physical mobility re
Noncardiopulmonary pathophysiology that im
lated to muscle weakness and partial paralysis, paraly
pacts upon cardiopulmonary function
sis, depressed level of consciousness, and anemia).
2. Immobility-loss of physical exercise stress
Physiological deficits are those deficits in oxygen
Recumbency-loss of vertical gravitational stress
transport, specifically, at the individual steps in the
3. Extrinsic factors (i.e., those related to the pa
pathway, and oxygen transpolt overall. Examples of
tient's care)
deficits at each step in the pathway appear in the
4. Intrinsic factors (i.e .. those related to the patient)
boxes on pp. 253-255.
Threatened oxygen transport

Although the complications of restricted mobility and
static body positions are well understood, the precise
prescription parameters for mobilization and body
(see box above), namely, the underlying cardiopul
positioning to avoid these complications have not
monary pathophysiology, restricted mobility (loss of
been defined in detail. With respect to cardiopul
physical exercise stress), recumbency (loss of vertical
monary complications, a one- or two- hourly turning
gravitational stress), extrinsic factors (i.e., those re
regi men is commonly accepted. For the flaccid or co
lated to the patient's care), and intrinsic factors (i.e.,
matose patient, range-of-motion (ROM) exercises
those related to the patient). These categories are ex
every several hours facilitates blood flow through de
panded and explained in detail in Chapter 17.
pendent areas and enhances alveolar ventilation as
Restricted mobility and recumbency:
special examples of extrinsic factors
well as mobilizes joints and muscles. Antiembolic

stockings and pneumatic compression devices are
routinely used to minimize circulatory stasis in the
Although bed rest can be considered an extrinsic
legs and the potential for thrombi formation.
factor (i.e., a therapeutic intervention that con
The PT has a major role in preventing infection of
tributes to cardiopulmonary dysfunction, the nega
all types but particularly cardiopulmonary infections.
tive sequelae of this intervention are often not fully
Both cardiopulmonary assessment and treatment in
appreciated clinically based on the widespread use
volves handling and close physical contact with pa
of rest in bed. Therefore to draw to the clinician's
tients. Thus the risk of nosocomial infection is high in
attention that the effects of this intervention need to
hospitalized patients. Some standard means of prevent
be considered in each patient, the effects of re
ing infection include meticulous hand washing before
stricted mobility and recumbency are analyzed sepa
and after every patient, and care of invasive lines and
rately (see Chapters 17 and 18).
catheters. The PT moves and repositions patients often,

thus it is essential that lines, leads, and catheters are
continuously monitored. The PT must consider when it
is appropriate to gown, mask and glove to protect and
Treatment Goals
Once the deficits and threats to oxygen transport have
been determined, the goals of treatment fall into three
be protected from the patient adequately.
categories: short-term, long-term, and preventive.
Factors that contribute to or
threaten oxygen transport
Short-term treatment goals include the following.

1. To correct or reverse acute cardiopulmonary
dysfunction
Those factors that can impair oxygen transport di

rectly or threaten it fall into four primary categories,
2. To reduce the rate of deterioration
16
3. To avoid worsening the patient's condition.
257
Common Treatment Goals in the Management of
Long-term treatment goals include:

I. To enhance the efficiency of the steps in the
oxygen transport pathway overall
the Patient With Cardiopulmonary Dysfunction

OVERALL GOAL: To optimize or preserve oxy
2. To enhance the efficiency of those specific
gen transport and gas exchange
steps in the oxygen transport pathway that com
Treatment directed at specific steps involved
pensate for impaired steps that may or may not
Object to enhance the efficiency of all steps in the
be reversibly affected
pathway
3. To maximize oxygen transport capacity to sus

tain maximal functional activity.
Augment medical management

Coordinate with nursing management (e.g., in criti
And preventive treatment goals include:
cal care)
I. To prevent cardiopulmonary dysfunction

2. To prevent multisystem organ complications
and nonpulmonary infection that will lead to
further restricted movement and recumbency,
hence the potential for further deterioration
Goals Directed at Specific Steps in the Oxygen

Transport Pathway
Maximize air entry and alveolar ventilation (mini

mize airflow resistance)
Maximize air distribution (optimize lung compli
3. To provide supportive palliative care.
ance and chest wall compliance)

Maximize ventilation and perfusion matching
WHAT IS THE TREATMENT AND WHY?
Optimize diffusion
Clinical Decision Making
Optimize oxyhemoglobin saturation
The basis for clinical decision making in the man

agement of the cardiopulmonary patient is to pair the
most efficacious treatments specificall y with im
paired or threatened steps in the oxygen transport
Reduce work of breathing (increased resistance, re

duced or excessive compliance)
Reduce work of the heart (increased preload, con
traction. increased afterload)
pathway. In addition, the patient spends considerable
Maximize efficiency of heart mechanics
time between treatments, thus optimal therapeutic ef
Minimize electrocardiogram (ECG) irregularities
fect is dependent on the efficacy of "between treat

ment" treatments (i.e., teaching the patient to carry
(identify factors that contribute to irregularities;

anticipate problems)
out prescriptive treatment whenever possible and
Optimize blood flow distribution
eliciting the assistance of the patient's family or
Optimize oxygen extraction ratio
nursing staff).
When confined to hospital, many patients spend
considerable time recumbent and in restricted body
Reduce excessive or unnecessary energy expenditure

Optimize carbon dioxide (C02) removal
positions, turn and move less frequently, and are up
Optimize blood volume
right and moving a smaller proportion of time. De
Optimize hydration
pending on the oxygen transport deficits, the body

positions the patient assumes can have a positive,
negative or neutral effect on oxygen transport. Thus,
the positions the patient assumes and his or her re
duced activity levels, must be monitored and any po
tential ill effects anticipated and countered.
goals and specific treatments are prioritized accord
Some examples of some common treatment goals

in managing the patient with cardiopulmonary dys
ing to the relative significance of the impact of each

on oxygen transport.
function are shown in the box above. Specific treat
A physiologically based treatment hierarchy is
ments are identified to address these goals and for
shown in the box on p. 258 and 259, and the box on
threat to oxygen transport. Treatment
p. 260, top right. The treatment hierarchy is based on
each deficit
or
258
PART III
Physiologic Treatment Hierarchy for Treatment of Impaired Oxygen Transport

PREMISE: Position of optimal physiological function is being upright and moving
I. Mobilization and Exercise
Goal: To elicit an exercise stimulus that addresses one of the three effects on the various steps in the oxygen trans
port pathway, or some combination
A. Acute effects
B. Long-term effect
C. Preventative effects
II. Body Positioning
Goal: To elicit a gravitational stimulus that simulates being upright and moving as much as possible i.e., adive. ac
tive assisted or passive
A. Hemodynamic effects related to fluid shifts

B. Cardiopulmonary effects on ventilation anti its distribution, pelfusion. ventilation. and perfusion matching
and gas exchange
III. Breathing Control Maneuvers
Goal: To augment alveolar ventilation, to facilitate mucociliary transport. and to stimulate coughing
A. Coordinated breathing with activity and exercise

B. Spontaneous eucapnic hyperventilation
C. Maximal tidal breaths and movement in three dimensions
D. Sustained maximal inspiration

E. Pursed lip breathing to end tidal expiration
F. Incentive spirometry
IV. Coughing Maneuvers
Goal: To facilitate mucociliary clearance with the least effect on dynamic airway compression and adverse cardio
vascular effects
A. Active and spontaneous cough with closed glottis
B. Active assist (self-supported or by other)
C. Modified coughing interventions with open glottis (e.g., forced expiratory technique, hulT)
V. Relaxation and Energy Conservation Interventions
Goal: To minimize the work of breathing. of the heart. and oxygen demand overall
A. Relaxation procedures at rest and during activity

B. Energy conservation, (i.e., balance of activity to rest, performing activities in an energy) efficient manner.
improved movement economy during activ:ty)
C. Pain control interventions
VI. ROM Exercises (Cardiopulmonary indications)
Goal: To stimulate alveolar ventilation and alter its distribution
A. Active
B. Assisted active
C. Passive
Continued.
16
259
Physiologic Treatment Hierarchy for Treatment of Impaired Oxygen Transport-cont'd

VII. Postural Drainage Positioning
Goal: To facilitate airway clearance using gravitational effects

A. Bronchopulmonary segmental drainage positions
VIII. Manual Techniques
Goal: To facilitate airway clearam;e in conj unction with specific body positioning
A. Autogenic drainage
B. Manual percussion
C. Shaking and vibration
D. Deep breathing and coughing
IX. Suctioning
Goal: To fac ili tate the removal of airway secretions collected centrally
A. Open suction system
B. Closed suction system
C. Tracheal tickle
D. Instillation with saline
E. Use of manual intlation bag (bagging)
the premise that physiologic function, including oxy

gen transport, is optimal when the human organism is
Treatment Plan
upright and moving. Thus the purpose of the hierar
The treatment plan consists of those interventions
chy is to exploit those treatments that are most physi
that will most expediently remediate the problems
ologic first (i.e., active mobilization and exercise in
that have been identified. These interventions are pri
the upright position). Therefore the hierarchy ranges
oritized according to the greatest effect they are pre
from the most physiologic interventions, that is, ac
dicted to have on remediating the oxygen transport
tive mobilization and exercise in the upright position,
deficit or minimizing any threat to oxygen transport,
to those interventions that are the least physiologic.
and on maximizing the benefit-to-risk ratio. Depend
The least physiological interventions, (i.e., conven
ing on the specific treatment goals and the adequacy
tional chest physical therapy techniques such as
of balance between oxygen supply and demand, coor
ROM, postural drainage and percussion) may simu
dinating physical therapy treatments with other care
late some of the physiologic effects of being upright
(e.g., nursing care and certain tests and procedures) is
and moving; however, their effects are more limited
often indicated.
and less scientifically well-substantiated, and affect

fewer steps in the oxygen transport pathway. Thus
they do not substitute for more physiologic interven
Treatment Prescription
tions higher up in the treatment hierarchy. All inter
Once the specific pathophysiological problems have
ventions featured in the hierarchy have some role in
been identified, they are differentiated as:
the management of cardiopulmonary dysfunction, but
that can be addressed by physical therapy (i.e., nonin
(I) those
(2) those that are
are recruited in descending order to ensure that the
vasive physical interventions) and
most physiological and efficacious interventions are
not amenable to physical therapy but need to be con
exploited first.
sidered during treatment to determine whether treat
260
PART III
ment is contraindicated or needs to be modified, and
Use of Modalities and Aids
specific outcome and treatment response measures

are indicated.
Goal: To incorporate the use of those modalities

and aids that enhance the ahove interventions
Problems amenable to physical therapy are priori

tized, the treatment is indicated for each problem, and
Modalities
its parameters are defined. The treatment goals are
Treadmill, ergometer, rowing machine
identified, that is, to reverse pathophysiological
Weights
mechanisms contributing to impaired oxygen trans
Pulleys
port, to compensate for irreversible pathophysiologi

cal deficits (improve efficiency of other steps in the
Nebulizers and aerosols
oxygen transport pathway), to decelerate deteriora
Flutter valve
tion, to avoid making patient worse palliative
BYPAP' and CPApt
care/support/comfort, and for prevention. Based on
Incentive spirometer
the goal of treatment, the parameters for the treatment

prescription are defined. Treatment parameters in the
Pharmacologic Agents
management of a cardiopulmonary patient are shown
Oxygen
in the box below.
Bronchodilators
Antiintlammatories
WHAT IS THE COURSE OF TREATMENT?
Mucolytics
Once a treatment has been prescribed, the prescrip
Surfactant
tion must be reviewed at each treatment and modified
Analgesics
accordingly, that is, change in the prescription para

meters, as the patient's condition changes. In addi
"Bilevel positive airway pressure
tion, the parameters may be modified within a treat-
"'Continuous positive airway pressure
Parameters of the Treatment Prescription in the Management of the Cardiopulmonary Patient

Define parameters of treatment based on history, laboratory investigations, tests, and assessment
Treatment type
Intensity (if applicable)
Duration
Frequency
Instruct patient in "between treatment" treatment, and if applicable the nurse. a family member. or both
Reassessment every treatment
Modify as necessary within each treatment
Progress between treatments as indicated
Define treatment outcomes
Determine when treatment is to be discontinued
Request for additional supportive information. tests, and investigations as indicated
Predict time course for optimal effects and course of treatment to determine treatment efficacy; modify as necess,u'y
In conjunction with other interventions (e.g., medical, surgical, nursing, respiratory therapy (weaning oxygen supplementation. sympathomimetic drugs, ADLs, balance with sleep and rest periods. peak of nutrition and feeds. peak
energy times. peak of drug potency and effects (e.g., pain, reduced sedation. reduced neuromuscular blockade)
16
261
Assessment and Treatment Outcome Measures Used in the Management of Deficits in Oxygen Transport
Pathway
Central Control of 8reathing
8 Iood-cont 'd
Central drive to breathe test
Platelets
Hemoglobin
Cerebral perfusion
Coagulability
Ambient Air
Viscosity
Partial pressures of 02. Nl and CO2
Stasis
Air pollution and quality
Hydration
Humidity
Immunological status
Airways
Clinical assessment including auscultation
Pullllonary function tests
Chest X-ray
Histamine challenge exercise tests
Lungs
Clinical assessment including inspection. percussion.
palpation and auscultation
Pulmonary function tests
Ventilation and perfusion scans
Diffusion capacity test
Chest X-my
lmmunulogical status
Respiratory muscle assessment
Assessment of the structure and integrity of chest
wall
Lung water studies
Blood
Circulating blood volume and cardiac output
Pulmonary Circulation
Pelfusion scan
Pulmonary artery balloon t1oatation catheter to assess
central venous pressure, pulmonary artery pres
sures, wedge pressure
Heart
Clinical assessment including percussion. palpation.
and auscultation
Inspection and clinical observation tests including
jugular venous distension test
Heart rate, systolic and diastolic blood pressures, and
rate pressure product
ECG
Hemodynamic studies to assess cardiac output, stroke
volume, cardiac distensibility. and ejection fraction
Ultrasound procedures to examine mechanical integrity
Scans
Coordination of electromechanical behavior of heart
Coronary artery perfusion studies
Stress test
Hemodynamic monitoring including central venous
pressure, pulmonary artery pressures and wedge
pressure
Arterial oxygen content
Angiography
Venous oxygen content
Chest X-ray
Plasma volume
Peripheral Circulation
Red and white blood cell counts
Clinical assessment
Protein constituents
Segmental blood pressures of the extremities
Cun/iIlLted.
262
PART III
Assessment and Treatment Outcome Measures Used in the Management of Deficits ill Oxygen Transport
Pathway-colll'd
Peripheral Circulation--cont'd
Tissue-colll'd
Ultrasound studies
Vascularization of tissue
Arterial and venous lab studies and investigations
Adequacy and efficiency of aJterial ,Uld venous tissue
Adequacy and efficiency of lymphatic drainage system
Blood now
of the healt and lungs, and pelipheml circulation
Tissue fluid balance; hydrostatic pressure, oncotic
Stress test
pressure, and lymphatic pressure
Tissue
Blood work including serum lactates and SV02
Enzyme studies
Tissue oxygenation and pH
Tissue biopsies
Nutritional and hydration status
ment based on the patient's treatment response. The
sential that these measures have certain characteris
PT also bases the decision when to discontinue a
tics. For example, measurements must be objective
given treatment as well as what overall cardiopul
and their procedures standardized to maximize test va
monary physical therapy to employ, based on treat
lidity and reliability. Although PTs specialize in non
ment response and outcome.
invasive assessment procedures as well as treatments,
Measures to assess treatment response and out
noninvasive measures are prone to imprecision, and
come are selected that reflect (J) the status of oxygen
hence measurement error and unreliability. It is there
transport overall, and (2) the integrity of the step or
fore essential that assessment measurements are per
steps in the oxygen transport pathway that were iden
formed in a systematic manner according to measure
tified as being the primary problems contributing to
m e n t guid elines to maximize their quality and
cardiopulmonary or cardiovascular dysfunction in the
usefulness in guiding and directing treatment (Chapter
original assessment (see box on pp. 261-262.) (see
6). Assessment measurements always precede any
Part II of this text). Cardiopulmonary dysfunction is
treatment to ensure that treatment is appropriate, that
determined based on the history, assessment and lab
is, the baseline measurements. Measurements during
oratory investigations, such as, pulmonary function
treatment provides information about the patient's re
testing, breathing pattern, cardiac function testing,
sponses, both beneficial and detrimental. This feed
fluid balance and renal function, anerial blood gases,
back determines the parameters of treatment, and
arterial saturation, vital signs, and hemodynamic
whether the treatment should be modified in some
variables, including heart rate and ECG, blood pres
way, or possibly discontinued. The overall treatment
sure, and rate pressure product. Subjective repOits are
response is established by further monitoring and as
also clinically relevant, such as subjective ratings of
sessment at the termination of treatment, and often at
perceived exertion, breathlessness, angina, and fa
peliodic intervals posttreatment so that delayed effects
tigue. These same measures are used to detect im
can be monitored. Frequent and periodic measure
proved oxygen transport and gas exchange.
ments over time are refelTed to as serial measurements
Considering that clinical decision making is based
and provide useful trend data. The pre- and posttreat
largely on the results of tests and measures, it is es
ment responses and any noteworthy responses during
16
treatment are charted with sufficient information

about the procedurcs that were used, that is, assess
ment as well as treatment procedures.
PTs often require the results of invasive tests such
as blood work or invasive hemodynamic monitoring
to establish treatment response and outcome; thus,
these need to be requested as required.
263
REVIEWaUESTlONS
I. Describe the use of the oxygen transport pathway
as a conceptual model of cardiopulmonary prac
tice and basis for defining problems related to
cardiopulmonary dysfunction.
2. Distinguish between short-term goals, long-term
goals and preventive goals of cardiopulmonary
physical therapy management.
SUMMARY
3. Explain and distinguish the
This chapter has provided a framework for clinical

problem solving and decision making based on oxygen
transport. The process includes diagnosis and treatment
prescription in the management of patients with car
diopulmonary dysfunction ranging from the medically
unstable critically ill patient to the medically stable pa
tient with cardiopulmonary dysfunction living in the
community. The purpose of a systematic approach to
clinical decision making is to maximize treatment effi
cacy and cost effectiveness by focusing on physiologi
cal and evidence-based practice. The clinical decision
making process involves diagnosis, that is, specific
analysis of the patient's problems in relation to the
physiology and underling pathophysiology, the contri
bution of restricted mobility and recumbency, and ex
four
categories of
factors (i.e., pathophysiology, restricted mobility

and recumbency, extrinsic, and intrinsic) that
contribute to cardiopulmonary dysfunction.
4. Describe the factors that need to be considered in
treatment prescription.
5. Desclibe the factors that must be considered In
determining the course of treatment.
Bibliography
&
and
Barlow, D.H., Hayes, S.c.,

practitioner. Research
Nelson, R.O. (1984). The scientist

accounlahiliry in clinical and edu
cational sellings. New York: Pergamon Press.
Cutler, P. (1985). Problem solving in clinical medicine. (2nd ed.).

Baltimore: Williams and Wilkins.
Dantzker, D.R. (1991). Cardiopulmonary critical care. (2nd ed.).
trinsic and intrinsic factors. Based on this analysis,
Dean, E. (1994). Oxygen transport: A physiologically-based con
treatment interventions and their parameters are pre
ceptual framework for the practice of cardiopulmonary physio

therapy. Physiotherapy,
rameters should have a clear, justifiable rationale.
80, 347-355.
& Henning R.1. (1993). Oxygen transpOlt variables
in the identification and treatment of tissue h ypox i a Heart &
L"ng, 22, 328-348.
Specific monitoring of the steps in the oxygen transport
Goldring, R.M. (1984). Specific defects in cardiopulmonary gas ex
sClibed that have the greatest physiological and scien

tific justification. Treatments and their prescription pa
pathway that are impaired is essential to establish and

confu'm the diagnoses, determine the most efficacious
treatment, evaluate the treatment response, refine and
progress the treatment, and determine when to discon
tinue a given treatment and cardiopulmonary physical
Epstein, C.D.,
change. American Review of Respiratory Diseases,
Hillegass, E.A.,
&
129, S57-S59.
Sadowsky, H.S. (1994). Essentials of cardiopul
monary physical therapy. Philadelphia: WB Saunders.

Irwin, S.,
& Tecklin, J.S. (1995).
Cardiopulmonary physical ther
apy (3rd ed.). SI. Louis: Mosby.
Patrick, D.E (1992). Clinical decision making. In Zadai C (Ed.).
therapy overall. The specific components of the treat
Clinics in physical therapy. P"lmonCllY management in physi
ment prescription include the treatment, its intensity (if
caltherapy. New York: Churchill Livingstone.
applicable), duration, and frequency, as well as its

course and progression. A problem-solving approach to
patient care has become essential in all health care pro
fessions, given the prohibitive cost of such care and the
need for all health care to be physiological, evidence
based, cost-effective and ethically justifiable.
Riegelman, R.K. (1991).
Minimizing
medical mistakes. Boston:
Little, Brown.
Schon, D.A. (1983). The rejlective practitioner. New York: Basic
Books.
Wasserman, K., Hansen,
J.E.,
Sue, D.Y.,
&
Whipp, B.1. (1987).
Principles of exercise testing and interpretation. Philadelphia:
Lea
& Fehiger.
Mobilization and Exercise
Elizabeth Dean
KEY TERMS
Exercise
Prescription
Metabolic demand
Recumbency factors
Mobilization
Restricted mobil ity
Oxygen transport
INTRODUCTION
port in a large proportion of patients. The sequelae of
The first purpose of this chapter is to define the terms
immobility and recumbency adversely affect all
mobilization and exercise and then to review the basis
steps in the oxygen transport pathway. An under
for prescribing mobilization and exercise as primary
standing of the effects of immobility and reduced ex
physical therapy treatment interventions to optimize
ercise stress on normal human physiological function
oxygen transport. The three distinct objectives of mo
provides the rationale for prescribing exercise for its
bilization and exercise for the purpose of maximizing
preventive effects.
oxygen transport are described. These include the ex

ploitation of their acute, long-term, and preventive ef
fects. Mobilization or exercise can be prescribed
specifically to elicit whjch of these effects is indicated.
The second purpose of this chapter is to review
DEFINITIONS
Mobilization is defined as the therapeutic and pre
scriptive application of low-intensity exercise in the
the negative effects of immobility and reduced exer
management of cardiopulmonary dysfunction usually
cise stress on multisystem function with special at
in acutely ill patients. Primarily, the goal of mobiliza
tention to cardiopulmonary and cardiovascular func
tion is to exploit the acute effects of exercise to opti
tion. Immobility and recumbency are major factors
mize oxygen transport. Even a relatively low-inten
contributing to impaired or threatened oxygen trans-
sity mobilization stimulus can impose considerable

265
266
PART III
metabolic demand on the patient with cardiopul
the submaximal exercise test have been less well-de
monary compromise. In addition, mobilization is per
fined (Dean and Ross, 1992a; Dean and Ross, 1993;
formed in the upright position, that is the physiologic
Shepherd et aI, 1968).
position (Chapter 18), whcnever possible, to optimize
The prescription of mobilization and exercise to
the effects of being upright on central and peripheral
optimize oxygen transport in the patient with acute
hemodynamics and fluid shifts. Thus mobilization is
cardiopulmonary dysfunction has been a relatively
prescribed to elicit both a gravitational stimulus and
neglected area of research compared with exercise
an exercise stimulus.
prescription in the management of chronic cardiopul
Exercise is the term used to describe the therapeu
monary dysfunction. This is surprising given that
tic and prescriptive application of exercise in the
"early mobilization" is a key component of car
management of subacute and chronic cardiopul
diopulmonary physical therapy in the management of
monary and cardiovascular dysfunction. Primarily,
acutely ill patients. Orlava (1959) was the first to re
the goal of exercise is to exploit the cumulative ef
port the beneficial application of mobilization in the
fects of and adaptation to long-term exercise and
management of acute cardiopulmonary compromise,
thereby optimize the function of all steps in the oxy
specifically, bronchopulmonary pneumonia. The
gen transport pathway.
physiologic literature supports an unequivocal role
In addition, mobilization and exercise can be pre
for therapeutic mobilization to maximize oxygen
scribed for their preventive effects. In this case, the
transport in patients with acute cardiopulmonary dys
parameters of the prescription focus on exploiting
function (Dean and Ross, 1992b). Despite this con
their multisystemic effects as well as their cardiopul
clusive body of literature, Orlava's work has not been
monary and cardiovascular effects.
extended significantly in the literature since her work

was published more than 35 years ago.
Unlike exercise prescription for the patient with
BASES FOR THE PRESCRIPTION
chronic cardiopulmonary and cardiovascular dys
OF EXERCISE STRESS
function, the acute patient cannot be exercise tested
The prescription of exercise is fundamental in the
in the conventional manner given the risks of an un
management of primary and secondary cardiopul
toward exercise response. Given the profound and di
monary and cardiovascular dysfunction. Exercise sci
rect effects of mobilization and exercise on car
ence has advanced exponentially over the past 30
diopulmonary and cardiovascular function, it is
years and is a primary basis for cardiopulmonary
essential that the physical therapist be able to identify
physical therapy. Guidelines have been developed for
the specific effects of exercise required and define the
prescribing exercise to maximize functional work ca
optimal therapeutic stimulus, ie, the stimulus that
pacity or aerobic capacity for healthy persons and in
yields the maximal benefit to oxygen transport with
dividuals with chronic heart and lung disease (Ameri
the least risk.
can College of Sports Medicine, 1994; Belman and
Acute and chronic cardiopulmonary and cardio
Wasserman, 1981; Blair, Painter, Pate, Smith and
vascular pathology have the additional problem of
Taylor, 1988; Froelicher, 1987; Hasson, 1994; Irwin
compromising functional capacity in two important
and Tecklin, 1985; Wasserman and Whipp, 1975;
ways. First, in acute illness, the patient tends to be re
Zadai, 1992). Exercise training is based on the find
cumbent in bed a greater propOition of time, and sec
ings of a maximum graded exercise test. Submaximal
ond, in both acute and chronic illnesses, the physical
exercise testing is often indicated for patients with se
activity of the patient is reduced. Recumbency and
verely impaired functional work capacity because of
immobility have physiologically distinct effects on
the inherent risks associated with maximal testing
oxygen transport and are the primary determinants of
(Compton, Eisenman, and Henderson, 1989). Guide
bed rest deconditioning (Chase, Grave, and Rowell,
lines for submaximal exercise testing, test interpreta
1966; Convertino, Hung, Goldwater, and DeBusk,
tion and prescription of exercise, however, based on
1982; Winslow, 1985). Thus dysfunction of oxygen
17
transport is further exacerbated in patients by the ad

ditional factors of recumbency and immobility. The
impact of these factors is further exacerbated in
smokers, the young, older adults, obese individuals,
and patients who are mechanically ventilated.
Even though the prescription of mobilization and
exercise for their acute effects ,is distinct from that for
its long-term effects, the efficacy of the acute exer
cise stimuli needs to be considered in terms of opti
mizing long-term benefit to oxygen transport as well
as the short-term acute effects. Both acute and long
term exercise needs to be prescribed specifically for a
given patient given the mechanisms of their underly
ing pathology (American College of Sports Medicine,
1994). The prescription parameters should include
(I) the type or types of mobilization or exercise,
(2) specific intensity, (3) duration, and (4) frequency.
These parameters are defined for each type of ex
ercise being prescribed. In addition, (5) the course of
the prescription, that is the time over which the pre
scription is designed to produce its maximum benefit,
and (6) the means of progression of the prescription
are defined.
Exercise has been reported to have beneficial ef
fects in the management of a multitude of conditions.
Its benefits range from enhancing all steps in the oxy
gen transport pathway to other peripheral and central
effects related to virtually every other organ system.
The preventive effects of exercise are central to
patient care across all conditions and physical therapy
specialties. Exercise is advocated preventively to
avoid the deleterious effects of immobility and to
provide optimal systemic health protection secondary
to cardiopulmonary conditioning.
Mobilization and exercise are the physical thera
pist's (PT's) "drug" with definable indications, con
traindications, and side effects for each patient. The
prescriptive parameters are determined by the effects
needed to address the patient's underlying problems
directly, whenever possible. Mobilization and exer
cise constitute the most potent and direct interven
tions affecting oxygen transport that are available to
the PT in that, unlike other cardiopulmonary physical
therapy interventions, they affect all steps in the oxy
gen transport pathway. Thus they need to be pre
scribed specifically as primary treatment interven
267
tions to remediate cardiopulmonary dysfunction, and

their effects exploited first.
OXYGEN TRANSPORT AND METABOUC
DEMAND IN PATIENTS
In health, when individuals have optimal physiologi
cal reserve, both the acute and long-term responses to
an exercise stimulus can be predicted. Specifically,
minute ventilation (vE) and cardiac output (CO),
hence oxygen delivery (002), increase commensu
rate with work rate and oxygen demand.
In patients, whose oxygen transport capacity is re
duced or threatened, mobilization and exercise con
stitute a significant additional metabolic demand that
is superimposed on various other factors that con
tribute to increased metabolic cost (see box on page
268). Hospitalized patients tend to be hypermeta
bolic. In addition to their basal metabolic demands,
their energy demands are increased secondary to such
factors as an increased body temperature, healing and
repair processes, increased work of breathing and of
the heart, and in response to routine interventions and
procedures including cardiopulmonary physical ther
apy. The goal, therefore, in prescribing mobilization
and exercise, is to ensure a safety margin wherein the
patient's demand for oxygen does not exceed the
available supply or delivery. In most situations, this
would be indicated clinically by worsening of the pa
tient's oxygen transport objectively and subjectively.
Of the physical therapy related interventions, mobi
lization, exercise, body positioning, arousal, breathing
control maneuvers, coughing, postural drainage, man
ual techniques, bagging, suctioning and range-of-mo
tion (ROM) exercises can significantly increase oxy
gen consumption and overall metabolic demand
(Dean, Murphy, Parrent, and Rousseau, 1995; Weiss
mann, Kemper, Darvask, Askanazi, Hyman, and Kin
ney, 1984). Therefore, the capacity of the oxygen
transport system to meet the patient's metabolic de
mands needs to be established in the physical therapy
assessment. Can the oxygen transport system support
the patient's metabolic demands? If so, what reserve
capacity is available to support a mobilization or exer
cise stimulus? The exercise stimulus is designed to ex
ploit the potential of the reserve capacity. Establishing
268
PART III
Factors That Contribute to Increased Metabolic Demand and Oxygen Consumption in Patient Populations
Pathophysiological Factors
Fever (e.g., secondary to an infectious agent or inflammation, surgery, multiple trauma, severe illness)
Thermoregulatory challenges (i.e., too hot or too cold, altered ambient temperature and humidity)
Healing and repairing (i.e., secondary to illness, trauma. surgery)
Com hatting infection
Interventions
Response to routine nursing, medical, and physical therapy inrerventions
Feeding: cnterally or parenterally
Physically being handled, e.g., by health care workers
Body positioning
Changing body position, i.e., passive. active assist, or active changes
ROM exercises, i.e., passive, active assist, or active
Mobilization and exercise
Noxious stimulation, e.g., injections, insertion of lines, procedures, neurological checks
Pharmacologic agents
Psychosocial Factors
Social contact, e.g., health care workers, family
Anxiety
Discomf0l1
Pain
Agitation
Miscellaneous
Noises
Disrupted circadian rhythms when ill, hospitalized or away from daylight
the availability of that reserve is essential to optimize
cedures need to be applied in the management of pa
the efficacy of the therapeutic exercise stimulus, that
tients with cardiopulmonary and cardiovascular dys
is, neither subthreshold or suprathreshold.
function in situations in which agitation, anxiety and
Metabolic demand and oxygen uptake are deter
pain contribute significantly to increased oxygen de
mined by multiple factors. In patients, the effect of
mand. This is especially true in intensive care, where
arousal, anxiety, pain, and noxious stimulation, in ad
oxygen transport is compromised or threatened in
dition to the hypermetabolic demands of recovery,
most patients (see Chapters 32 and 33).
contribute significantly to the energy cost and de

mand on the oxygen transport system. Thus relaxing
and calming patients is a central component of car
diopulmonary physical therapy as these interventions
CElLULAR ENERGETICS IN RESPONSE

TO MOBILIZATION AND EXERCISE
can minimize oxygen demand. Although relaxation,
The cardiopulmonary unit supports oxygen transport
often coupled with analgesia is central to physical
and cellular respiration (Weber, Janicko, Shroff, and
therapy management in other settings, relaxation pro
Likoff, 1983). Oxygen is continually being Llsed by
17
every cell in the body for oxidative phosphorylation
269
layed rather than eliminated. In disease states, anaer
and the synthesis of adenosine triphosphate (ATP).
obic metabolism occurs when a patient's oxygen
The splitting of a phosphate bond from ATP to form
transport system cannot meet the metabolic demand
adenosine diphosphate yields a considerable amount
required, e.g., patients with sepsis and multisystem
of energy for metabolism. The e nergy for this
organ failure. Serum lactate levels are significantly
process comes from the reduction of hydrogen in the
elevated in these patients, resulting in metabolic aci
formation of water and carbon dioxide, which is the
dosis, which is extremely unfavorable to the mainte
end products of the respiratory or electron transfer
nance of homeostasis.
chain. These metabolic processes which comprise
During exercise, the cellular P02 is lower than the
oxidative phosphorylation, take place in the mito
surrounding interstitial fluid P02. Oxygen diffuses
chondria of the cells (Chapter I).
rapidly through cell membranes. At the onset of
The balance of oxygen consumption to delivery
physical exercise, the increased metabolic demand of
is precisely regulated to ensure that there is not
the muscle and supporting tissues increases the oxy
only an adequate supply of oxygen, but also that
gen diffusion gradient. Feedback mechanisms are
under normal resting conditions approximately four
triggered to increase oxygen delivery, which de
times as much oxygen is delivered to the tissues as
pends primarily on arterial oxygen content and car
is used. This safety margin permits the immediate
diac output. The first line of defense is the response
availability of oxygen when the system is perturbed
to an increase in pericellular pH. The concentration
by physical, gravitational, and mental challenges
of carbon dioxide is increased which, as a result of
(see Chapter I).
the decrease in pH, facilitates the dissociation of
Anaerobic metabolism occurs during all out short
oxygen from hemoglobin, that is, it shifts the oxyhe
sprint type activities, e.g., hockey, soccer and volley
moglobin dissociation curve to the right. The cardiac
ball. Although PTs tend to focus on aerobic rather than
output (CO
anaerobic training, in conditions where oxygen deliv
with overall metabolic demand. The immediate re
SV x HR) increases commensurate
ery is significantly compromised, patients may rely on
sponse to oxygen deficit is an increase in CO to in
anaerobic metabolism to sustain ATP production and
crease oxygen delivery. This averts arterial desatura
break down to provide energy. Although anaerobic ex
tion which is not normally observed in health even
ercise implies that the exercise is pelformed in the ab
with extreme exertion.
sence of oxygen, anaerobic metabolism provides a
The increase in systemic CO results in increased
short-term means of supporting phosphorylation using
venous return and pulmonary CO. To oxygenate a
substrates other than oxygen to generate and split ATP.
greater volume of blood in the lungs, an increased
If insufficient oxygen is available, the amount of ATP
volume of air must be inspired. To effect an increase
that can be generated anaerobically is limited. Thus
in VE, tidal volume (VT) and respiratory rate (RR)
this process can only be sustained for a short period.
are increased. At low intensities of exercise, VT in
Lactic acid accumulates in the blood during anaerobic
creases disproportionately to RR, whereas at moderate
metabolism. In healthy, untrained individuals, lactic
to high intensities, VT plateaus and further increases
acid increases exponentially at an exercise intensity of
in VE are effected by an increase in RR (Jones and
about 55% of maximal aerobic capacity (McArdle,
Campbell, 1982). Exercise is associated with a small
Katch, and Katch, 1994). Anaerobic capacity and
but significant increase in airway diameter and length
specifically the anaerobic threshold can increase with
of pulmonary structures, hence, a reduction is airway
training, however, anaerobic training effects are less
resistance. Zone 2, that is, the zone of greatest ventila
significant compared with the training effects achieved
tion to pelfusion (V/Q) matching of the lungs, is in
with aerobic training.
creased as a result o
Anaerobic metabol ism is thought to be triggered
pulmonary capillary dilatation
and recruitment. Diaphragmatic excursion is enhanced
by tissue hypoxia. The term anaerobic is a misnomer
and the distribution of ventilation and perfusion is
in that oxygen is needed to pay the oxygen debt that
more uniform throughout the lung, which helps mini
it creates. Thus in health, the need for oxygen is de
mize atelectasis and airway closure. Exercise in
270
PART III
creases the excursion, hence, inflation of the lungs in

three planes (i.e., anteroposterior, transverse, and
cephalocaudal, particularly in the upJight positions).
Rhythmic inflation and deflation of the lungs as
EFFECTS OF MOBILIZATION AND EXERCISE

ON OXYGEN TRANSPORT
In health, optimal function of oxygen transport de
pends on the integrity of each step in the oxygen trans
sociated with physical activity has several clinically
port pathway and the interdependent function of all the
important physiologic effects. First, this action in
steps. As a result of cardiopulmonary and cardiovascu
creases alveolar ventilation by a primary increase in
lar dysfunction, one or more steps in the oxygen trans
tidal volume. Second, exercise-induced lung motion
port pathway can be affected. Because of the interde
facilitates lymphatic flow and drainage. Optimal
pendence of the steps in the pathway and the ability of
lymphatic drainage is essential to maintain optimal
functional steps to compensate for dysfunctional steps,
lung fluid balance with the increased volume of
gross measures of the efficacy of gas exchange and
blood being processed through the pulmonary circu
oxygenation can be normal. The number of steps af
lation and lung parenchyma. This action may ex
fected by disease and the severity of the disease deter
plain, in part, the beneficial effect of mobilization on
mines the degree of impairment of oxygen transport
the distribution and function of pulmonary immune

factors (Pyne,
1994). The increased movement of the
overall and the degree to which this is reflected in

gross measures of oxygen transport as a whole.
lungs during exercise has a primary effect on mu
To optimize the capacity of the various steps in the
cociliary transport and mucus clearance (Wolff,
oxygen transport pathway, the oxygen transport sys
1977). Related
tem needs to be exposed to two principal stressors:
to its effects on mucociliary transp0l1, physical activ
(I) gravitational stress and (2) exercise stress. These
Dolovich, Obminski, and Newhouse,
ity may help minimize bacterial colonization in the
stressors are tantamount to life in that they enhance
airways, hence, reduce the risk of pulmonary infec
the biochemical, physical and mechanical efficiency
1989). Finally,
of the various steps in the oxygen transport pathway,
tion (Skerrett, Niederman, and Fein,
lung movement stimulates surfactant production and
and the patient's ability to respond rapidly to changes
its distribution over parenchymal tissue. Surfactant is
in the physical environment.
essential for reducing surface tension in the alveoli,
The fact that the absence of gravitational stress
maintaining alveolar stability, maintaining lung com
and exercise stress are the two primary factors con
pliance, thereby, minimizing airway closure and
tributing to bed rest deconditioning supports the ex
areas of lung collapse.
ploitation of both gravitational and exercise stress in
The heart and peripheral circulation are primed
remediating cardiopulmonary dysfunction. Therefore
and respond to the increased demands of acute exer
mobilization and exercise are the two most physio
cise. Hemodynamic adjustments occur immediately
logic interventions available to the PT for remediat
with the onset of exercise stress. To maximize the
ing cardiopulmonary dysfunction.
CO available, blood moves from the venous capaci

tance reservoirs such as the venous compartments of
the gut and extremities, particularly the legs. At rest,
most of the circulation,
70%, is contained within the
PRESCRIPTION OF MOBILIZATION AND EXERCISE:

ACUTE RESPONSES
highly compliant venous circulation. The Starling
The clinical decision-making process involved in
Law of the heart regulates the forward movement of
defining the optimal mobilization and exercise stimu
blood commensurate with the volume of blood that is
lus is multifactorial. Based on the patient's history,
received. The heart chambers are normally distensi
history of the present illness, assessment, and results
ble and adjust to changing volumes of blood return
of the lab tests and procedures, the integrity of each
ing to the heart and pump more forcefully to eject it
step in the oxygen transport pathway is determined,
through the pulmonary and peripheral circulations.

Muscle enzymes that extract oxygen at the cellular
level are also primed and are produced commensurate
and the integrity of this system overall to preserve ar

terial oxygenation and pH. The box on p.
271 shows
some common conditions associated with acute car
with chronic metabolic demand.
17
271
exploited are directed at each patient's specific
Acute Pathophysiological Conditions
pathophysiological deficits. Once the specific ef
That Benefit From the Acute Effects
fects of acute mobilization or exercise that are
of Mobilization alld Exercise
needed are identified and matched to the patient's
Atelectasis
pathophysiology, then the mobilization or exercise
Pulmonary consolidation
stimulus can be prescribed (see box on p. 273).

The increased metabolic demand of acute exer
Pulmonary intiltrates
cise results in a slight increase in airway diameter,
Bronchopulmonary and lobar pneumonias
increased VE, alveolar ventilation (VA), VT, RR,
Bronchiolitis
air flow rates, CO, SV, HR, blood pressure (BP),
Alveolitis
rate pressure product (RPP), that is, product of heart
Pleural effusions
rate and systolic blood pressure (RPP is highly cor

related with myocardial oxygen consumption, and
Acute lung injury and pulmonary edema
therefore myocardial work) oxygen consumption
Hemothorax
(V02), and carbon dioxide production (VC02). The
Pneumothorax
area of greatest ventilation to petfusion matching in
Cardiopulmonary insufficiency
the lungs, zone 2, is increased secondary to in
Cardiopulmonary sequelae of surgery
creased dilatation and recruitment of pulmonary
Cardiopulmonary sequelae of immobility
capillaries (West, 1995).

The hemodynamic benefits of exercise are maxi
mized in the upright position compared with recum
bent positions in that exercise alone fails to counter
the loss of volume regulating mechanisms associated
with recumbency (Sandler, 1986) See Chapter 18 for
diopulmonary dysfunction for which a rational basis

can be made for exploiting the acute effects of mobi
the effects of position changes.

Mobilization and exercise stimulate the endocrine
system. Catecholamines, released to support the car
lization as a primary treatment intervention.

If the patient presents with acute cardiopul
diovascular system, sustain a given exercise work
monary dysfunction, then primarily the acute ef
rate. Increased sympathetic activity secondary to mo
fects of mobilization are indicated. These effects
bilization can help reduce the patient's need for sym
are distinct from those that occur on assuming the
pathomimetic pharmacologic agents (Bydgeman and
upright position. The majority of patients benefits
Wahren, 1974). Sympathetic nerve stimulation, for
most from a mobilization and exercise stimulus
example, is increased and sympathetic neurotransmit
when they are in the upright position. The effects of
ters are processed more efficiently. This is a signifi
being upright vs. exercise. however, need to be
cant effect that can be used as a goal for the prescrip
considered separately so that the benefits of their
tion of mobilization.
individual and combined contributions can be de
Central nervous system (CNS) responses to mobi
termined as well as any adverse reactions. The
lization include arousal and priming of the various
physiological benefits of acute exercise are shown
organ systems involved (Browse, 1965).
in the box on p. 272. The principal effects that re
The prescription of mobilization and exercise to
mediate acute cardiopulmonary dysfunction are in
stimulate their acute benefits parallels that of the pre
creased VE secondary to increased VT, RR, or
scription of exercise for its long-term, central and pe
both; improved air flow rates and mucus transport.
ripheral aerobic effects. The exercise parameters to
Cardiac output is increased secondarily to increased
achieve long-term adaptations in healthy people have
stroke volume (SV), heart rate (HR) or both, and
been well-defined by the American College of Sports
increased tissue perfusion. The particular benefits
Medicine (1994) (Table 17-1) and are well-accepted.
of acute mobilization and exercise that need to be
The individual engages in aerobic exercise at a heart
272
PART III
Acute Physiological Effects of Mobilization and Exercise

Pulmonary System
Lymphatic System----<oll't
Regional ventilation
Regional perfusion
Hematologic System
Regional diffusion
i Circulatory transit times
i Zone 2 (i.e., area of ventilation perfusion matching)

i Tidal
i or !-
volume
Pulmonary lymphatic drainage
!- Circulatory stasis
Neurological System
Breathing frequency
Arousal
Cerebral electrical activity
Minute ventilation
Efficiency of respiratory mechanics
!-
Stimulus to breathe
Airtlow resistance
Sympathetic stimulation
Postural reflexes
i Flow
rates
Strength and quality of a cough
Mucociliary transport and airway clearance
Distribution and function of pulmonary immune
Neuromuscular System
factors
Venous return
Stroke volume
Heal1 rate
Myocardial contractility
i
i
Circulating blood volume
i Chest tube drainage

Peripheral circulatory effects
!- Peripheral vascular resistance
i
Peripheral blood flow
Peripheral tissue oxygen extraction
Lymphatic System
Pulmonary lymphatic flow
di s t ribution,
and
degradation
of
catecholamines
Genitourinary System
Stroke volume, heart rate and cardiac output
i Coronary perfusion
i Oxygen extraction
i R e l e ase,
effects
flow
Endocrine System
Cardiovascular System
Hemodynamic
i Regional blood
Glomemlar tiltration
Urinary output
Gastrointestinal System
Gut motility
!- Constipation
Integumentary System
i Cutaneous circulation for thermoregulation

Multisystemic Effects
!-
Effects of anesthesia and sedation
!-
Deleterious cardiopulmonary effects of surgery
!-
Risk of loss of gravitational stimulus (when in con

junction with the upright position) and exercise
stimulus
17
273
Clinical Decision Making and Prescription of Acute Mobilization and Exercise
Step 1
Identify ALL factors contributing to deficits in oxygen transp0l1 (Chapter I), that is, those factors contributed to by:
I. The underlying pathophysiology of the disease or condition

2. Imillobility and recumbcncy
3. Extrinsic factors related to the patient's care, and
4. Intrinsic factors related to the individual patient
Step 2
Determine whether mobilization and exercise are indicated, and if so, which form of either will specifically address
the oxygen transport deficits identified in Step I.
Step 3
Match the appropriate mobilization or exercise stimulus to patient's oxygen transport capacity.
EXAMPLES:
activities of daily living (ADLs). walking unassisted, standing erect with assist and taking a few steps,
transferring from bed to chair*, seated dangling position over bed side, moving in bedt
Step 4
Set the intensity within therapeutic and safe limits of the patient's oxygen transport capacity.
Step 5
Combine the various body positions especially in the erect position with the following maneuvers:
I. Thoracic mobility exercises. that is, flexion, extension, side tlexion, and rotation
2. Active. active assist, or passive ROM exercises
3. Breathing control exercises especially coordinated with body movements
4. Coughing, spontaneous and voluntary, supported by self or others
Step 6
Set the dUnltion of the mobilization sessions based on the patient's responses (i.e., changes in measures and indices
of oxygen transport) rather than time.
Step 7
Repeat the mobilization session as often
as
possible based on its beneficial effects and on is being safely tolerated by
the patient.
Step 8
Increase the intensity of the mobilization stimulus. duration of the session, or both comml!l1surate with the patil!nt's
capacity to maintain optimal oxygen transport when confronted with an increased mobilization stressor, and in the
absence of distress; monitored variables to remain within predetermined threshold range.
':'AII sitting positions requ i re upright ereci

u pri gh t position are NOT physiologically
silting; propped up, semi recumbenl, slouched or slumped posit ions although approximaling the
comparable
i-No amount of movement or activity is too sm.,lIlo derive benefits acutely or over long-Ierm
274
PART III
TABLE 17-1
Exercise Prescription Parameters to Elicit Long-Term Aerobic Benefits In Healthy Persons
SPECIFICATIONS
Parameter
Exercise Type
Rhythmic activity, involving the large muscle groups; the legs, arms or both
InLensity
Duration
70% to 85% of the age predicted maximum heart rate or observed maximum heart rate
20 to 40 minutes
Frequency
Three to five times a week
Course
6 to 8 weeks
Adapted from the American Col lege of Sports Medicine, (1994). Guidelines for exerc ise testing and
Williams and Wilkins .
prescription. (6th ed.). Philadelphia:
rate intensity of 70% to 85% of a maximum heart rate,
Mobilization Stimuli
for 20 to 40 times three to five times a week. Aerobic
Ambulation-independently, with one or more

assisting
training effects are usually observed within 2 months.

In severely deconditioned individuals and in some
Cycle ergomelly-Iower and upper extremity
patient populations, however, such a prescription
ADLs-independently, with one or more assisting
would not be realistic, ethical, or indicated. Thus exer
Standing-independently, with one or more assisting

Transferring-independently, with one or more
assisting
Dangling-independently, with one or more assisting
Cycle ergometry in bed (lower extremity)
cise is prescribed that is sufficient to elicit progressive

physiological adaptation within defined limits of cer
tain objective and subjective responses, such as per
ceived exertion, shortness of breath, angina, discom
fort/pain, and general fatigue. Considerable research,
however, is needed to refine the prescription of mobi
Turning in bed
lization and exercise for their acute effects in patients
Bed exercises
with acute cardiopulmonary and cardiovascular dys
Supplemental Aids and Devices for Mobilization
For the patient:

Walking aids, such as crutches, cane, intravenous
(IV) pole, wheelchair, orthoses
Weights
Pulleys
function. Furthermore, the specifications for low level

exercise needed to affect long-term acrobic adaptation
have not been elucidated in dctail. However, based on
physiological understanding of acute exercise re
sponses and cardiopulmonary pathophysiology, prin
ciples for prescribing mobilization for acute car
diopUlmonary conditioning can be formulated.
Monkey bar
Grab bars
Grab rope
For the PT:

Transfer belts
Mechanical lifts for patients
Mobilization Testing
Evaluating a patient's response to a mobilization
stimulus can be assessed in two ways. First, the pa
tient can be exposed to a mobilization challenge test.
The patient is monitored before, during, and after
mobilization activities (see box at left). Relatively
low-intensity activities such as bed exercises, moving
in bed, changing body position, sitting up, dangling
17
over bed side, transfer to chair, chair exercises, and
275
in the previous couple of hours, be as attentive and
short walks with assistance, constitute a sufficient
aroused as possible and be experiencing minimal
stimulus to elicit the acute effects of exercise. The de
pain or discomfort. Review of a patient's medication
gree of assistance required to perform the activity
schedule will ensure treatments are well-timed with
should be noted, since this significantly influences
respect to pain medications, and medications that in
the patient's individual effort. Second, if the patient's
terfere with a good treatment response, such as nar
status is unstable and oxygen transport is severely
cotics. The patient's clothing should not be restric
jeopardized, then monitoring a patient during stan
tive, and any lines, leads, and catheters should not be
dard care and procedures, such as turning the patient,
taut. Any equipment, monitors, and IVs need to be
ADLs, nursing and medical procedures, can provide
appropriately positioned to avoid disconnections or
an indication of the patient's physiological responses
mishaps. Mobilizing the patient in intensive care re
to mobilization and the capacity of the oxygen trans
quires positioning of the mechanical ventilator and
port system to meet the metabolic demands imposed.
other supports before moving the patient. The PT
No movement is too small. Any movement that is
must prepare personnel before moving a patient par
sufficient to perturb the oxygen transport system, no
ticularly if one or more assists are required. Despite
matter how minimal, is sufficient to elicit short- and
the number of persons assisting, the goal is usually
long-term gains.
to have the patient perform as much of the mobiliza

tion activity as possible. Even small degrees of phys
ical movement can provide sufficient stress to the
Monitoring
cardiopulmonary system to be beneficial.
Patients for whom mobilization is prescribed require
The basic components of the mobilization session
monitoring. Because of the stress to the oxygen trans
are comparable to the components of an exercise ses
port system that mobilization elicits, the following
sion described by the American College of Sports
variables in addition to the oxygen transport vari
Medicine for long-term training effects (Figure 17-1).
ables, are most useful to monitor: heart rate (HR),
Wherever possible, the session should include the
systolic and diastolic BP, RPP, RR, Sa02, arterial
following components: warm-up, steady-rate, cool
blood gases, ECG and subjective responses.
down, and recovery. These components are less dis

tinct when a patient has minimal functional capacity
or is being mobilized to remediate acute cardiopul
Mobilization Prescription
monary dysfunction. The rhythmic movement of
Prescribing a mobilization stimulus for its acute ef
large muscle groups is ideal. Prolonged static maneu
fects parallels the prescription of exercise for its long
vers are usually avoided particularly if the patient is
term effects with some important differences. In an
severely ill, because of their disproportionate hemo
acute patient, a mobilization or stimulus often results
dynamic response. The movements that are usually
in a greater response gain than such a stimulus in
considered when mobilizing a patient include: turn
subacute and chronic patients. In addition, to the
ing, sitting up, shifting, transferring, standing and
rapid favorable response an acute patient may have to
taking some steps. These can be extremely metaboli
acute exercise, the patient may exhibit a negative re
cally demanding for patients with significant acute
sponse just as quickly. Thus judicious monitoring of
cardiopulmonary dysfunction. Thus pacing the mobi

lization session allows the patient to rest between
treatment response in these patients is essential.

The scheduling of and preparation for a mobiliza
stages. The patient is reassured and encouraged to
tion session is crucial to the response that can be ex
relax and coordinate deep breathing and coughing
pected. The following conditions should be adhered
with the activity. Throughout the session, attention is
to as closely as possible; and their details should be
given to the patient's biomechanical alignment, and
recorded so that any factor that significantly influ
postural erectness and stability. Back extension or
ences the response to treatment can be identified.
body positioning minimizes slumping of the chest
The patient should be rested, not have eaten heavily
wall and compromised ventilation. In this way, chest
276
PART III
L """1J
0..
1
200r
.Q 1 ?
L.. 1 E
1 0
L..
1 8011
1
.:.c 1
'
1601-
g 1
U 1
Over time, exposure to an acute exercise stimulus

of an appropriate intensity, for an appropriate duration
.:.c
u
and at an appropriate frequency will stimulate long
120f-
I\
scribing the exercise stimulus results in less potent ef

fects and overprescribing results in an excessive,
:\ :
I
'
term exercise adaptation to that stimulus, Underpre
140r Trai in
100'
bility, or respiratory distress.
L..
"""1J
1
without arterial desaturation, hemodynamic insta
"""1J
1 .Q
deleterious effect. Although the latter may be toler

ated in the short run, the patient's well-being may be
'01
\ I
1'>"
jeopardized, such as suboptimal treatment rc"ponse,

ovettraining signs and symptoms, and injuries.
80
The duration of the session and the frequency of

sessions should be response-dependent rather than
60
time-dependent. The optimal mobilization threshold,

that is, physiological variables increased but not in
o
Start
exerCise
Time (minutes)
35 40
Stop
exercise
45
FIGURE 17-1
Components of the exercise training session (i,e., stretching,
warmup, training zone, cool down, and stretching,
excess of predetermined acceptable and safe limits,

should be maintained for as long as possible within
the patient's fatigue and comfort levels, and in the
absence of adverse responses. The mobilization ses
sion should be repeated as often as the patient can
tolerate, that is, exhibits a beneficial response or no
deterioration and adequately restores between treat
men ts. Treatmen t sessions for acu te cardiopu 1monary dysfunction are usually shorter and more
wall expansion is maximized in three dimensions.
common than for the patient with chronic cardiopul
The erect position is efficient and requires the least
monary dysfunction. The patient's condition changes
amount of energy to maintain. Less demand is placed
rapidly both with respect to improvement as well as
on the accessory muscles of respiration in erect sit
deterioration. Progression of mobilization for its im
ting, and this effect is enhanced further with leaning
mediate acute effects is usually rapid. Progression of
forward and support of the arms.
exercise for its long-term effects may occur every

several weeks whereas progression of mobilization
for its acute effects may range from as frequently as
Mobilization Training
every treatment to every few days. Over time, expo
With respect to oxygen transport, the purpose of
sure to a progressive mobilization stimulus leads to
the mobilization session is to elicit the immediate
long-term physiological adaptations throughout the
effects of an exercise stimulus, no matter how min
oxygen transport pathway,
imal. The optimal therapeutic dose of the stimulus

is based on the patient's presentation and history
and the specific parameters are determined by the
goals of the treatment and the acute effects of exer
Monitoring
The more acute the patient's condition, the more
cise that are indicated. The intensity of mobiliza
physiologic variables usually need to be recorded,
tion for many patients, for example, is that intensity
More objective measures are available in special care
that elicits optimal tidal volumes and VA, increased
and intensive care units (ICUs), Subjective responses
breathing frequency and air flow rates, enhanced
are also vital components of determining the ade
mucocil i a r y transport, and cough stimulation,
quacy of the mobilization stimulus; however, se
17
verely ill patients are often unable to respond effec
277
a response-dependent duration and frequency, there is
tively. Compared with the condition of chronic pa
a cumulative adaptive response to that repeated stimu
tients, the condition of acute patients tends to vary
lation, or a long-term, training response. In decondi
more within and between sessions and afterward,
tioned individuals with low functional work capacity,
which necessitates greater monitoring.
or whose oxygen transport system has been compro
Monitoring needs to be performed continuously
mised by disease, the exercise intensity associated
for patients for whom acute mobilization has been
with relatively low-intensity mobilizing activities such
prescribed. First, a baseline of the patient's resting
as bed exercises, moving in bed, sitting up, dangling
metabolic state needs to be established. Second, the
over bed side, transferring to chair, chair exercises,
metabolic responses to stimuli that perturb oxygen
and short walks with assistance, constitute a sufficient
transport and the lability of this response needs to be
stimulus for long-term adaptation. However, optimal
established. Obtaining such a profile provides some
adaptation only occurs if these activities are pre
indication of the upper limit of the target intensity
scribed at a requisite intensity, duration, and fre
range for mobilization. The target intensity range can
quency and the exercise prescription progressed com
be defined in terms of an upper and lower level of
mensurate with the individual's adaptation.
various physiologic variables. The most commonly
Mobilization activities prescdbed to enhance oxy
used are HR, BP, RPP, RR, perceived exertion or
gen transport, can be coupled with resistive muscle
breathlessness. Monitoring during nursing procedures
work to increase muscle strength and endurance (e.g.,
and other types of routine care provides an indication
weights, use of a monkey bar for moving in bed and
of the patient's functional capacity without having to
sitting up, manual resistive exercise, the use of wrist
conduct a modified exercise test.
or ankle weights, ergometry, and walking). Coordi
Alternatively, a mobilization or exercise challenge
nating postural, thoracic mobility and upper extrem
can be given. The patient's response is compared
ity exercises with inspiratory and expiratory efforts
with resting baseline measures. The quality as well as
can be effective in stimulating increased VT, and im
the immediacy of the response is documented. The
proved ventilation and perfusion matching. Chapters
characteristics of the quality of response is also
2l and 22 illustrate how such movement and breath
recorded. Is the response commensurate with the in
ing patterns can be coupled to maximize oxygen
tensity of the exercise stimulus? With cessation of
transport in neurological patients. Such coordinated
exercise do the responses revert to baseline? If so,
exercise, however, can also be used with patients
how fast? Do the variables return to baseline or re
with acute cardiopulmonary conditions. Isometric
main above baseline?
type exercises, postures that require increased muscle
The variables to be measured depend on the pa
work for stabilization, and activities that elicit the
tient (see Chapters I and 16). Most commonly, HR,
Valsalva maneuver produces disproportionate hemo
ECG, BP, RPP, RR, and subjective symptoms, are
dynamic responses, which could be detrimental. The
basic measures and indices of exercise response that
capacity of the patient to respond appropriately to
require no invasive procedures. At the other end of
these loads needs to be established beforehand.
the spectrum is the critically ill patient who has vari
In the management of acute cardiopulmonary dys
ous invasive lines and monitoring equipment, includ
function, the parameters of mobilization stimuli in
ing hemodynamic monitoring and intracranial pres
clude a relatively low intensity (although often per
sure monitoring. This patient requires more specific
ceived as intense by the patient), short duration, and
and frequent measures of oxygen transport.
high frequency of sessions. If the patient is severely

compromised (e.g., end-stage heart or lung disease)
interrupted or interval training is indicated. This type
Adaptation to an Acute Mobilization Stimulus
of training is characterized by either on-off exercise,
When an individual is exposed to repeated exercise
which allows for rest in between bouts of exercise, or
stress, that is, of a specific threshold intensity, and for
high-low intensity of activity. The volume of work
278
PART III
TABLE 17-2
Relationships Among Mobilization and Exercise Prescription Parameters
Activity and Relative Intensity
SESSION DURAnON
SESSION FREQUENCY
Mobilization activities
5to 20 min
Interval continuous aerobic exercise
5to 20 min
Continuous aerobic exercise (light)
5to 20 min
Continuous aerobic exercise (moderate)
20 to 40 min
20 to 40 min
I time per I to 2 hours to 4 to 6 times per day

I time per I to 2 hours to 4 to 6 times per day
I time per I to 2 hours to 4 10 6 times per day
2 to 3 times daily to once daily
Daily to 3 to 5times per week
Continuous aerobic exercise (heavy)
that can be achieved in an interrupted protocol by a
beds with lines and leads is crucial, because it is these
severely compromised patient, is significantly greater
patients who benefit significantly from exercise stress
than during continuous activity. With physiological
and also succumb most severely to its removal.
adaptation over time, the exercise period can be in
The goal is to adapt the patient to multiple ShOl1 mo
creased and the rest period decreased, and possibly
bilization sessions per day, as frequently as once per
eliminated. When high- and low-intensity exercise is
hour, and progressively increase the intensity of these
alternated the work load can be progressed by either
sessions, reduce the duration and conespondingly re
increasing the respective loads in each phase or by in
duce the frequency of sessions. Table 17-2 illustrates
creasing the duration of the higher load period. If the
the inverse relationsrup between mobilization and exer
patient has low functional work capacity but suffi
cise intensity, duration, and frequency of the sessions.
cient physiological reserve, adaptation can be rapid,

necessitating small, frequent progressions. As the pa
tient's aerobic capacity increases, the response gains
Multisystem Effects of Mobilization
are correspondingly smaller. If the patient has both
Acute exercise affects most organ systems in addition
poor functional capacity and poor physiological re
to the cardiopulmonary and cardiovascular systems.
serve capacity, progress would be correspondingly
The neurological system is primed for activity. To
slower and less significant.
counter postural perturbations, reflexes and postural
When mobilization activities are being prescribed
control adjustments are activated. Blood flow is in
to remediate acute cardiopulmonary dysfunction, par
creased to the working muscles commensurate with
ticularly in patients in the leU, extensive and often
the intensity and duration, and therefore overall meta
invasive monitoring is required. This permits detailed
bolic demand of the work. The endocrine system also
assessment, and ongoing metabolic assessment of the
adjusts to largely stimulate the cardiopulmonary and
patient's treatment responses and recovery. With
cardiovascular systems through a complex system of
these supports, mobilization and exercise can be pre
neurotransmitters to support the oxygen demands re
scribed effectively in these patients. Judicious moni
quired of the work rate imposed.
toring minimizes any inherent dangers of either under

or over prescribing the intensity of the exercise stim
ulus (Part II). Special consideration has to be given to
the fact that various monitoring leads, lines, and

lONG-TERM RESPONSES
catheters may restrict certain body positions and ac
In health, the long-term effects of exercise occur in re
tivities. Such encumbrances, however, do not pre
sponse to a specific and sufficient exercise stimulus to
clude most activities including ambulation. Moving
which the individual is exposed for a finite period. With
relatively immobile patients who are tied to their
respect to aerobic training or adaptation, the essential
17
279
Long-Term Physiologic Effects of Mobilization and Exercise

Cardiopulmonary System
Neuromuscular System
J,
Submaximal minute ventilation
Enhanced neuromotor control
Efficiency of postural retlexes associated with type
Reflex control
Movement efticiency and economy
of exercise
i Collateral ventilation
i
Pulmonary vascularization
Cardiovascular System
i Myocardial muscle mass
Musculoskeletal System
Muscle vascularization
Myoglobin
Myocardial efficiency
Exercise-illduced bradycardia
J Stroke volume
J,
J..
at rest and submuximal work rates
Resting heart rate and blood pressure

Submaximal heart rate. blood pressure, and rate
pressure product
Muscle metabolic enzymes
Glycogen storage capacity
Improved biomechanical efficiency
Movement economy
J..
Submaximal perceived exertion and breathlessness
Efliciency of thermoregulation
J..
Muscle strength and endurance
Orthostatic intolerance when performed in the up-
Ligament tensile strength
Muscle hypertrophy
right position
Maintain bone dellSity
Hematologic System
i Circulating blood volume

i Optimize number of red blood
Endocrine System
i Efficiency
cells
of hormone production and degradation
to support exercise
Optimize hematocrit
J..
Cholesterol
Immunological System
J..
Blood lipids
Resistance to infection
Central Nervous System
Integumentary System
Sense of well-being
i Efficiency
Concentration
of skin as a heat exchanger
Sweating efficiency
training parameters appear in the box above. As adapta
tion and hemodynamic responses to submaximal exer
tion to the exercise stimulus occurs, each step in the
cise are decreased. The subjective experience of exer
oxygen transport system becomes more efficient facili
cise stress is also reduced. These training effects are
tating oxygen delivery, uptake and extraction at the cel
commensurate with increases in the efficiency of oxy
lular level. The long-term effects of aerobic exercise
gen transport at each step in the pathway.
are summarized in the box above. In addition to an in
As the body adapts to the exercise training stimu
crease in maximal oxygen consumption, training results
lus, the intensity needs to be increased to elicit fur
in an exercise-induced bradycardia and increased stroke
ther training benefit. This is the basis for the physio
volume at rest and a reduction in the physiological de
logical adaptation to an exercise training stimulus.
mands of submaximal work rates. Specifically, ventila-
Depending on the goals of the exercise prescription, a
280
PART III
Chro1lic Pathophysiological Conditions That Benefit From the Long-Term Effects of Mobilizatio1l and Exercise
Cardiovascular Conditions
Neurological Conditions-<o1l't
Congenital heart disease
Multiple sclerosis
Acquired heart disease
Poliomyelilis
Postsurgical heart conditions
Endocrine Conditions
Angina
Thyroid dysfunclion
Hypertension
Diabeles mellitus
Hyperlipidemia
Neoplastic Conditions
Hypercholesterolemia
Conditions Requiring Organ Transplantation
Congesti ve heart failure
Pre- and postsurgical siages
Heal1 transplantation
Musculoskeletal Conditions
Peripheral vascular disease
OSleoarthrilis
Cardiopulmonary Conditions
Rheumatoid al1hrilis
Chronic obstructive pulmonary disease
Ankylosing spondylitis
Chronic ventilatory failure
Osteoporosis
Interstitial lung disease
Connective Tissue Conditions
Asthma
Systemic lupus erythelllatosis
Cystic fibrosis
Nutritional Disorders
Postthoracotomy conditions
Obesity
Lung transplantation
Anorexia
Neurological Conditions
Other Systemic Conditions
Siroke
Chronic fatigue syndrome
Parkinson's disease
Chronic depression
Quadriplegia
Alcoholism
Paraplegia
P regnanc y
Cerebral palsy
Renal disease
Down syndrome
Liver disease
decision is made after several weeks whether the ex

ercise intensity needs to be increased to further in
EXERCISE TESTING AND TRAINING

IN PATIENT POPULATIONS
crease aerobic capacity, or whether a maintenance
Numerous conditions including nonprimary car
program is indicated. The training program is pro
diopulmonary conditions have been shown to bene
gressed by establishing a new exercise intensity usu
fi t from the long-term effects of aerobic exercise
ally based on 70% to 85% of the maximal heart rate
(see box above). For eacll patient, however, with
achieved in a repeat of the initial exercise test.
each of these conditions, the exercise prescription
17
Common Indications for Exercise
Relative and Absolute Contraindications
Testing in Patient POpuUltiOIlS
to Exercise Testing
Diagnosis
Absolute Contraindications
Coronary artery disease and vasospasm
Congestive heart failure (CHF)
281
Hyperreactive airway disease
Acute EKG changes of myocardial ischemia
Cardiac vs. pulmonary limitation to exercise
Unstable angina
Ventricular or dissecting aneurysm
Assessment
Ventricular tachycardia
Maximal functional work capacity
Multifocal ectopic beats
Chest pain
Repetitive ventricular ectopic activity
Dyspnca
Untreated or refractory tachycardia
Endurance
Supraventricular arrhythmia
Ability to work
Recent thromboembolic event (pulmonary or other)
Employmelll options
Uncontrolled asthma
Cardiopulmonary and cardiovascular conditioning
Uncontrolled heart failure
Movement economy
Pulmonary edema
Limitations to exercise
Uncontrolled hypertension (above 250 mm Hg

systolic, 120
Effect of medication
mm
Hg diastolic)
Acute infections
Adequacy of diabetes management
Relative Contraindications
Prescription
R e c e n t m y ocardial inf a rction (M!) (l e s s than
Exercise program
4 weeks ago)
Medications
Aortic valve disease

Severe cardiomegaly
Pulmonal), hypertension
differs. Comparable with prescribing mobilization

in acute conditions, prescribing exercise for long
Resting tachycardia
Resting electrocardiogram (ECG) abnormalities
term adaptations is based on the patient's presenta
Poorly controlled diabetes
tion, history, premorbid status and conditioning
Severe electrolyte disturbance
level, lab and investigative reports related to physio
Severe systemic hypertension
logic reserve capacity, the exercise test and the
Significant conduction disturbance
goals of the exercise prescription.
Complete atrioventricular block

Fixed rate pacemakers
Exercise Testing
Acute cerebrovascular disease (CVD)
Exercise testing no matter how modified can pose a
Respiratory failure
potential risk to the patient, therefore exercise testing
Left ventricular failure
must have clear indications, and any contraindications
Epilepsy
must be ruled out. The indications for exercise testing

are numerous (see box above, at left). They range
from quantifying maximum functional capacity to as-
Adapted from Jones. N.L. (1988). Clinical Exercise Testing.

(3rd Ed.). Philadelphia: WB Saunders.
282
PART III
TABLE 17-3
Subjective Scales of Exercise Responses Based on the Borg Scale of Rating of Perceived Exertion
0
0.5
1
2
3
4
5
6
7
8
9
10
PERCEIVED EXERTION
BREATHLESSNESS
DlSCOMFORTIPAIN
Nothing at all
Nothing at all
Nothing at all
Nothing at all
Very very weak
Very very light
Very very weak
Very very light
FATIGUE
Very weak
Very light
Very weak
Very light
Weak
Light
Weak
Light
Moderate
Moderate
Moderate
Moderate
Somewhat strong
Somewhat hard
Somewhat strong
Somewhat hard
Strong
Hard
Strong
Hard
Very strong
Very heavy
Very strong
Very heavy
Very very strong
Very very hard
Very very strong
Very very hard
Maximal
Maximal
Maximal
Maximal
sessing endurance during low level ADLs. Contraindi
the ratings can be used to compare the patient's sub
cations are classified as either relative or absolute (see
jective exercise responses over repeated tests.
box on p. 281, at right). Absolute contraindications
Depending on the functional impairments and ca
prohibit the safe conduction of an exercise test,
pacity of the patient, the exercise test can be one of
whereas the presence of relative contraindications re
various types depending on the objective of testing
quires that the test, protocol, physiological variables
and potential training. If exercise training is an objec
monitored, or the end point of the test be modified.
tive of the exercise test, the activity used in the test
Both the indications for the test and any contraindica
should be comparable with that to be used in training.
tions must be clearly established before performing an
Physiological responses and adaptation to exercise
exercise test.
are highly specific to the training stimulus (the speci
The guidelines used to test and train healthy peo
ficity of exercise principle). Thus if walking is to be
ple with no disease states are not directly generaliz
the training activity, the test should be a walking test
able to chronic medically-stable patient populations.
rather than cycling.
Because of functional impairments in these patients
There are numerous variants of standard exercise
(e.g., secondary to cardiopulmonary, cardiovascular,
tests (Table 17-4). These are categorized as continuous
neuromuscular, and musculoskeletal dysfunction) ex
and interrupted tests. Continuous tests include maxi
ercise testing and training must be modified. More
mal and submaximal incremental tests and steady-rate
over, patients who are physically challenged experi
tests, and interrupted tests include maximal interval
ence more subjective symptoms in response to
and submaximal interval tests. Interrupted tests are de
exercise compared with healthy people, therefore
signed for patients with low functional work capacity
monitoring the subjective responses to exercise is es
who cannot sustain prolonged periods of aerobic exer
sential. The Borg scale of rating of perceived exertion
cise. These patients can perform more work over time
can be modified for clinical use to score breathless
when the work load is administered in an interrupted
ness, discomfort, pain, and fatigue (Table 17-3)
or periodic manner. Specifically, the test alternates
(Borg, 1970; 1982). If the endpoints of the scale are
fixed periods of work and rest, or high and low intensi
well-described and understood by the patient, then
ties of exercise. The proportions of work-to-rest or
17
283
TABLE 17-4
Exercise Tests That Can Be Applied to Patient Populations
TEST TYPE
INDICA TlONS
Continuous Tests
Maximal
. Generally medically-stable patient

No significant musculoskeletal abnormalities
Test maximal functional capacity
Basis for aerobic exercise program
Incremental
Incremental work rates usually 2 to 5 minutes in duration
Steady-rate
Endurance test at a given work rate; usually a comfortable walking or cycling speed
Submaximal
For patients for whom maximal testing is contraindicated
Incremental
Approximate maximal exercise testing

Test of near maximal functional capacity or some significant propOition of maximum
Steady-rate
Establish baseline of response to steady-rate exercise usually at 60 to 75% of predicted

maximum heart rate
Establishes an index of endurance, cardiopulmonary conditioning and may give an
index of movement economy
Interrupted Tests
Maximal or Submaximal
Establish level of functional capacity in patients with extremely low functional

work capacity
On-off protocol or high-low intensity protocol, such as 5 min on to I min off; alternate
high- and low-intensity exercise in cycles, such as I minute high to 15 seconds low
high-to-low exercise intensity is set according to the
treadmill or ergometer, which jeopardizes stringent
patient's level of impairment. One patient, for exam
test control (Dean and Ross, 1992a).
ple, may be able to tolerate 3 to 5 minutes of relatively
Like other diagnostic or testing procedures, the va
high intensity work to I to 2 rrlinutes of low-intensity
lidity and reliability of the exercise test depend on the
work, whereas another patient may be able to tolerate
quality of the procedures used. The preexercise test
only 1 minute of low intensity work to 10 to 20 sec
conditions and the preparation and testing procedures
onds of rest.
need to be standardized (see boxes on pp. 284-285).
For maximal standardization and the capacity to
The test is terminated as soon as the sign or symptom
perform more comprehensive monitoring, stationary
criteria for terminating the test is reached or the crite
exercise modalities such as the treadmill, ergometer,
ria for prematurely terrrlinating the test is reached (see
or step are recommended. However, there may be in
box on p. 286). Recording the test conditions and pro
dications to perform an exercise test without a modal
cedures in detail is essential. An example of an exer
ity, such as the 12-minute walk test or some variant
cise test data sheet that can be modified to any testing
like 6 or 3 minutes (McGavin, Gupta, and McHardy,
protocol using an exercise modality is shown in the
1976). Standardization of such tests, however, is
box on p. 287, at left. Many patients are unable to be
more difficult. Practice has a significant effect on the
exercise tested using a modality. These patients can
results of the 12-minute walk test, thus this test needs
walk on a marked circuit. An example of an exercise
to be repeated several times to achieve a valid test.
test data sheet is shown in the box on p. 287, at right.
Also, the instructions for this test are less well
Systematic and detailed record-keeping will maximize
standardized clinically compared with those for the
the test validity and its interpretation as well as ensure
284
PART III
Preexercise Test Conditions

Establish the indications for an exercise test.
Determine absolute and relative contraindications to conducting an exercise test.
Ensure patient is free of any acute illnesses including influenza and colds for 48 hours.
Ensure patient understands the purpose of the test and provides signed consent.
Ensure patient has not eaten heavil y . has avoided caffeinated beverages and has refrained frolll smoking for at least 3
hours before testing.
Ensure patient is rested and has not e x ercised, or is not being excessively exerted for at least 24 hou rs before testing .
Ensure patient is app ro priate ly dressed, for exampl e , shorts, n onbindi n g clothes, short-sleeve shil1. socks, running or
walking shoes that have proper SliPPOI1, and secured laces or fastenings.
Orthoses should be worn unless the test is evaluating changes in functional capacity with and without nn orthosis.
Ensure patient understands the subjective rating scales and is able to read them when held at an nppropr i ate distance.
Select the type of exercise test, the pr otoc 01 and the exercise test termination criteria beforehand.
Ensure the patient is familiar with and has practiced performing the test
or
test activity preferably before the test day
to reduce arollsal, improve movement efficiency . and maximize test validity.
that the same procedures are used in follow up tests
exercise capacity and are unable to tolerate being
thereby maximizing the abi Iity to compare test results.
tested on an exercise modality. A major disadvan
It is imperative that retests are conducted comparably
tage, therefore is that the patient cannot be as com
in every respect to the original test with respect to pa
prehensively monitored. Thus patients need to be se

lected carefully to undergo a 12-minute walk test or
tient preparation and the procedures.
one of its variants.

Knowledge of the patient's functional ability
Exercise Tests and Protocols
based on verbal report can be useful and can serve as
Depending on the functional capacity of the patient,
a guideline for determining the exercise test, its para
the exercise test can be a continuous maximal, sub
meters, and what tile patient's termination criteria
maximal incremental or steady-rate, or an interrupted
should be. Although these verbal reports do not re
maximal or submaximal test. The protocol for the test
place an exercise test, they can be used as an adjunct.
and the end points to be used in terminating the test
The oxygen cost diagram is shown in the box on p.
are determined beforehand depending on the indica
290, at left. This visual analog scale is constructed of
tions for the test and the objectives. Some commonly
a 100 mm line; the high end of the scale represents
used protocols are shown in Figure 17-2 along with a
strenuous activity, that is, walking briskly uphill, and
comparison of the energy expenditure of the various
the low end of the scale represents no activity, or
work stages in their protocols.
sleep. The patient crosses the line at the point where
The 12-minute w a lk test a n d i t s varian ts, 6
breathlessness does not allow continuation when at
minute- and 3 minute-walk tests, were designed to
the patient's best. Figure 17-3 shows an incremental
test patients with lung disease (McGavin, Gupta,
ladder of workloads associated with step increments
and McHardy, 1976). These tests have been favored
in metabolic cost, (hat is, multiples of resting or near
clinically, because they are functional and do not re
resting metabolic rate (resting metabolic rate
quire exercise equipment. However, these tests are
MET, or 3.5 ml 02/mink

i g
often used for patients who have extremely impaired
of metabolic costs ranges from very light to very
17
285
PreparaJion and General Procedures for an Exercise Test

Preparation
Patient ch,mges into exercise clothes and shoes (not new); ensure laces are secure.
If the ergometer is used. the seat-to-pedal distance must be established before the test, and the seat should be adjusted
to allow for 15 degrees or knee extension when the foot is lowennost in the pedal in the revolution cycle; the knee
must not extend fully.
Patient sits quietly in a supported chair to establish a resting baseline.
Monitors are allached (e.g., heart rate, ECG, blood pressure cuff, pulse oximeter) and the subjective rating scales are
explained.
Testing procedures are explained and demonstrated; the patient has an opportunity to answer questions.
General Procedures
Unnecessary conversation and interaction with the patient is kept to a minimum throughout all stages of the test, in
cluding postexercise recovery, to optimize the validity of the measurements and the test results overall.
Resting baseline measures are taken over 5 minutes or ulltil they have plateaued.
Patient stands
011
treadmill or sits erect on cycle ergometer with feet securely strapped into place on the pedals; the
metatarsal heads should be positioned comfortably over the pedals.

Patient uses two fingers for balance on one side if possible when walking on the treadmill rather than a hand grip, or
ir on the ergometer, not the excessively grasp the handle bar.
Additional baseline measures are recorded in this position for 2 to 3 minutes or until the baseline is stable.
The test timer is started.
The warm-up portion of the protocol begins.
The selected protocol is calTied out.
Patient is monitored objectively and subjectively at least every couple of minutes throughout all stages of the test. in
cluding postexercise recovery.
The test is terminated when the preset exercise test termination criteria or any of the criteria for prematurely terminat
ing an exercise test are reached.
The cooldown begins.
When the cooldown portion of the protocol is complete, the patient moves to the supported chair for the postexercise
recovery phase with legs slightly elevated and uncrossed.
Postexercise recovery continues until resting baseline measures have been reached or are within 5% to 10%.
Obtain a report from patient about how patient feels.
Disconnect the monitoring equipment.
Continue to observe patient for any untoward postexercise signs or symptoms.
heavy actIVItIes. One limitation of such charts on
Monitoring
metabolic costs of various activities and exercise is
Common variables measured during an exercise test in
that they can only be used as a rough g uide in pa
clude HR, ECG, systolic and diastolic BP, RPP, RR,
tients with cardiopulmonary compromise, as they do
Sa02 and subjective responses such as perceived exer
not take into consideration the increased work of
tion, breathlessness, discomfort, pain, and fatigue. Mea
breathing and work of the heart observed in patients
sures are taken every few minutes after the patient has
with cardiopulmonary dysfunction.
been exercising at a given intensity for a few minutes.
286
PART III
Criteria/or Prematurely Terminating an Exercise Test

Miscellaneous
Wish of individual for any reason
Failure of monitoring equipment
General Signs and Symptoms

Fatigue
Lightheadedness, confusion, ataxia, pallor. cyanosis, dyspnea, nausea, or peripheral vascular insufficiency
Onset of angina
ECG Signs
Symptomatic supraventricular tachycardia
ST displacement (3
mm) horizontal or downsloping from rest
Ventricular tachycardia
Exercise-induced left bundle branch block
Onset of second- or third-degree atrioventricular block
R=wave on T=wave premature ventricular contractions (one)
Frequent multifocal premature ventricular contractions (frequent runs of three
or
more)
Atrial fibrillation when absent at rest

Appearance of a Q wave
Cardiovascular Signs
Any fall in blood pressure below the resting level
Exercise hypotension
(> 20 mm Hg drop in systolic blood pressure)
Excessive blood pressure increase (systolic
220 or diastolic
110 111111 Hg)
Inappropriate bradycardia (drop in heart rate greater than 10 beats/minute with increase or no change ill work load)
Adapted from the American College of Sports Medicine, (1994). Guidelines for exercise testing and prescription.
(6th ed.). Philadelphia: Williams and Wilkins.
Adapted from Jones, N.L. (1988). Clinical Exercise Testing. (3rd Ed.). Philadelphia: WE Saunders.
Exercise Training Prescription
tion of the heart rate response, or some other response,
One of the most conunon indications for exercise test
to a maximum or near maximum work i'ate that was
ing is to establish whether a training program is indi
safely tolerated during the exercise test. The training in
cated and, if so, what the training parameters should be.
tensity for a patient who is able to tolerate several in
The components of exercise training for patients is the
cremental work stages on a graded exercise test may be
same as for healthy people, specifically, selection of the
optimal between 70% to 85% of the peak heart rate
type of exercise. and its intensity, duration, and fre
achieved in the test. A patient who is unable to tolerate
quency; and the course of training and its progression.
a couple of increases in work stage, is more likely to
The selection of the type of exercise for training and
benefit from an exercise intensity range of 60% to 75%
that used in the exercise test, is based on the objectives
of the peak heart rate achieved. In some patients. heart
of training. The intensity is usually set at some propor
rate is an invalid indicator of exercise intensity either
17
Exercise Test Data Sheet for Treadmill
Exercise Test Data Sheet for a Walk Test
or Ergometer
on a Circuit
Patient name:
Patient name:
Patient number:
Patient number:
Date:
Date:
Weight (kg)
Weight (kg)
Height (em)
Height (cm)
Body mass index
Body mass index

Reason for test:
FEY\
Reason for test:
Type of test:
Fye
FEY\lFye
FEY\
Fye
Type of test:
FEY/Fye
Minute
287
Work rate
Minute
HR BP RPP RR Sa02 RPE
speed/grade
Work rate
HR BP RPP RR Sao2 RPE
speed/grade
(work/rpm)
(work/rpm)
Review of preexercise checklist
Review of preexercise checklist
Level of hand support
Level of hand support
Use of orthoses: type and side
Use of orthoses: type and side
How often docs the patient experience the level of
How often does the patient expelience the level of
exertion reached in the test (e.g., lx/ wee k ,
exertion r e a c h e d in t h e test (e.g., I x/week,
lx/month, 3x/day. etc.)
lx/month. 3x/day. etc.)
Reason for test termination
NOTE:
Reason for test termination
'Relevant notes and comments include abnormal ECG
NOTE:
'Relevant notes and comments i nclude abnormal ECG
changes, comments by patient, observations about coordination,
changes, comments by patient, observations about coordination,
and anxiety.
and anxiety.
I\)
CD
CD
Functional
class
Clinical
status
02 cost
ml/kg/minute
::0
>-l
-
Bicycle
Bruce
1 Watt
60 KPDS 3=minute
stages
mph %Gr
For
=
2::-
Normal
and
1
0
Q)
C>
0
c
0
56.0
52.5
49.0
45.5
42.0
38.5
1-
35.0
>..
-
-0
31.5
28.0
Q)
...r:::.
r->..
24.5
\..
2
3
4
5.5
.2
c
Q)
\J
Q)
V)
"]
'E
u
0"5
E
.2
Cl..
>--V)
21.0
17.5
16
15
14
13
12
11
10
9
8
7
14.0
10.5
3.5
7.0
KPDS
1500
1350
1200
1050
900
750
600
450
300
150
5.0
%Gr
at
3.3 MPH
1 20
4.2
18
1 16
3.4
2.5
14
12
1.7 1 10
1
1.7 1
1.7
Balke
Ware
Kattus
ETS
"slow"
Ellestad USAFSam
McHENRY Stanford
USAFSam
3/2/3=
minute
stages
Imph %Gr
4
4
4
1 18
1 14
1 10
1
1
15 mph %Gr
21
20
19
18
17
16
15
14
13
12
11
10
9
8
7
6
5
4
3
2
15
1 10
23
22
22
10
10
l-
1 10
1.7
10
1 10
"0
=
3"
o
::J
.,
'<
26
25
24
3.3
1 25
3.3
3.3
l 15
mph %Gr
3.3
1 10
3.3
1 21
3.3 1 18 22.5
20.0
3.31 15 t---
mph %Gr
1 25
1 20
1 15
1 10
2
2
2
3.3
2.0
1
3.3 1
3.3 1
33
.
20
.
17.5
12 1 15.0
9 12.5
10.0
6
7.5 14
5.0 10.5
2.5 7
0.0 3.5
FIGURE 17-2
permission from Froehlicher YF: Exercise and the heart, ed 2, Chicago, 1987, Year-Book.)
'"
;:;.
e:..
>-l
"0
'<
::J
-.lL
-.!L..
8
3
1
Oxygen cost of work stages of some commonly used exercise test protocols. (Reprinted with
'<
::J"
...
.,
33
.
20
(j
.,
Q.
%Gr %Gr
at
at
2
3
mph mph
2=or3=
minute
stages
1 =minute
stages mph %Gr
};
Q)
\J
c
Q)
Cl..
Q)
\J
>..
:c
70 kg
bod
weig t
Treadmill protocols
METS ergometer
"
.,
0(
...
a
o
5l
17
FIGURE 17-3
Energy cost in METS of activity and exercise.
(From Underhill, SL
et
at: Cardiac nursing, ed 2,
Philadelphia, 1989, JB Lippincott.)
9 METs
10 + METs
Swimming
(crawl,55
yard/minute
Skiing, fast
downhill
Walking up
hill,5 mph
8 METs
7 METs
Cycling, 13 MPH
Swimming, 40 + yard/ minute
Level ski touring, 4 MPH
Cross-country running
Walking on level,5 to 6 mph
6 METs
5 METs
Shoveling snow
Digging vigorously
Sawing wood
Tennis
Skiing
Walking on level, 5 mph
4 METs
3 METs
Self-care
washing
dressing
Gardening (weeding)
Ballroom dancing
Canoeing, golF
Bedmaking
Woodworking (drilling, sawing)
Walking on level ground, 4 mph
2 METs
Light calisthenics
Driving (can be more MET under stressful conditions)
light housework (sweeping, ironing, mopping)
Walking, 2.2 mph
1 MET
Resting
Eating
Writing
Handsewing
Knitting
Very light activity
Light activity
Moderate to heavy activity
289
Very heavy activity
290
PART 1II
Oxygen Cost Diagram Used to Assess
Patient's Check List Before Exercise Testing or
Breathlessness on Exertion
Training Session
Brisk walking uphill
Feeling well over the past 48 hours
Medium walking uphill
No cold or influenza
No temperature
Brisk walking on the level

Slow walking uphill
No unaccustomed muscle or joint discomf0l1 or pain

Heavy shopping
No chest tightness or pain
Medium walking
No unaccustomed breathing difficulty or fatigue

Adequate night's sleep
Bedlllaking
Have not eaten heav i ly within past 3 hours
Light shopping
Best time of day
Washing yourself
Slow walking on the level
Wearing or using orthoses, walking aids. and devices
Sitting
Clothing appropriate for exercise conditions. such as

indoors
Standing
well-fitting and secured laces <double-knotted)
Have water within reach

Taken preexercise medications at specified time
M, Naoe H, and McHardy GJR: Dysp
nea, disability, and distance walked: Comparison of estimates of ex

ercise performance in respiratory disease. 8M}
outdoors
Appropriate socks and footwear that is comfonable.
Sleeping
From McGavin CR, Anvinli
or
Have nitroglycerine within reach (cardiac patients)
1:822-823, 1978.
Have inhaler within reach (pulmonary patients)

Have sugar supply within reach (diabetics)
because of the pathology or medications (Dean, 1993;
ExerCise Training
Dean and Ross, I 992b). Thus other responses such as
General procedures
blood pressure, arterial saturation, or subjective para

rating of perceived exertion or breath
Before an exercise session, the patient needs to review
lessness can be used. The duration and frequency of the
a checklist to ensure that exercise is not contraindi
exercise program are established based on the patient's
cated on that day. This is particularly important for
meters such
as
functional capacity, physiological reserve capacity and
patients whose conditions change rapidly or whose
exercise responses (see Table 17-2, for general guide
disease course tends to fluctuate, such as multiple
lines). Patients with low functional capacities but with
sclerosis, cystic fibrosis, and chronic fatigue syn
adequate physiologic reserve capacity respond to a
drome. The box above includes guidelines in prepara
training stimulus quickly (short training course), thus
tion for exercise testing and training sessions. Such a
need to be progressed accordingly. Patients with low
checklist, however, must be tailored to each patient.
functional capacities, however, with limited physio
Specific procedures
logic reserve capacity, adapt more slowly (long training

course). The shorter the training course, the sooner a
In the supervised setting, the general procedures
retest is indicated to progress and reset the training pa
used in exercise training are comparable to those
rameters. To ensure that the patient continues to be
used for testing. Specifically, the patient prepares
trained safely and optimally, the training parameters
for the training session in a standardized manner,
should be progressed based on an exercise retest.
and is monitored according to his or her condition.
17
The components of the session are the same with re

spect to a warm-up, cool-down, and recovery. The
main part of the exercise program, however, will
usually be steady-rate or interrupted exercise. Vary
ing work rates may be indicated for some patients.
In the majority of situations, the goal is to transfer
the responsibility of surveillance and monitoring
from the PT to the patient. Depending on the pa
tient's pathology and ability to learn how to monitor
291
Physiological Consequences of Bed Rest

I. Fluid volume redistribution
Decreased plasma and blood volume
Decreased total heart and left ventricular volumes
Increased hematocrit and hemoglobin
Diuresis and natriuresis
II. Muscular inactivity
exercise responses accurately, this process may take
Insulin resistance
varying amounts of time.
Loss of muscle mass
Monitoring
Loss of muscle strength
L(lSS of muscle endurance
For safety reasons and ensuring that the patient is
III. Altered distribution of weight and pressure
within the target training range of the variables selected
Venous stasis
to set exercise intensity, the patient must be closely
Urine stasis, retention. tendency toward calculus
monitored. This is particularly true if the patient has
formation
any risk of untoward or adverse reactions to exercise. If
Hyperca1ciuria
patients are considered to be at any fisk, then exercise

training should only take place in a supervised setting.
Stable patients may begin an exercise program in a su
pervised setting, but with training and education they
usually can be transfelTed to an unsupervised setting.
Education includes self monitoring of exercise re
sponses, maintaining exercise intensity within the ap
Bone demineralization
Local skin changes
IV. Mixed or unknown etiology

Increased heart rate at rest and at all levels of
activity
Decreased resting and maximum stroke volume
propriate limits, and keeping a record of the details of
Decreased maximum cardiac output
their exercise sessions. When the patient is safely carry
Increased venous compliance
ing out the exercise program independently in the com
Increased risk of venous thrombosis and throm
munity some mechanism is needed to follow-up on the

patient's progress. If the objective is continued condi
tioning, then the patient needs to be rescheduled for a
retest. If the patient is on a maintenance program, the
PT is responsible for reminders about exercise and in
boembolism
Decreased orthostatic tolerance
Cardiovascular deconditioning
Decreased V02 max
jury precautions, and notifying the PT or physician if
Anorexia
significant adverse effects are observed.
Constipation
Increased sensitivity to thermal stimuli; increased
sweating and hyperemia
Alteration in clearance of some drugs
PREVENTATIVE EFFECTS
Increased anxiety, hostility, depression
Humans are designed to be upright and moving.

When they are recumbent and inactive, gravitational
stress (the vertical gravitational gradient) and exer
cise stress are removed. Bed rest is one of the most
Increased auditory threshold

Increase in focal point. decreased near point
of visual acuity
commonly used yet unquestioned therapeutic prac

tices. Despite its widespread acceptance, the body po
From Underhill SL. Woods SL. Froehlicher ES, and Halpenny
sitions it promotes, namely, being supine and immo-
Cardiac 1Illl'.I'illg,
ed 2. Philadelphia,
1989,18
Lippincotl.
CJ:
292
PART III
bile, is nonphysiologic (Chapter 18). The harmful se
1951). Thus alveolar-arterial oxygen difference and
quelae of this posture have been well-documented
arterial oxygen tension are reduced during periods
(Dean and Ross, I 992b) yet the more severely ill the
of bed rest (Cardus, 1967; Clauss, Scalabrini, Ray,
patient, the more-confined that individual is to the
and Reed, 1968; Ray et aI, 1974). Closing volumes
bed, and the greater the risk of multisystem complica
are increased precipitating arterial desaturation in
tions (see box on p. 291).
recumbent positions.
The immediate effects of immobility that are ob
Cardiovascular sequelae of prolonged recumbency
served are those associated with recumbency; these
include an increase in resting and submaximal heart
are followed within 24 to 48 hours by cardiopul
rate (Deitrick, Whedon, and Shorr, 1948), a decrease
monary and musculoskeletal changes. Within 24
in maximum oxygen uptake (Saltin et ai, 1968), and a
hours, significant fluid shifts occur and blood vol
decrease in total blood volume, plasma volume, and
ume is reduced by 10% to 15%. Within days, these
hematocrit (Deitrick et aI, 1948; Saltin et aI, 1968;
effects can significantly impair oxygen transport.
Friman, 1979). The combination of an increase in
These systemic effects are more profound in pre
blood viscosity and a decrease in venous blood tlow
mature infants, young and older people, smokers,
results in an increased risk of thromboemboli (Lentz,
obese and deconditioned individuals. These effects
1981; Wenger, 1982).
are further compounded when a patient has either
Musculoskeletal changes that occur with bed rest
primary or secondary cardiopulmonary and cardio
deconditioning include loss of muscle mass and
vascular compromise. The less aerobically fit an
strength, muscle and ligament shortening, joint contrac
individual, the less physiological reserve is avail
tures, skin lesions, and decubitus ulcers (Rubin, 1988).
able in the cardiopulmonary and cardiovascular
CNS changes include slowed electrical activity of
systems. In the event of a medical or surgical in
the brain, emotional and behavioral changes, slowed
sult, such a patient will have an increased risk of
reaction times, sleep disturbances, and impaired psy
morbidity and mortality than a more fit counter
chomotor performance (Rubin, 1988; Ryback, Lewis,
part. Thus tl1e importance of aerobic fitness cannot
and Lessard, 1971; Zubeck and MacNeil, 1966).
be overemphasized.
Metabolic changes that occur during periods of
A primary effect of mobilization and exercise on
bed rest include reduced insulin sensitivity and glu
the cardiopulmonary system is enhanced mucocililary
cose intolerance (Mikines, 1991), increased calcium
transport and clearance (Wolff, Dolovich, Obminski,
excretion from bone loss and increased nitrogen ex
and Newhouse, 1 977). Frequent body position
cretion secondary to protein loss from atrophying
changes are essential to maintain optimal bronchial
muscle (Deitrick et ai, 1948; Donaldson, Huliey, and
hygiene and avoidance of pooling and stagnation of
McMillan, 1969; Hulley, Vogel, Donaldson, Bayers,
bronchial secretions, hence, airway obstruction and
Friedman, and Rosen, 1971).
airt10w resistance (Chapter 18).
Bed rest has been associated with a reduction in
The primary effects of bed rest on the cardiopul

monary system result from recumbency. Pulmonary
antibody counts, hence an increased risk of infection

(Ahlinder, Birke, Norberg, and Plantin, 1970).
sequelae of recumbency included reduced lung vol
Of clinical significance is the fact that car
umes and capacities, particularly functional residual
diopulmonary and cardiovascular deterioration
capacity (FRC), residual volumes (RV) and forced
occur at a faster rate than musculoskeletal deterio

'
ration, and that the rate of recovery from the ill ef
expiratory volumes (FEVs) (Blair and Hickman,

1955; Craig, Wahba, Don, Couture, and Becklake,
fects of bed rest is generalJ y slower than the rate of
1971; Hsu and Hickey, 1976; Powers, 1944; Risser,
impairment (Kottke, 1966; Sandler, Popp, and Har
1980; Svanberg, 1957). A reduction in FRC in
rison, 1988).
supine position compared with the sitting position
The negative effects of bed rest are accentuated in
has been attributed to both a decrease in thoracic
older adults (Harper and Lyles, 1988), and are likely
volume and an increase in thoracic blood volume,
to further compound the oxygen transport and other
hence pulmonary venous engorgement (Sjostrand,
deficits of patients with pathology.
17
293
tural alignment, stiffness, and soreness. Bed rest allo
HAZARDS OF BED REST

The literature on the negative sequelae of bed rest has
been unequivocal for 50 years (Chobanian, et aI.,
1974; Dean and Ross, 1992b; Dock, 1944; Harrison,
1944; Ross and Dean, 1989). Thus the use of bed rest
as a primary medical intervention requires consider
able justification. The recumbent, immobile positions
associated with bed rest adversely affect every organ
system and palticularly compromise oxygen transport
by its direct negative effects on the cardiopulmonary
and cardiovascular systems. This is particularly signifi
cant in that in conventional patient management there
is a direct relationship between how sick the patient is
and the amount of time confined to bed. In addition,
the musculoskeletal and neurological systems are ad
versely affected.
The cardiovascular sequelae of bed rest primarily
include the loss of fluid volume regulating mecha
nisms, diuresis, and loss of plasma volume. In turn,
the hematocrit is increased, and the risk of develop
ing deep vein thromboses and thromboemboli is in
creased. This is exacerbated by increases in blood
viscosity, platelet count, platelet stickiness, plasma
fibrinogen (Browse, 1965), and stasis of venous
blood flow. The work of the heart is increased in the
immobile, recumbent patient as is the work of breath
cates various body parts to being weight bearing.

Skin breakdown most commonly occurs over boney
prominences such as the sacrum, trochanters, elbows,
scapulae, and heels. Muscles imbalance may result
from poor postural alignment. Patients are at risk of
bone demineralization. Of particular importance in
older populations, patients with disabilities, post
menopausal women, and patients on steroids is cal
cium loss secondary to bed rest or sedentary lifestyle.
Bed rest affects psychological status. Patients may
become depressed, sensorily deprived, or develop a
psychoneurosis with prolonged bed rest.
The evidence supports the following:
I. Evidence supporting the wide spread use of bed
rest as a therapeutic intervention is lacking.

2. Currently the use of bed rest is excessive and
nonspecific.
3. Bed rest has multisystem negative effects and
therefore must be used judiciously and specifically.
4. Alternative means of managing very ill pa
tients, such as those in the intensive care, must
be developed.
ALTERNATIVES TO THE NONSPECIFIC

USE OF BED REST
ing. The work of the heart is increased as a result of
With respect to developing alternative means of man
the increased filling pressures and heart rate associ
aging very ill patients rather than in the recumbent
ated with recumbency, and increased blood viscosity.
immobile positions, physical therapists need to be
The work of breathing is increased by the decreased
come vocal in designing furniture and devices that
lung volumes secondary to visceral encroachment on
are better suited to the patient's normal physiologic
the underside of the diaphragm, increased intratho
functioning and to the needs of that patient's course
racic blood volume, and restricted chest wall motion.
of recovery. Such appliances would include a greater
With bed rest, the blood vessels of the muscles and
number of neurologic and cardiac chairs in ICUs,
splanchnic circulation dilate. With prolonged bed rest,
which enable easy transfer of patients from bed to
they may lose their ability to constrict. The ability of
chair and upright positioning, greater availability of
these vessels to constrict is essential to prevent the
patient-lifting devices, and increased number of or
pooling of blood and maintain circulating blood vol
derlies to assist with moving patients.
ume in the upright position. Thus following bed rest, a

patient may feel lightheaded or dizzy, or may faint.
Rotating beds are electromechanical beds that turn

the patient through an arc of about 30 degrees to ei
With only a few days of bed rest, skeletal muscle
ther side from supine over a 3-minute period (Schim
atrophies leading to weakness, discoordination and
mel, Civetta, and Kirby, 1977). These beds are used
balance difficulty (Lentz, 1981; Saltin, et aI., 1968).
for heavy care critically ill patients who are unable to
With severe weakness, excessive strain may b e
turn themselves or are difficult to turn. Even though
placed o n ligaments and joints. The limited position
studies have shown these beds can enhance oxygena
ing alternatives in bed may contribute to poor pos
tion in severely c o m promised patients such a s
294
PART III
patients with adult respiratory distress syndrome
agement of such patients. However, 30 years ago re
(Summer, Curry, Haponik, Nelson, and Elston, 1989;
striction to a chair was reported to be significantly
Yarnel, Helbock, and Schwiter, 1986), they need to
more beneficial than restriction to bed in heart dis
be used selectively to avoid reliance on passive posi
ease patients (Levine and Lowe, 1954). Despite this
tioning with the bed vs. more active and active as
finding, many coronary patients continue to recline in
sisted patient positioning.
beds rather than chairs. Mobilizing coronary patients
The use of tilt tables to promote mobilization can be
and permitting bathroom privileges has also been re
hazardous in that leg movement is minimal. Passive
ported to be less stressful than being confined to bed
standing on a tilt table constitutes a greater physiologi
and having to use
bedpan (Andreoli et ai, 1994).
cal stress than active standing. Upright sitting postures

with the legs dependent may elicit greater physiologi
cal benefit than passive standing with less risk.
Prescription of an Adequate Stimulus to Elicit

the Preventative Effects of Exercise
Although much is known about the protective bene
INDICATIONS FOR BED REST
fits of cardiopulmonary fitness and conditioning and
Despite the uni versal acceptance of bed rest as a
about the negative effects of bed rest and immobility,
medical therapeutic intervention, indications for its
little has been documented about defining the appro
therapeutic use have not been documented. FUlther
priate exercise stimulus to optimize the preventive ef
more, considerably more is known about the adverse
fects of exercise for a given patient. The preventive
and potentially life-threatening hazards of bed rest
effects of an exercise stimulus can be defined as that
than about its potential benefits. Bed rest should
exercise dose that will maintain the patient's condi
clearly be used as selectively as other medical inter
tioning level and prevent deterioration. At present,
ventions to ensure that specific benefits are being de
the presCliption of preventative mobilization and ex
rived and the multisystemic negative sequelae are
ercise is nonspecific. Research is needed to make ex
being minimized. Many procedures such as surgery
ercise prescription for the preventative effects of ex
are associated with considerable pain, thus being rel
ercise more scientifically based. For example, the
atively immobile and recumbent in bed is believed to
following questions need to be answered:
minimize postsurgical discomfort. In some cases,
however, relative immobilization rather than confine

ment to bed may offer the same benefits without the
How do different types of exercise compare with

respect to preventative aspects?
Does exercising in some body positions elicit
dire risks. Patients who are severely limited are phys
better preventive effects than other body
ically supported by a bed and do not have to work
positions?
against the force of gravity. Minimizing the effects of

gravity and the need to weight bear is often indicated
What principles establish which exercise intensity
What principles establish how often the patient
and duration are best?
in patients following orthopedic surgery. The bed en

ables a patient with multiple wounds and fractures to
be immobilized and supported in a fixed position that
should be mobilized or should petform exercise?
is believed to promote healing. Conditions that are
The question arises as to what constitutes an ade
associated with edema require minimizing the effect
quate stimulus to maximize the preventive effects of
of gravity on the affected limbs. Whether edema can
exercise for a given patient. Although the preventive
be controlled by localized elevation rather than bed
effects of exercise are accepted, this important ques
rest must be established. Some conditions particularly
tion has not been adequately researched. Some gen
in the acute stages to reduce the work of the heart,
eral practices, however, have become accepted clini
such as MI, require some activity restriction, thus the
cally. These include turning patients. The turning
use of the bed has been a mainstay of the early man
frequency that is widely accepted is every 2 hours.
17
295
There is no literature, however, to support greater
individual steps in the oxygen transport pathway
preventive effects turning a patient every 2 hours vs.
that are primarily affected, and oxygen transport as
hourly or every 4 hours. Sitting up and ambulation
a whole, such as oxygen delivery, oxygen consump
are two other practices that are also widely used. The
tion, and oxygen extraction at the tissue level, are
timing of these interventions, however, is often based
fundamental. Of considerable clinical relevance is
on convenience and what else may be happening with
the adequacy of tissue oxygenation; however, to
the patient, or on a once or twice daily regimen rather
date, there are no clinically expedient means of as
than on a prescriptive basis. Patients who are sitting
sessing tissue oxygenation.
or walking for preventive reasons often assume sub

optimal and even deleterious slumped or malaligned
postures. Patients and their caregivers need to be re
SUMMARY
minded about the importance of proper body position
This chapter described three distinct goals associated
at all times and be provided with appropriately sup
with the prescription of mobilization and exercise in
ported chairs, firm bolsters, and adjustable beds that
the management of impaired oxygen transport,
maintain optimal body positions.
namely, to exploit their acute, long-term, and preven
Like exercise prescribed for its beneficial acute and
tive effects.
long-term effects, exercise to elicit its optimal preven
The PT needs a comprehensive and detailed un
tive effects should be prescribed based on the individ
derstanding of how mobilization and exercise have
ual (e.g., age; premorbid functional work capacity; the
potent and direct effects on oxygen transport acutely,
type, distribution, and severity of disease; and within
in the long-term, and preventively. The specific mo
capabilities of patient). Such preventive mobilization
bilization or exercise prescription is based on a com
or exercise must also be prescribed to avoid any dele
prehensive multisystem assessment and the treatment
terious effects on the patient's overall condition.
goals for a given patient. If the acute effects of mobi
Frequent ambulation constitutes preventive exer
lization or exercise on oxygen transport are indicated,
cise. Provided the patient does not require undue
the prescription specifies the parameters of an appro
monitoring and has been cleared as a risk, preventive
priate mobilization or exercise stimulus, lIsually, of
exercise can be encouraged by all team members.
relatively low intensity, shOtt duration and high fre
This role of exercise is quite distinct and separate
quency. The treatment effects are often immediate.
from the therapeutic interventions of mobilization
Because treatment responses can be dramatic, the
and exercise for their specific acute and long-term ef
prescription is progressed relatively quickly based on
fects that are prescribed for the remediation of acute
the treatment response measures. Prescribing mobi
and chronic cardiopulmonary dysfunction. The appli
lization to remediate acute cardiopulmonary dysfunc
cation of mobilization and exercise for optimizing
tion requires the same precision and specificity as
oxygen transpott is the specific expertise and within
prescribing exercise for chronic cardiopulmonary
the unique domain of the PT.
dysfunction. If the long-term effects of exercise are

indicated, the exercise stimulus is defined in an ap
propriate prescription, i.e., generally higher intensity,
ASSESSMENT OF MOBILIZATION
longer duration, and less frequent compared with the
AND EXERCISE RESPONSES
prescription for the acute effects, and designed to be
To prescribe mobilization and exercise for optimal
followed for several weeks or more before significant
therapeutic effect, resting baseline measures of rele
physiologic adaptation can be observed and progres
vant physiologic oxygen transport responses need to
sion of the stimulus is indicated. If the preventive ef
be recorded so that any perturbation of oxygen
fects of mobilization or exercise are required, then
transport and homeostasis caused by exercise can be
the prescription focuses on maximizing these benefits
identified. Measures that rencct the function of the
for a given patient by prescribing exercise, that is of
PART III
296
sufficient intensity, duration, and frequency, to pre

serve adequate aerobic capacity and endurance for a
given patient. The principles for prescribing mobi
lization and exercise for their optimal preventive ef
fects have not been scientifically elucidated. These
three levels of prescription of mobilization and exer
cise are physiologically distinct and need to be pre
scribed specifically for each patient.
Borg, G. (1982). Psychophysical basis of perceived exertion. Med

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Browse, N.L. (1965). The Physioiogy lind Pa/hol08Y of Bed Res/.
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REVIEW QUESTIONS
14, 377-381.
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(j( Applied
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I. Distinguish between mobilization and exercise.

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Rowell, L.B. (1966). Independence of
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Chobanian, A.V., Lillc, RD., Tercyak,A., Blevins, P (1974). The
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for its (l) acute effects,
Chase, G.A., Grave,
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Clauss, R.H.,
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4. Explain the effects of mobilization on enhancing
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Craig, D.B., Wahba, W.M., Don, H., Couture, J.G.,
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(1978). Dyspnea, disability, and distance walked Comparison

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298
PART III
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Zadai, c.c. (ed). (1992). Pulmonary Management in Physical
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ogy, 20, 316-336.
Body Positioning
Elizabeth Dean
KEY TERMS
Cardiopulmonary function
Prescriptive body positioning
Gravity
Routine body positioning
Oxygen transport
INTRODUCTION
prescriptions, because no specific patient is being con
The purpose of this chapter is threefold. First, thera
sidered. Understanding the physiological effects of
peutic body positioning, which is prescribed to opti
body position on oxygen transport and how patho
mize cardiopulmonary function and oxygeQ transport
physiology disrupts these normal processes is funda
is differentiated from routine
mental to prescribing body positioning. However, an
dY'l'ositioning. Sec
ond, the physiological effects of different body posi
optimal body position can only be prescribed based on
tions and changing body positions on cardiopulmonary
consideration of all the factors that impact on oxygen
function and oxygen transport, are described. And
transport, that is, effects of the patient's pathophysiol
third, the prescription of therapeutic body positioning
ogy and its specific presentation in that individual, the
is described. Body positions that simulate normal
effect of immobility, the effect of extrinsic factors re
physiological effects of gravity and position change on
lated to the patient's care and the effect of intrinsic
oxygen transport are the priority, that is, being upright
factors related to the patient (Chapter
and moving. A hierarchy of body positions ranging
an integrated analysis of these factors collectively that
from the most to the least physiological is presented.

scribing therapeutic body positioning and body posi
(1) the most beneficial body positions can be pre

(2) the least beneficial body positions can be
identified and used minimally, and (3) the appropriate
tion changes. The chapter does not provide treatment
treatment outcome measures can be selected.
This chapter concentrates on the principles of pre
IS). It is only by
dicted,
299
300
PART III
GRAVITY AND NORMAL PHYSIOLOGIC FUNCTION:

IMPLICATIONS FOR CARDIOPULMONARY
PHYSICAL THERAPY
The human is an orthograde animal. From moment to
-fl .> '0
(%)
moment, gravity exerts its influence on the human
(L minute)
body and importantly on oxygen transport. The com

bined effects of gravity on the lungs, hea11, and pe
ripheral circulation is central to their interdependent
I
II
/
/
I
Knowledge of the effects of gravity on cardiopul

monary function in health and the deleterious effects
of pathophysiological states on cardiopulmonary func
tion provide a foundation for the clinical application
of body positioning as a primary therapeutic interven
tent and direct effect
011
oxygen transport, therapeutic
13
N
O
Z
0....
u
0....
t0
U
therapy intervention that can augment arterial oxy

genation so that invasive, mechanical, and pharmaco
logical forms of respiratory support can be postponed,
/r-",
I\
I'
t
"
\
.\
\
\
\ f\
\ '\
/ \ 1\
.82 1.29 0.63 89 1'42 582 19.21149 739 60 39

/'
"'::j J.- \.....
V
/
"I
"\
I
A patient is continually exposed to gravity, thus
be improved, maintained or worsened with changes in

body position. Despite being essential to normal car
diopulmonalY function, gravity is the principal contribu
tor to signjficant inhomogeneity of physiological func
tion down the lungs (West,
1995). Figure
I
\
\
1'0
the singlemost important objec
gravity on oxygen transport, thus, oxygen transport can
in out
(ml/minut
tive of cardiopulmonary physical therapy.

every position the patient assumes reflects the effect of
N
0
:r:
0..
content
(mil
100 ml)
(mm Hg)
N
o
__
body positioning is a primary noninvasive physical
reduced, or avoided
o
0....
7 .24 .07 3.3 132 28 553 200 42 751 4
function and establishing normal oxygen transport.
tion to optimize oxygen transport. Because of its po
""-
. :;;
FIGURE 18-1
Regional physiologic differences down the upright lung.
VA
alveolar ventilation, Q
perfusion, V NQ
ventilation perfusion ratio. (Reprinted with permission from

West JB: Respiratory physiology-rhe essenrials, ed 5,
Baltimore, 1995, Williams & Wilkins.)
18-] illustrates
the effect of this gradient with respect to alveolar venti
hydrostatic, gravitational and compression forces act
lation (V A), perfusion (Q), ventilation and perfusion
ing on the heart, blood volume, lymphatic system,
ratio (V A/Q), Pao2, Peo2, PN2, oxygen content, CO2
lungs, and chest waJi, including the diaphragm, wiJi
content, pH, and the flow of oxygen and CO2 in and out
eventually compromise oxygen transport, and any ben
of the lungs. Thus the lungs should not be likened to
eficial effect will be offset. Therefore monitoring is es
balloons either physiologically or anatomically.
sential to ensure the patient is turned to another posi
Based on a thorough analysis of all factors con
tion before detrimental effects are observed. Frequent
tributing to impaired oxygen transport and gas ex
changes in body position and avoidance of prolonged
change (Chapter 16), those body positions that will
periods in any single position will minimize the risk of
have an optimal effect and those that may be deleteri
diminishing returns, which are inevitable. The time
ous must be discriminated. In this way, a greater pro
course differs according to pathology, type, severity,
portion of time can be spent in beneficial positions and
and other factors. The duration a patient assumes a
response-dependent
less time spent in deleterious body positions. When
body position should be primarily
beneficial positions are assumed for too long, however,
rather than time-dependent. Knowledge of the dekteri
18
ous effects of prolonged periods in a single position
Body Positioning
301
deleterious to oxygen transport. The side-lying positions
supports the prescription of both frequent body posi
have an effect that is intermediate between upright and
tion changes and extreme consecutive body positions.
supine. The prone position which is under utilized clini
These perturbations simulate the nOimal perturbations
cally, has such a significant beneficial effect on oxygen
that the cardiopulmonary and cardiovascular systems
transport that a good rationale should be made for not
are exposed to in health during normal mobility and
incorporating this position into the treatment prescrip
body position changes. The ability to weigh the rela
tion rather than for using this position.
tive beneficial and deleterious effects of each possible
The indications for therapeutic body positioning
body position, that is, over 360 degrees in the horizon
and the indications for frequent body position changes
tal plane and 180 degrees in the vertical plane (ranging
to optimize oxygen transp0l1 are shown in the boxes
from 20 degrees head down to 20 degrees lean for
on pp. 302-303. For each of the indications listed, an
ward) on a given patient's gas exchange, is critical in
optimally therapeutic body position can be selected
prescribing body positioning therapeutically.
for a given patient. A description of the physiological

effects of several primary body positions follow,
namely, the upright supine, side lying, head down,
PRESCRIPTIVE VS. ROUTINE BODY POSITIONING
and prone positions. This information, howevcr, can
The literature supports the benefits of frequent body po
not be applied out of context. The specific positions
sition changes particularly for the patient who is rela
prescribed for a patient are based on a consideration
tively immobile, severely debilitated, obtunded, breath
of the multiple factors that impair oxygen transport
ing at low lung volumes, obese, aged, very young or
(Chapter 16) in conjunction with a physiological
who has lost the sigh mechanism. The practice of rou
analysis of the most justifiable positions.
tinely turning patients every 2 hours is widely accepted.
Because of the potent and direct effects of body po
This practice is based on the belief that the deletelious
sitioning on various steps in the oxygen transport path
consequences associated with assuming a static posi
way in health and in disease, it is unknown whether the
tion for a prolonged period will be prevented. Recent
beneficial effects reported with the use of postural
evidence, however, supports that more frequent turning
drainage are attributable to enhanced mucociliary
can have greater physiological benefits in criticaJiy ill
transport, or to the direct effect of positioning the good
patients (Dean and Suess, 1995) which suggests less se
lung down on improving the gas exchange of that lung,
verely ill patients may also benefit. The preventive ef
by increasing alveolar volume of the affected, nonde
fects of a routine turning regimen are distinct from the
pendent lung, or both. Typically, studies evaluating
acute effects of body positioning on oxygen transport
conventional chest physical therapy, including postural
which is the primary focus of this chapter.
drainage, have failed to control for the direct effect of

body positioning on cardiopulmonary function, or for
the direct effects of increased arousal and mobilization
PHYSIOLOGICAL EFFECTS OF
that occur when changing a patient's body position
DIFFERENT BODY POSITIONS
(Dean, 1994a). This is an extremely serious method
Body positioning has potent and direct effects on most
ological problem that pervades the literature evaluating
steps of the oxygen transport pathway, thus can be pre
conventional chest physical therapy, and one that
scribed to elicit these effects specifically. Because hu
needs to be considered when interpreting the results of
mans function optimally when upright and moving,
studies on these procedurers. Unless these potent con
therapeutic interventions that elicit or simulate being
founding variables are controlled, the degree to which
upright and moving (i.e., elicit both gravitational and
conventional chest physical therapy had a beneficial
exercise stress) are most justified physiologically. The
effect over and above the effects of positioning as well
recumbent supine position, a common position assumed
as mobilization and increased arousal cannot be deter
by hospitalized patients, is nonphysiological, therefore
mined (Dean, I 994b).
PART III
302
Indications/or Body Positioning To Optimize Oxygen Transport

Cardiopulmonary
Facililate viscerodiaphragmatic breathing
i Regional alveolar volume

i
Change the pattern of breathing
Regional ventilation
Cardiovascular
i Regional perfusion
i
..l. Preload and afterload
Regional diffusion
..l. Work of the heal1
Optimize area of optimal ventilation to perfusion

matching
Improve systolic ejection fraction to pulmonary and

systemic circulations
..l. Pulmonary shunting

i Lung volumes and capacities particularly, functional
Alter venous return
..l.
residual capacity, vital capacity and tidal volume
..l. Closure of dependent airways
astinal structures. and lymphatic system
Alter breathing frequency
Optimize t1uid shift from central to dependent areas

(extremities) and vice versa to maintain nuid vol
Alter minute ventilation
ume regulating mechanisms
Alter position of the hemidiaphragms
Other Systemic Effects
Respiratory muscle efticiency
..l.
Airway resistance
Lung compliance
Air now rates
Optimize chest tube drainage

Facilitate urinary drainage
Reduce posturally increased muscle tone
Facilitate patient arousal
Stimulate cough
Gravitational. mechanical a n d compression

forces on the myocardium. great vessels, medi
Biomechanical efficiency of cough, its strength
Promote relaxation
Promote comfort
and productivity
..l. Work of breathing
Control pain
Improve arterial blood gases, gas exchange and oxy
Promote biomechanically optimal body positions
genation
lntraabdominal pressure
i Mucociliary transpOit and mucus clearance
Intracranial pressure
..l. Gravitational, mechanical and compression forces

on the lungs, chest wall, diaphragm and the gut
Upright Positions
exercise stimulus. The upright standing position max
The physiological position for the human organism is
imizes lung volumes and capacities with the excep
the same as the anatomical position-upright. The
tion of closing volume, which is decreased (Svan
upright positions include walking, standing, and sit
berg, 1957). Functional residual capacity (FRC), the
ting. The upright position coupled with movement
volume of air remaining in the lungs at the end of a
(e.g., walking and cycling) optimizes oxygen trans
normal expiration, is slightly greater in standing com
port to the greatest degree in that ventilation and per
pared with sitting and exceeds that in supine by ap
fusion are more uniform than without the additional
proximately 50% (Figure
18-2). Maximizing FRC is
18
Indications for Frequent Changing

of Body Position
Body Positioning
303
associated with reduced airway closure and maximal

arterial oxygenation (Hsu and Hickey, 1976; Ray et
ai, 1974). Figure 18-3 illustrates the relationship of
Cardiopulmonary
FRC and closing capacity as a function of age. Be
Alter chest wall configuration
cause of age-related changes, closing capacity of the
Shift distribution of alveolar volume

Shift distribution of ventilation
Shift distribution of perfusion
Shift distribution of diffusion
dependent airways increases with age; this effect is

further accentuated with recumbency. Airway closure
is evident in supine in the healthy 45-year-old person,
and in the upright position in the healthy 65-year-old
person (Leblanc, Ruff, and Milic-Emili, 1970). These
Shift distribution of ventilation to perfusion matching
effects are further accentuated in patient populations,
Shift mechanical physical compression of the heart
thus the upright position is favored and the supine po
on adjacent alveoli
Shift position of the heart thereby alter chamber end
disastolic filling pressures. preload, afterload, and
work of the heart
sition should be minimized to prevent airway closure

and impaired gas exchange.
With respect to pulmonary function testing, the up
right sitting position with legs dependent is the stan
Shift distribution of mucus transport and accumulation
dard reference position (American Thoracic Society,
Stimulate effective and productive cough
1987). When upright, the diameter of the main air
Facilitate lymphatic drainage

Perturb pattern of monotonous tidal ventilation
Alter breathing pattern
Shift gravitational, mechanical and compression forces
on the lungs, chest wall. diaphragm, and the gut
Simulate normal inflation-deflation sigh cycles
Shift intraabdominal pressure
Cardiovascular
Shift gravitational. mechanical, and compression
forces on the myocardium, great vessels. medi
astinal structures. and lymphatic system
Stimulate fluid volume shifts particularly to the de
pendent limbs
Other Systemic Effects

Optimize chest tube drainage
ways increases slightly. If the airways are obstructed

even small degrees of airway narrowing induced by
recumbency can result in significant airway resistance
(Figure 18-4). The vertical gravitational gradient is
maximal when upright, the anteroposterior dimension
of the chest wall is the greatest, and compression of
the heart and lungs is minimal (Weber, Janicki,
Sllroff, and Likoff, 1983). The shortened position of
the diaphragmatic fibers is countered by an increase in
the neural drive to breathe in the upright position
(Druz and Sharp, 1982).
The distribution of ventilation is determined pri
ll)arily by the effect of gravity, which changes down
the lung due to the anatomical position and suspen
sion of the lungs within the chest. At FRC in the up
right position, the intrapleural pressures at the apex is
-10 cm H20 and at the base -2.5 cm H20 (Figure 18
Promote urinary drainage
5). The intrapleural pressure is less negative in the
Shift abnormal postural tone patterns
base because of the weight of the lung. Because of
Alter arousal state

Promote relaxation
Promote comfort
Control of pain
Prevent skin breakdown, risk of infection. and re
sulting positioning limitations
Limit lying on a preferred side
the greater negative intrapleural pressure in the

apices, thus low compliance, these lung units have a
larger initial volume, thus smaller volume changes
occur during respiration. Because the lung units at the
base have a smaller initial volume, thus high compli
ance, larger volume changes occur during respiration.
Therefore depending on their relative position with
respect to gravity, different regions of the lung are at
different parts of the pressure volume curve.
304
PART III
Mean height
Cf)
0I
a:I
1.S8
. 300 =-- 30. ,

::i'::.__
----- SO_:s:.
0
3.5
'u
'"
c.
3.0
'"
:l
1:>
'v;
'"
c
2. 5
.9
U
c
:l
u..
2.0
Bars indicate
:!: 1
standard deviation
---1
1.5 'L..
FIGURE 18-2
Changes in functional residual capacity in various body positions. (Data reprinted with permission
from Nunn JF: Applied respiratory physiology, London, 1987, Butterworths.)
FRC upright
FRC supine
'"
..
!;
..
E
.2
o
:>
at
c
:l
-'
OJ
__
30
________
40
______
________
50
______
60
__
70
Age yearsl
FIGURE 18-3
Functional residual capacity (FRC) and closing capacity as a function of age. (Data reprinted with
permission from Nunn JF: Applied respiratory physiology. London, 1987, Butterworths.)
18
Erect
Body Positioning
305
-10 em H20
Supine
Intrapleural
pressure
Bronchus
100%
<1l
Mucus
50%
FIGURE 18-4
Effect of body position on bronchiolar diameter. (Reprinted
with permission from Browse NL: The physiology and
+10
pathology of bed rest, Springfield, III. 1965, Charles C.
Intrapleural pressure (cmH20)
Thomas.)
FIGURE 18-5
A common clinical concern is the patient breathing
Schematic of the regional differences in ventilation down
at low lung volumes (e.g., the patient in pain, the sur
the upright lung. (Reprinted with permission from West 18:
gical patient with thoracic or abdominal incisions,
Ventilation! bloodflow and gas excfumge,
older and younger patients, obese patients, pregnant
1985, Blackwell Scientific.)
ed 4, Ox ford,
patients, patients with gastrointestinal dysfunction

-4 em H20
such as paralytic ileus and ascites, organomegaly, in

trathoracic and intraabdominal masses, patients who
are malnourished, mechanical ventilated patients and
Intrapleural
pressure
patients with spinal cord injuries. Breathing at low
(RV)
lung volumes reverses the normal intrapleural pres

sure gradient such that in the upright lung the apices
-.,100%
have a negative intrapleural pressure compared with

the bases, which have a positive intrapleural pressure,
that is, exceeds airway pressure (Figure 18-6). This
results in the apices being more compliant, thus better
<1l
E
50% .2
ventilated than the bases. The bases are prone to air

way closure in patients breathing at low lung volumes.
An other f a c t o r t h a t r e v e r s e s t h e n o r m a l in
trapleural pressure gradient is mechanical ventilation.
Despite its necessity in the management of patients in
respiratory failure, mechanical ventilation contributes

to hypoxemia in several ways. First, it reverses the
normal intrapleural pressure gradient so that the up
permost lung fields are preferentially ventilated. Be
-30
Intrapleural pressure (cmH20)

FIGURE 18-6
Schematic of the regional differences in ventilation at low
cause the dependent lung fields are preferentially per
lung volumes. (Reprinted with permission from West 18:
fused, ventilation perfusion mismatch is promoted.
Ventilation/ bloodflow and gas exchange,
Positive pressure ventilation has the additional com
1985, Blackwell Scientific.)
ed 4, Oxford,
306
PART III
Cardiopulmonary Physical Therapv Interventions
of
intrathoracic pressure and re-
the recruitment of pulmonary vessels. Arterial pres
venous return and cardiac output. These fac
sure exceeds alveolar pressure and blood flow. Zone
open the
to
pressure
tors in addition to the
3, in the lower area of the
reflects the blood
valve can increase the work of
flow from the distension of pulmonary vessels; arter
associated with mechanical ventilation
ial and venous pressures exceed alveolar pressure.
and
Arcos, and Hiriart, 1984).
of the
gravity is the primary determinant of in

differences in the distribution of ventila
tion in the
secondary to differences in
lung
has minimal to no pulmonary
blood flow because of interstitial pressure acting on

the pulmonary blood vessels
1995).
Ventilation (V) and
and resistance
and Abboud, 1992). These effects are eXa)!,)!,CI
Both V and Q increase down
(989).
V increases disproportion
The distribution of perfusion down the upright

lung is also
(Figure 18-
gravity
The pressures affecting blood flow through the

pulmonary capillaries and
(Q) matchl!1g re-
of the distributons of V and Q
also contribute
populations
a compression
force
lung, imrareg ional
of
in the most
zone 4
1990;
in the
18-8). As a
ately more than Q
the
mal area for VIQ matching is in the mid zone where

the ratio is about 1.0 (West,
un
The uoril!ht position is associated with
even distribution of blood flow are alveolar pressure,
effects. These effects reflect primarily
and the arterial and venous pressures. Zone 1, at the
the central blood volume that is shifted from the tho
apex, alveolar pressure predominates arterial and ve
racic compartment to the dependent venous compart
nous pressures, thus has minimal to no blood flow.
ments on
Zone 2, in the
reflects the blood flow from
the
(Blomqvist and Stone,
position from
Gauer and Thron,
---+
FIGURE 18-7
Schematic of pressures affecting the pulmonary
permission from West 1B:
and blood flow. (Reprinted with
VentilaliOIl/bloodjlolV and gas exchange, ed 4, Ox ford, 1985,
Blackwell
18
15
Body Positioning
I/minute
% Lung volume
10
Blood flow
2
Ventilation
05
Rib number
BaHam
Top
FIGURE 18-8
Distributions of ventilation and blood flow down the upright lung and the distribution of ventilation
perfusion matching down the upright lung. (Reprinted with pennission from West JB:
Ventilationlbloodflow and gas exchange, ed 4, Oxford, 1985, Blackwell Scientific.)
45
15
Blood
4
flow
ml/minute/
3
1 00 m l
2
Calf
Ai
0'
Foot
FIGURE 18-9
Effect of body position on peripheral blood flow. (Reprinted with permission from Browse NL:
The physiology and pathology of bed rest, Springfield, 111., 1965, Charles C. Thomas.)
307
308
PART III
Erect
Supine
Stagnant area
FIGURE 18-10
Effect of body position on drainage from the pelvis of the kidney. (Reprinted with permission from
Browse NL: The physiology and pathology of bed rest, Springfield, III., 1965, Charles C. Thomas.)
Sandler, \986). End diastolic and stroke volumes are
Supine Position
decreased, which results in a compensatory increase
The supine position is clearly not a physiological
in heart rate (Thandani and Parker, 1978). Cardiac
position for humans unless sleeping, and is physio
output is correspondingly decreased. The net effect of
logically the least justifiable position for ill patients
these physiological changes is a reduction in myocar
regardless of whether they exhibit cardiopulmonary
dial work (Langou, Wolfson, Olson, and Cohen,
dysfunction (Dock, 1944; Moreno and Lyons, 1961;
1977). This finding in corroborated by the observation
Powers, 1944; Winslow, 1985). The nonspecific use
that anginal threshold is increased in cardiac patients
and overwhelming acceptance of bed rest has devel
in this position (Prakash, Parmely, Dikshit, Forrester,
oped historically over the past 130 years. In the
and Swan, 1973). Peripheral vascular resistance in
mid-1800s, that internal organs could be rested as a
creases and blood flow decreases, with the assumption
therapeutic intervention comparable with immobi
of the upright position greater than 45 degrees to off
lizing and resting injuries of the limbs was the pre
set dependent fluid shifts and potential blood pressure
vailing medical philosqphy. The injudicious appli
drop (Figure 18-9). Another important effect of body
cation and overuse of bed rest to cure all medical
position on fluid volume is the promotion of urinary
problems was critically challenged by Harrison
drainage from the renal pelvi to the bladder in the up
(1944) and Browse (1965). Although there has been
right positions as a result of the reduced area for uri
a significant decrease in use of prolonged periods of
nary stasis in this position compared with supine (Fig
bed rest based on innumerable studies of the nega
ure 18-10). Optimal renal function is essential in
tive sequelae of bed rest over t h e past several
preserving normal hemodynamic status.
decades (Dean and Ross, 1992b), the merits of bed
18
Body Positioning
309
rest as a therapeutic modality and the parameters for

its prescription, that is, indications and specifica
Erect
Supine
tions to achieve healing and recovery without deteri

oration, have not been scientifically established.
This void in our scientific knowledge seems incon
gruous given the exponential rate of medical re
search and advances over the years in understanding
obscure diseases and treatments. Because recum
bency in bed is nonphysiologic and therefore associ
ated with dire side effects, rest in bed needs to be as
scientifically investigated and judiciously prescribed
as any medication.
The supine position alters the chest wall configu
ration, the anteroposterior position of the hemidi
aphragms, the intrathoracic pressure, and the intraab
0
0,
,
:.
:..
.:: "," . .:::.'.
dominal pressure secondary to the shifting of the

abdominal viscera in this position (Behrakis, Baydur,
FIGURE 18-11
Jaeger, and Milic-Emili, 1983; Craig, Wahba, Don,
Effect of body position on the distribution of mucus within
Couture, and Becklake, 1971; Don, Craig, Wahba,

and Couture, 1971; Druz and Sharp, 1981; Klingstedt
et ai, 1990; Roussos, Fukuchi, Macklem, and Engel,
the bronchi. (Reprinted with permission from Browse NL:

The physiology and pathology of bed rest, Springfield, IJI.,
1965, Charles C. Thomas.)
1976; Saaki, Hida, and Takishima, 1977). The normal

anteroposterior configuration becomes more trans
verse. The hemidiaphragms are displaced cephalad,
Several significant cardiovascular changes occur
which significantly reduces FRC in this position (Hsu
on assuming the supine position. A central shift of
and Hickey, 1976). Excess secretions tend to pool on
blood volume from the extremities to the central cir
the dependent side of the airway. Thus the upper side
culation initiates orthostatism (Sandler, 1986). This
may dry out, exposing the patient to infection and ob
fluid shift increases both the preload and afterload of
struction (Fig. 18-11).
the right side of the heart. This increased volume
An increase in intrathoracic blood volume also
tends to distort the interventricular septum, and re
contributes to a reduction in FRC, lung compliance,
duces left ventricular volume and preload. Prefaut
and increased airway resistance in the supine position
and Engel (1981) observed that hypoxic vasocon
(Nunn, 1987; Sjostrand, 1951). Collectively, these ef
striction secondary to closure of the dependent air
fects predispose the patient to airway closure and an
ways in the supine position contributed to preferential
increase in the work of breathing. Although a healthy
perfusion of the nondependent lung zones. The rela
person can accommodate to these physiological
tively increased central blood volume inhibits the re
changes, a healthy person does not assume this posi
lease of antidiuretic hormone. Ten to 15 percent of
tion for prolonged periods without shifting. A hospi
fluid is lost within 24 hours (Sandler, 1986), which
talized patient, however, is less likely to adapt to these
can manifest clinically as cardiac underfilling, ortho
immediate changes and their long-tenn effects. In ad
static intolerance, and a negative fluid balance (Dean
dition, they may be less responsive to the need to shift
and Ross, 1992a).
position or unable to respond to afferent stimuli
Because of a reduction in the vertical gravitational
prompting a need to change position. These effects are
gradient, and therefore the intrapleural pressure gra
accentuated in older people whose arterial oxygen ten
dient of the lung in supine, the distribution of V/Q
sions progressively diminish with age (Ward, Tolas,
matching appears more uniform and evenly matched
Benveniste, Hansen, and Bonica, 1966; Nunn, 1987).
in the supine position (Bates, 1989). These changes,
310
PART III
Erect
Supine
cm
Above 20
iliac
crest
15
FIGURE 18-12
Effect of body position on the level and movements of the diaphragm during respiration.
(Reprinted with permission from Browse NL: The physiology and pathology of bed rest,
Springfield. Ill.,
1965, Charles C.
Thomas.)
I
1.:I.::'
/':-:
,..:-::L:':
r:-::::,:
(: :' :
---....
::
nnn rtn<..:<
,
Awake spontaneous
:':
r::::'
j
-:
7':
.:- -.,
:':::i
>1
....
/
nnnqn
:
<
___
Anasthelized spontaneous
nn n\n
Paratyzed
FIGURE 18-13
Position of the diaphragm in an awake spontaneously breathing subject, and in an anesthetized
subject with and without paralysis. The broken line is the end-expiratory position of the diaphragm
in the awake state in the supine position. The shaded area shows the excursion of the diaphragm
during inspiration and expiration.
(From Froese AB, Bryan AC: Effects of anesthesia and paralysis on diaphragmatic mechanics in
man. Anesrhesio[ogy
41 :242-255.)
18
however, must be considered in conjunction with
Body Positioning
311
Functional
other changes associated with supine, namely re
Maximal
residual
duced FRC, reduced vital capacity, reduced flow
inspiration
capacity
rates, increased area of dependent lung, and increased

closure of the dependent airways. These deleterious
factors offset any theoretical benefit of the supine po
sition on VIQ matching (Ross and Dean, 1992).
The position of the diaphragm and its function, is
dependent on body position. Figure 18-12 illustrates
the effect on body position on the level and movement
of the diaphragm. In the supine position, the resting
Maximal
level of the diaphragm is influenced differentially by
inspiration
Functional
residual
anesthesia and neuromuscular blockade (Froese and

Bryan, 1974). Figure 18-13 illustrates these effects. In
the spontaneously breathing subject, the excursion of
the diaphragm is greater posteriorly because the de
pendent viscera beneath the posterior portion of the
diaphragm. During anesthesia with or without paraly
sis, the diaphragm ascends 2 cm into the chest. When
paralysis is induced, the loss of diaphragmatic tone re
sults in greater excursion of the nondependent rather
than the dependent part of the diaphragm.
FIGURE 18-14
Outlines of the lungs at two lung volumes in a conscious
spontaneously breathing subject in the right side-lying
Side-Lying Positions
Compared with the supine position, side lying is
more physiological, thus a more justifiable position
position. (Reprinted with permission from Nunn JF:

Applied respiratory physiology, London, 1987,
Butterworths.)
in terms of i t s t h e r a p e utic b e n e f i t (Hu rewitz,

Susskind, and Harold, 1 985; Ibanez, R a u r i ch,
Abizanda, Claramonte, Ibanez, and Bergada, 1981;
right side lying. Although effective ventilation is en
Ross and Dean, 1992; Roussos, Martin, and Engel,
hanced to the dependent lung, inspiratory lung vol
1977). The side-lying position accentuates anteropos
ume and FRC are significantly reduced.
terior expansion at the expense of transverse excur
There is evidence to suggest that side lying results
sion of the dependent chest wall. In this position, the
in increased end diastolic ventricular pressure on the
dependent hemidiaphragm is displaced cephalad be
dependent side secondary to compression of the vis
cause of the compression of the viscera beneath it.
cera beneath the diaphragm, and reduced lung com
This results in a greater excursion during respiration,
pliance on that side (Lange, Katz, McBride, Moore,
and greater contribution to ventilation of that lung
and Hillis, 1988). Although such changes can be
and to gas exchange as a whole. The FRC in side
readily accommodated in health, for the patient with
lying falls between that in upright and supine. Simi
compromised oxygen transport, they may impair gas
larly, compared with supine, compliance is increased,
exchange fUl1her.
resistance is reduced, and the work of breathing re
Optimal V/Q matching occurs in the upper one
duced, whereas these are reversed when comparing
third of each lung in the side lying position (Kaneko,
this position with upright. Figure 18-14 illustrates the
Milic-Emili, Dolovich, Dawson, and Bates, 1966).
difference in lung volumes between maximal inspira
The total area therefore for optimal V/Q matching is
tion and FRC in a spontaneously breathing subject in
likely greater than that in the upright position, which
312
PART III
contributes to an improved V IQ matching. These ap
those with respiratory muscle fatigue may have in
parent improvements, however, are offset by reduced
creased respiratory distress in this posi tion due to
lung volumes and air flow rates in this position.

In both healthy people and patients, arterial oxy
the resistive loading of the diaphragm from the

weight of the viscera beneath.
gen tension is greater in side lying compared with

supine (Clauss, Scalabrini, Ray, and Reed, 1968).
This is true both for patients receiving supplemental
Prone Position
oxygen as well as those who are not. Thus sidelying
There is considerable physiological justification for
can be used to enhance the efficiency of oxygen
the use of the prone position to enhance arterial oxy
transport and thereby minimize or avoid the use of
genation and reduce the work of breathing in patients
supplemental oxygen. Arterial blood gases are im
with cardiopulmonary dysfunction. Specifically, the
proved in patients with unilateral lung disease (Re
prone position increases arterial oxygen tension, tidal
molina, Khan, Santiago, and Edleman, 1981; Sonnen
volume and lung compliance (Albert, Leasa, Sander
blick, Meltzer, and Rosin, 1983) when positioned
son, Robertson, and Hlastala, 1987; Schwartz, Fen
with the good lung down and worsened with the af
ner, and W o lfsdorf, 1975; Wagaman, Shutack,
fected lung down. When lung pathology is bilateral,
Moomjiam, Schwartz, Shaffer, and Fox, 1979). These
arterial blood gases are improved when patients lie
benefits have also been observed in critically ill pa
on the right side compared with the left. This can be
tients (Langer, Mascheroni, Marcolin, and Gattinoni,
explained by the greater size of the right lung and the
1988). In one study (Douglas, Rehder, Beynen,
reduced compression of the heart on the lung in this
Sessler, and Marsh, 1977), supplemental oxygen was
position compared with left side lying (Dean, 1985;
reduced in four out of five mechanically ventilated
Zach, Pontoppidan, and Kazemi, 1974).
patients whose positioning regimen included the

prone abdomen-free position. The two common vari
ants of the prone position are prone abdomen-re
Head Down Position
stricted and abdomen-free. Prone abdomen-restricted
The head down position augments oxygen transport
refers to lying prone with the abdomen in contact
in some palients by improving pulmonary mechan
with the bed, whereas in the prone abdomen-free po
ics. Patients with chronic airflow limitation, for ex
sition the patient's hips and chest are elevated so that
ample, tend to have hyperinflated chests and flat
the abdomen is free.
tened diaphragms in which the contraction of the
W h i le both prone positions augment gas ex
diaphragm is inefficient because of the position of
change, the prone abdomen-free position, comparable
its muscle fibers on the length tension curve. The
with the hands and knees position (Mellins, 1974),
head down position causes the v iscera to be dis
enhances lung compliance, tidal volume, FRC and di
placed cephalad beneath the diaphragm. The di
aphragmatic excursion to a greater degree. Although
aphragm is positioned more normally and rests at a
patients in respiratory failure have been shown to
higher and more mechanically efficient position in
benefit significantly from the prone position, certain
the chest (Barach and Beck, 1954; De Troyer,
precautions must be observed. The patient must be
1983). In this position, patients may experience re
positioned so that all pressure points particularly on
lief from dyspnea, reduced accessory muscle use,
the head and face, and stress on the mechanical venti
reduced upper chest breathing patterns and reduced
lator tubing and circuitry is minimized. The patient
minute ventilation. Patients with pathology to the
should be monitored continuously and not be unat
bases may also benefit from the head down position
tended. A semiprone position can provide many of
in that this position favors gas exchange in the more
the physiological benefits of a full prone position,
functional upper lung fields and promotes alveolar
and minimize some of the risks, particularly in me
distension of bases, which are uppermost in the head
chanically ventilated patients and patients with cervi
down position. Other patients, however, such as
cal spine pathology. In addition, the semiprone posi
18
Body Positioning
313
tion simulates the prone abdomen-free position. The
constituent distributions of ventilation, perfusion, and
scmiprone position may be more conservative, safer,
ventilation and perfusion matching. Areas of depen
and comfortable for the patient who is severely ill,
dent atelectasis, physiologic dead space and shunting,
potentially hemodynamically unstable, older, or who
and mucus distribution are dramatically shifted. The
has a protruding abdomen.
"stir-up" correspondingly s t i mulates lymphatic
For patients who are not able to be effectively mo
drainage, surfactant production and distribution, and
bilized some variant of the 'prone position is even
the distribution and function of pulmonary immune
more important. Excessive recumbency, particularly
factors (Pyne, 1994). Frequent physical perturbations
in patients who are being positioned through a re
also inhibit bacterial colonization (Skerrett, Nieder
stricted arc (e.g., supine and one-quarter turns to ei
man, and Fein, 1989). F r e q u e n t b o d y position
ther side) needs to be offst by some variant of the
changes redistribute compression forces acting on the
prone position and this position needs to be incorpo
diaphragm, myocardium, and mediastinal structures,
rated often. [nevitably, patients exposed to a re
and the compression of the lungs by the myocardium
stricted arc of positioning will develop atelectasis in
and mediastinal structures.
the dependent lung fields. The only means of pre
Frequent body position changes have significant
venting and countering compression and hydrostati
effects on stimulating the patient and increasing
cally induced atelectasis is by placing those depen
arousal and a more wakeful state (Figure 18-15). The

more upright the patient is positioned the greater the
dent areas uppermost.

The time course for the development of such hy
neurological arousal and greater the stimulus to
drostatic complications is dependent on the patient.
breathe; this effect is augmented by encouraging the
Although objective measures of oxygen transport and
patient to be self-supporting. Concomitant with an in
the adequacy of the steps in the oxygen trans[lort path
crease in arousal, the patient is stimulated to take
way are essential to monitor, functional changcs will
deeper breaths, and hence increase alveolar ventila
likely precede the appearance of objective changes.
tion. When body positioning is coupled with mobi

lization, vasodilatation, and recruitment of the pul
monary capillaries is stimulated, which in turn
PHYSIOLOGIC EFFECTS OF FREQUENT

CHANGES IN BODY POSITION
improves the even distributions of ventilation and

perfusion, and hence augments VIQ matching.
The box on p. 303 lists some of the significant physi

ological effects of frequent changes in body position
that are largely mediated through their effects on res
piratory mechanics, cardiac mechanics, airway clo
PRESCRIPTION OF THERAPEUTIC BODY POSITIONS

AND BODY POSITION CHANGES
sure, mucociliary transport, lymphatic drainage, and
Prescription of body positioning is based on an analy
altered neural activation of the diaphragm. These ef
sis of the factors that contribute to impaired oxygen
fects resulting from the changc in position are distinct
transport. Specific positions are selected to simulate
from the benefits derived from a particular body PoS!
as closely as possible the physiologic function of the
tion. The benefits of changing position can be en
normal healthy upright cardiopulmonary unit, and the
hanced by moving to an extreme position, ie, moving
perturbations and "stirring up" that occurs in the car
from supine to prone compared with supine to side
diopulmonary system during normal mobility and
lying. Extreme body position changes simulate, but
being upright. A hierarchy of body positioning alter
do not replace, the physiological "stir-up" and pertur
natives based on the physiologic justification of the
bations that occur with normal mobility and being
various positions, appears in the box on p. 3 14. These
upright. When the "stir-up" regimen was originally
positions range from the most to the least physio
proposed, Dripps and Waters ( 1941) did not appreci
logic. The hierarchy is based on the premise that oxy
ate fully its physiological implications. The net effect
gen transport is optimal when upright and moving.
of changing body position is a "stirring up" of the
Mobilization in the upright position increases tidal
314
PART III
Physiological Hierarchy of Body Positions

Most Physiologic Therapeutic Body Positions
Normally moving upright in a I G gravitational field and exposed to a range of body positions and body position
changes over the course of several hours
Relaxed erect standing (not too prolonged)
Erect sitting (self supported or with assist) with feet moving (e.g., active, active assisted or passive cycling motion)
Erect silting (self-supported or with assist) with feet dependent
Lean forward sitting with arms supported and feet dependent
24S degree sitting with legs dependent

Erect long sitting (legs non dependent)
<
4S degrees sitting (legs non dependenl)
Prone and semiprone/side lying

Supine
Least Physiological Therapeutic Body Positions
Provisos
The upright erect position implies the back, head and neck are vertical and aligned with flexion only at the hips: the
patient is not slumped
or
recumbent.
The less able the patient is to assist in positioning the greater the need for more extreme positions and greater the
turning frequency.
If the patient is totally unable to move, that is, in coma or paralyzed, extreme body positions arc also indicated if not
contraindicated because of hemodynamic instability or increased intracerebral pressure. The upright position is
used as much as possible provided the patient is physically supported for safety and monitored in terms of treat
ment response. Passive standing on a tilt table is hemodynamically questionable; preferably patients should be
placed in
high Fowler's position with legs positioned dependently using the knee breaks in the bed.
Regimens of 360-degree horizontal tuming and ISO-degree vertical turning (ranging from 20 degrees head down to
20 degrees lean forward) are used unless contraindicated. Positioning through a maximal arc simulates as closely as
possible three dimensional movement of the chest wall during normal respiration.
volume, respiratory rate, and hence minute volume,
right state. Furthermore, even the mobilized patient
flow rates, mucociliary transport, and clearance, and
can benefit from therapeutic body positioning be
enhances the efficiency and effectiveness of airway
tween mobilization sessions.

Body position needs first to be exploited when
clearance and coughing. Thus incorporating active

movement into the body position change is optimal.
Despite the well-documented benefits of the judi
coupled with movement followed by the erect sitting

positions with legs dependent. Figure 18-16 illus
cious application of therapeutic body positioning to
trates several variants of the sitting position. Each of
enhance oxygen transport, it does not replace the
these positions has distinct effects on oxygen trans
more physiological intervention of mobilization and
port, thus the specific upright position has to be pre
exercise to maximize oxygen transport. Rather, once
scribed specifically as the supported and "propped
the effects of mobilization/exercise have been ex
up" positions in bed do substitute for upright erect
ploited maximally, then body positioning is the next
sitting. These variants only have a role when the pa
best physiological approximation to a mobilized up
tient will deteriorate by attempting to position in the
18
Body Positioning
315
Asleep
Aroused
Cortical
activating
impulses
AFFerent impulses from
sense organs, with collateral
tracts to the reticular formation
FIGURE 18-15
Effect of arousal on cerebral activity. (Reprinted with permission from Browse NL: The physiology
and pathology of bed rest, Springfield, III., 1965, Charles C. Thomas.)
upright erect position, or the patient immediately de
prone or semiprone positions. Patients can be posi
teriorates once in the position. Sitting with the feet
tioned safely, with appropriate supervision and moni
down is preferable to long sit because of the hemody
toring, and comfortably in these full positions by ob
namic benefits associated with this position. Sitting
serving the normal precautions of passive positioning.
up in bed fails to position the patient in a perfectly
A common practice is to progressively turn pa
vertical upright position. Fowler's position in bed can
tients in one-quarter turns, such as supine to side
be maximized and the use of knee breaks in the bed
lying and back to supine and so forth. However, the
provides a gravitational stimulus to the circulating
use of extreme positions and extreme position
blood volume.
changes may yield greater benefit with respect to the
A major difficulty with positioning patients in bed is
degree of perturbation and "stir-up" elicited (Piehl
the tendency to lose the position. Patients lose optimal
and Brown, 1977). Extreme position changes result in
positions in bed very quickly and thus need to be moni
significant alterations in the distributions of V, Q,
tored to ensure the specific positions are maintained.
and V and Q matching. Mucociliary transport is stim
Pillows should not be used to maintain a body position,
ulated, and secretion accumulation and stagnation is
since these are easily compressed and shifted. Blankets
minimized. In addition, the more extreme the body
and sheets tightly rolled and secured with tape, and spe
position, the greater degree of arousal stimulated par
cially made bolsters are considerably more effective in
ticularly in the upright positions, which is essential in
maintaining a patient's body position.
critically ill patients.
Although there is a role for modified positions,
Another impo r t a n t consideration is the time
such as half side lying these positions are often
course of changes in ox.ygen
overused at the expense of full turns to each side, or
and position changes. There are three plausible out
316
PART III
1984; Fink, Helsmoor

1990; Gentillelo, Thomp
patients (Brackett and Condon,
f=4
Supine
HI
h
Recumbent
Propped-up
hi
Sitting
FIGURE 18-16
Approximations of the upright position from supine. The

recumbent and propped-up positons are not comparable
physiologically to the upright sitting position. (Reprinted with
permission from Browse NL: The physiology and pathology

of bed rest, Springfield, 111., 1965, Charles C. Thomas.)
tel, Stein, Lee, and Cohn,
1988; Gonzalez-Arias, Goldberg,

1983; Kelley,
Vi b u l srest, Bell, a n d D u n c a n, 1987; Mein ig,
Leininger, and Heckman, 1986; Summer, Curry,
Haponik, Nelson, & Elston, 1989). These beds are in
son, Tonnesen,
Baumgartner, Hoopes, and Rubin,
dicated for patients who are moderately hemodynami

cally u nstable and on neuromuscular blockers, and
thus tolerate manual turns poorly. Such turning frames
are contraindicated, however, for patients who are less
ill. Even for those patients who require multiple assis
tants and extra caution and time to turn and position
effectively, these issues should never deny a patient a
much needed treatment with proven efi'icacy.
The benefit of these beds on oxygen transport in
critically ill patients has implications for the manage
ment of less critically ill patients. The continuous me
chanical rotation of the Rotobed can be simulated
by increasing the frequency and arc of positions
when manually positioning patients.
PRACTICAL CONSIDERATIONS IN
POSITIONING PATIENTS
Prescriptive body positioning takes
significant
amount of the PTs time as well as other team mem

bers' time. Such prescriptive positioning is based on
clear indications and well-defined parameters; it is
not to be confused with 'routine' positioning. For any
hospitalized patient who is recumbent and inactive
comes: a favorable response, no response, an unfa
compared with being out of hospital, body position
vorable response. With the passage of time, all three
ing is a 24 hour concern, ie, a concern both during
outcomes will deteriorate. The specific time depends
treatment and between treatments. Such patients are
on the multitude of factors contributing to impaired
at risk of impaired oxygen transport.
oxygen transport.
Despite the time and labor involved in turning a pa
Because of the significant changes that can be ex
tient to prone, particularly if mechanically ventilated,
pected with positioning and positioning changes, the
the benefits of this position outweigh the time and ef
(PT) has a prime therapeutic oppor
fort required to prone a p tient even for short periods.
tunity to assess and treat the patient before, during,
Gi ven the considerable benefits that can be derived
and after position changes.
from the prone position, a good case needs to be made
physical therapist
for not turning a patient prone. Frequently, therapeutic

body positioning can be effectively coordinated with
Mechanical Body Positioning
nursing interventions and other procedures.
Mechanical turning beds such as the Rotobed have
Extreme body positions and body position changes
significant benefits On oxygen transport in severely ill
are the goal. However, when these are less feasible,
18
Body Positioning
317
modified positions may be used. Even though the
tient includes subjective and objective evaluation of
greatest benefits will be derived from extreme
indices of the adequacy of oxygen transp0l1 (Part II).
changes as these simulate the normal range o f
Among the most imp0l1ant are oxygen delivery, oxy
changes the human body is exposed to in health,
gen consumption, oxygen extraction, and gas ex
small changes can be effective in altering intrapleural
change indicators such as the A-a02 difference and
gradients slightly so that previously closed alveoli
Pa02/PA02. Subjectively, the patient's facial expres
will be opened even though previously opened ones
sion, respiratory distress, dyspnea, anxiety, discomfort
may be prone to closure. Although modified posi
and pain are assessed. Objectively, heart rate, blood
tions and small degrees of position change should not
pressure, respiratory rate, Sa02, flow rates, beside
be relied upon their effects should not be minimized
spirometry are readily assessed. The appropriate stan
in patients for whom extreme positions are con
dardization and procedures need to be used to ensure
traindicated. Before and after every position change
that the measures are both valid and reliable (see
are prime opportunities to assess the patient, and to
Chapter 6). Because physiological variables are
encourage deep breathing and coughing, or suction
changing from moment to moment, serial measures

over a period of time should be taken to establish an
the patient as indicated.

Another important consideration is the time course
of change in oxygen transport with positions and po
average value rather than using peak or discrete mea

sures which may misrepresent a treatment effect.
sition changes. There are three possible outcomes: a
In order to interpret and compare various mea
favorable response, no response, an unfavorable re
sures, the Fi02 and any change in FI02 must be
sponse. With the passage of time, all these outcomes
recorded. The use of the ratio Pa02/Fl02 enables
will deteriorate. The specific time depends on the
comparison of gas exchange within and between pa
multitude of factors that contribute to the patient's
tients when patients Fi02s differ or are changed

(Dean and Ross, 1992c). Similarly, for mechanically
oxygen transport and the patient's responses.
ventilated patients, any changes in the ventilatory pa

rameters must also be noted, in addition to other in
MONITORING THE RESPONSE TO A BODY
POSITION OR POSITION CHANGES
terventions that have a direct effect on oxygen trans
The prescriptive parameters of body positioning and
conclude within reasonable doubt that the position or
port. Only in this way will the clinician be able to
body position changes include the positions selected,
position change was instrumental in enhancing car
the duration spent in each position, the sequence of
diopulmonary function.
position changes, the cycle of all positions, and posi
Measures are recorded before (pretreatment base
tion changes overall. Because a patient necessarily
line), during, and at periodic intervals following the
assumes a body position at all times, positioning pa
treatment. A valid stable pretreatment baseline is es
tients between treatments can contribute as much to
sential to determine the therapeutic effect of a given
the overall treatment response as the treatment itself
position on oxygen transport. Variables monitored
as the patient is likely to spend more time in the be
during the treatment are focused on ensuring that
tween-treatment positions than in the within-treat
the treatment is having a beneficial effect, in addi
ment positions.
tion to its not having any deleterious effect on the
The duration and frequency of the positions and
patient subjectively or with respect to any parameter
the frequency of body position changes are response
of oxygen transport. As long as beneficial effects
dependent rather than time-dependent. Monitoring is
are being recorded a position can be safely main
the basis for defining and modifying the body posi
tained, however, diminishing returns can be ex
tioning prescription. The physiological variables to be
pected as the period becomes prolonged. Patients
monitored depend on the patient's specific presenta
maintained in static positions for more than one to
tion, cardiopulmonary dysfunction, and its severity
two hours need to be monitored closely. A position
and distribution. Monitoring of the noncritically ill pa
change is physiologically defensible after this dura
318
PART III
tion rather than the risk of diminishing returns and
ations presented. Thus this chapter has presented prin
potentially worsening the patient's condition.
ciples that must be considered in the decision-making
Although sicker than a noncritically ill counter
process behind the prescription of therapeutic body
part, the critically ill patient has the advantage of
positioning, rather than a treatment prescription for a
having more monitoring lines in place. These lines
given patient.
give access to several measures and indices of oxy

gen transport, and certain hemodynamic and pul
monary variables are available continuously.
REVIEW QUESTIONS
In summary, the prescription of therapeutic body

positions is based on a detailed analysis of each pa
I. Describe the effects of gravity on cardiopul

monary function and oxygen transport.
tient's unique presentation and the factors contributing

to impairment of oxygen transport or threatening it.
2. Distinguish between prescriptive and routine

body positioning.
Then those positions that are predicted to result in the

best therapeutic outcome are selected and applied, and
3. In reference to the seated upright position, describe
those that are predicted to lead to an adverse result are
the effects of different body positions (i.e., supine,
used minimally and with appropriate monitoring.
side lying, head down, and prone) on cardiopul
Monitoring is an essential component to body position
monary function and oxygen transport in health.
prescription in that it confirms the prediction of benefi
4. In reference to the seated upright position, describe
cial and deleterious positions, establishes when a posi
the effects of different body positions (i.e., supine,
tion change is indicated, and helps the PT anticipate
side lying, head down, and prone) on cardiopul

monary function and oxygen transport in disease.
the point of diminishing returns of any given body po

sitions. The specific physiological variables monitored
5. Explain how a physiologically ideal body posi
are those that reflect the steps in the oxygen transport
tion with respect to oxygen transport can be dele

terious over time.
pathway that are most affected in a given patient.
6. Distinguish between the prescription of therapeu

tic body positions and frequency of body posi
SUMMARY
tion changes.
The purpose of this chapter was to differentiate rou
7. Describe the principles of monitoring oxygen

transport variables during body positioning.
tine and therapeutic body positioning designed to op

timize oxygen transport. The physiological effects of
different body positions and changing body positions
on cardiopulmonary and cardiovascular function and
oxygen transport, were described. The primary goal
is to strive toward the physiological position for opti
mizing oxygen transport, that is, upright and prefer
ably moving. Issues related to optimizing the pre
s c r i p t i o n of t h e r a p e u t i c b o d y p o s i t i o n i n g and
monitoring treatment outcome were presented.
This chapter focused on the physiological effects
of body positioning, an intervention that has well-doc
umented, direct and potent effects on oxygen trans
port. Establishing a clear rationale for prescribing a
specific body position or body position changes is es
sential. The rationale, however, is based on multiple
other factors in addition to the physiological consider
References
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Physiological Basis for Airway

Clearance Techniques
Anne Mejia Downs
KEY TERMS
Active cycle of breathing technique (ACBT)
Percussion
Airway clearance techniques (ACTs)
Positive expiratory pressure (PEP)
Autogenic drainage (AD)
Postural drainage (PD)
Flutter
Shaking
Forced expiratory technique
Trendelenburg
High frequency chest compression (HFCC)
Vibration
Manual hyperventilation
INTRODUCTION
Research studying the results of airway clearance
Techniques for assisting the mobilization of secre
are often difficult to evaluate because the components
tions from the airways have long been advocated for
of a given treatment have not been standardized.
use in the patient with an impairment in mucociliary
Availability of equipment or education about a tech
clearance or an ineffective cough mechanism. The
nique as well as cultural differences in its application
goals of this therapy are to reduce airway obstruction,
confound the results. Differences in the outcome
improve mucociliary clearance and ventilation, and
measures for a given technique also occur-some
optimize gas exchange.
studies use wet or dry (dehydrated) sputum volume
Airway clearance techniques have been referred
or radioaerosol clearance, whereas other studies use
to in the literature in a variety of ways, including
pulmonary function tests, radiographic evidence or
chest p h y s i o t h e r a p y , c h esl ph y s i c a l t h e r a p y,
arterial blood gases to asses the effectiveness of an
bronchial drainage, postural drainage therapy, and
airway clearance technique. Although a treatment has
bronchial hygiene.
been shown to be effective in one cross section of pa

321
322
PART III
tients with pulmonary disease, care must be taken not
may interfere with this process. Retained secretions
to generalize the effectiveness of the treatment across
or mucus plugs in the airways may interfere with the
other groups of patients or differing time frame
exchange of oxygen. The secretions need to be mobi
(acute vs. chronic). The majority of secretion clear
lized from the peripheral or smaller airways to the
ance research has been focused on patients with cys
larger, more central airways where they may be re
tic fibrosis, as the need for ongoing secretion removal
moved by coughing or suction.

The following conditions are indications for air
is apparent in this population.

Recently the "gold standard" of airway clearance,
way clearance:
namely a combination of postural drainage, percus
I. Cystic fibrosis-In this multisystem genetic
sion, and vibration with cough, has been challenged
disease, copious (often purulent), thick secre
(Lapin, 1994). The indications for routine airway
tions and mucus plugs block the peripheral and
clearance with certain diagnoses have been ques
central airways. Even infants diagnosed with
tioned and the conditions leading to effective applica
cystic fibrosis, whether symptomatic or not,
tion have been examined. Postural drainage and per
show evidence of small airway obstruction in
cussion has been shown to be ineffective in some
the form of bronchial mucus casts (Wood,
cases, and in fact, to be detrimental to the pulmonary
1989). Recurrent bacterial infections combined
status of some patients. Caregivers have also been
with this mucus hypersecretion in the lungs
shown to suffer from the performance of percus
leads to destruction of the bronchial walls, or
sion-repetitive motion injuries of the wrists have
bronchiectasis. Airway clearance continues to
been documented as a result of regular performance
be an important therapy in the treatment of
of percussion (Ford, Godreau, Burns, 1991, MMWR
cystic fibrosis. This practice is supported by
Publication 1989).
evidence of deteriorating lung function when
Alternate techniques have arisen out of the need to
regular treatments of postural drainage and
find effective methods for those patients not respon
percussion have been stopped (Desmond,
1983, Reisman, 1988).
sive or not tolerant of traditional methods. A desire to

increase compliance with airway clearance (Currie,
2. Bronchiectasis-This condition results in a
1986), especially in those patients approaching ado
breakdown of the elastic tissue in the bronchial
lescence and adulthood has led to an investigation of
walls, causing severe dilation. Inflamed mucosa
more independent techniques. Many of these tech
and copious, purulent secretions are present in
niques have been practiced for years in European
this condition. Airway clearance has been
countries, but are more recently being introduced to
shown to benefit patients with bronchiectasis in
practitioners in the United States.
the mobilization of sputum (Mazzocco, 1985,

Gallon, 1991).
It is important to remember, however, that secre

tion clearance is but one step to take toward realizing
3. Atelectasis-This condition is caused by the
effective gas exchange in the complex oxygen trans
collapse of an alveolar segment, often by re
port pathway (Dean, 1992). Airway clearance, when
tained secretions. It is a documented sequela of
indicated, should be integrated into a total approach
patients who have undergone surgery under

general anesthesia, especially thoracic or ab
to optimize oxygen transport.
dominal surgery. Airway clearance techniques

are indicated where atelectasis is suspected to
INDICATIONS FOR AIRWAY CLEARANCE
be caused by mucus plugging (Marini, 1979,

Hammon, 1981).
Oxygen transport is the primary purpose of the car

diopulmonary system (see Chapter 1). Ventilation of
4. Respiratory muscle weakness-Many patients
the alveoli is an important step in the oxygen trans
with neurological or metastatic diseases or gen
port chain that allows optimal delivery of oxygen to
eral debilitation, tend to hypoventilate or have an
the tissues. Several medical and surgical conditions
increased work of breathing. They are unable to
Physiological Basis for Airway Clearance Techniques
19
323
maintain adequate control of respiratory secre
tance of gravity (Figure 19-1). Positioning the patient
tions and often have a weak, ineffective cough
to enable gravity to assist the flow of bronchial secre

standard treatment
(Massery, 1987). This is especially true in pa
tions from the airways has been
tients with diminished diaphragm innervation re
for some time in patients with retained secretions
sulting from spinal cord injuries (Wetzel, 1990).
(Zadai,1981).
5. Mechanical ventilation-Patients on ventilatory
Knowledge of the anatomy of the tracheobronchial
support for any reason, including obtunded or
tree is vital to an effective treatment. Each lobe to be
comatose patients, are at risk for atelectasis and
drained must be aligned so that gravity can mobilize
are unable to independently manage their secre
the secretions from the periphery to the larger, more
tions (Dickman, 1987).
central airways. The mechanism of postural drainage
6. Neonatal respiratory distress syndrome-These
is considered to be a direct effect of gravity on
infants are born lacking surfactant in the lungs,
bronchial secretions, although a study by Lannefors
which results in atelectasis. Airway clearance
(1992) observing that gravity influences regional
techniques may be useful in clearing secretions
lung ventilation and volume suggested these other
and preventing atelectasis but must be moni
mechanisms are also involved.
tored carefully in this population (Finer, 1978).
Postural drainage (also k n o w n as b r o n c h i a l
7. Asthma-This condition is characterized by the
drainage) has been shown t o b e effective i n mobiliz
presence of hyperreacti ve airways and mucus
ing secretions in patients with cystic fibrosis (Wong,
plugging. Airway clearance techniques may be
1977, Lorin, 1971), bronchiectasis (Mazzacco, 1985),
beneficial to assist with the mobilization of
and other pulmonary diseases (Bateman, 1981; Zaus
mucus plugs but are not helpful in treating un
mer, 1968). Other treatments such as percussion, vi
complicated acute exacerbations (Eid, 1991).
bration, and the active breathing cycle (ACB) tech
Chest physical therapy techniques appear not to be
nique may be used while the patient is in postural
beneficial in the treatment of patients with pneumo
drainage positions.
nia or chronic bronchitis without large amounts of se
There are many contraindications to optimal posi
cretion production. No differences were found with
tioning for PO, especially the head down or Trende
the inclusion of postural drainage and percussion in
lenberg positions required for the lower lobes.
these populations (Britton, 1985; Sutton, 1982;

Rochester, 1980; Wollmer, 1985).
Viral bronchiolitis is an asthma-like lung disease
Percussion
occurring in infants less than 2 years of age. These
Percussion, sometimes referred to as chest clapping,
patients do not appear to benefit from airway clear
is a traditional approach to secretion mobilization. A

rhythmical force is applied with cupped hands to the
ance techniques (Webb, 1985).

Also of little benefit, and possibly harmful, is the
patient's thorax over the involved lung segments with
inclusion of chest physical therapy in the routine care
the aim of dislodging or loosening bronchial secre
of postoperative patients without extensive secretions
tions. This technique is performed with the patient in
(Eid, 1991). Even in patients with a history of lung
postural drainage positions and requires a caregi ver
disease, the use of airway clearance techniques have
to administer. In the United States,percussion in con
failed to affect the incidence of atelectasis as a post
junction with postural drainage continues to be a
operative complication (Torrington, 1984).
mainstay of treatment of the person with pulmonary

disease, especially in neonates or patients who are
unresponsive.
Postural Drainage
The proposed mechanism of action of percussion
Postural drainage (PO) is a passive technique, in
is the transmission of a wave of energy through the
which the patient is placed in positions that allow the
chest wall into the l u n g . T h e resulting motion
bronchopulmonary tree to be drained with the assis
loosens secretions from the bronchial wall and
324
PART III
Normal
Phase: 1
FIGURE 191
Phases of autogenic drainage shown on a spirogram of a normal person. Phase 1: unstick phase 2:
collect, phase 3: evacuate.
volume,
FRC
(VT
ERV expiratory reserve volume. RV reserve

IRV inspriatory reserve volume; fRV + VT + ERV
tidal volume,
Punctual residual capacity,
vital capacity)
moves them proximally where ciliary motion and

cough (or suction) can remove them. The combina
tion of postural drainage and percussion has been
shown to be effective in secretion removal (Denton,
1962; May, 1979, Radford, 1982). A study by Ross
man et al. (1982) is in disagreement, finding that me
c h a n i c a l p e rcussion did n o t enhance postural
drainage in secretion removal.
A handheld mechanical percussor may be used by
a caregiver to decrease fatigue or by the patient for
self-administration of percussion. The effectiveness
of mechanical versus manual percussion has been
studied. Maxwell and Redmond (1979) found me
chanical percussion equivalent to manual percussion
in affecting removal of secretions. This is supported
by Pryor et a1. (1979) in patients using the forced ex
piration technique, although there was a significant
increase in pulmonary function with manual tech
niques (Pryor, Parker, and Webber, 1981).
There are many contraindications to percussion. If
the patient's pulmonary status is of greater concern
than the relative contraindications, it may be decided
to modify and administer the treatment.
Vibration
Vibration is a sustained cocontraction of the upper
extremities of a caregiver to produce a vibratory force
that is transmitted to the thorax over the involved
lung segment. Vibration is applied throughout exha
lation concurrently with mild compression to the
chest wall. Vibration is often applied in postural
drainage positions following percussion to the area.
A mechanical vibrator may be used by the patient or
a caregiver in place of manual vibration.
Vibration is proposed to enhance mucociliary
transport from the periphery of the lung fields to the
larger airways. Since vibration is used in conjunction
with PD and percussion, many studies do not separate
out the effects of vibration from the other compo
nents. In fact in multiple studies, the techniques of
PD, percussion, and vibration are described as a single
entity and referred to as chest physical therapy (CPT),
pulmonary therapy, or postural drainage therapy.
Pavia (1976) demonstrated a higher, though not sta
tistically significant, rate of secretion clearance and
sputum production with vibration. However, this study
was conducted with subjects in an upright position
19
325
only, not a replication of the use of vibration clinically.
applies shaking or vibration at the very beginning of
Mackenzie et al. (1980) used measurement of total
exhalation to mobilize secretions. The timing of this
lung/thorax compliance to assess the effect of secre
sequence is important to achieve the desired effect
tion clearance. Significant improvement in total
(Webber, 1988). It has been likened to simulation of a
lung/thorax compliance was demonstrated after treat
cough----deep inspiration, pause, and forceful exhala
ment with postural drainage, percussion, and vibra
tion. Saline may be instilled into the airway at the be
tion in mechanically ventilated patients. Feldman et
ginning of the cycle, with suctioning a component at
al. (1979) demonstrated improved ventilatory func
the end of treatment of each side. Manual hyperventi
tion by showing a significant improvement in expira
lation is peIt'ormed in postural drainage positions and
tory flows at lung volumes in patients receiving pos
requires two competent caregivers to peItorm.
tural drainage, percussion, vibration, and coughing.
The inspiration provided by the manual ventilation

bag, which is deeper than the patient could generate,
promotes aeration of the alveoli. The compression of
Shaking
the thorax augments the high expiratory flow rate
Shaking consists of a bouncing maneuver sometimes
from the bag, accelerating the movement of the secre
referred to as "rib splinging" against the thoracic wall
tions from the smaller airways to the larger bronchi
in a rhythmic fashion throughout exhalation. A concur
(Clement, 1968).
rent pressure is given to the chest wall, compressing
Clement (1968) reports this method of airway
the thorax. Shaking is similar in application to vibra
clearance enables patients to be maintained on ventila
tion, with shaking being on one end of the spectrum in
tors for long periods with normal lung function. It has
application of force, and vibration being on the oppo
been demonstrated that hyperinflation and suction in
site end, supplying a gentler amount of pressure. Many
the treatment of atelectasis was enhanced by the addi
variations exist throughout the spectrum between these
tion of positioning and vibrations (Stiller, 1990).
techniques. Shaking may be used in place of percus

sion or intermittently with percussion and vibration.
Shaking may be used in postural drainage positions
Active Cycle of Breathing

Thompson (1973) in New Zealand described clearing
and requires the assistance of a caregiver.

Shaking is proposed to work in the same manner
bronchial secretions in patients with asthma by a
as vibration, mobilizing secretions to the central,
technique of forced expirations and diaphragmatic
larger airways from the lung periphery. Since the
breathing. British physiotherapists have modified the
compressive force to the thorax is greater, producing
technique and further described it in the literature,
increased chest wall displacement, the stretch to the
first as the forced expiration technique (FET) (Pryor,
respiratory muscles may produce an increased inspi
1979) and later as the ACB technique (Webber and
ratory effort and lung volume (Levenson, 1992).
Pryor, 1993).
The same relative contraindications for percussion
As described by Webber and Pryor (1993), the
should be observed for shaking, since it does involve
ACB consists of repeated cycles of three ventilatory
application of force to the thorax.
phases: breathing control, thoracic expansion exer

cises, and the FET. Breathing control is described as
gentle tidal volume breathing with relaxation of the
Manual Hyperinflation
upper chest and shoulders. The thoracic expansion
This technique is used on patients with an endotra
phase consists of deep inspiration, and may be ac
cheal or tracheostomy tube that can be attached to a
companied by percussion or vibration peIt'ormed by a
manual ventilation bag. One caregiver uses the bag to
caregiver or the patient. This phase helps to loosen
hyperinflate the lungs with a slow, deep inspiration
secretions. The forced expiration technique involves
and after a short inspiratory pause, provides a quick
one or two huffs (forced expirations). Webber and
release to allow rapid exhalation. A second caregiver
Pryor (1993) report huffing from a mid-lung volume
326
PART III
Cardiopulmonary
(a medium sized breath
and continued down to
the
hV[)OSiCn tlOn. This sug
low-lung volume will move secretions from the pe

to the upper
tions may be cleared
ume (a
breath
a huff from
effective in gravity assisted
1990). The
bronchospasm
o f thoracic expansion,
which increases
described the
in a relaxed state without use of
aohragmatic breathing to mobilize secre
airflow. It consists of three
at low-lung volumes to "unstick"
is the point in the airways
where the pressure is
nMtn ,,1
(Chevaillier,
of "equal
to the pleural pressure.
The forced expiratory maneuver
PD and cJap-
AD is an antidyspnea technique based on
pressure point," which is the basis for the FET. The

pressure point
the day,
mucus was mobilized better than
Mead et at
1967 for treat
ment of asthmatic patients. He observed that during
behind secretions and
assist in their mobilization
was in
Chevaillier in Belgium in
sleep, as well as playing and laughing
collateral
ventilation, allowing air to
(1
(AD) or
troduced
The period of breathing control is essential be

(Lapin,
Autogenic Drainage
drainage) posi
1992).
tween the other phases to
retention of
little sputum.
lung vol
The ACB may be performed
in the sitting position, but has been shown to be more

tions (Steven,
nJY'HmcrPfl
secre
peJ]DJ1eral secretions,
(2) breathing at low- to mid
volume (tidal volume) to collect the mucus in the
compres
(3) breathing at mid- to
sion of the airway peripherally to the EPP. A huff
middle
from high lung volume causes compression within
volumes to evacuate the mucus from the central air
the trachea and bronchi to move secretions from
ways
these
laxed position and exhales actively with the mouth and
airways. A huff continued to low lung
volume shifts the EPP more oeripherallv to move
and
1984). The patient is seated in a re

open and listens for the movement of mucus
while
a wheeze. The phases in the AD techdelJ'ict<d in
a patient
nhU ;AIA""
by pa
by Shoni
tients independently has been shown to clear more

sputum in a shorter amount of time than PD with selfcombined with
and shaking by
a physical therapist (PT)
1986) and sputum
clearance (Sutton,
1983) have been demonstrated in
patients with cystic fibrosis who
the FET
ensure
of lung segments by collateral fill-
serve volume range. By lowering mid-tidal volume

below functional residual capacity
lapsible bronchial wails, it increases the expiratory
tidal volume is lowered in the range of normal

tory reserve volume. The second
air
of tidal volume
Another benefit of this
from
flow in patients with obstruction without
lies in its ability to maintain oxygen satura

tion. The decrease in oxygen saturation that has been
demonstrated with postural
secretions
from peripheral lun!:! regions are mobilized

alveolar ducts.
Because huffing has been shown to stabilize col
(Hietpas,
re
and then a deep exhalation into the
into their postural drainage treatments.
way
has been ex
(1989). The first
starts with an inspiration, followed by a breath hold to
Improvement
in pulmonary function
19-1.
of AD's three
and percussion
has been prevented with the use of the ACB technique
1990). Hassani et al. (1994) has recently shown
of AD consists
so that
is
reserve volume into the in-
reserve volume range to mobilize secretions

from the
of the lungs. The
of the
so
airflow must be adjusted at each level of
that the maximal expiratory ailflow is reached without

being high enough to cause collapse of the
that unproductive cough and FET resulted in the
Flow volume curves show that higher flows of
movement of secretions proximally from all regions of
duration can be achieved with AD (Dab.
19
demonstrating that mucus can be moved further and at

a faster rate. The third phase consists of deeper inspira
tion into the inspiratory reserve volume, with huffing
often used to help in evacuating the mobilized secre
tions. Control of ailflow during this final phase is es
sential to avoid uncontrol led, unproductive coughing.
The Belgian method has been modified by German
practioners to use a combination of diaphragmatic and
costosternal breathing in a treatment that is not delin
eated into phases (David, 1991). The patient varies his
or her mid-tidal volume in a passive exhalation followed
by an active exhalation through pursed lips or through
the nose. The German method includes other maneuvers
in conjunction with autogenic drainage, including in
halation therapy, FET, chest wall exercises, and sports.
Autogenic drainage has been compared with posi
tive expiratory pressure and PD with percussion/
vibration. More sputum was produced with AD in pa
tients with hyperreactive airways (Davidson, 1988).
In a 2-year crossover trial, AD was found to be as ef
fective as conventional CPT among patients with cys
tic fibrosis for improving pulmonary function
(Davidson, 1992). However, patients exhibited a
strong preference for AD, increasing the likelihood of
compliance. Miller (1993) showed greater clearance
of inhaled radioisotope with AD vs. the ACB tech
nique, with no significant differences in sputum
weight, spirometry, or transcutaneous oxygen satura
tion. Giles (1993) also studied oxygen (02) saturation
in AD and found an increase in O2 saturation with
AD over PD with percussion and greater sputum re
covery with AD.
The learning of AD requires tactile and auditory
feedback and continued modifications of the patient's
technique is necessary, at least initially, to achieve a
good result. AD takes considerable time to learn and
requires a great deal of cooperation from the patient.
Therefore it is not suitable for the very young or dis
tractable patient.
Positive Expiratory Pressure

The development and utilization of positive expira
tory pressure (PEP) breathing came about in the
1980s in Denmark and is now widely used in Europe
with increasing acceptance in the United States.
327
The application of PEP consists of a mask or

mouthpiece connected to a one-way breathing valve
to which expiratory resistors are attached. This re
sults in positive pressure in the airways during exha
lation. A manometer in the circuit determines and
monitors the correct pressure generated by the pa
tient. A patient uses PEP in a cycle of about 10
breaths at tidal volume with slightly active expiration
followed by huffing or coughing to expectorate secre
tions (Falk and Kelstrup, 1993).
High- or low-pressure PEP may be prescribed. In
low-pressure PEP, the resistance is regulated to
achieve 10 to 20 cms of water pressure during expira
tion. The pressure should be sustainable during only
slightly active expiration. The prescription for high
pressure PEP requires the patient to perform forced
vital capacity maneuvers through the range of expira
tory resistances with the mask connected to a spirome
ter. The appropriate resistor is one that produces a flow
volume curve demonstrating a maximal forced vital
capacity, good plateau, and no curvilinearity (Prasad,
1993). In general, the range of pressure generated with
high pressure PEP is 50 to 120 cms of water pressure.
Low-pressure PEP is used more often, as it offers
equal effectiveness at a lower risk of pneumothorax.
It is theorized that PEP allows more air to enter
through collateral channels, allowing reinflation of
collapsed alveoli. Pressure is built up distal to an ob
struction, promoting the movement of secretions to
wards the larger airways (Anderson, 1979; Groth,
1985). Airway stability is maintained with PEP pro
moting improved ventilation and gas exchange, as
well as airway clearance (Hardy, 1994). Supplemen
tal oxygen can be supplied during treatment with PEP
and nebulized medication has been shown to be ef
fectively delivered with this treatment as well (An
derson, 1982).
PEP has been shown to benefit patients at risk for
postoperative atelectasis but has also gained wide
practice in the area of airway clearance, especially for
patients with cystic fibrosis (MaJhmeister, 1991). Nu
merous studies have demonstrated PEP's effective
ness. Tyrrell (1986) has shown the PEP mask to be as
effective as conventional physiotherapy over a 1
month period with no difference in pulmonary func
tion. Falk (i 984, 1993) demonstrated increased spu
328
PART III
tum production and clearance with the use of PEP
Recently approved by the FDA for use by patients
over FET alone. However. Hofmeyer (1986) found
with cystic fibrosis, the Flutter'M continues to be the
FET produced a greater quantity of sputum without
focus of study in the United States. Konstan et a!.
the addition of PEP. Oberwaldner (1986) evaluated
(1994) compared the amount of sputum expectorated
lung function during 10 months of regular treatments
with use of the Flutter'" vs. vigorous voluntary cough
with high-pressure PEP and found reduced pul
vs. PD, percussion and vibration. More than three
monary hyperinflation and airway instability and
times the amount of sputum was produced by subjects
conventional CPT.
with cystic fibrosis using the Flutter'" than with the
higher flow rates with PEP
VS.
These improvements in lung function deteriorated
other two methods and no adverse effects were re
only 2 months after a return to conventional CPT. A
pOited. Ambrosino (1991) has reported success in the
study by Plfeger et a!. (1992) compared PEP to AD
treatment of COPD patients with the device.
and found that PEP produced the highest amount of
Reports in the European literature advocate the
sputum and an increase in lung function when added
use of the Flutter'" for airway clearance (Althaus,
to both techniques. Finally, decreased duration of
1989). In comparison with AD, the Flutter'" was
hospitalization has been cited as a benefit of PEP for
found to be equal in amount of mucus expectoration
airway clearance (Simonova, 1992).
(Lindemann, 1992). When compared with the PEP
Increased independence for the patient and pre
m ask, the Flutter'" showed a small increase i n
sumably, better compliance have been cited as advan
spirometry, whereas the PEP-mask did not, but the
tages of this technique. However, frequent assess
two techniques were otherwise comparable (Schw.
ment of patient technique and appropriate level of
Med. Wschr. 1989).
resistance is recommended (Lapin, 1990). A PEP
The advantages of the Flutter'" device lie in its
mouthpiece (Resistex) has recently been FDA ap
pOltability and ease of learning. Young children can
proved, but the PEP mask has not yet been approved
be taught to use the device effectively, and because
by the FDA.
of its small size, it can easily be used for multiple
A form of PEP in combination with high fre
treatments throughout the day.
quency oscillation is available in a device developed

in Switzerland. which is quickly gaining popularity in
the United States. The Flutter VRP1 (VarioRaw SA,
High Frequency Chest Compression
Aubonne, Switzerland) is a handheld device that in
EffOits aimed at mucus clearance by creating a differ
terrupts the expiratory flow and decreases the col
ential air flow rate, that is, greater expiratory than in
lapsability of the airways. The pipe-like device con
spiratory flow rate, led to the development of a high
sists of a steel ball, a plastic cone, a pertorated cover,
frequency chest compression (HFCC) systcm.
and a mouthpiece. The patient completes about lO to
Hansen and Warwick (1990) designed a large-vol
15 deep breaths keeping the cheeks flat while the
ume variable frequency air-pulse delivery system to
Flutter'M is tilted to achieve the maximum effects of
be used by patients with obstructive lung disease to
the vibration in the chest. This is followed by huffing
promote mucus clearance.

The ThAIRapy'" Vest (American Biosystems,
to eliminate the airway secretions.

Exhalation through the Flutter'M device causes air
Inc.) system consists of an inflatable fitted vest con
way vibrations and oscillating endobronchial pres
nected to an air-pulse. generator by flexible tubing.
sures (Althaus, 1993) to ease the expectoration of
This device provides oscillation of the entire thoracic
mucus. The PEP maintained by the Flutter (5 to 35
cavity at varying frequencies (5 to 25 Hz) and is used
cms of water pressure) prevents dynamic airway
while sitting upright. The lung volume expired tends
compression and improves airflow acceleration.
to increase with lower frequencies (less than to to 12
Therefore the improvement in expectoration is based
Hz), whereas the flow rates tend to increase with
on the increase in airway diameter, as well as on the
higher frequencies (12 to 20 Hz). Three frequencies
improvement in airflow acceleration (Schibler, 1992).
are selected for large volume and three for high
19
329
flows. Each frequency is used for 3 to 5 minutes with
Hospitalized patients with acute exacerbation of
conti I1UOUS ul:J"osolized medication or saline to assist
their lung disease have been shown to tolerate HFCC
secretion Illohilil.ation (Warwick, 1992).
well (Burnett, 1993), and safety and tolerance of this
Two probahlc mechanisms of action have been of

fered to explain the significant increase in sputum mo
method has been demonstrated in long-term mechani

cally ventilated patients (Whitman, 1993).
bilizJlion (Kious, 1(94). The first mechanism pro
Expense of the apparatus may be a significant de
poses that oscillatory airflow leads to changes in the
terrent to its use; it is more costly than other mechan
con.;islency of mucus, which result in increased spu
ical aids for airway clearance. However, in a study of
tum mobilil.ation. Significant decreases in mucus vis
HFCC users insured by Blue Cross and Blue Shield,
coelasticity were observed during administration of
a 49% reduction in health care costs was shown in
oscillatory aitflow (Tomkicwicz et aI, (994). The sec
the year following initial use of the vest as compared
ond mechanism proposes that the difference between
with the year prior to HFCC use (Ohnsorg, 1994).
the expiratory and inspiratory velocities produces
The impact of the llse of the HFCC device in a hospi
enough to move muclls. Chang et
tal department was analyzed with a substantial sav
al. (1988) lkmonstrated that nonsymmetrical airflow
ings resulting from therapy self-administration
(peak expiratory flow rates greater than inspiratory
(KIous, 1993).
shear forces
s lrong
flow ratt:s) could be a significant factor leading to en

harlCed mllcus clearance during the administration of
HFCC. Each chest compression produces a transient
Exercise
flow pulse similar to that observed during coughing
In addition to its many effects on health and well
and by using those flows with the greatest rates and
being, exercise has been shown to assist in secretion
volumes, sufficient force is obtained to move mucus
clearance. It has been suggested that exercise can re
in the airway (Warwick, 1991).
place all or pmt of a conventional chest physiotherapy
High frequency chest wall compression has been

shown to inc re as e mucus clearance rates in dogs,
routine in some patients or at some stages of lung dis

ease (Zach, 1982; Andreasson, 1987; Cerny, 1989).
with the most pronounced effect in the II to 15Hz
Exercise increases mucociliary transport in pa
frequency range (King, 1983). Radford et al. (1982)
tients with chronic bronchitis (Oldenberg, 1979).
used bronchoscopy to demonstrate a marked increase
Higher transpulmonary pressure with aerobic exer
in speed and flow of mucus by oscillations at even
cise may open closed bronchi as well as increase col
higher frequencies not attainable by manual percus
lateral ventilation to allow mucus to be movcd (An
sion. Results of short-term use of the ThAIRapy'"
dreasson, 1987). It has also been shown that exercise
vest have been mixed, but show HFCC to be at least
induced hyperventilation is more effecti ve than eu
as effective as conventional CPT. Robinson (1992)
capnic hyperventilation in mobilizing bronchial se
showed no significant i m pro vement or deterioration
cretions (Wolff, 1977). The contribution of expira
of lung function with its use. In two different studies,
tory ailflow and exercise-induced coughing are other
Kluft (1992) and Faverio (1994) demonst rated in
factors in more effective secretion removal.
creased wet and dry sputum weights using HFCC vs.
Some studies conclude that exercise alone is not
manual CPT, and Arens (1993) showed similar dry
sufficient and recommend its use to complement
sputum weight, but an increase in wet sputum weight
other forms of airway clearance. Airway clearance
and a significant improvement in pulmonary function
using PD and FET was shown to be more effective
with HFCC vs. conventional CPT. One 2-year study
than exercise with a cycle ergometer at inducing spu
showed improved lung function and greater sputum
tum expectoration (Sath, et ai, 1989). Results from
production in subjects with cystic fibrosis with the
Bilton et al (1992) demonstrated that any modality
use of HFCC vs. manual CPT (Warwick, 1991). No
which included the ACB technique in PD positions
adverse effects were ohsL rvcd with long-term use of
alone or in combination with exercise is better than
the ThAIRapy'" vest.
exercise alone at clearing sputum.
330
PART III
Other studies have suggested that some forms of
1990). However, if the patient develops atelectasis,
exercise may serve as a replacement for chest physio
the stress of respiratory embarrassment may also in
therapy, citing a lack of decrease in lung function fol
crease intracranial pressure. In this instance, the deci
lowing the cessation of CPT and continuing with an
sion may be made to tip the patient to clear the at
exercise program (Zach, 1984; Andreasson, 1987). In
electasis and then subsequently return to a modified
hospitalized patients with cystic fibrosis, no signifi
conservative regimen (Frownfelter, 1987).
cant change in pulmonary function was reported
A fall in arterial O2 saturation has been reported
when exercise was substituted for two treatments of
with the use of postural drainage from additional in
PD, percussion and vibration, and the weight of spu
chest physiotherapy, although the effects of PD were
tum produced was equivalent (Cerny, 1989).
not separated techniques (Selsby, 1990; Huseby,
When mucous clearance was studied, no signifi

cant differences were found between exercise on a
cycle ergometer, postural drainage, and PEP mask
Contraindications for Postural Drainage
breathing (Lannefors, 1992). Increases in sputum ex

pectoration on exercise vs. nonexercise days have
All Positions Are Contraindicated
been reported (Zach, 1981; Baldwin, 1994). For pa
for the Following:
tients with cystic fibrosis who demonstrate compli
Intracranial pressure (ICP)
ance with an exercise program alone or in addition to
>
20 mm Hg
Head and neck injury until stabilized
another form of secretion mobilization, there is evi
Active hemorrhage with hemodynamic instability
dence of positive prognostic value (Nixon, 1992).
Recent spinal surgery (e.g
It is difficult to compare these studies across the

board; however, because the mode and length of ex
spinal injury
ercise differs, as does the measurement of effective
Active hemoptysis
ness of airway clearance. Exercise as an airway clear
Empyema
ance technique is not suitable for the very young (less
Bronchopleural fistula
than 4 to 5 years of age), patients with neuromuscular
laminectomy) or acute
Pulmonary edema associated with congestive heart
limitations, or patients with severely limited exercise
failllJ'e (CHF)
tolerance. Moreover, the potential need for supple
Large pleural effusions
mental oxygen during exercise should be monitored.
Pulmonary embolism
Nonetheless, evidence suggests that an exercise pro

gram, in addition to clearing secretions, may decrease
Aged, confused, or anxious patients
morbidity and mortality t J improving exercise ca
Rib fracture. with or without flail chest
pacity (Lapin, 1993).
Surgical wound or healing tissue
Contraindications/Precautions to Airway Clearance
Trendelenburg Position is Contraindicated

.
for the Following:
General precautions and contraindications
Patients in whom increased ICP is to be avoided
to postural drainage positioning
Uncontrolled hype11ension
It is essential that the therapist and the health care
Distended abdomen
team discuss treatment priorities. A decision to use
Esophageal surgery
postural drainage might be made despite a contraindi
Recent gross hemoptysis related to recent l ung

carcinoma
cation, if the benefits were thought to outweigh the

risks in a particular case.
Uncontrolled airway at risk for aspiration
For example, it is known that use of the Trende

lenburg (head down) position increases intracranial
AARC Clinical Practice Guideline.
pressure in neurosurgical patients (Humberstone,
apy.
(1991). Postural drainage ther

RespiraIOI)' Care, 36 (12), 1418-1426.
19
Physiological Basis ror Airway Clearance Techniques
331
[976). Therefore O2 saturation levels should be mon
show an intolerance for percussion as part of chest
itored during treatment, most importantly in those pa
physiotherapy. Campbell et a1. (1975) demonstrated
tients with known [ow Pa02 values.
a fall in FEV I associated with percussion that was
Caution must also be used in treating the patient
not evident when percussion was omitted. Adminis
with end-stage lung disease in postural drainage posi
tration of a bronchodilator before treatment with per
tions because of the risk of hemoptysis (Hammon,
cussion abolished the fall in FEV I. Wheezing has
1979; Stern, [978).
also been associated with percussion and vibration in
Decreased cardiac output (Laws, 1969; Barrell,

[978) has been associated with chest physiother
1975; Feldman, 1979).
patients with cystic fibrosis and COPD (Tecklin,
apy treatment; however, the effects of postural
The box below summarizes the precautions and
drainage were not separated from those of percus
contraindications for external manipulation of the

thorax associated with percussion, shaking, and high
sion and vibration.

In the pediatric population, some experts recom
frequency chest compression. Vibration involves less
mend caution with the position used to treat the ante
force to the thorax and may be better tolerated than
rior lower lobes because of the risk of gastroe
the aforementioned techniques. A nebulized bron
sophageal reflux. The box on p. 330 summarizes the
chodilator may be administered during a treatment of
precautions and contraindications for postural
high frequency chest compression to avoid the conse
drainage.
quences of hyperreactive airways.
General contraindications and precautions
to external manipulation of the thorax
Other precautions
Manual hyperinflation has been shown to cause sig
In patients who are very young, who have limited
nificant depression of cardiac output in patients who
ability to cooperate, or who are not compliant with

other airway clearance techniques, percussion, shak
ing, and vibration offer a method to dislodge retained
secretions. Because of the force transmitted to the
thoracic cage with these techniques, there are many
precautions and contraindications to consider. The
therapist should not make this decision alone, but
needs direction from the medical team. Chest physio
therapy is not a completely benign procedure and
should not be peliormed in the absence of good indi
cations (McDonnell, 1986).
Percussion has been shown to contribute to a fall
Contraindications to External
Manipulation of the Thorax
In Addition to Contraindications for Postural
Drainage:
Subcutaneous cmphysema
Recent epidural spinal infusion or spinal anesthesia
Recent skin grafts, or flaps, on the thorax
Bums. open wounds. and skin infections of the thorax
in Pa02 in acutely ill patients (Connors, 1980), espe
Recently placed pacemaker
cially in patients with cardiovascular instability (Oor
Suspected pulmonary tuberculosis
menzano, 1972) and in neonates (Fox, 1978). The

factor that seems most associated with or predictive
of the effect is the baseline or before-therapy Pa02
(McDonneJl, 1986).
Cardiac arrhythmias have been associated with
Lung contusion
Bronchospasm
Osteomyelitis of the ribs
Osteoporosis
chest percussion for bronchial drainage (Hammon,
Coagulopathy
1981). Huseby (1976) hypothesizes that hypoxemia
Complaint of chest-wall pain
may be the underlying mechanism of CPT-caused

cardiac arrhythmias.
AARC Clinical Pracli ce Guideli'ne. (1991). Postural drainage ther
Patients with hyperreactive airways (e.g., asthma)
apy. Respil'(l/ory Care,]6 (12),1418-1426.
332
PART III
are unable to compensate hemodynamically with lit
Factors to Be Considered When Selecting
tle cardiac reserve (Clement, 1968; Laws, 1969). Sig
an Airway Clearance Technique
nificant and deleterious increases in ICP have also

been demonstrated (Garradd, 1986). Webber (1988)
Motivation
offers these additional contraindications to manual
Patient's goals
hyperinflation: severe hypoxemia with few bronchial
Physician/caregiver's goals
secretions as in ARDS, acute pulmonary edema, air
Effectiveness (of considered technique)
leak (e.g., pneumothorax), severe bronchospasm as in
Patielll's age
acute asthma, and hemoptysis.
Patient's abiliLY to concentratc
The use of PEP for airway clearance carries an in

creased risk of pneumothorax (Oberwaldner, 1986).
Ease (of learning and of teaching)
Bronchodilator premedication should be considered
Skill of therapists/teachers
when applying PEP in patients who show clinical
Fatigue or work required
and/or physiological signs of airway hyperreactivity
Need for assisLants or equipmelll
(Pfleger, 1992).
LimiLations of technique based on disease type and
The increased aitilow produced by the huff cough,
severity
as in the ACB technique, may aggravate bron

chospasm (Hietpas, 1979). Additionally, Hietpas cau
Costs (direct and indirect)
tions that spontaneous explosive coughing may be
Desirability of combining methods
precipitated by the movement of secretions into the

Hardy, K.A. (1994). A review of airway clearance: new techniques,
larger airways by the huff cough.

Several precautions must be observed when using
indications, and recommendations. Re.ljJimlorv Care, 39 (5), 440-452.
exercise as a form of airway clearance. Desaturation

has been shown to occur with exercise in people with
pulmonary disease (Lane, 1987; Henke, 1984), and
a prescribed treatment has a negative influence on pa
therefore it becomes prudent to monitor oxygen satu
tient adherence. It has been suggested that enhanced
ration, providing supplemental oxygen for the exer
compliance might be achieved if the treatment were
cise period when indicated. Exercise-induced bron
specifically tailored to the individual patient's needs
chospasm must also be considered when pulmonary
with regard to clinical status, family functioning, and
compromise is seen with exercise, especiall y with
family concerns. Negotiation between the patient and
higher intensity exercise (Godfrey, 1975). When indi
the caregiver to agree on follow-through with the pre
cated, it is recommended to provide an inhaled bron
scribed treatment regimen is also effective (Shultz,
chodilator 20 to 30 minutes before exercise to allevi
1980). For this reason, it is imperative to consider
ate this symptom (Orenstein, 1985). Andreasson
multiple factors in the recommendation of a specific
(1987) reports a risk of pneumothorax in conjunction
technique of airway clearance, especially in the pa
with exercise in those patients with extensive bullae.
tient with a chronic disease (see box above).

The age of the patient will affect the usefulness of
a particular technique. Infants and very young chil
Factors Affecting Selection of
dren are limited to conventional physical therapy
Airway Clearance Techniques
(postural drainage, perc'ussion,
In the pulmonary population, lack of compliance in
they are not able to cooperate with other methods of
performing airway clearance on a regular basis has
airway clearance. After the age of 3 or 4, a youngster
been well documented (Currie, 1986; Passero, 1981;
may be taught huffing and brcathing control, and as
Muszynski-Kwan, 1988; Litt, 1980). The problem is
sisted with the ACB technique. A vest for use with
worse in the adolescent group. Litt (1980) has also
HFCC is now available for children as young as 2 or
shown that the complexity and increased duration of
3 years of age. PEP, FlutterT' and exercise also are
19
333
suitable for this age group, depending on the child's
Accessibility of equipment or trained personnel
attention span and cooperation. Children 12 years of
limits the use of some airway clearance techniques.
age and older are capable of using any of the airway
Many of these techniques are new or not available to
clearance techniques, including AD, which requires
many health care centers, especially in the United
more concentration than a younger child is typically
States, since they were pioneered in Europe. Proper
able to exhibit.
instruction and review of a patient's technique is im
The lack of an assistant to provide airway clearance
perative to achieve optimal results, and in the case of
is a factor that prompts many patients to seek methods
PEP, the reassessment of resistance is recommended.
other than postural drainage and percussion. HFCC,
In the case of AD, the method is limited by the num
PEP, Flutter''", ACB, exercise and AD are techniques
ber of instructors available to teach the technique to
that provide independence from a caregiver. These
patients and requires a great deal of time on the part
methods have been chosen by adults living on their
of the health care team member to learn. The patient
own, students away at school, and adolescents eager
must possess motivation and the time to learn the
for independence. For optimal results, each tech
technique and be willing to "fine tune" the technique
nique's effectiveness must be regularly reevaluated by
with the therapist periodically.
a health care team member skilled in the area of air
In this area of cost containment, the financial re
way clearance after it has been agreed that a patient ex
quirements of a technique must also be taken into con
hibits independence in a given technique.
sideration, especially in the case of a chronic condi
The clinical status of the patient during each hos
tion. The availability of any given method then, could
pital admission must be evaluated to determine the
be determined by the insurance coverage or additional
appropriateness of an ACT. For example, airway hy
financial resources of the patient. If several methods
perreactivity might be worsened by PO and percus
prove to be equally effective, it would be prudent to
sion, and care must also be taken when using ACB in
select the methods requiring the least expense. Al
this case. HFCC, Flutter''", and exercise should be
though the most common form of airway clearance in
preceded with an inhaled bronchodilator in this case,
the United States continues to be postural drainage
and PEP can be performed concurrently with bron
and percussion by a caregiver, this often proves to be
chodilator administration. AD lends itself well to use
quite expensive, especially if a family member is not
by patients with airway hyperreactivity.
available for ongoing home treatments. The equip
Gastroesophageal reflux prohibits patients from
ment needed for ACTs varies. The generator required
performing airway clearance in conventional PO po
for HFCC is expensive to purchase or rent on a
sitions. In this instance, AD, Flutter''', PEP, HFCC,
monthly basis. Mechanical percussors or vibrators are
and exercise, or ACB in upright positions, are the
moderately priced, and PEP and the Flutter valve are
preferred treatments. In infants or neurologically im
the least expensive of those techniques requiring
paired patients where PO and percussion is the treat
equipment. A patient independently using ACB or AD
ment of choice, modified PO positions are used and
consumes the least financial resources.
sufficient time allowed between a feeding and a treat

ment with PD.
Ultimately, the regular use of a particular ACT by

a patient is governed by personal belief in the effec
The severity of a patient's lung disease will affect
tiveness of the method for his or her own disease
the choice of ACT. Specifically, a patient with end
process, the manner in which the method affects the
stage lung disease or an acute exacerbation might not
patient family's life habits, and the patient's willing
have the required energy level to carry out an active
ness to use the technique on a daily basis. Compli
airway clearance technique such as AD or PEP effec
ance is ultimately the best measure of any airway
tively. A more passive technique would be appropri
c1earancc technique's effectiveness.
ate, at least temporarily. Also a marked decrease in
Clinical outcome measures to assess the effective
PFT's limits the airflow control necessary for AD,
ness of an airway clearance technique can be fol
F1utter, or PEP.
lowed during clinical appointments or periods of hos
334
PART III
pitalization. Radiographic changes, arterial blood gas
must consider many factors in recommending an
values, O2 saturation, and pulmonary function tests
alternate form of airway clearance. Age of the pa
may demonstrate adequate airway clearance or the
tient is a prime factor in the appropriateness of a
need to reassess the appropriateness of the technique
selected technique. For infants, PO, percussion,
or the application of it by the patient. Though it is
and vibration remain the mainstay of secretion
difficult to quantify, many patients subjectively rely
clearance. In older children, the active cycle of
on amount of sputum production to guide their choice
breathing may be initiated, positive expiratory
of secretion clearance method. This measure provides
pressure and Flutter'" may be taught, and high fre
immediate feedback to the patient without visiting the
quency chest compression is available for children

after about age 3 or 4. Exercise should be included
hospital or clinic.
in treatment as well. Children 12 years of age or

older and adults have the complete range of airway
SUMIVIARY
clearance techniques at their disposal, including
The goals of airway clearance are to decrease airway
autogenic drainage.
obstruction, improve secretion clearance, and im
Treatments aimed at secretion clearance require an
prove ventilation and gas exchange. Routine applica
individualized approach to tailor the treatment to the
tion of airway clearance techniques in many condi
patient's condition and lifestyle, to continuously
tions has not been shown to be effective in achieving
reevaluate the patient's status, and to monitor the re
these goals. ACTs are not without side effects or
sponse to treatment.
complications; routine use of these methods is not
Acceptance of the specific treatment technique by

the patient and family is paramount; compliance is
recommended without clear indications.

Indications for ACTs have been divided into
those for acute illness and chronic disease states.
the key to achieving effective treatment, especialJy in

chronic lung disease.
In acute illness, traditional chest physical therapy,
Further research in the area of airway clearance
that is, PO, percussion, and vibration, has been
is certainly needed. Studies with consistent applica
shown to be beneficial in patients with copious se
tion of techniques, similar outcome measures, and
cretions and in the treatment of atelectasis (Kir
consistent study design will assist practitioners in
iloff, 1985). For patients with cystic fibrosis, treat
evaluating and recommending a given technique of
ment with PEP and exercise in conjunction with
airway clearance.
PO, percussion, and vibration were also shown to

be effective in an acute exacerbation (Boyd, 1994).
Acute asthma, bronchitis, and pneumonia without
copious secretions, bronchiolitis, and routine post
REVIEW QUESTIONS
I. What kinds of pulmonary conditions would not
be likely to benefit from ACTs?
operative conditions were not shown to benefit

from PO, percussion, and vibration (Sutton, 1982;
2. Which ACTs would be the easiest (for the thera

pist and the patient) to incorporate into a routine
Eid,1991).
of conventional PO and percussion?
In chronic disease states, patients with cystic fi

brosis and bronchiectasis were found to benefit from
3. What possible factors could be considered a con
PO, percussion, and vibration (Kiriloff, 1985). Posi
traindication to chest percussion with PO in a
tive expiratory pressure and exercise were also shown
trauma or postoperative patient?
to be effective in the chronic management of patients
4. What factors might make it difficult for a patient

to accept a new method of airway clearance?
with cystic fibrosis (Boyd, 1994).

In those patients for whom traditional chest
5. Which ACTs would be most appropriate during
physical therapy is not effective, the caregiver
an acute exacerbation of a pulmonary disease?
19
335
Chang, H.K., Weber, M.E., King, M. (1988). Mucus transport by
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cl
al. (1993). Preliminary evaluation of high-fre
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Physio logy: Respirolory
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48, 586591
Clinical Application of Airway

Clearance Techniques
Anne Mejia Downs
KEY TERMS
Active cycle of breathing technique (ACBT)
Manual hyperventilation
Airway clearance techniques (ACTs)
Percussion
Postive expiratory pressure (PEP)
Dynamic air therapy bed
Flutter
Shaking
Forced expiratory technique (FET)
Trendelenburg
High frequency chest compression (HFCC)
Vibration
INTRODUCTION
The previous chapter addressed the physiological
Oxygen transport from the lungs to body tissues can
basis of each technique, the history of its use, and re
be limited in patients that possess an ineffective
search to establish its effectiveness. This chapter pro
cough or an impairment of normal mechanisms of
vides an introduction to the application of these tech
mucociliary clearance. The caregiver must augment
niques to patients and addresses the benefits and
these mechanisms using the array of techniques avail
liabilities of each technique.
able for airway clearance. Each technique has a phys
Airway clearance techniques differ with respect to
iological basis for improving the mobilization of
equipment needs, the skill level required to perform
secretions. The caregiver must consider the patho
them, and their usefulness with various clinical prob
physiology and the symptoms of the disease, the
lems. Matching a patient with an appropriate method
availability of the technique to the patient, and the
or combination of methods may increase effective
patient's acceptance of the technique in prescribing
ness, reduce complications, and promote adherence
an optimal method of airway clearance.
to the long-term treatment.

339
340
PART III
Cardiopulmonary Physic.al Therapy Interventions
UTILIZATION OF AIRWAY CLEARANCE TECHNIQUES
of tube feedings or meals. The inhalation of bron
This section will deal with the application of airway
chodilator mcdications should take place before air
clearance techniques (ACTs) with specific instruc
way clearance maneuvers. Inhaled antibiotics are best
tions for patient treatment. Contraindications and pre
scheduled after airway clearance has taken place for
cautions for each ACT are addressed in Chapter 21.
optimal deposition of medication. Adequate pain con
This section will speak to practical concerns regard
trol is necessary to receive a patient's best effort and
ing patient care.
cooperation with a treatment. It is also impOitant to
Preparation for any secretion removal technique

should include evaluation of the patient's pulmonary
status (see Chapter
15)
have all necessary equipment and personnel available

at the start of the treatment.
so that measures may be com
pared before and after a treatment is completed. A

physical examination, including inspection, palpa
POSTURAL DRAINAGE
tion, measurement of vital signs, and chest ausculta
Postural drainage (PO) is accomplished by position
tion provides assessment of a treatment's effective
ing the patient so that the position of the lung seg
ness. Laboratory tests including chest x-ray, arterial
ment to be drained allows gravity to have its greatest
20- I
20-5).
blood gas measurements, and pulmonary function
effect (see Figures
studies should be reviewed, since these may be used
sitions are used when a precaution or relative con
as measures of treatment effectiveness.
through
Modified po
traindication to the ideal position exists. For example,
Scheduling an optimal time for patient treatment
if an increase in intracranial pressure is a concern, the
must take into account several factors. At least I half
head of the bed should remain flat instead of being
hour to I hour should be allowed for the completion
tipped into Trendelenburg (head down) position.
Both Upper Lobes

Apical Segments
Right Upper Lobe

Anterior Segment
- hIps .:Ire in external rotiltJon,
smilH pillow under knee:s for
:support 0' JoInts and comfort.
----
KPS.
FIGURE 20-1
Upper lobes.
,;,1>(1,.,
20
Clinical Application of Airway Clearance Techniques
Right Upper Lobe

Posterior Segment
Left Upper Lobe Lingula
Both Lower Lobes

Superior Segments (Apicall
Right Middle Lobe
FIGURE 20-2
Upper, middle, and lower lobes.
Both Lower Lobes

Anterior Segments
Right Lower Lobe

Lateral Segment
Both Lower Lobes

Posterior Segments
Left Lower Lobe

Lateral Segment,
RLL Cardiac (Mediall
FIGURE 20-3
Lower lobes.
341
342
PART III
FIGURE 20-4
A, right upper lobe-posterior segment (anterior view-patient positioned three-fourths prone).
B, right upper lobe-posterior segment (posterior view).
NOTE:
Upper extremities toward prone,
underneath arm pulled free from under patient's body. This position may also be a modified
position for right lower lobe posterior segment.
FIGURE 20-5
Both lower Jobes-posterior segments (shown using teJeJphone books or piJlows for home use). A
beanbag chair is also helpful for home treatments.
20
Equipment Required For Postural Drainage
343
specific lobe. Extended times in a position may
I. For the hospitalized patient, there exists a vari
be used by coordinating the positioning with
ety of beds that employ manual or electric de
nursing care for skin pressure relief. If postural
vices to position the patient. Air therapy beds,
drainage is used in conjunction with another
most often used in the intensive care unit (lCU),
technique, the time in each position may be de
are valuable aids allowing ease of positioning,
creased. For example, if percussion and vibra
especially in large or unresponsive patients.
tion are performed while the patient is in each
2. Make use of pillows or bedrolls to support
PO position, 3 to 5 minutes is sufficient.
3. A patient who requires close monitoring should
body parts or relieve pressure areas.
3. For home treatmcnt, aids in positioning might
not be left unattended in a Trendelenberg posi
include pillows, a slant board (or ironing board
tion, but this may be appropriate if patients are
if the patient is small), a foam wedge, sofa
alert and able to reposition themselves.
4. It is not necessary to treat each affected lung
cushions, or a bean bag chair.
segment during each treatment; this may prove

to be too fatiguigg for the patient. The most af
Preparation for Postural Drainage
fected lobes should be addressed with the first
l. Nebulized bronchodilators before PO may fa

cilitate the mobilization of sputum.
treatment of the day, with the other affected

areas addressed at a subsequent treatment.
2. An adequate intake of fluids (if allowed) de
5. The patient should be encouraged to take deep
creases the viscosity of the secretions, allowing
breaths and cough after the treatment and if
easier mobilization.
possible after each position. Having the patient
3. Become familiar with the workings of the

model of bed the patient is occupying, espe
cially the movement of the bed into the Trende
sit upright or lean forward optimizes this effort

(Frownfelter, 1 987).
6. Secretions may not be mobilized immediately

after the treatment but possibly 1 half hour to
lenberg position.
4. In the ICU, it is imperative to be familiar with
1 hour later. The patient should be thus in
the multiple lines, leads, and tubes attached to
formed and requested to clear secretions then.
the patient. Allow enough slack from each de
The nurse or family member should be in
vice to position
cluded in this aspect of treatment, especially
patient for postural drainage.
5. Make sure there are enough personnel to posi

tion the patient with as little stress to both pa
with difficult patients who need such encour

agement (Frownfelter, 1987).
tient and staff as possible (Frownfelter, 1987).
6. Have suctioning equipment ready to remove se

cretions from an artificial airway or the pa
tient's oral or nasal cavity after the treatment.
Advantages and Disadvantages of PO

PO is relatively easy to learn; the patient and/or care
giver must be familiar with the appropriate position
ing for the affected lung fields. Treatment in the hos
Treatment with PO
p i t a l m a y be c o o r d i n a t e d w i t h o t h e r p a t i e n t
1 . After determining the lobe of the lung to be
activities-po sitioning for s k i n pressu r e relief,
treated, position the patient in the appropriate po
bathing, or positioning for a test or procedure. Home
sition, using pillows or bed rolls as needed to sup
treatment may be coordinated with activities such as
port the patient comfortably in the position indi
reading or watching television.
cated. See figures 20-1 through 20-5, p. 340-342.
2. If postural drainage is used exclusively, each
However, for many patients, optimal PO positions

will be contraindicated for a variety of reasons (see
position should be maintained for 5 to 1 0 min
Chapter 21). Compliance with PO may be reduced
utes, if tolerated, or longer when focusing on a
because of the length of the treatment, especially in
344
PART III
FIGURE 20-6
A and B, If children are able to role play the treatment, they will better understand what is expected
and be more cooperative with therapy.
the pediatric population, who will require consider
breathing. Percussion is used in postural drainage po
able distractions to maintain a desired position.
sitions for increased effectiveness (Sutton, 1985;
The cost of the equipment required for PD is mini

mal; inexpensive items may be used for home treat
Bateman, 1979) and may also be used dUling the ac

tive cycle of breathing (ACB) technique.
ment. However, the cost of a caregiver's time to pro

vide the treatment, especially in the case of a chronic
disease, may be substantial. A family member may
Equipment Required for Percussion
be willing to learn the procedure, which would pro
1. The only equipment required for manual per
vide a benefit in terms of expense, as well as flexibil
cussion is the caregiver's cupped hands to de
ity in scheduling (Figure 20-6).
liver the force to mobilize secretions.
2. For the adult and older pediatric population,

electric or pneumatic percussors that mechani
PERCUSSION
cally simulate percussion are available. This
Percussion is performed with the aim of loosening re
enables a patient to apply self-percussion more
tained secretions from the airways so they may be re
effectively. Several models have variable fre
moved by suctioning or expectoration. A rhythmical
quencies of percussion, as well as different lev
force is provided by clapping the caregiver's cupped

hands against the thorax over the affected lung seg
els of intensity.
3. Several devices may be used to provide percus
ment, trapping air between the patient's thorax and
sion to infants: padded rubber nipples, pediatric
the caregiver's hands (Figure 20-7). It is performed
anaesthesia masks, padded medicine cups, or
during both the inspiratory and expiratory phases of
the bell end of a stethoscope.
20
345
FIGURE 20-7
Chest percussion.
Preparation for Percussion
thema occurs with percussion, it is usually a re
1. Placing the patient in appropriate PD positions

(as the patient's condition allows) enhances the
effect of percussion.
sult of slapping or not trapping enough air be

tween the hand and the chest wall (Imle, 1989).
3. An even, steady rhythm will best be tolerated
2. Place a thin towel or hospital gown over the pa
by the patient, and the rate of manual percus
tient's skin where the percussion is to be ap
sion is normally between 100 and 480 times per
plied. The force of percllssion over bare skin
minute (lmle, 1989).
may be uncomfortable; on the other hand,
4. The force applied to the chest wall from each
padding that is too thick absorbs the percussion
hand should be equal. If the nondominant hand
without benefit to the patient.
is not able to keep up with the dominant hand,
3. Adjust the level of the bed so that proper body
the rate should be slowed to match that of the
mechanics may be used during the treatment.
slower hand. It might also be helpful to start
Fatigue or injury of the caregiver may be the
with the nondominant hand and let the domi
result of lengthy or numerous treatments if
nant hand match the nondominant (Frownfelter,
1987). The force does not have to be excessive
proper body mechanics are ignored.
to be effective; the amount of force should be

adapted to the patient's comfort.
Treatment With Percussion
5. If the size of an infant does not allow use of a
I. Position the hand in a cup with the fingers and
full hand, percussion may be done manually
thumb adducted. It is important to maintain this
with four fingers cupped, three fingers with the
cupped position with the hands throughout the
middle fi nger "tented," or the thenar and hy
treatment, while letting the wrists, arms, and
pothenar surfaces of the hand (Crane, 1990).
shoulders stay relaxed.
6. Hand position should be such that percussion
2. The sound of percussion should be a hollow
does not occur over bony prominences. The
sound as opposed to a slapping sound. If ery
spinous processes of the vertebrae, the spine of
346
PART III
the scapula, and the clavicle should all be
The expense of a mechanical device for percus
avoided. Percussion over t h e floating ribs
sion is minimal compared with the ongoing cost of a
should also be avoided, since these ribs have
caregiver to provide percussion and PD in the hospi
only a single attachment.
tal setting or a home care situation. In the case of
7. Percussion should not be performed over breast
young children or unresponsive patients, there are
tissue. This would produce discomfort and di
few choices for airway clearance. For other popula
minish the effectiveness of the treatment. In the
tions, however, a more independent method would
case of very large breasts, it may be necessary
also prove to be more cost-effective if adequate com
to move the breast out" of the way with one
pliance was achieved.
hand and percuss with the other hand.
8. A patient may be taught to perform one-handed

self-percussion to those areas that can b e
reached comfortably, either manually o r with a
VIBRAnON/SHAKING
The techniques of vibration and shaking are on oppo
mechanical percussor. This does however, vir
site ends of a spectrum. Vibration involves a gentle,
tually preclude the treatment of the posterior
high frequency force, whereas shaking is more vigor
lung segments.
ous in nature. Vibration and shaking are performed

with the aim of moving secretions from the lung pe
Advantages and Disadvantages of Percussion
riphery to the larger airways where they may be suc

tioned or expectorated. Vibration is performed by co
The addition of percussion to a PD treatment may en
contracting all the muscles in the caregiver's upper
hance secretion clearance and shorten the treatment.
extremities to cause a vibration while applying pres
Patients often find the rhythm soothing and are re
sure to the chest wall with the hands. Shaking is a
laxed and sedated by percussion, especially young
stronger bouncing maneuver, which also supplies a
children and infants.
concurrent, compressive force to the chest wall.
Patients with chronic lung disease, who have used
Like percussion, vibration and shaking are lIsed in
PD and percussion for many years and have found it
conjunction with PD positioning. Unlike percussion,
effective, are reluctant to try an alternative method of
they are performed only during the expiratory phase
airway clearance. Compliance with this method is de
of breathing, starting with peak inspiration and con
pendent on the availability of a family member or
tinuing until the end of expiration. The compressive
other caregiver to provide the treatment. Mechanical
forces follow the movement of the chest wall.
percussors allow the patients more independence or

decrease fatigue of a caregiver, and are especially use
ful in patients requiring ongoing treatment at home.
Equipment Required for Vibration/Shaking

I. For manual techniques, the only equipment re
Percussion is not well-tolerated by many patients

postoperatively without adequate pain control. The
quired is the caregiver's hands.
2. Mechanical vibrators are available to administer
force of percussion is also a threat to patients with os

teoporosis or coagulopathy. Other contraindications
the treatment and are useful for self-treatment
are listed in Chapter 21. Percussion has been associ
by a patient or to reduce fatigue in the caregiver.
ated with a fall in oxygen saturation, which can be
3. For infants, a padded electric toothbrush is an
eliminated with concurrent thoracic expansion exer
alternative (Crane, 1990).
cises and pauses for breathing control (Pryor, 1990).

Delivering percussion for extended periods on an
ongoing basis can result in injury to the caregiver,
Preparation for Vibration/Shaking
whether a family member or a health care provider.
I. Place the patient in the appropriate PD posi
Repetitive motion injuries of the upper extremities
tion or modified position as the patient's sta
may occur in long-term delivery of percussion for
tus allows.
airway clearance.
2. Place a thin towel or hospital gown over the
20
patient's skin. The material should not be

thick enough to absorb the effect of the vibra
347
ment of chest deflation.

4. If the patient is mechanically ventilated, the
previously described techniques must be timed
tion or shaking.
3. Proper body position of the caregiver is impor
tant to deliver an effective treatment and to de
crease caregiver fatigue.
with ventilator-controlled exhalation.

5. If the patient has a rapid respiratory rate, either
voluntary or ventilator-controlled, it may be
necessary to apply vibration or shaking only
during every other exhalation.
Treatment with Vibration/Shaking
6. The frequency of manual vibration is between
I. Conventional chest physical therapy is often re

ferred to as a combination of postural drainage
12 and 20 Hz; shaking is 2 Hz (Gormezano,

1972; Bateman, 1981).
7. A mobile chest wall is necessary to apply a com
and percussion, vibration, or shaking.
2. For shaking, with the patient in the appropriate
pressive force without causing discomfort. If a pa
PO position, place your hands over the lobe of
tient has limited chest wall movement, vibration
the lung to be treated and instruct the patient to
will probably be tolerated better than shaking.
take in a deep breath. At the peak of inspiration,
8. Mechanical vibrators may be used by patients
apply a slow (approximately 2 times per sec
themselves, realizing that limited attention can
ond), rhythmic bouncing pressure to the chest
be paid to the posterior portions of the lungs.
wall until the end of expiration. The hands fol

low the movement of the chest as the air is ex
haled.
3. For vibration, the hands may be placed side by
Advantages/Disadvantages of Vibration/Shaking
The use of vibration or shaking with PO may enhance
side or on top of one another as shown in Fig
the mobilization of secretions. Shaking or vibration
ures 20-8 and 20-9. As with shaking, the pa
may be better tolerated than percussion, especially in
tient is instructed to take in a deep breath while
the postsurgical patient.
in a proper PO position. A gentle but steady co
Manual vibration and shaking allows the caregiver
contraction of the upper extremities is per
to assess the pattern and depth of respiration. The
. formed to vibrate the chest wall, beginning at
stretch on the muscles of respiration during expira
the peak of inspiration and following the move-
tion may encourage a deeper inspiration to follow. A
FIGURE 20-8
FIGURE 20-9
Vibration-hands positioned on both sides of the chest.
Vibration-hand p)acement one on top of the other.
348
PART III
mechanical vibrator, more commonly used with pedi
Equipment Required for Manual Hyperinflation

I. A manual ventilation bag, such as the Ambu, at
atric patients, may be preferred by a caregiver to de
tached to an oxygen source is needed for lung
liver long-term airway clearance.

The patient cannot apply these techniques her
inflation. A positive-end expiratory pressure
self, except in a limited manner with a mechanical
(PEEP) valve may be attached. This is recom

mended when greater than 10 cm PEEP is being
used for mechanical ventilation (Webber, 1993).
vibrator, so compliance and regular administration

of vibration depends on caregiver availability.
The same contraindications for percussion apply,
2. A second trained caregiver is necessary to pro
since compression to the thorax is involved with shak
vide shaking or vibration in an appropriate se

quence with lung inflation.
ing and vibration. The technique of vibration is less
3. Normal saline should be available for installa
constrained by these contraindications than is shaking.
tion into the airways to assist with loosening

secretions.
MANUAL HYPERINFLATION
The technique of manual hyperinflation is used in pa
tients with an artificial airway, who are mechanically
Preparation for Manual Hyperinflation
ventilated or who have a tracheostomy. This method of
1. It may be necessary to premedicate the patient
airway clearance promotes mobilization of secretions
with a sedative or analgesic so that airway
and reinflates collapsed areas of lung. Two caregivers
clearance may be better tolerated.
are necessary to provide this treatment and the coordina
2. The two caregivers providing the treatment
tion between these two people is key to achieving satis
should be positioned on opposite sides of the
20-10.
bed to allow greater freedom of movement and
factory results. This technique is shown in Figure
FIGURE 20-10
Simulated cough using self-inflating bag and chest compression with vibration.
20
improved observation of the patient's response
349
Advantages/Disadvantages of Manual Hyperinflation

Manual hyperinflation may be helpful in managing air
to treatment.
3. Normal saline (2 to 3 mL) may be used before
way secretions in those patients requiring long-term me
hyperinflation to assist with loosening, thick se
chanical ventilation. In this patient population, the
cretions (Webber, 1993).
choice of airway clearance techniques is limited, espe
4. The positions for treatment will be primarily
cially when the patient is unresponsive. Manual hyperin
side-lying with the head of the bed flat or
flation simulates a cough by augmenting the inspiratory

effort, momentarily maintaining a maximal inspiratory
slightly elevated to patient tolerance.
hold, and causing an increased expiratory flow.

However, hyperinflation has the potential to cause
Treatment With Manual Hyperinflation
significant barotrauma. There are a number of con
1. One caregiver squeezes the manual ventilation
traindications to this technique including unstable he
bag slowly to inflate the lungs. A pause i s
modynamics, pulmonary edema, air leak, and severe
maintained momentarily at the peak o f inflation
bronchospasm (Webber, 1988). In addition, it is not
to allow collateral ventilation to fill underex
appropriate for infants with increased pulmonary resis
panded areas of the lung. Release of the bag
tance requiring high inflation pressures or in preterm
should be rapid, resulting in a high expiratory
infants at risk of pneumothorax (Webber, 1993). Other
flow rate (Clement, 1968).
contraindications are discussed in Chapter 21.
2. A second caregiver provides thoracic compres

sion with shaking or vibration to assist with the
Thus manual hyperinflation requires two well-trained

caregivers. This may be its biggest disadvantage.
mobilization of secretions. The compression

phase should begin just before the inflation
pressure has been released and continue until
the end of the expiratory phase.
ACTIVE CYCLE OF BREATHING TECHNIQUE

The active cycle of breathing (ACB) technique involves
3. In a patient who is breathing spontaneously,
three phases repeated in cycles: breathing control, tho
"bag squeezing" with the manual ventilation
racic expansion, and the forced expiratory technique
bag should be timed to augment the patient's
(FET). This method encourages active participation of
inspiratory effort, making vibration more effec
the patient and has been shown to be as effective when
tive (Imle, 1989).
perfonned by the patient alone as with the aid of a care
4. After about six cycles of inspiration/expiration,
giver (Pryor, 1979). Postural drainage positions may be
the patient's airway is suctioned using sterile
used in conjunction with ACB technique. This method
technique. The length of treatment is individu
of airway clearance may be used with some children as
alized and depends on the amount of secretions
young as 3 or 4 years of age. The sequence of ACB
present in the airways and the areas of the
technique is shown in the box on p. 350.
lungs affected.
5. Manual hyperint1ation may be performed with

intubated infants or children using an appropri
Equipment Required for ACB Technique
ately sized ventilation bag. Care must be taken
1. The only equipment required for this manual
to apply slow inflation, so as to avoid a high
technique is the patient's or caregiver's hands
peak inspiratory pressure, which carries the risk
to percuss or shake/vibrate the chest wall dur
of barotrauma (Webber, 1993).
ing the thoracic expansion phase.
6. When manual hyperinflation is contraindicated,
2. Mechanical percussors or vibrators may be
shaking or vibration may be timed with the expi
used during the thoracic expansion phase, ei
ratory phase of the ventilator without additional
ther for self-percussion by the patient or for use
inflation during inspiration (Webber, 1988).
by the caregiver.
350
PART III
ACB Technique
Breathing control
Diaphragmatic breathing at no nnal tidal volume
3-4 Thoracic expansi on exercises

Deep inhalation with relaxed exhalation at
vital capacity
with or without chest percussion
Breathing control
Three to four thoracic e xp an sion exe rcises

Breathing control
Forced exp iratory technique
One to two huffs at mid to low lung volume
Abdominal muscle contracti on to produce
forced exhalation
Breathing control
J. (1993). Physiotherapy skills:

B. Pryor, J. (eds.). (1993).
Physiotherapy for respiralory and cardiac problems. Churchill
Adapted from Webber,
B.,
FIGURE 20-11
Peak flow meter mouthpiece.
Pryor,
techniques and adjuncts. In Webber,
ducti ve area of the lungs. The entire treatment
Livings\one: Edinburgh.
may also be done in the sitting position.
3. A minimum of 10 minutes in any productive

position may be necessary to clear a patient
3. If PD positions are used, equipment for posi
with a moderate amount of secretions. Patients
tioning will be required.
after surgery or with minimal secretions may
4. To teach the huffing maneuver (part of the
not require as much time, and very ill patients
FET), it may be helpful to use a peak flow
may fatigue before optimal treatment is given
meter mouthpiece to keep the mouth and glottis
(Webber, 1993).
open (Figure 20-11). Young children may be

taught games of huffing at cotton balls or tissue
to improve the technique (Webber, 1993). To
help them focus on the expiratory maneuver,
Treatment With the Active Cycle

of Breathing Technique
small children may also be taught to flap their

arms to their lateral chest as they perform the
I. Breathing
control-The
patient is instructed to
breathe in a relaxed manner using normal tidal
huff, a technique referred to as the "chicken
volume. The upper chest and shoulders should
breath" (Mahlmeister, 1991).
remain relaxed and the lower chest and ab

domen should be active. The phase of breathing
control should last as long as the patient re
Preparation for ACB Technique
quires to relax and to pr epare for the next
I. Treatment of two or three productive areas during

one session may be tolerated by most patients.
phases, usually 5 to J a seconds.
2. Thoracic expansion
The emphasis during this
2. The patient is positioned or positions herself in
phase is on inspiration. The patient is instructed
a PD position to stimulate drainage of a pro-
to take in a deep breath to inspiratory reserve;
20
Ineffective Huffing
Effective Huffing
Mouth half or almost closed
Mouth open, O-shaped to keep glottis open
Expiratillfi always starting from high lung volume
Forced expiration
Abdominal muscles not used
From mid to low lung volume moves periph

eral secretions
Sound more like hissing or blowing
from high to mid lung volume moves proxi
Mouth shaped ;)s for "E" sound
mal secretions
Incorrect quality of expiration
Too vigorous or long. producing paroxysmal
Muscles of the chest wall and abdomen contract.
Sound is like a sigh. but forced.
Rate of expiratory flow varies with the following:
coughing
Too gentle
Too short
351
The individual
The disease
"Catching" or "grunting" at the back of the throat
The degree of airflow obsu'lIction
Crackles heard if excess secretions are present
From Partridge, et ai, Physiotherapy, March 1989, Vol. 75, No.3

expiration is passive and relaxed. The caregiver
or the patient may place a hand over the area of
the thorax being treated to further encourage in
creased chest wall movement.
breath in will be effective. This huff will be
3. Chest percussion, shaking, or vibration may be
longer and quieter. To clear secretions that
performed in combination with thoracic expan
have reached the larger, proximal airways, a
sion as the patient exhales. For surgical pa
huff after a deep breath in will be effective.
tients or those with lung collapse, a breath hold
This huff will be shorter and louder.
or a sniff at the end of inspiration encourages
6. The patient must pause for breathing control
collateral ventilation to assist with reexpansion
after one or two huffs. This will prevent any in
of the lung.
crease in airflow obstruction.
4. FET: This phase consists of huffing inter
7. The ACB technique may be adapted to the indi
spersed with breathing control. A huff is a
vidual patient's needs. If secretions are tena
rapid, forced exhalation but not with maximal
cious, two cycles of the thoracic expansion
effort. This maneuver can be compared with
phase may be necessary to loosen secretions
fogging a pair of eyeglasses with warm breath
before the FET can follow. In a patient with
so they may be cleaned. Unlike a cough in
bronchospasm or unstable airways, the period
which the glottis is closed, a huff requires the
of breathing control may be as long as 10 to 20
glottis to remain open. In an effective huff, the
seconds (Webber,
muscles of the abdomen should contract to pro
tient may be shown how to support the incision
1993). After surgery, the pa
vide greater expiratory force. Other characteris
with their hands during the FET to achieve suf
tics of effective vs ineffective huffing are
ficient expiratory force.
shown in the boxes above.
8. When a huff from a medium-sized inspiration
5. Two different levels of huffing are character
through complete expiration is nonproductive
ized in the FET. To mobilize secretions from
and dry sounding for two cycles in a row, the
peripheral airways, a huff after a medium-sized
treatment may be concluded (Pryor,
1991).
352
PART III
Advantages and Disadvantages of ACB Technique
quired for the patient in whom percussion or shaking

during the thoracic expansion phase increases the ef
Incorporation of the ACB technique into a treatment
fectiveness of the treatment.
of PO and percussion allows the patient to participate
Care must be taken to adapt the ACB technique for
actively in a secretion mobilization treatment and of
patients with hyperreactive airways or after surgery.
fers the prospect of independently managing airway
This individual approach will be helpful with all pa
clearance. The ACB may be introduced at
3 or 4
tients using the technique to optimize effectiveness.
years of age, with a child becoming independent in

the technique at 8 to 10 years of age.
The technique may be adapted for patients with
gastroesophageal reflux, bronchospasm, and an acute
AUTOGENIC DRAINAGE
Autogenic drainage (AD) is a breathing technique
exacerbation of their pulmonary disease. A decrease
that uses expiratory airflow to mobilize bronchial se
in oxygen saturation caused by chest percussion may
cretions. It is a self-drainage method that is per
be avoided by using the ACB technique (Pryor,
formed independently by the patient in the sitting po
[990). When the technique is performed indepen
s i t i o n . AD c o n s i s t s of three phases:
dently, the cost of using ACB technique for the long
"unsticking" phase. which loosens secretions in the
term is minimal.
peripheral airways,
However, in young children and in extremely ill
(1) the
(2) the "collecting" phase, which
moves the secretions to the larger, more central air
(3) the "evacuating" phase, which results
adults, a caregiver wi/I be necessary to assist the pa
ways, and
tient with this technique. An assistant will also be re-
in the removal of the secretions. This technique of

airway clearance requires much patience and concen
tration to learn and is therefore not suitable for young
children. It is ideal, however, for the adolescent or
adult who prefers an independent method.
Equipment Required for AD

1. No equipment is needed for a patient to perform
the technique of AD. The patient must possess
good proprioceptive, tactile, and auditory per
ception of the mucus moving; this feedback
makes it possible to adjust the technique of AD.
2. To teach this method to a patient, a caregiver

requires keen tactile and auditory senses to
coach a patient to move between the phases by
listening to and feeling the location and the
quality of the secretions.
FIGURE 20-12
Autogenic drainage: German method. Autogenic drainage
Preparation for AD
shown on a spirogram of a normal person. The method is

not divided into separate phases. (Vt=tidal volume,
ERV=expiratory reserve volume, RV=reserve volume,
FRC=functional residual capacity, IRV=inspiratory reserve
volume, IRV
Vt
ERV = vital capacity). (From David,
A. (1991). Autogenic drainage-the German approach. In
I. The patient should be seated upright in a chair

with a back for support. The surroundings should
be devoid of distractions, allowing the patient to
concentrate on the breathing technique.
2. The upper airways (nose and throat) should be
Pryor, J. (Ed.), Re pir{/{orv Care, Edinburgh: Churchill
cleared of secretions by huffing or blowing
Livingstone.)
the nose.
20
3. The caregiver should be seated to the side and
353
5. The evacuating phase-In this phase, the pa
slightly behind the patient, close enough to hear
tient increases inspiration into the inspiratory
the patient's breathing. One hand should be
reserve volume range. This middle-to-high
placed to feel the work of the abdominal mus
lung volume breathing continues until the se
cles and the other hand placed on the upper
cretions are in the trachea and are ready to be
chest (see Figure 20-12).
expectorated. The collected mucus can be

evacuated by a stronger expiration or a high
volume huff.
Treatment With Autogenic Drainage
Nonproductive coughing should
be avoided, since it may result in collapse of
l. In all phases, inhalation should be done slowly,
airways.
though the n o s e if possible, using the di
6. Compression of the airways should be avoided.
aphragm or lower chest. A 2- to 3-second
If wheezing is heard, the expiratory t10w rate
breath hold should follow, allowing collateral
must be decreased. Beginners may have to use
ventilation to get air behind the secretions.
p u rs e d l i ps to a v o i d a i r w a y c o m p r e s s i o n
2. Exhalation should occur through the mouth
(Chevaillier, 1992). Instructing the patient t o
with the glottis open, causing the secretions to
roll the tongue (if possible) may assist i n con
be heard. The vibrations of the mucus may also

be felt with the hand placed on the upper chest.
trolling the expiratory flow rate.

7. A German modification of AD resulted from
The frequency of these vibrations reveals their
the observation that many patients had diffi
location. High frequencies mean that the secre
culty breathing in the expiratory reserve vol
tions are located in the small airways; low fre
ume range. In the simplified procedure, the pa
quencies mean that the secretions have moved
tient begins by varying the mid-tidal volume
to the large airways (Chevaillier, 1992).
without excessive effort. After a passive but
3. The umticking phase-This phase mobilizes
rapid expiration, an actively performed expira
mucus from the periphery of the lungs by lower
tion follows, achieving exhalation to a low ex
ing the mid-tidal volume below the functional
piratory reserve volume (David, 199 1). See
residual capacity level (Schoni, 1989). In prac
Figure 9- 1, p. 155. for the difference between
tice, inspiration is followed by a deep expiration
the two methods of AD.
into the expiratory reserve volume. The patient
8. The duration of each phase of AD depends on
attempts to exhale as far into the expiratory re
the location of the secretions. The duration of
serve volume as possible, contracting the abdomi
a session depends on the amount and viscos
nal muscles to achieve this. This low lung volume
ity of the secretions. A patient who is experi
breathing continues until the mucus is loosened
enced in autogenic drainage will clear secre
and starts to move into the larger airways.
t i o n s in a s h o r t e r a m o u n t of t i m e t h a n a
4. The collecting phase: This phase collects the

mucus in the middle airways by increasing the
beginner. An average treatment wiiJ be 30 to
45 minutes in length.
lung volume over the unsticking phase. Tidal

volume breathing is then changed gradually
from expiratory reserve volume toward the in
Advantages and Disadvantages of AD
spiratory reserve volume range (Schoni, 1989)
After instruction in the technique of AD has been
so that the lungs are expanded more with each
completed, it may be performed independently by pa
inspiration. The patient increases both inspira
tients over 12 years of age and requires no additional
tion and expiration to move a greater volume of
equipment. Since it does not require the use of pos
air. This low to middle lung volume breathing
tural drainage positions, it is appropriate for patients
continues until the sound of the mucus de
with gastroesophageal ret1ux. It is also recommended
creases, signaling its movement into the central
f o r use in patients with airway hyperreactivity
airways to be evacuated.
(Pfleger, 1992).
354
PART III
Although it is widely used in Europe, the use of
PEP is performed in the upright position and can
AD in the United States is limited by the lack of
be used during acute episodes, as well as chronic pul
trained caregivers but is growing in popularity.
monary conditions. Children over 4 years of age may
To learn this technique, patients must demonstrate
be instructed in the technique, and PEP may provide
good self-discipline and possess the ability to concen
an independent method of airway clearance in older
trate. This method takes more practice than others. A
children and adults.
patient must also be available for periodic reevalua

tion and refinement of the technique.
AD is not the treatment of choice for a patient who
is unmotivated or uncooperative, and the study of
Equipment Required For Positive

Expiratory Pressure
flow volume curves suggests that AD would not be
I. A PEP mask is manufactured by Astra Tech in
appropriate for small children even if they are coop
Denmark, but is not approved by the Federal
erative (Dab,
Department of Agriculture (FDA) and is not
1979).
The period of hospitalization for an acute pul
available in the United States. However, a self
monary exacerbation is a difficult time for a patient
made PEP mask system may be assembled
to learn AD. In fact, patients who are skilled in the
using a soft ventilation mask, a T-piece, a one
technique choose a more passive (less energy-con
way valve, and resistors of various sizes or an
suming) form of airway clearance at such a time until
adjustable resistor valve (Figure
they return to their baseline pulmonary status.
mask should fit tightly but comfortably over the
20-13). The
mouth and nose.
2. Another form of PEP delivery consists of a
POSITIVE EXPIRATORY PRESSURE
mou thpiece attached to a one way valve (for
Positive expiratory pressure (PEP) creates a back
use with noseclips) with adjustable expiratory
pressure to stent the airways open during exhalation
resistance. The Resistex
and promotes collateral ventilation, allowing pressure
Medical, Clearwater, Fla.) has recently been
to build up distal to the obstruction. This method of
valve (from Mercury
FDA-approved.
airway clearance prevents collapse of the airways,
3. A manometer is placed proximal to the resistor
which eases the mobilization of secretions from the
in the initial stages of instruction in the use of
periphery toward the central airways. A mask or
PEP. First, the manometer helps to determine
mouthpiece apparatus provides a controlled resis

tance
(10 to 20 cm water pressure) to exhalation and
and monitor the appropriate level of resistance

needed for the patient to achieve
10 to 20 cm of
requires a slightly active expiration; tidal volume in
water pressure throughout exhalation. Sec
spiration is unimpeded.
ondly, the visual display of the manometer
A variation of positive expiratory pressure, known

as high-pressure PEP, uses the same mask apparatus
but at much higher levels of pressure
serves as feedback to assist the patient in mas

tering the technique (Mahlmeister,
1991).
(50 to 120 cm
4. Aerosol medication by nebulizer or metered
water pressure). Inspiration is performed to total lung
dose inhaler may be placed inline to be deliv
capacity; this is followed by a forced expiratory ma
ered simultaneously with PEP for airway clear

ance. Deposition .of medication improves with
neuver against the PEP mask.

A form of intermittent PEP is provided by a de
vice called the FlutterT". This pipe like device pro
PEP (Andersen,
1982; Frischnecht-Christensen,
1991).
(I) positive expiratory pressure, (2) oscillation

6 to 20 Hz) and
5. Supplemental oxygen may also be placed inline
(3) accelerated expiratory flow rates to loosen secre
6. With high-pressure PEP mask therapy, spirom
vides
of the airways (at frequencies of
for patients who are hypoxic.

etry is used to determine the appropriate resis
tions and move them centrally.
20
355
FIGURE 20-13
Self-made PEP mask system.
2. If aerosolized medication is to be used simulta
tance for each patient individually.

7. The Flutter'M VRPI valve (from VarioRaw,
neously, the patient should be instructed in how
Switzerl and), recently FDA - a p p roved, is
to stop the flow of the aerosol when the mask
marked in the United States (by Scandipharm
or mouthpiece is removed during the PEP treat
Pharmacy, Birmingham, Ala.). It is a pipe-like

device consisting of a mouthpiece, a plastic
cone, a steel ball, and a petforated plastic cover.
ment session.
3. To determine the correct level of resistance for

low-pressure PEP, the patient inhales using
8. The PEP mask, mouthpiece, and the Flutter
tidal volume and exhales actively into the
should be cleaned regularly with hot, soapy
mask/mouthpiece. Different resistors are tested
water. The one-way valve should be cleaned
(or the resistor valve is adjusted) while the
with hot water only; soap may cause it to stick
level of PEP is monitored on the manometer.
or become brittle. In the hospital, the equip
The resistance is gradually decreased until the
ment will need to be sterilized according to in
PEP level supplying 10 to 20 cm of water pres
fection control recommendations.
sure
has
been
identif i e d
(Falk
1993).
Mahlmeister (199 J) reports most patients

achieve this pressure range with flow resistors
Preparation for PEP
of 2.5 to 4.0 mm in diameter. Selection of the
1. For PEP therapy, the patient should be seated
proper resistor produces the desired inspiratory
upright with elbows resting on a table. Use of a
to expiratory ratio of l:3 to 1:4 (Mahlmeister,
mask may require securing the device with both
1991). The use of too great a resistance will
hands for a tight seal (Figure 20-14).
create too Iow a pressure or an increased respi
356
PART III
FIGURE 20-15
Use of Flutrer (R) valve.
pressure and frequency while movement of the
device downward results in lower pressure and
frequ e n c y (Al t h a us, 1993). The Flutter
reaches frequencies of between 6 and 20 Hz.
FIGURE 20-14
Treatment With PEP
Preparation for PEP therapy.
1. The patient should be instructed to breathe into

ratory rate, whereas too small of a resistor will
the mask or mouthpiece to tidal volume using
create too high a pressure or a slow respiratory
the lower chest and abdomen. Exhalation into
rate (McIlwaine, 1993).
the mask or mouthpiece should be slightly ac
4. For high-pressure PEP, appropriate resistance is
tive but not forced.
determined by connecting the outlet of the PEP
2. The patient continues breathing into the mask
mask to a spirometer. Forced vital capacity ma
or mouthpiece for 10 to 15 breaths, using a nor
neuvers are peliormed through different expira
mal respiratory rate. Initially, the patient and
tory resistors. The resistor producing the highest
caregiver monitor the effort by means of the
forced vital capacity through the PEP mask is
manometer, ensuri'ng that a pressure of 10 to 20
selected for continued use (Oberwaldner, 1986).
cms of water pressure is achieved throughout
5. To use the Flutter'" valve, the patient should be
exhalation. After the technique is mastered with
seated upright (Figure 20-15). The full effects
the appropriate resistor, the manometer may be
of the vibration induced by the Flutter may be
removed from the system. The appropriate re
received by changing the angle of the device.
sistance should be rechecked periodically dur
Movement of the Flutter'M upward increases the
ing clinical visits or periods of hospitalization.
20
the mucus is mobilized (Mcllwaine, 1993).
6. The recommended procedure for use of the Flut
Inhale deeply and hold breath for 2 to ) seconds.
ter'''' is shown in the box at left. The device is
Place Flutter"" in mouth and, keeping cheeks as
held horizontally with the lips tightly around the
stiff as possible, exhale through Flutter'M adjust

ing the degree of tilt to maximize vibrations.
mouthpiece. After a deep inspiration through the

nose, the breath is held for 2 to 3 seconds before
Exhalation need not be forced. Patient best deter
exhaling deeply through the Flutte r'''. The
mines "speed" of exhalation.
cheeks must be kept flat and to use the abdomi
Perform multiple exhalations through the Flutter'"
nal muscles for effective exhalation. The vibra
(usually 5 to 15) with breath hold to maximize
tion of the chest may be palpated by the patient
mobilization of mucus.
Ajier pelforminR
multipl e
" lo o s e ning "
357
against the PEP mask. This is repeated until all
Technique for Using FlutterT"
and caregiver to provide feedback as to the opti
breaths,
mal angle of the device. A Flutte,:'''' session con
increase depth of breath and speed of exhalatioll

'"
Ihrough F/uller to Ilrecipilllle coughing and
sists of I 0 to 15 breaths followed by huffing
mucus expectoration,
(this may be done into the device), with a ses

sion lasting about 15 to 20 minutes. To avoid
Repeat entire sequence until "clear,"
dizziness due to hyperventilation. a patient
For more information abollt Flutter"". contact' Sandipharl11; 22 In

verness Center Parkway; Birmingham, AL 35242; (205) 991-8085.
should refrain from forced exhalation. It may be

necessary to pause every 5 to to exhalations be
fore resuming the session (Althaus, 1993).
Advantages and Disadvantages of PEP

3. After a series of 10 to 15 breaths, the mask is
PEP therapy does not possess some of the limitations
removed from the face and the patient performs
of conventional PD and percussion for secretion clear
a series of huffs (and coughing if necessary) to
ance and is therefore applicable to a wider patient pop
expectorate any mucus that has been mobilized.
ulation. It is relatively easy to learn in one or two ses
4. The series of PEP breaths followed by huffs
sions, and may be applied equally to the pediatric and
should be repeated about four to six times. The
adult populations. PEP is appropriate for use in hospi
total treatment lasts about 15 to 20 minutes and
talized patients, as well as long-term use at home.
should be repeated twice to three times during
The expense of the equipment is minimal and once
the day. The frequency and duration of the
the patient is competent in the technique. it provides
treatment must be individualized for each pa
independence (except for small children). All of the
tient. During periods of pulmonary exacerba
PEP devices (the Flutter'" in particular) are quite
tion, patients are encouraged to increase the
portable, making airway clearance easier to perform
frequency of PEP treatments, rather than ex
during travel or when away from home during the day.
tending the length of individual s e s s i o n s

(Mahlmeister, 1991).
Although rare, pneumothorax has been reported

with high-pressure PEP (Oberwaldner, 1986). A deci
5. The procedure for use of high-pressure PEP
sion to use PEP should be carefully evaluated in
differs from that of low-pressure PEP. The ex
cases of acute sinusitis, ear infection, epistaxis, recent
piratory pressure used in this method usually
oral or facial surgery or injury (Mahlmeister, 199/).
ranges between 50 and 120 cms of water pres
For PEP therapy to be effective, a patient should be
sure. The patient breathes in and out through
able to cooperate and actively participate with the
the mask at tidal volume for 6 to LO breaths,
treatment. Pfleger (1992) recommends that patients
then inspiration is done to total lung capacity
with airway hyperreactivity should take a bron
and a forced expiratory maneuver is performed
chodilator premedication before the use of PEP.
358
PART III
Low-pressure PEP is more commonly used i n

North America, because it is felt t o be a s effective,
easier, and safer to use and monitor than high-pressure
PEP. In those patients in whom PEP is an appropriate
airway clearance technique, a high degree of accep
tance has been shown (Falk, 1984; Steen, 1991). This
may translate into better adherence in the long term.
HIGH FREQUENCY CHEST COMPRESSION

The ThAIRapy (from American Biosystems, Inc.,
St. Paul, Minn.) system of high frequency chest com
pression (HFCC) (also refelTed to as high frequency
chest wall oscillation) consists of a vest linked to an
air-pulse generator. Figure
20-16 shows a patient
using HFCC. Although the sensation of the device is

somewhat akin to mechanical percussion, it differs
significantly in its mechanism of action. HFCC
works by differential airtlow, that is, the expiratory
flow rate is higher than the inspiratory flow rate, al
lowing the mucus to be transported from the periph
ery to the central airways for expectoration. HFCC
has also been shown to decrease the viscosity of
mucus, making it easier to mobilize.
FIGURE 20-16
Patient using high frequency chest compression.
Equipment Required for High Frequency

Chest Compression
I. The air-pulse generator, required for a treat
ment of HFCC, weighs just over
100 Ibs, but
should not feel restricted while the vest is de
can be wheeled from one room to another.
flated. A single layer of clothing should be
2. The inflatable vest is constructed to fit over the
worn under the vest.
entire thorax and should extend to the top of the
2. The pressure control setting should be adjusted
thigh when the patient is sitting upright. Five
to either the high or the low setting according
different sizes are available (from child to large

adult). For use in a hospital setting, adjustable
to patient comfort.
3. The foot/hand control may be placed on the
vests are available, which are fitted to subse
floor to be activated by stepping on it, or placed
quent patients with velcro straps.
under the thigh to be activated by leaning onto
3. Simultaneous use of an aerosolized medication
it, or pressed with the hand.
or saline is recommended throughout the treat

ment. This humidifies the air to counteract the
drying effect of the increased airflow.
Treatment With HFCC

I . The treatment should progress through different
frequencies, from low (7 to 10 Hz) to medium
(10 to IS Hz) and then to high (IS to 25 Hz), to
Preparation for HFCC

1. The patient should be seated upright in a chair.
achieve both higher flow rates and increased
The vest should fit properly, but breathing
lung volume. Warwick (1991) reported that the
20
359
frequencies associated with the highest flow
successfully in reclining patients who are unable to
rates were usually greater than 13 Hz, whereas
tolerate the upright sitting position.
those associated with the largest volume were
Use of HFCC may result in time savings at home

as well as in a hospital or long-term care facility.
usually less than 10Hz.

2. The recommended protocol (American Biosys
Nebulized medications are administered concurrently
tems, Inc., 1994) gives the option of intermit
with the airway clearance treatment, and all lobes of
tent or continuous us e . For the intermittent
the lungs are treated simultaneously. The amount of
(only on exhalation) method, the patient should
time for patient contact required for a hospital care
inhale deeply and depress the foot/hand control
giver is much less with this method than with con
at peak inspiration. Exhalation should be pas
ventional PD and percussion.
sive and relaxed while the vest is pulsating. For
A disadvantage of this method of airway clearance
the continuous method, the foot/hand control
is the cost of the equipment. A monthly rental fee is
should be depressed while breathing normally.
reimbursed by most insurance companies. However,
At least once per minute, the patient should in
a study by Ohnsorg (1994) demonstrated a decline in
hale to total lung capacity.
t o ta l h e a l t h care costs for t h e y e a r a f t e r t h e
3. The average length of time spent at each fre

quency is 3 to 5 minutes, but this will vary ac
ThAIRapy Vest was put into use b y I I patients. A

study of the impact of the device in a hospital setting
cording to patient tolerance, amount, and con
(KIous, 1993) showed a substantial savings as a result
sistency of secretions, and the phase of the
of therapy self-administration. A disadvantage of
patient's illness (acute or chronic).
HFCC is its lack of portability. Although the device
4. After treatment at each frequency for the pre
can be readily moved from room to room in the
scribed length of time, the foot/hand control
house, i t does not accommodate use away from
should be released and the patient instructed to
home.
huff or cough to clear loosened secretions. The
In those patients for whom it is appropriate (and
control is adjusted to the next prescribed fre
reimbursable), HFCC is an effective method of air

way clearance. It provides independence for long
quency, and the procedure is repeated.

5. HFCC has been used on a smaller scale with
patients requiring long-term mechanical venti
term use at home as well as for acute exacerbations in

the hospital.
lation. Whitman et al. (1993) found use of the

ThAIRapy'M vest to be safe and effective, and
resulted in time savings over conventional PD
EXERCISE FOR AIRWAY CLEARANCE

A regular program of exercise has been shown to im
and percussion.
6. Patients requiring central intravenous (IV) ac
prove many variables in patients with lung disease.
cess such as a Porta-cath or Hickman are able
Peak oxygen consumption, maximal work capacity,
to use the ThAIRapy"''' Vest with sufficient
respiratory muscle endurance, and exercise tolerance
padding (such as a foam doughnut pillow) to
all improve with an exercise program (Orenstein,
relieve pressure around the access site.
1981, Andreasson, 1987). Secretion clearance is also

improved with exercise (Zach, 1981; Oldenburg,
1979). Based on improvement in pulmonary function,
Advantages and Disadvantages of HFCC
exercise has been recommended as a replacement,
This method of airway clearance allows indepen
partial or complete, for conventional chest physical
dence and is easy to learn in a short period. The
therapy (PD and percussion) (Zach, 1982; Cerny,
ThAIRapy Vest is now designed to accommodate
1989; Andreasson, 1987).
children as young as 3 years of age, and a vest may
Exercise for secretion clearance has focused on
be custom-made for very large or obese adults.
aerobic or endurance exercise to increase ventilation.
HFCC is appropriate with those patients in whom PD
The many forms of exercise must be adapted to the
positions are contraindicated, and it has been used
individual patient's status and abilities.
360
PART III
Equipment Required For Exercise
5. Supplemental oxygcn and oxygen delivery sup
I. A walking program requires nothing more than
plies will be necessary for those patients who

demonstrate oxygen desaturation during exercise.
a suitable pair of shoes and a safe location.

2. The following exercise equipment may be suit
able for a patient who is beginning an exercise
Preparation for Exercise
program: treadmill, bicycle ergometer, mini

I. Patients with hyperreactive airways should be
trampoline, or arm ergometer.
premedicated with a prescribed bronchodilator
3. For more accomplished exercisers or patients
before exercise.
with a higher exercise tolerance, equipment
2. Baseline vital signs should be recorded before
may include a stair climber, cross-country ski
beginning the exercise. In a home setting, pa
machine, or rowing machine.

4. Tools to monitor a patient's response to exer
tients should be knowledgeable in pulse taking
cise include a blood pressure monitor, heart
and estimating their level of perceived exel1ion.
rate monitor, pulse oximeter, and a scale to
For those patients who require closer monitor
measure patient's level of perceived exertion
ing, a pulse oximeter may be rented from an
(Figure 20-17).
oxygen supply company.
6
7
8
9
1
0
1
1
1
2
1
3
1
4
1
Treatment With Exercise
Very, very light
1. The principles of an excrcise prescription ad

dressing intensity, duration, and frequency, as
well as principles of warm up and cool down
Very light
are addressed in Chapter 24 and should be fol
Fairly light
for each patient is important.
lowed when using exercise as a form of airway

clearance. Individualizing an exercise program
2. Patients in the hospital for an acute exacerba

tion may not be able to perform endurance ex
Somewhat hard
ercise for the first couple of days. They should

be started slowly and progressed as tolerated.
Monitoring of heart rate, blood pressure, oxy
gen saturation, respiratory rate, and level of
Hard
perceived exertion at periods before and during

exercise, and during recovery, will allow titra
tion of the workload and duration for optimal
Very hard
performance.
3. The patient should be instructed in huffing or
Very, very hard
coughing (productive, not prolonged) to expec

torate secretions as they are loosened.
4. A regular, consistent program of exercise must
be scheduled around the patient's daily activi
FIGURE 20-17
ties to achieve adherence (e.g., walking the
Perceived exertion scale. (From Borg, G., 1982.
dog, sports at school, stopping by the health
Psychophysical basis of perceived exertion, Med Sci Sports
club after work).
Exer,
14(5),377.)
20
361
TABLE 201
Airway Clearance Techniques Applied to Patients
TYPE
Traditional
INDEPENDENCE
No
EQUIPMENT
REFLUX
REACTIVE
NEEDED
<4
>4
>12
PRESENT
SEVERE
EXACERBATION
PD board
Yes
Yes
Yes
Modified
Modified
No
Yes
Yes
Yes
Yes
May include
No
Yes
Yes
Yes
Yes
May include
Yes
Yes
Modified
Modified
AGE
percussor
CPT"
AIRWAYS
May cause
bronchospasm
HFCC
Yes
Vest and
PEP
Yes
Mask or
ACB
Yes
PD board
No
Yes
None
No
No
Yes
Yes
No
Good results
Yes
Variety
No
Yes
Yes
Yes
No
Bronchodilator
generator
bronchodilator
bronchodilator
mouthpiece
Needs care
Technique
AD
Exercise
Premedication
*Includes pOSlural drainage, percussion, shaking, vibralion, and coughing.
Modified from Maggie Mcllwaine, 1993, unpublished.
Advantages and Disadvantages of
Andreasson (1987) observed that regular contact
Exercise For Airway Clearance
with a caregiver seems to be necessary for success
Exercise has the advantage of being the only airway
ful exercise training as does family support, espe
clearance technique that is peliormed regularly by
cially in young children. Compliance will also be
people without lung disease. This factor that makes it
affected by a patient's preference for a particular
appealing to those patients who do not want to call
activity, scheduling conflicts, and commitment by
attention to their differences from their peers. Exer
friends and family members.
cise may improve self-esteem, a sense of well-being,

and quality of life. The level of exercise tolerance in
patients with cystic fibrosis has been demonstrated to
SELECTION OF AIRWAY CLEARANCE TECHNIQUES

The process of prescribing an appropriate technique
be of prognostic value (Nixon, 1992).

Because the amount or frequency of exercise re
for secretion mobilization should be ongoing, with pe
quired to achieve its benefits would not be tolerated
riodic reevaluation of the method and its effects on the
by many patients, it is often recommended as an ad
patient. Because of the low compliance reported with
junct to other forms of airway clearance. This is par
conventional chest physical therapy (Passero, 1981), it
ticularly true during an acute exacerbation when ac
is necessary for caregivers to address the many factors
tivity tolerance is limited, or in infants or patients
that may alter a patient's adherence to a particular
with neurological or muscular limitations.
method. These factors include the availability of both
Care must be taken in prescribing exercise to pa
the caregiver to teach the technique and the patient to
tients with hyperreactive airways or with a tendency
learn it; the effectiveness of the technique (subjective
toward oxygen desaturation. Use of bronchodilator
and objective); support for the technique from family,
medication and supplemental oxygen delivery may
friends, and health care personnel; and the cost of the
be necessary to achieve exercise tolerance, but these
treatment. Table 20-1 summarizes factors that influ
patients require close monitoring as well.
ence the choice of an airway clearance technique.
362
PART III
Cardiopulmonar)' Physical Therapy Interventions
AVAILABILITY
A patient's subjective response to the treatment

has implications for adherence to any technique. The
Many techniques of airway clearance are new to health
ease of sputum mobilization and the quantity of spu
care providers in the United States although they have
tum are useful feedback for a patient. How much ef
been used in Europe for some time. Use of a method
fort the treatment requires, or more importantly, how
may be limited by the lack of caregivers trained to in
much energy remai ns after completion of the treat
struct patients in a particular technique. This is espe
ment, will affect the patient's willingness to continue.
cially tllle for AD, which takes longer for a caregiver
Complications that occur as a result of a technique
to learn to teach than does use of the FlutterT" or
or precautions to be observed must guide a patient
ThAIRapyTM Vest. The ACB technique is easily incor
and caregiver to find an alternate technique in many
porated into conventional chest physical therapy by
instances. A patient hospitalized with an acute pul
learning the FET and modifying the use of percussion
monary exacerbation may need to be assisted with a
or shaking. Manual hyperinflation, on the other hand,
more passive method of secretion clearance until the
because of increased precautions for its use, requires
patient's condition allows a return to a more indepen
more study and observation before implementation.
dent technique. A patient with hyperreacti ve airways
Exercise for airway clearance may be out of the realm
may find that bronchospasm renders percussion inef
of a caregiver who is trained in respiratory care but not
fective. The presence of gastroesophageal reflux may
exercise therapy.
force the decision to use a technique which can be
The patient's availability must also be taken into
pelformed in an upright position. Sinus surgery may
consideration. An outpatient clinic visit does not lend
make use of a PEP mask intolerable. Placement of a
itself to instruction in AD, but instruction in PEP,
chest tube may necessitate a temporary replacement
ACB technique, HFCC, or Flutter"< can be initiated,
for HFCC.
with further training during return visits. On the other

hand, if a patient is admitted for exacerbation of a
pulmonary disease, the patient is a captive audience
for instruction of AD or a home exercise program
SUPPORT
When airway clearance must take place on a daily
basis, it becomes necessary to accommodate a pa
once the acute stage has passed.

Reevaluation of any airway clearance technique is
tient's schedule. A patient may have a preference for
key to its success. The patient and caregiver must be
the most effective treatment performed in the shortest
available to demonstrate and review the technique pe
amount of time. A patient may also be interested in
riodically so that modifications can be made. A
performing another activity during the airway clear
change in a patient's level of independence or motiva
ance treatment: AD or Flutter'M may be performed
tion, a decline or marked improvement in pulmonary
while riding in a car (as a passenger); HFCC can be
status, or a decrease in the effectiveness of a technique
conducted while studying for an examination; and
all necessitate reevaluation of the current method.
while running on a treadmill or during percussion by

an assistant, a patient can be watching the news.
Many patients adopt a multifaceted approach to
EFFECTIVENESS
secretion clearance, becoming adept at several meth
The prime consideration in selecting a technique is
ods and using them as conditions dictate. Patients
the effectiveness of the technique measured both sub
who use AD or exercise primarily will need to use an
jectively and objectively. Objective measures in
alternate form of airway clearance during an acute
clude: pulmonary function studies, chest x-rays,
exacerbation of an illness. Use of HFCC at home
blood gas values, changes in mechanical ventilator
may necessitate use of a more portable technique
settings, changes in auscultation, and quantity of spu
when away from home for long periods. Patients who
tum produced. A patient's response to treatment can
rely on an assistant to perform percussion may need
be evaluated by changes in heart rate, respiratory rate,
to learn a more independent method for occasions
oxygen saturation, and level of fatigue.
when the assistant is not available.
20
363
In a home where more than one family member re
The effectiveness of these newer techniques com
quires ongoing airway clearance, as can be the case for
pared with more established methods are just begin
parents of children with cystic fibrosis, spending the
ning to be studied. Health care providers have anec
least amount of time for the greatest benefit becomes of
dotally reported their effectiveness, but long term,
primary importance. For an infant or young child, per
well-designed studies are needed.
formance of secretion mobilization must be carried out

by an adult. As the child grows older and the choices of
a technique increase, close supervision remains neces
sary. In the adolescent, even when physical assistance
INTRAPULMONARY PERCUSSIVE VENTILATOR (IPV)

The intrapulmonary percussive ventilator (IPV) (from
is no longer required, emotional support from family
Percussionaire Corp., Sandpoint, Idaho) is an airway
and friends is paramount to continued success with a
c l e a r a n c e device t h a t s i m u l t a n e o u s l y delivers
technique. Finally, the support received from health
aerosolized solution and intrathoracic percussion
care providers is vital to the patient's motivation to con
(Homnick, 1994). The functional component in the

IPY is an apparatus known as the phasitron. The pha
tinue with a technique, or to learn a new one.
sitron was originally developed by Bird in 1979 for

the volumetric diffusive respiration (VDR) ventilator.
COST
It is used with thermally injured patients in place of
In this age of health reform, especially in long-term
conventional mechanical ventilation. The VDR venti
care or chronic disease, cost of a treatment must be
lator functions by accumulation of subtidal volume
considered. The initial cost of equipment, replace
breaths, which build to an oscillatory equilibrium that
ment costs, and the expense of assistance required, all
is followed by passive exhalation (Rodenberg, 1992).
figure into the total cost of treatment.
Figure 20-18 shows a YDR ventilator waveform.
The generator for HFCC is the most costly piece
In the IPV, the phasitron provides high-frequency
of equipment presented here, but replacement should
impulses during inspiration, and positive expiratory
not be necessary. The vest itself should not require
pressure maintained throughout passive exhalation.
replacement except for growth of a child. PEP masks
The pressure generated is 10 to 30 cms. of water
and mouthpieces, and the FlutterT" are relatively inex
pressure. Treatment with IPV is titrated for patient
pensive, with replacement of equipment expected to
comfort and visible thoracic movement.
occur occasionally during a lifetime of use (more
Homnick et a!. (1994) performed a 6-month study
often for a one-way valve in a self-made PEP). AD
using the IPV for airway clearance in patients with
and ACB require no equipment.
cystic fibrosis. No significant differences were
Payment of a trained assistant for home use of
demonstrated in pulmonary function studies, body
postural drainage and percussion when family sup
weight, use of antibiotics, or hospital days between
port is not available is at great expense. Depending
the IPV and conventional chest physical therapy
on the duration and frequency of treatment, this cost
group. Three fourths of the patients estimated in
may outweigh that for other airway clearance tech
creased sputum production with IPY and satisfaction
niques on a long-term basis.
was high for comfort and independence.
Often the choice of an airway clearance technique

is limited by the reimbursement available for equip
ment or assistance. Nonetheless, the caregiver must
DYNAMIC AIR THERAPY BED
strike a balance between economic and clinical con
The E FICA CC'" Dynamic Air Therapy bed (from
siderations in choosing a mode of therapy.
HILLROM, Batesville, Indiana) is used in hospital

ized patients, primarily in an intensive care setting.
The modes available from the bed are continuous lat
FUTURE TRENDS IN AIRWAY CLEARANCE
eral rotation, percussion, vibration, and the ability to
A recent resurgence of interest in airway clearance
position the patient in postural drainage positions.
has led to the introduction of additional techniques.
Use of the bed demands less time of the caregivers
364
PART III
11111AlII
1 AI
IUUIUU'IUV
'II I" I"
\
I,
IIIIHulI,
!nll,I"HUIVUU UU
IlIUVIII' I"
frI
11
I
I
llIlHIIH
UlnllIHVIIVUI
UUM
.JIII" I" II 'I
AI
fI
I,
'VY 'VIII
till, IAIlAllA
uAflJUVIIIUVIIVVIIUI
m '" "
AI
I'
I
I
'YV
.11
AI
"
,yv
FIGURE 20-18
VDR ventilator waveform. (From Rodeberg, D.A., (1992). Decreased pulmonary barotrauma with
the use of volumetric diffusive respiration in pediatric patients with burns: The 1992 Moyer Award,
Journal of Burn Care Rehabilitation 13, 506-511.)
presented by patients and choose a technique or combi
for hands on airway clearance treatment.

A smaJi pilot study by Samuelson et al.
(1994)
nation of techniques that best suits each patient's needs.
compared the bed to manual percussion and postural
An individualized approach to airway clearance re
drainage in adult patients with cystic fibrosis. Patients
quires consideration of the multitude of variables, both
were randomized to receive four treatments a day with
physiological, psychological, and practical that affect a
either the Dynamic Air Therapy bed or manual chest
patient's response to treatment. Health care providers
physical therapy for I week and then switched to the
are challenged to keep abreast of techniques and their
other modality for an additional week. Outcome mea
modifications to best provide for the patient's needs.
sures included pulmonary function studies, 6-minute
The role of the caregiver involves more than tech
walk distance, dyspnea score, and a Quality of WeJl
nical expertise. The caregiver is uniquely positioned
Being Scale. Both therapies demonstrated a positive
to simplify medical language for a patient and en
effect from baseline, but a significant improvement
courage adherence to airway clearance. Support of a
was found only in the 6-minute walk distance of those
treatment by a health care provider can increase the
patients treated with the bed therapy first.
benefit derived from the treatment.
Studies on more appropriate patient populations,
Further study is needed to compare and standardize
especiaJly nonambulatory, critically ill patients, for
techniques, follow long-term outcomes, and establish
whom the Dynamic Air Therapy beds are generally
optimal treatment guidelines. This information will
prescribed, are necessary to demonstrate the most ef
assist both patients and caregivers to maximize treat
fective use of this expensive equipment.
ment with airway clearance techniques.
SUMMARY
REVIEW QUESTIONS
Numerous airway clearance techniques have been
1. Which ACTs can be performed without acquir

ing additional equipment?
shown to reduce obstruction, enhance mucociliary

clearance, and improve ventilation, accomplishing the
2. Are there any ACTs that are not suitable for use
in an intensive care unit?
goal of improved oxygen transport. Their effectiveness

has been demonstrated in controlled situations and eval
3. What are the airway clearance methods most
uated with sophisticated equipment. Caregivers must in
suited for instructing a patient/family in during a
corporate this information into the real life situations
single outpatient clinic visit?
20
4. What outcome measures do you have at your dis

posal for evaluating the effectiveness of airway
clearance?
5.
How would you encourage adherence of a pre

scribed method of airway clearance in:
365
Gormenzano,J . Branthwaite,M.A. (1972). Pulmonary physiother

apy with assisted ventilation. Anaeslhesia, 27, 249-257.
Homnick, D., SpiJlers, e., White,F. (1994). The intrapulmonary
percussive ventilator compared to standard aerosol therapy and
chest physiotherapy in the treatment of patients with cystic ti
brosis. Abstracted in Pedialr Pulmonology, Suppl. 10,266.
a fiercely independent adolescent with a spinal
[mle, P.e., (1989). Percussion and vibration. In Mackenzie, (Ed.).

CheSi Physical Therapy in the Inlensive Care Unil, 2nd Ed.
cord injury?
a 3 year old newly diagnosed with cystic fibrosis?
an older patient with bronchiectasis?
(pp. 134-152). Baltimore: Williams
& Wilkins.
Kious,D.,et al. (1993). Chest vest and cystic fibrosis: Better care
for patients. Advanced RespiralOry Care Management, 3,44-50.
Kious, D.R. (1994) High-jrequency chest wall oscillation: Princi
ples and appiicalions. Published by American Biosystems,
Inc.. St. Paul. 626-630.
References
Mahlmeister,M.J.,et al. (1991). Positive-expiratory-pressure mask

Althaus, P. (1993). Oscillating PEP. [n Bronchial Hypersecretion:
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tion of nebulized bronchodilator in severe bronchospasm. Euro
63, 119,97-100.
Andreasson,B., et al. (1987). Long-term effects of physical exer

cise on working capacity and pulmonary function in cystic fi
fresher Class. Presented at Seventh Annual North American

Cystic Fibrosis Conference, DaJlas.
Nixon, P.A. (1992). The prognostic value of exercise testing in pa
tients with cystic fibrosis. New England Jo umal of Medicine,
327, 1785-1788.
Oberwaldner,
brosis. ACIO Paedialr Seal/d, 76,70-75.21-38.

Bateman, 1.,et al. (1979). Regional lung clearance of excessive
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B., Evans, J.e.. Zach, M.S. (1986). Forced expira
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Ohnsorg, F. (1994). A cost analysis of high-frequency chest waH
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FJ. (1989). Relative effects of bronchial drainage and exer
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Cerny,
36 (11), 1218-1229.
Mcllwaine, M. (1993). Airway clearance techniques (ACT) Re
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ALNATS International Conference, Boston.
Oldenberg. FA.,et al. (1979). Effects of postural drainage,exer
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Orenstein, D.M., et al. (1981). Exercise conditioning and car
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Chevaillier,1. (1992). Airway clearance techniques. Course Pre
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Passero, M.A., Remor, B., Salomon,
J. (1981). Patient-reported
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Pryor, J.A., et al. (1979). Evaluation of the forced expiration tech
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Dab,I., Alexander,F. (1979). The mechanism of autogenic drainage
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Pryor,J.A., Webber B.A., Hodson, M.E. (1990). Effect of chest
studied with flow volume curves. Mon Paed, 10,50-53.

David, A. (1991). Autogenic drainage-the Gelman approach. In Pryor.
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Falk,M.,el al. (1984). Improving the ketchup bottle method with
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65, 423-32.
Frownfelter D. (1987). Postural drainage. In Frownfelter, D. (Ed.).
ClTesl Physical Thempy (lnd Pulmol/Qly Rehabilil{lIion (2 nd
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Dise(lses,
Frischknecht-Christensen E., Norregaard,
0., Dahl, R. (1991).
Treatment of bronchial asthma with terbutaline inhaled by
brosis,45, 77.
(Ed.), Respiralory Care (pp. 79- 100). Edinburgh: Churchill
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Rodeberg, D.A., et al. (1992). Decreased pulmonary barotrauma
with the use of volumetric diffusive respiration in pediatric pa
tients with burns: The 1992 Moyer Award. Joumal of Burn
Care Rehabilitation, 13. 506-5 I
Samuelson, W., Woodward.
I.
F, Lowe,V. (1994). Utility of a dynamic
conespacer combined with positive expiratory pressure mask.
air therapy bed vs. conventional chest physiotherapy in adult CF
CITesI, 100 (2), 317-321.
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10, 266.
366
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Cardiopulmonary
SchonL M.H. (1989). Autogenic drainage: A modern approach to
Cystic Fibrosis (CF). Published by International Physiotherapy
physiotherapy in cystic fibrosis. Journal of the Royal Society of
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Webber, BA, Pryor, JA (1993). Physiotherapy skills: techniques
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Steen, H.F., et aL (1991). Evaluation of the P E P mask in cystic fi
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Sutton, P.P., et aL (1985), Assessment of percussion, vibratory
Whitman, J"
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10
expiration and sputum clearance in
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Zach, M" OberwaJdner, R, Hausler, F. (1982), Cystic
chanical ventilation. In Webber, B,A, (Ed,) The BromplOn Hos

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et aL (1993). Preliminary evaluation of high-fre
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phYSical
eases of/he Child,
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57. 587-589,
Facilitating Airway Clearance

With Coughing Techniques
Mary Massery
Donna Frownfelter
KEY TERMS
Airway clearance deficits
Mucous blanket
Assisted cough
Reflex cough
Complications with coughing
Smokers cough
Cough
Swallowing disturbance
Cough pump
Throat clearing
Cough stages
INTRODUCTION
Cough truly serves many purposes: a therapeutic technique,
a
diagnostic signpost, and a social necessity. If it didn't al
ready exist, we would have to invent it.
of food goes "down the wrong hole" or into the tra

chea rather than the esophagus, a cough is not the
usual mechanism to clear mucus.
Glen A. Lillington, MD
A nervous cough or throat clearing may also sig
The cough is an interesting phenomenon. A cough
nal that the airways are irritated, mucus is not clear
can either be a reflex or a voluntary action. Gener
ing normally, or the person is in an uncomfortable
ally, in healthy individuals a cough is rarely heard
situation. This is something to be aware of especialJy
unless the person has a cold or an irritant is inhaled
when treating asthmatics, patients with cystic fibro
and a sneeze or a cough ensues to evacuate the for
sis, or patients with psychological problems.
eign body. The mucociliary escalator functions to
In reality the mucous blanket and the cough
clear secretions and inhaled particulate matter. Unless
mechanism are the two ways the lungs have of pro
the mucus is very thick, such as in individuals with
viding airway clearance under normal everyday cir
dehydration, inhalation of a foreign body, or a bolus
cumstances.
367
368
PART III
It is interesting how many people are unaware of
Airway clea rance techniques, such as postural
their coughing. For example, when asked if they
drainage, autogenic drainage, or active cycles of
cough, smokers with typical morning and ongoing
breathing, need to be used to mobilize the secretions
smoker's coughs will deny that they do. Spouses will
to the area where the cough will be effective (see
chime in, "He coughs and hacks all the time." An in
Chapter 20).
dividual might constantly clear his or her throat and

swallow mucus but will claim to be unproductive of
mucus and free of coughing. It is important for thera
COUGH ASSOCIATED WITH EATING OR DRINKING
pists to be aware of both the reflex and voluntary na
If a cough is associated with eating or drinking or
ture of their patients' coughs.
taking medications, the patient should be evaluated
Frequent coughing or throat clearing may also in
for a swallowing disturbance. This usually consists of
dicate other problems than airway clearance deficits.
a "cookie swallow," a fluoroscopy study where the
For example, a patient may have postnasal drip from
patient is given barium or
a sinus infection or allergy. When the mucus drips
liquids and solids to swallow and observed to see if
variety of consistency
down into the back of the throat, it can cause a reflex
aspiration into the respiratory tract occurs. Patients
cough to clear it. Other causes include bronchogenic
may have dysfunction after a cerebrovascular acci
carcinoma, nervousness, and smoking. In a pediatric
dent (CY A) or prolonged intubation or because high
patient, a foreign body or object inserted or inspired
placement of a tracheostomy tube inhibits the proper
into the nose or airway should be ruled out.
function of the larynx during swaJlowing. Speech
Cigarette smoking paralyzes the cilia so airway
language pathologists working with patients with
clearance is altered. It has been noted that for every
dysphagia can help patients learn techniques to pre
cigarette an individual smokes the cilia are paralyzed
vent aspiration. They also help the patient and spouse
for approximately 20 minutes. Many individuals are
(significant other) to understand cognitively proper
chain smokers and light up one cigarette after the
positioning (usually sitting up in semi-Fowler's) and
other. Consequently, coughing is the only means of
proper head and neck position (usually chin tuck and
clearing the lungs. This is understandable when a
slight neck flexion) during swallowing. If a patient
smoker coughs up a large amount of mucus in the
has dysphagia and cannot or will not follow a safe
early morning on arising. After sleeping for hours the
swallowing retraining program and continues to
individual's cilia are able to clear secretions; a cough
choke and aspirate food and liquid, aspiration pneu
assists in airway clearance. During the day the
monia will occur and can lead to the patient's condi
smoker who chain smokes must cough regularly to
tion deteriorating and even to death. In a situation
clear secretions because the cilia are paralyzed by the
such as this, alternative feeding would need to be
smoke.
considered.
COUGH PUMP
COMPLICATIONS OF COUGHING
One must appreciate the complexity and intricacy of
The act of coughing can be hazardous to the patient.
the cough pump. Mucus is transported up against
A patient should never be asked to cough repeatedly
gravity by the mucous blanket and propelled cepha
as a routine part of treatment. The irritation and pos
lad by the action of the cough.
sible narrowing of the airways during the forced ex
In general the cough is most effective at high expi
halation may cause bronchospasm. If a patient is
ratory flow rates and at high volumes. The cough is
sounding dry and unproductive, do not encourage fre
of limited value beyond the sixth or seventh genera
quent coughing. This is especially true in patients
tion of airway branching. Consequently when a pa
with asthma.
tient has a lower lobe pneumonia or atelectasis,
If a patient demonstrates retained secretions on x
coughing alone will not clear the retained secretions.
ray, encourage hydration (drinking water), use airway
21
Facilitating Airway Clearance With Coughing Techniques
clearance mobilization techniques, and carefully eval
369
for a forceful cough. Generally, adequate inspiratory
uate the cough. Instruct the patient in controlled
volumes for a cough are noted to be at least 60% of
coughing when mucus is felt in the throat or upper
the predicted vital capacity for that individual. The
airways. The patient may try to cough in a controlled
second stage involves closing of the glottis (vocal
fashion after a postural drainage session or use the
folds) to prepare for the abdominal and intercostal
forced expiratory technique. The forced expiratory
muscles to produce positive intrathoracic pressure dis
technique uses midlong volume ventilation followed
tal to the glottis. The third stage is the active contrac
by one to two huffs, which can include chest com
tion of these muscles. The fourth and final stage in
pression with the arms. Forced coughing can also in
volves opening of the glottis and forcefully expelling
crease blood pressure and Jower cardiac output. Tus
the air. The patient should be able to cough three to
sive syncopy can occur when a patient goes into a
six times per expiratory effort. A minimal threshold of
series of coughs in which the intrathoracic pressure
a FEY) (forced expiratory volume in I second) of at
becomes so high that venous return to the heart is im
least 60% of the patient's actual vital capacity is a
paired. The cardiac output falls and the patient be
good indicator of adequate muscle strength necessary
comes very dizzy, progressing to unconsciousness.
for effective expUlsion (Figure 21-1). During a cough,
Care must be exercised, especially with patients with
alveolar, pleural, and subglottal pressures may rise as
primary lung disease; they must learn to control their
much as 200 cm H20 (Bach, 1993; Jaeger, 1993; Lin
coughing to prevent untoward side effects.
der, 1993).
Stages of Cough
COUGH EVALUATION
There are four stages involved in producing an effec
How do you assess whether a patient's cough is ef
tive cough (Linder, 1993). The first stage requires in
fective? The answer appears to be obvious: ask the
spiring enough air to provide the volume necessary
patient to cough. However, the obvious answer often
FIGURE 21-1
Cough mechanics. A, Stage I: adequate inspiration. B, Stage 2: glottal closure; Stage 3: b u i l ding up of intrathoracic and
intraabdominal pressure. C, Stage 4: glottal opening and expUlsion.
370
PART In
does not adequately analyze the functional perfor
inspiration or expiration cycle? Did the patient sponta
mance of a cough, especially for a neurologically im
neously use trunk extension, an upward eye gaze, or
paired patient. The clinician must first take time to
the arms to augment the inspiratory effOlt? Did the pa
set up the patient for successful evaluation of their
tient take enough time to fully inspire before cough
cough. Guidelines for setting up the patient follow:
ing? If the patient inspires adequately, he or she should
I. Do not ask the patient to cough in whatever
be able to sustain two to six coughs per expiratory ef
posture you happen to find him or her in. Ask,
fort for a cascade effect. Neurologically impaired pa
"What position do you like to cough in when
tients who have inadequate inspiratory effol1s usually
you feel the need to cough?" Then ask the pa
present with only one or two coughs per breath and
tient to assume that posture, or assist him or her
generally produce a quieter cough (Hoffman, 1987).
in assuming a posture as close to the preferred

posture as possible. Listen closely to his or her
answers. A patient should s po n t a n e o u s l y
Stage 2: Glottal Closure
choose a posture that lends itself to trunk flex
Did the patient hold his or her breath at the peak of
ion, which is necessary for effective expulsion
inspiration before the expulsion phase or did the pa
and airway protection. A red flag or inappropri
tient go directly from inspiration to expiration? Did
ate choice would be a preference for coughing
you hear a cough or a huff? A huff (or a complete ab
while supine, which involves the opposite:
sence of a hold between inspiration and expiration),
trunk extension and poor mechanical alignment
when the patient intended to give you a cough, is an
for airway protection.
indication of insufficient glottal closure. This can re
2. Now the patient is ready to demonstrate cough
sult from a wide variety of situations including glottal
ing. Do not make the mistake of asking a pa
edema after prolonged intubation, partial or full
tient to "show me a cough" or he or she may
paralysis of the vocal folds, hemiparesis of the vocal
simply "show you" a cough. It may not be the
folds, or timing or sequencing difficulty secondary to
way the patient coughs to clear secretions. In
brain injuries to name a few. A complete lack of glot
stead continue to set the patient up for success
tal closure will not produce any cough sound because
by asking him or her to "show me how you
the vocal folds are not approximating.
would cough if you had secretions in your chest

and you felt the need to cough them out." With
these instructions you are asking the patient to
show you something functional not theoretical.
Stage 3: Building up of Intrathoracic

and Intraabdominal Pressure
Cough effectiveness can now be accurately as
Did you see active contraction of the intercostal
sessed. Guidelines for objective evaluation with pul
and abdominal muscles? D id the patient sponta
monary function tests have been indicted. This sec
neously move into trunk flexion during this phase?
tion focuses on analyzing the movement during all
Did the cough have a low resonant sound? Inade
four stages. An effective cough should maximize the
quate force is usually heard as a higher pitch cough,
function of each individual stage. Thus the clinician
often called a throaty cough. The sound is quieter
should see a deep inspiratory effort paired with trunk
overall and does not produce as many coughs per
extension, a momentary hold, and then a series of ex
expiratory effort. It is sometimes associated with
piratory coughs on a single breath while the patient
neck extension rather than flexion as the patient at

tempts to clear the upper airway only. The air ap
moves into trunk flexion.
pears to leak out rather than being propelled out of

the larynx during the cough. Like inadequate lung
Stage 1: Adequate Inspiration
volumes, inadequate pressure also prevents the pa
Did the patient spontaneously inspire a deep breath be
tient from coughing more than once or twice on one
fore coughing or did he or she cough regardless of the
expiratory effort.
21
371
Stage 4: Glottal Opening and Expulsion
tient to take a deep breath and cough because this can
Timing of the opening of the glottis and forcefully ex
cause more air trapping, which does not facilitate ex
pelling the air is directly tied into the function of the
pulsion of secretions. Patients will be more effective
third stage. During expulsion, does the patient appear
trying to take controlled small or medium breaths fol
to gag before successfully allowing the air to be ex
lowed by huffs or a small series of coughs.The active
pelled? Does the patient seem to get stuck holding his
cycles of breathing and forced expiratory pressure
or her breath? Deficiencies in this area are often re
technique is also a good choice for these patients.
lated to brain injuries and coordination difficulties. The
Several ideas are presented because the therapist
opposite can also occur. Some patients will get stuck at
needs a bag of tricks. Some techniques work well
the end of expulsion, especially those with severe neu
for some patients and not for others. Try several
rological impairments or bronchospasms and may
with each patient and let him or her determine what
have difficulty initiating the next inspiratory effort.
works best.
Another variation that decreases stress on the pa
tient is to use a series of coughs starting with a small
PATIENT INSTRUCTION
breath and a small cough, then a medium breath and a
When working with patients, especially those with
medium cough, then a larger breath and a large
primary pulmonary disease or primary disease super
cough. This is a good technique to use with postoper
imposed on secondary disease (i.e., a patient with a
ative patients, who get fatigued trying to maximally
CY A and asthma), there are some helpful techniques
cough each time.

For patients with transient or permanent neuromus
to make secretion mobilization more effective.

Patients with asthma tend to go into an expiratory
cular weakness or paralysis, further instructions may be
1993; Braun, 1984). These patients
wheeze when they force and prolong exhalation.This
necessary (Jaeger,
can lead to bronchospasm and respiratory distress.
must use every physical trait to maximize the function
The patient can be taught a pump cough, a variation
of each stage of the cough (see Figure
on a huff technique. A huff may be used when pa
the box on p.
tients have had an endotracheal tube in for an ex
during the expulsion stage of the cough only addresses
tended time. The vocal folds are swollen and irri
one aspect (Slack,
tated. Consequently, they will not close and form a
taken to look at all four stages to maximize the airway
21-1, p.369, and

372). Physically assisting these patients
1994; Fishburn, 1990). Care must be
tight seal to build up pressure and cough. The patient
clearance potential of any assistive cough technique.
is instructed to huff rather than cough to mobilize se
First, the patient must be positioned for success.The
cretions.It is done with more open vocal folds, a low
beginning of any cough requires trunk extension or in
sound, and less effort, yet it is quite effective in mo
spiratory movement to maximize inhalation, whereas

the expulsion stage requires trunk flexion or expiratory
bilization of secretions.
The pump cough extends the huff and is more ef
movement to maximize exhalation (Massery,
1994).
fective. The patient is instructed to take three short
Thus for any given posture, the clinician must assess
huffs and follow it with three short, easy coughs at
the following:
lower lung volume, not deep breaths or deep lung
trunk movements,
(1) whether the posture allows for both

(2) whether flexion and extension
volumes. Three or four sequences are done ...huff,
are possible, which movement is more important for
huff, huff, cough, cough, cough, huff, huff, huff,
that particular patient, and whether that posture facili
(3) how gravity is effecting the
cough, cough, cough, huff, huff, huff, cough, cough,
tates this occunence,
cough.Usually if secretions are present a sponta
patient's muscle strength and function in this posture,
(4) whether the patient can still protect the airway
neous cough might occur or the secretions will mobi
and
lize with the small cough.
in this posture. When these questions are answered sat
Patients with emphysema have overdistel')ded lungs

and difficulty with exhalation. Do not instruct the pa
isfactorily, the clinician is ready to instruct the patient

in the act of coughing.
372
PART III
Positioning and Patiellt Instructioll to Improve

Cough Effectiveness
scribed previously, these subtle motions may signifi

cantly increase the patient's inspiratory effort and pro
vide a more active means for the patient to participate
Position the patient for success, especially in
Maximize inspiratory phase through verbal cues,
Improve hold stage through verbal cues and
loud command to "hold it" at the peak of inspiration,
positioning.
may be sufficient to facilitate closure. Remember to
Maximize intrathoracic and intraabdominal
allow enough time for the patient to take in a deep
regard to trunk alignment.

positioning, and active arm movement.
pressures with muscle contractions, physical

assist, or trunk movement.

Instruct the patient in appropriate timing and trunk

movements for expulsion.
in his or her own coughing program.

Stage two involves closing the glottis. For some
patients with weakness or timing problems, a sharp
inspiratory effort before asking them to "hold."

Some clinicians rush the first phase, by saying in
quick succession: "take a deep breath and hold it,"
Make the procedure physically active on the
thus unintentionally limiting the time of the inspira
patient's part.
tory effort. A more appropriate verbal cue would be:

"take a deep breath in . . .
in .. .in. . .in ... , and
now hold it," allowing adequate time for the patient
to inhale.
Stages three and four (building up pressure and ex
pulsion) are discussed together because their timing is
An example may provide the best illustration of
interdependent. The patient now needs to move into
these instructions. A clinician may pick a modified
trunk flexion, with or without the clinician's assis
sitting position for a patient with generalized weak
tance, to maximize expulsion. For those patients who
ness (e.g., incomplete spinal cord injury, developmen
can assist, they can be asked to do the opposite of stage
tal delay, or temporary weakness or exhaustion after a
one:
medical or surgical procedure). The patient looks
of your arms down to your hips as you cough."
slumped, so the clinician places a lumbar support
(3) "Roll your shoulders forward while you cough."

(4) "Bend your trunk forward while you cough." like
(e.g., a lumbar roll, a towel, or a pillow) behind the
(I) "look down while you cough." (2) "Pull both
lower back to increase trunk extension in that posi
wise, patients with more limited aim function can be
tion. The patient is asked if he or she is comfortable
asked to do the following:
and if he or she can swallow safely. Next the clinician
your chest while coughing." (2) "Roll your shoulders
(1) "Squeeze your arms to
tries to maximize the first cough stage by asking the
and arms inward while coughing."
patient to take in a deep breath. Observing that the pa
hands down while coughing."
(3) "Turn your
tient did not appear to take in as deep a breath as the
In this manner the clinician has used every con
clinician perceived capable, the clinician adds further
ceivable resource to maximize a voluntary cough.
(1) "look upward
Even the weakest cough can be made more effective
instructions such as the following:
(I) posi
(3) ask
while you inhale." (2) "Raise both of your arms up
by applying the following simple concepts:
over your head as high as you can while you inhale,"
tion for success, (2) maximize inhalation first,
(3) "Squeeze your shoulders back while you inhale."

(4) "Straighten or extend your back while you inhale."
racic and intraabdominal pressures,
for a breath hold,
(4) encourage maximal intratho

(5) instruct the
For those with more limited arm function, apply ap
patient in appropriate timing and trunk movements
propriate ventilatory strategies detailed in Chapter 22.
for expulsion, and
Very subtle movements can then be requested, such as
as possible for the patient. However, even with excel
(6) make the procedure as active
(I) "Bring your arms up and out while
lent instructions, many neurological patients require
you inhale." (2) "Rotate your arms outward while you
the clinician's physical assistance to inhale deeper or
(3) "Turn your forearm up while you inhale."
to exhale more forcefully because of muscle weak
the following:
inhale."
Although less dramatic than the larger movements de
ness or paralysis (Maclean,
1989).
21
ACTIVE ASSISTED COUGH TECHNIQUES
If after instruction and modification in the patient's

cough as described previously, the patient still can not
produce an effective cough, then one of the following
assistive cough techniques may be appropliate. How
ever, a patient who needs some assistance to improve
a cough is not excused from an active role in cough
ing. Keep the act of coughing as active as possible for
each patient. whether that is accomplished by adding a
few verbal cues to improve overall timing or posture
while the patient independently performs the cough,
or whether it is accomplished by adding eye gazes for
a very weak patient who cannot move the upper ex
tremities and breathes with the assistance of a ventila
tor. Encourage the patient to be responsible for his or
her own care by teaching the concepts involved in
producing an effective cough (Estenne, 1990). In that
manner, you will help the patient develop the problem
solving skills necessary for modifications later. Mod
ify and develop additional techniques on the princi
ples presented thus far. See the box below for tech
niques presented in this chapter.
Manually Assisted Techniques
Costophrenic assist
The first assistive cough technique, the costophrenic

assist, can be used in any posture. After assessing the
most appropriate position for the patient (most often
sitting or sidelying) and giving the patient instruc
tions to maximize all four coughing stages, the thera
373
pist places his or her hands on the costophrenic an

gles of the rib cage (Figure 21-2). At the end of the
patient's next exhalation, the therapist applies a
quick manual stretch down and in toward the pa
tient's navel to facilitate a stronger diaphragmatic
and intercostal muscle contraction during the suc
ceeding inhalation. The therapist can also apply a se
ries of repeated contractions from proprioceptive
neuromuscular facilitation (PNF approach (Sullivan,
1982). throughout inspiration to facilitate maximal
inhalation. The patient may assist the maneuver by
actively using his or her upper extremities, head and
neck, eyes, trunk, or all of the above to maximize the
inspiratory phase. The patient is then asked to "hold
it." Just a moment before asking the patient to ac
tively cough, the therapist applies strong pressure
through his or her hands, again down and in toward
the navel. In this manner the therapist is assisting
both the build up of intrathoracic pressure and the
force of expiration. Of course, the patient would also
actively participate by using his or her arms, trunk,
or other body parts throughout the entire procedure
(see Chapter 22).
This technique's obvious use would be for patients
with weak or paralyzed intercostal or abdominal mus
cles. The therapist must remember to evaluate the ef
fect of gravity and posture in each position for the ap
propriateness of this technique (Massery, 1987). It is
Assisted Cough Techniques

Manually assisted lechniques
I.
2.
3.
4.
Costophrenic assist
H ei m li ch-type or abdominal thrust assist
Anterior chest compress i on assist
Counlerrotation assist
Self-assisted techniques
I.
2.
3.
4.
5.
Prone on elbows head flexion sel f-assisted cough

Long-silting self-assisted coughs
Short-sitting self-assisted coughs
Hands-knees rocking self-assisted cough
FIGURE 21-2
Standing self-assisted coughs
Assisted cough techniques in supine position; costophrenic

assist.
374
PART III
helpful for lower airway clearance but does not di
the heel of his or her hand, as in a Heimlich choking
rectly assist in upper chest clearance unless the pa
maneuver. The patient is instructed to assist with ap
tient is able to move his or her upper body indepen
propriate trunk movements to the best of his or her
dently while the therapist assists the lower chest. This
ability. TechnicalJy, this procedure is very effective
technique is easy to learn and teach and can usually
at forcefully expelling the air (Braun, 1984), as in a
be used from the acute phase through the patient's re
cough, but it can be extremely uncomfortable for the
habilitation phase, thus accounting for its popularity.
patient because of (1) its concentrated area of contact,
Heimlich-type assist or abdominal thrust assist

The second technique, the Heimlich-type assist or an
(2) the abrupt nature, which may elicit an undesired

high neuromuscular tone response or worse when
combined with the sensory input that the therapist's
abdominal thrust, requires the therapist to place the
manual contacts supply, (3) the force, which may
heel of his or her hand at about the level of the pa
cause an abdominal herniation. Because of its limited
tient's navel, taking care to avoid direct placement on
usefulness, the Heimlich type of assist or abdominal
the lower ribs (Figure 21-3). After appropriate posi
thrust should only be used when the patient does not
tioning, the patient is instructed to "take in a deep
respond to other techniques and the need to produce
breath and hold it." Unfortunately, manual facilita
an effective cough is imminent. Patients with low
tion of inhalation is not feasible with this technique.
neuromuscular tone or flaccid abdominal muscles
As the patient is instructed to cough, the therapist
fare best with this procedure.
quickly pushes up and in, under the diaphgram with
FIGURE 21-3
Hand position for Heimlich-type assist or abdominal thrust.
21
The therapist can simultaneously use both of the
375
enhance the first two cough stages. The therapist then
above techniques in sidelying. If the patient is hemi
applies a quick force through both arms to simulate
plegic or suffered from an unilateral lung or thorax
the force necessary during the expulsion phase. The
disease or trauma, emphasizing one side of the thorax
directions of the force are
over the other may be an appropriate focus during
upper chest, and
airway clearance treatments. One upper extremity is
or abdominal arm. Performed together the compres
used to perform the Heimlich"type of assist while the
sion force from both arms makes the letter V.
(l) down and back on the

(2) up and back on the lower chest
other does an uni lateral costophrenic assist. In this
The anterior chest compression technique is more
manner the therapist can compress simultaneously all
effective than the costophrenic assist for patients with
three planes of ventilation in the lower chest. The
very weak chest wall muscles because of the added
possibilities of combining techniques and positions
compression of the upper anterior chest wall. These
are almost endless once the therapist understands the
authors have found sidelying or 3/4 supine position to

be the most effective position for this technique.
principles on which they were developed.
However, the anterior chest compression technique is
Anterior chest compression assist
not appropriate for patients with a cavus condition of
The third assistive cough is called the anterior chest
the upper anterior chest because it promotes further
compression assist, since it compresses both the
collapsing of the anterior chest wall.
upper and lower anterior chest during the coughing

maneuver. This is the first single technique thus far to
Counterrotation assist
address the compression needs of the upper and
The most effective assistive cough for the widest
lower chest in one maneuver. The therapist puts one
cross-section of neurological patients, in these au
arm across the patient's pectoralis region to compress
thors' clinical experience, is the fourth and final
the upper chest and the other arm is either placed par
method described in sidelying, the counterrotation as
21-4) or
sist. The positioning and procedures required for the
placed like in the Heimlich type of maneuver (Figure
counterrotation technique are described in detail in
allel on the lower chest or abdomen (Figure
22 and apply for both the patient and the ther

21-6). The therapist should recall that
21-5). The commands are the same as in the other
chapter
techniques. Because of the direct manual contact on
apist (Figure
the chest, inspiration can be easily facilitated first,
orthopedic precautions of the spine, rib cage, shoul
followed by a "hold." Thus the therapist can readily
der, and pelvis still persist for this technique.
FIGURE 21-4
FIGURE 21-5
Assistive cough techniques in supine position; variation of
Assistive cough techniques in supine position; variation of
the anterior chest compression assist.
the anterior chest compression assist.
376
PART III
FIGURE 21-6
Counterrotation assist; A, Hand placement during expulsion phase; B, Hand placement during
inspiration phase.
21
377
The therapist begins by following the patient's
tion before passively coughing in a comatose
breathing cycle with his or her hands positioned over
patient can reduce high tone and frequently re
21-6).
duce a high respiratory rate. Both of these re
The therapist then gently assists the patient in inhala
duce the possibility of the patient keeping his
the patient's shoulder and pelvis (see Figure
tion and exhalation to promote better overall ventila
or her glottis closed during the expulsion phase.
tion. This sequence is generally repeated for three to
2. Counterrotation is an excellent mobilizer for a
five cycles or until the patient appears to have
tight chest, which in itself can facilitate sponta
achieved good ventilation to all lung segments.
neous deeper breaths. Tidal volumes (TVs) can
At this point, the patient is ready to begin the

coughing phase of the procedure. The patient is
asked to take in as deep a breath as possible with the
therefore be increased for many patients by mo

bilizing the chest walls.
3. Finally, rotation can be a vestibular stimulator
therapist assisting the patient in chest expansion
and may assist in arousing the patient cogni
21-6, 8). The patient is then instructed
tively, allowing him or her to take a more ac
(see Figure
to "hold it" at the end of maximal inspiration. The
tive role in the procedure.
patient is then commanded to cough out as hard as
The true beauty of the technique is the fact that no
possible while the therapist quickly and forcefully
active participation on the part of the patient is re
compresses the chest with his or her hands in their
quired for success. Incoherent or unresponsive pa
flexion phase positions (see Figure
21-6, A).
tients, such as those patients with low functioning
The importance of following a true diagonal plane
following a head trauma, CVA, or cerebral palsy, will
of facilitation during both the flexion and extension
still demonstrate good secretion clearance with this
phases of this technique cannot be overemphasized.
technique. The mechanics of the procedure dictate
Failure to do so will result in shifting of the air within
that the air within the lungs be rapidly and forcefully
the chest cavity rather than the desired forcing out.
expelled regardless of the patient's level of active
This air shifting can occur to varying degrees, when
participation. Obviously, patient participation is de
the upper and lower chest are not used together, as in
sirable to clear secretions even more effectively and
all the other assistive cough techniques. When done
for teaching the patient to eventually clear his or her
properly, the counterrotation assist is the only one to
own secretions, but it is not critical.
rapidly close off the chest cavity in all three planes of
Clinical experience has demonstrated with patients
ventilation in all areas of the chest. Unless the patient
who have extremely tenacious secretions, use of vi
voluntarily closes his or her glottis, it is impossible to
bration instead of quick chest compression during the
withhold the air from being forcefully expelled.
cough itself may be more effective. This prolongs the
However, a common mistake made by the therapist is
cough phase and gives the secretions time to be
pulling the patient back into trunk extension during
moved along the bronchi for successful expUlsion.
the expUlsion phase rather than into trunk flexion. A
These patients may also require a series of three or
good rule of thumb: if you can see your patient's face
four cough cycles before clearing most of their secre
when you are applying the compression force, you
tions. In general, patients from all the diagnostic
have pulled them into extension. The head and neck
groups discussed thus far with or without good cogni
should stay forward and flexed, thus only a facial
tive functioning are appropriate for this procedure.
profile should be seen.
The majority of them find it to be the most comfort
Other effects of countcrrotation make this proce

dure particularly beneficial to patients with low levels
able and effective assistive means of expectorating

secretions.
of cognitive functioning.
I. The rotation component is
natural inhibitor of
high tone. Thus this is the least likely of all
Self-assisted Techniques
techniques discussed so far to elicit an increase
The coughing techniques d iscussed in this section
in abnormal tone during the coughing phase. In
are intended to be used as self-assisted procedures,
fact the opposite usually prevails. Gentle rota
thus usually taught later in a patient's rehabilitation
378
PART III
process. Five different techniques will be presented
capitalize on the functional increase in chest expan
in detail. Suggestions for variations are included.
sion and compression abilities. For the population of
All self-assisted cough techniques can start out as
patients who can assume a prone on elbows posture
physically assisted techniques; however, because
independently (i.e., some patients with tetraplegia),
they are more active and require greater gross motor
this t ec hniquc may be used functionally. Here, they
movement, they lend themselves to self-assisted
can assist their own coughs when the need arises,
techniques.
rather than wait for someone to assist them in a posi
Prone on elbows head flexion self-assisted cough
tion change.
The head flexion assist requires good use of head
Prone is not frequently used as a posture for coughing
and neck musculature, scen in patients sustaining a
because the position itself inhibits fuJI use of the di
spinal level injury below C4 (e.g., spinal cord injuries
aphragm by preventing lower anterior chest and ab
(SCIs), spina bifida). It can be used either as a self
dominal excursion following a neurologic insull. This
assisted or therapist-assisted procedure, using the
forces the patient to use an alternate breathing pattern
principles of trunk extension to facilitate inspiration
that facilitates greater accessory muscle use. Because
and trunk flexion to facilitate expiration. With the pa
this change in breathing patterns often occurs sponta
tient prone on elbows, the therapist instructs him or
neously, prone on elbows can be an effective posture
her to bring the head and neck up and back as far as
for promoting spontaneous use of the accessory mus
possible, breathing in maximally (Figure 21-7). The
cles in a more difficult activity (coughing). However,
patient is then instructed to cough out as hard as pos
without the full use of the diaphragm, the resultant
sible while throwing the head forward and down
cough will be weaker than in other postures. Prone on
(Figure 21-8). This head-and-neck pattern can be ini
elbows should not be the exclusive posture for assist
tially assisted by the therapist to establish the desired
ing a cough. After mastering the timing of the proce
movement pattern, and gradually progressed to a re
dure, most patients move back to another posture,
sisted pattern to promote increased accessory muscle
usually sitting or sidelying, and to other techniques to
participation and to strengthen those muscle groups.
FIGURE 21-7
Head flexion assistive cough in prone on elbows; extension and inspiratory phase.
21
379
FIGURE 21-8
Head flexion assistive cough in pTone on elbows; flexion and coughing phase.
FIGURE 21-9
FIGURE 21-10
Tetraplegic-self-assisted cough in long sitting: maximizing
Tetraplegic-self-assisted cough in long sitting: maximizing
the inspiration phase.
the expiration or coughing phase.
inhalation, whereas the flexion aspect is used to max
Long-sitting self-assisted cough
imize expiration. The self-directed chest compression
For the first procedure, tetraplegic-Iong-sitting self
occurs mainly on the supetior-inferior plane of venti
assist, the patient is positioned on a mat in a long-sit
lation only.
ting posture (legs straight out in front of the patient)
The second procedure, the paraplegic-long-sit as
and with upper extremity support. The therapist in
sist, uses the same principles as the techniques de
structs the patient to extend his or her body backward
scribed for the tetraplegic-long-sit assist. These pa
while inhaling maximally (Figure 21-9). The thera
tients have active spinal extension musculature and
pist then tells the patient to cough as the patient
can achieve greater trunk extension and flexion
throws his or her upper body forward into a com
safely, achieving greater chest expansion before the
pletely flexed posture, using shoulder internal rota
cough and greater chest compression on a superior
tion if possible (Figure 21-10). Once again, the exten
inferior plane during the cough. The patient positions
si0n aspect of the procedure is used to maximize
his or her upper extremities in a butterfly position or
380
PART III
self-assist, is typically performed in a wheelchair or

over the edge of a bed. The patient is instructed to
place one hand over the other at the wrist and place
them in his or her lap. As in the previous technique,
the patient is then asked to extend his trunk backward
while inhaling maximally, followed by a strong vol
untary cough. During the cough, the patient pulls his
or her hands up and under the diaphragm, resembling
the motion of a Heimlich maneuver (Figure 21-13).
The hands mimic the abdominal muscles, which
would ordinarily contract to push the intestinal con
tents up and under the diaphragm to aid its recoil
ability. This short-sitting technique uses the di
FIGURE 21-11
aphragm more substantially than the long-sitting pro
Paraplegic-self-assisted cough in long-sitting: inspiration.
cedure and is therefore generally more effective as an

assistive cough. It is an effective self-assisted method
for patients who have weak diaphragms or abdominal
musculature. Most SCI or spina bifida patients, Cs or
b e l ow , c a n s u c cessf u l l y l e a r n t h i s t e c h n i que.
Tetraplegics usually require trunk support from their
wheelchairs to perform it independently and safely,
whereas most paraplegics can perform it from an un
supported short-sitting position. Patients who lack
good upper-extremity coordination. such as many
Parkinson's and multiple sclerosis (MS) patients,
cannot perform the procedure quickly or forcefully
enough to make it effective and usually require assis
tance from another person.
Variations on all sitting techniques can be readily
FIGURE 21-12
made. Use the concepts explained in the introduction
Paraplegic-self-assisted cough in long-sitting: expiration.
to cough techniques to develop techniques that work
uses elbow retraction, depending on the level of in
your patient to lift his or her arms up while inhaling,
jury (Figure 21-11). During the flexion phase, pa
hold, and then cough while he or she throws the arms
tients throw themselves onto their legs, thereby com
down toward feet or lap using maximumlrunk flexion.
for your patients. For example, in a wheelchair, ask
pressing both the upper and lower chest (Figure
(Use a seat belt for safety.) Another idea is to have the
21-12). This can be taught very successfuJly to pa
patient hook one arm on a push handle of the wheel
tients with paraplegia, provided they do not have an
chair, move the other upper extremity up and back (as
interfering tone problems. If the patient lacks hip
in a PNF D2 pattern), watch the patient's moving hand
flexion or is worried about bony contact or skin in
to maximize trunk rotation, inhale during the move
jury, place a pillow (or two as needed) on the legs.
ment, hold, and again cough as he or she throws trunk
This will limit the hip flexion and minimize trauma
and upper extremity down toward opposite knee.
from the quick thrust onto the legs.
When devising the most appropriate self-assisted

cough for your patient, remember to look for combina
Short-sitting self-assisted cough
tion of trunk, upper extremity, head, neck, and eye pat
The third assistive cough in sitting, the short-sitting
terns that will maximize all four phases of the cough.
21
381
FIGURE 21-13
Assisted cough in short sitting. A, Hand
position for patient with good hand function;

B, Hand position for patients with only wrist
function.
Hands-knees rocking self-assisted cough

The last assistive cough to be discussed is performed
most frequently as a multipurpose activity to increase
the patient's balance, strength, coordination, and func
tional use of breathing patterns (including quiet breath
ing and coughing) simultaneously. The patient as
sumes an all-fours position (hands-knees). He or she is
then instructed to rock forward, looking up and breath
ing in as he or she moves to a fully extended posture
(Figure 21-14). After this, the patient is told to cough
out as he or she quickly rocks backward to the heels
with a flexed head and neck (Figure 21-15). Once
again, the importance of flexion and extension compo
nents of a cough are noted. The rocking can be done
with or without a therapist's assistance. For patients
with generalized or spotty weakness throughout (e.g.,
some SCI, head traumas, Parkinson's, MS, cerebral
palsy, or spina bifida patients), this method is perfect
for incorporating many functional goals into a single
activity. It can help prepare them for more challenging
respiratory activities that they will undoubtedly meet
after their discharge from a rehabilitation center.
For patients with limited lower-extremity range of
movement or skin concerns associated with a quick
force, a pillow can be placed on the lower legs, thus
FIGURE 21-14
restricting knee flexion and preventing direct contact
Assisted cough in hands-knees position; extension or
of bony prominences.
inspiratory phase.
PART III
382
5. What is a smoker's cough, and why does it

L
I. .
::
I .
....
. .!
'
't .
occur?
6. What are the stages of a cough?
7. What should the therapist interpret when a pa

tient's cough is associated with eating or drink
ing?
8. What effect does coughing have on the blood

pressure and cardiac output?
9. What special techniques can be taught to asth
matic patients to mobilize secreations?
10. What manual techniques are most effective in
FIGURE 21-15
spinal cord patients?
Assisted cough in hands-knees position; flexion or

coughing phase.
References
Standing self-assisted cough
Bach. J.R. (1993). Comparison of peak expiratory flows wilh man
Standing uses the same concepts and can be readily

used for self-assisted coughs, provided the patient has
adequate standing balance and/or upper extremity
support. Use any technique previously described and
modify for this higher developmental posture. Com
binations of trunk, head, and extremity movements
during the cough maneuver is almost endless, thus
specific techniques are not itemized.
ually assisled and unassisled coughing techniques. Chest
104(5): I 553-{i2.
Braun. S.R.. Giovannoni, R.,
& O'Connor, M. (1984). Improving
cough in patients with spinal cord injury. American Journal of
Physical Medicine 63( I): 1-10.

Estenne, M .. Detroyer, A. (1990). Cough in letraplegic subjects: an
active process. Annals of Internal Medicine 12(1):22-28.
Fishburn,
M.J.. Marino, R.J., & Dittuno, J.F. (1990). Alelectasis
and pneumonia in acute spinal cord injulY Archives of Physical
Medicine and Rehabilitation 71: 197-200.

Hoffman, L.A. (1987). Ineffeclive airway clerarance related
10
neuromuscula.r dysfunction. Nursing Clinics of North America
SUMMARY
22(1):151-66.
In all postures and in all techniques, both for assisted

and self-assisted coughs, the importance of initial po
sitioning and ventilatory strategies is of utmost im
portance to the success of the airway clearance tech
nique. There is an effective i dea waiting to be
incorporated for all patients to improve their cough,
from the tiniest postural change to full body move
ments and physical assists. Be creative in applying
the concepts to all patient populations.
Jaeger, R.J., Turba, R.M., Yarkony, G.M.,
& Roth, E.J. (1993).
Cough in spinal cord injured patients: comparison of three

methods to prodoce cough. Archives of Physical Medicine and
Rehabilitation 74: I 358-{i1.

Linder.
S.H. (J 993). Functional electrical slimulation
cough in quadriplegia. Chest 103( I): 166-9.

MacLean, D., Drummond.
10
enhance
c., & Macpherson, C . et a!. (1989).
Maximum expiratory airflow during chest physiotherapy on

ventilated patients before and after the application of an ab
dominal binder. Intensive Care Medicine 5:396-399.
Massery, M.P. (1987). An innovative approach to assistive cough
techniques. Topics in Acute Care Trauma Rehabilitation
(3):73-85.
REVIEW QUESTIONS
Massery, M.P. (1994).. What's positioning got to do with it? Neu
rology Report 18(3):11- I 4'.
1. What is the purpose of a cough?
Slack, R.S., Shuca11.
2. W h a t a r e t h e two m e c h a n i s m s f o r a i rw a y
Medicine 15(4):739-49.
clearance?
3. Why would a therapist assist a patient to cough?
4.
What techniques are most effective to assist

coughing?
W. (1994). Respiratory dysfunction wilh trau
malic injury to the central nervous system. Clinics in Chest

Sullivan, R.E., Markos, P.D.,
& Minor. A.D. (1982). An integraled
approach to therapeutic exercise: Theory and clinical applica

tion. Reston, Va.: Reston Publishing.
Facilitating Ventilation Patterns

and Breathing Strategies
Mary Massery
Donna Frownfelter
KEY TERMS
Controlled breathing
Ventilatory strategies
Diaphragmatic breathing pattern
Work of breathing
Jacobsen's progressive relaxation
INTRODUCTIOtJ
tient. No single technique is appropriate in all cases.
Attaining optimal ventilatory patterns requires the use
Sound clinical judgment and experience must be exer
of a variety of techniques. Some are passive in nature,
cised when applying these ideas with each patient. It
such as passive positioning of the patient or applica
is the hope of these authors that the techniques identi
tion of an abdominal binder for better diaphragmatic
fied in this chapter will stimulate the clinician's cre
positioning. Some require very active participation on
ative talents, and that they will extrapolate and im
the part of the therapist and/or patient, such as in as
prove on the techniques according to specific patient
sisted-cough techniques or in glossopharyngeal
population needs. See the box on next page for spe
breathing instruction. Other techniques are subtly in
cific areas covered in the chapter.
corporated into the patient's total physical rehabilita

tion program, requiring little overt attention to the pa
tient's respiratory performance, such as when using
POSITIONING CONCERNS
ventilatory strategies. All of these diverse aspects of
All patients spend some portion of the day in a hori
treatment play an important role in the total develop
zontal position for rest or sleep. Using this opportunity
ment of a successful respiratory rehabilitation pro
to assist the patient in passive drainage of lung secre
gram for the neuromuscular and musculoskeletal pa
tions is a natural beginning in the development of a pa

383
PART III
384
Just as passive positioning of the patient in bed
Categories of Therapeutic Interventions

Presellted in this Chapter to Optimize
Ventilation Patterns
helps to maintain bronchial hygiene and improve

ventilation potential, passive positioning of the pa
tient's skeletal frame in an upright posture (sitting,
standing) helps to maximize the patient's mechanical
I. Positioning concerns
advantage of breathing. For example, patients with
2. Ventilatory and movement strategies
spinal cord injuries (SCIs) resulting in tetraplegia
3. Manual facilitation techniques
Fac i l i tating contr olled breathing patterns

(diaphragmatic)
expansion of the chest in all three planes of ventila
Mobilizing the thorax
Facilitating upper chest breathing patterns

(accessory muscles)
Promoting symmetrical breath ing patterns

(unilateral dysfunction)
will be unable to support their intestinal contents

properly under the diaphragm to al]ow for maximal
tion (see Chapter 37). Use of an abdominal support
from the iliac crest to the base of the xiphoid process
provides positive pressure support to restore intesti
nal positioning in an upright position (Figure 22-1).
Research has documented well the significant im
Reducing high respiratory rates
provements in vital capacity, inspiratory capacity,
4. Glossopharyngeal breathing
and tidal volume in sitting with use of a strong ab

dominal support. These binders have also been used
S. Enhancing phonation skills
in nursing care to provide for better circulation and

in the prevention of hypotension.
The abdominal binder's value in cosmesis may be
underrated. Many of these neurological patients were
tient's long-term respiratory program. Specific pos
once normal, healthy individuals with high self-es
tural drainage positions are covered extensively in this
teem who took great pride in their appearances. They
book (see Chapter 21). Using a combination of these
now present with a protruding belly (the anterior and
positions in your patient's bed position rotation, in the
infelior shift of the intestines resulting from flaccid
hospital, or at home can help to achieve multiple goals.
abdominal muscles), which may be psychologically
First, they can assist the patients in clearing secretions
disturbing to them. Thus the use of a binder may
passively that they may have difficulty performing ac
greatly aid in the restoration of that person's self-es
tively. Second, these position changes provide for skin
teem, which should be a high-priority goal in any re
relief and better circulation. Finally, they assist in re
habilitation program.
tarding the development of joint contractures or other
A rigid type of abdominal support can be used
musculoskeletal abnormalities. A four-position rota
when the vertebral column and the abdominal viscera
tion (i.e., supine, prone, side-to-side) is usually an ef
need support. These are called body jackets or total
fective and reasonable means of incorporating these
contact thoracic lumbar sacral orthosis (TLSOs).
goals into a long-term prophylactic program.
(Figure 22-2). A TLSO is a rigid trunk support
Simple adaptations may make ventilation easier in
molded individually to the shape of the patient's en
each of these postures. For example, in supine, plac
tire trunk from the axilla down to the pubis. It is
ing the arms lip over the patient's head facilitates

greater anterior upper chest expansion. Likewise, po
made up of two separate front and back pieces, with

'
an anterior cutout in the abdomen to allow for normal
sitioning the pelvis in a slight posterior tilt facilitates
diaphragmatic displacement of the viscera. Many of
more diaphragmatic excursion. See Chapter 40 for
these jackets also use a strong elastic support across
more detailed explanations. Observation of all pre
the cutout to allow for diaphragmatic motion but to
cautions and contraindications to passive positioning
minimize excessive displacement of the abdominal
is still warranted.
contents. This is very appropriate for the growing
22
Facilitating Ventilation Patterns and Breathing Strategies
385
"
FIGURE 22-1
A, Abdominal binder-Velcro fastener. B, placement of
abdominal binder.
child who needs more spinal stability or the com
as well as many other areas of rehabilitation, depends
pletely flaccid tetraplegic patient who may also re
on good alignment of the body against the forces of
quire the same support. Because head and neck posi
gravity. Symmetry must be strived for through the
tioning are so interdependent on trunk positioning, a
use of a body jacket, lateral trunk supports in the
body jacket may be the difference to these patients
wheelchair, abdominal binders, or some other means
between being dependent or independent in an up
(Figure 22-3). This is especiaJly important for pa
right posture. It may result in significantly better head
tients with hemiplegia where habitual asymmetrical
control, eye contact, longer phonation, and possibly
posturing leads to musculoskeletal problems later.
better articulation. However, because it limits trunk
Symmetrical breathing patterns and uniform aeration
movement, its usefulness for each patient must be as
of all lung segments are augmented by careful up
sessed carefuII y.
right positioning. Therefore everything from the type
Logically, the next consideration under passive
of neck support to the height and width of the arm
respiratory techniques is proper wheelchair position
rests to the length and type of the foot supports must
ing. Optimal performance in respiratory functioning,
be carefully analyzed for each patient.
386
PART III
FIGURE 22-2
A, patient with CS congenital tetraplegia independent long sitting. B, long sitting with body jacket
support. Note changes in head position and eye contact, hip alignment, and shoulder rotation.
22
VENTILATORY AND MOVEMENT STRATEGIES
387
ally, these simple concepts take no more than I to
FOR IMPROVING FUNCTIONAL OUTCOMES
additional minutes of therapy, with no additional
Once the patient is positioned for success, motor ac
equipment costs other than a few extra pillows or
tivities should be introduced that improve the pa
towels. Therefore time or money are not mitigating
tient's ventilatory support, or the therapist should
factors. However, these ideas do require the practi
capitalize on the patient's good ventilatory support to
tioner to look carefully at the patient before begin
improve the motor activity. Using ventilatory strate
ning any therapy, asking "Have J positioned my pa
gies to improve motor performance or movement
tient for respiratory success?" "Am J simply treating
strategies to improve ventilation performance enables
the patient in whatever position J found them in?"
patients to achieve their functional goals sooner than
and "Have I carefully chosen my verbal cues to in
other patients; patients also get sick less often. Gener
clude a respiratory response and a functional re

sponse?" The practitioner must actively include res
piration in every single activity to help the patient
understand that breathing transcends all activities.
See the box below for a summary of the most impor
tant ventilatory-movement strategies.
Incorporating Simple Therapy Tasks
Inspiration
After the patient has been carefully positioned for
respiratory success, as described previously, begin
the patient's therapy or daily-living activities. From
an anatomical perspective, the pattern of inspiration
(1) trunk
(2) shoulder flexion, abduction, and exter
is naturally associated with the following:

extension,
nal rotation movements, and (3) an upward eye gaze.

Expiration is logically associated with the opposite:
(I) trunk flexion,
(2) shoulder extension, adduction,
and internal rotation movements, and (3) a downward
Significant Ventilatory-Movement Strategies

J. Pair trunk extension activities with inspirati o n
2. Pair trunk flexion activities with exhalation
3. Pair shoulder flexion, abduction and/or external
rotation activities with inspiration
4. Pair shoulder extension, adduction and/or inter

nal rotation activities with exhalation
5. Pair upward eye gaze with inspiration

FIGURE 22-3
6. Pair downward eye gaze with exhalation
Wheelchair alignment considerations.
388
PART III
Ca.-diopulmonary Physical Therapy Interventions
eye gaze. Accordingly then, the simple task of pas
nity to learn from the beginning of his or her rehabili
(ROM) can easily include
tation process that movement and breathing go hand
the active goal of increasing ventilation by asking the
in hand. C1inicaJly, incorporating appropriate breath
sive range of movement
patient to breathe in and look up every time his or her
ing pattems with movement early in the rehabilitation
arm is raised up into shoulder flexion. This encour
process discourages the development of Valsalva pat
ages the patient to breathe in when his or her chest
tems or shallow breathing pattems when the motor ac
wall muscles are being maximally stretched and the
tivities become more difficult and complex.
ribs are naturally opening up, causing both activities

to be more successful. It also begins to teach the pa
tient to use ventilatory strategies to optimize potential
functional movement, such as in reaching up to a
kitchen cabinet.
Dynamic Activities
Inhalation promotes trunk extension and exhalation
promotes trunk flexion and vice versa. This basic
theme occurs naturally in all motor activities but
Expiration
may have ceased to become spontaneous after a
Likewise, active or passive exhalation should be co
neuromuscular or musculoskeletal insult. Valsalva
ROM pat
maneuvers during transitional movements, such as
ordinated with the reverse upper extremity
tern (i.e., the arm returning from flexion back to the
rolling or coming to sitting
patient's side). This can be done using all types of ex
noted with these patients. By teaching them strate
or
standing, are often
halation patterns, including the following:
(1) passive
(2) forceful exhalation as in blow
ing, coughing, or pursed-lips exhalation, or (3) vocal
gies that incorporate breathing into their motor
quiet exhalation,
plans for all motor activities, Valsalva patterns can
ization patterns. Thus the therapist may ask the pa
promoting beller cardiac function.
be eliminated or minimized while simultaneously
tient to slowly count out loud to 10 while the arm is
Every activity of daily living cannot be described
being returned to his or her side. Subconsciously, the
in this book, however, suggestions for typical gross
patient learns to correlate exhalation with shoulder
motor activities using ventilatory strategies as a
extension while simultaneously learning a much
means to improve these motor tasks are presented.
more complex idea-that of controlling his or her
Extrapolation of these concepts to all other motor ac
rate and volume of expiration by including deliberate
tivities should be carefully analyzed by each therapist
speech during exhalation maneuvers.
for each individual patient.
To improve exhalation potential, increase the pa

tient's relative trunk flexion alignment. While sti II
Rolling
ROM, this
Ask patients to attempt to roll and assess whether
can be simply accomplished by asking the patient to
they tend to move with trunk extension or flexion to
supine and performing upper-extremity
lift his or her head and watch the hand as it returns to
begin the roll. If they roll with a trunk extension pat
his or her side, which increases abdominal and inter
tern ask them to breathe in while they roll and to look
costal activation, or by increasing knee flexion,
up. If they roll with trunk flexion as their primary
which increases posterior pelvic tilting and trunk
movement pattern, instruct them to roll while blow
flexion. Pairing trunk flexion with exhalation com
ing out and tucking their chin. In doing
pletes the ventilatory-trunk movement strategy.
work with, not against natural whole patterns of
Combining positioning with respiratory verbal
ROM activities, changes passive

upper-extremity ROM exercises to dynamic upper-ex
tremity ROM exercises. It encourages increased inspi
:\0,
patients
movements to increase the likelihood of success.
cues, as described in
Coming up to sitting
Pushing up to sitting from sidelying should be evalu
ratory and expiratory capacities, develops early func
ated in much the same manner. If patients are more
tional motor planning strategies, and facilitates trunk
effective in coming upright when using trunk exten
mobility. In this manner the patient has the opportu
sion, have them inhale as they push up to sitting.
22
Asking them to "look up" as they move will reinforce
389
independent one. Returning to sitting should be ac
the upper chest movements through the use of the
companied with slow controlled exhalation, such as in
symmetrical tonic neck reflex (STNR). If they have
pursed-lips blowing or counting out loud, to maximize
more success pushing up with trunk flexion, have
the body's controlled descent into gravity's influence.
them blow out and tuck the chin while moving.
FACILITATING A CONTROLLED DIAPHRAGMATIC
Dressing
Dressing activities can benefit from the same con
BREATHING PATTERN
cepts. While putting on lower-extremity items such
Why woul.d a therapist want to change a patient's
as pants, socks, and shoes in a long sitting position,
breathing pattern? The answer is simple-when the
have the patient first take in a deep breath while ex
pattern being used is ineffective. Patients generally use
tending his or her trunk. Then have the patient blow
a pattern of breathing that is the most efficient for them.
out, huff out, or cough while flexing the trunk to
A healthy person uses approximately 5% of the
reach his or her toes. This combines the functional
total oxygen consumption for the muscular work of
daily task of dressing with improving breath control,
breathing and 10% of their vital capacity. Conse

quently, breathing at rest is generally perceived as ef
trunk control, and airway-clearance techniques.

Upper-extremity dressing and upper-extremity ex
fortless under normal conditions.
ercising can incorporate the same ideas. All move
However, in patients that physical therapists evalu
ments should be coordinated with harmonious chest
ate and treat (often after surgery, respiratory disease, or
wall movements to maximize upper-extremity tasks.
dysfunction secondary to neurological insult or injury),
Thus every time the arm is moving up above 90 de
the vital capacity may be significantly decreased and
grees of shoulder flexion, the patient should be asked
the oxygen consumption may be greatly increased re
to breathe in, allowing for the normal shoulderlrib
sulting from the use of accessory muscles or the extra
cage rhythm to occur. Full shoulder flexion requires
effort needed to breath or cough. In the example of a
opening of the intercostal spacing and the separation
patient with tetraplegia the vital capacity may be re
of the individual ribs. Many neurological patients
duced to 1000 to 1500 m!. If the normal tidal volume
have lost the intrinsic mobility of the chest wall and
(normal volume of breathing) is 500 ml that would
thus may have lost some functional shoulder ROM as
mean that with each breath the patient would use 33%
well. Not pairing inspiration with shoulder flexion is
to 50% of his or her vital capacity (maximal inspiration
likely to limit the patient's shoulder ROM to approxi
followed by maximal exhalation). This would greatly
mately 140 to 150 degrees. It may also encourage
increase the oxygen consumption just for normal quiet
Valsalva maneuvers during the activity and may
breathing. The patient would have little pulmonary re
cause more shoulder pain.
serve. During exercise or stress, the patient would have

an increased subjective feeling of shortness of breath
Coming up to standing
(dyspnea) and feel an increase in their work of breath
Coming up to standing requires both trunk move
ing. There are specific terms to describe breathing pat
ments, thus the patient should initiate the forward
terns, the most common are listed in the box on p. 390
trunk lean with exhalation and initiate the standing
at top. Also see the box on p. 390 at bottom for indica
phase with inhalation and neck extension. Active neck
tions for teaching controlled-breathing techniques.
extension during assumption of standing not only fa
It should be appreciated that breathing comfort
cilitates greater inhalation but, along with the influ
ably and in control is associated with wellness and a
ence of the tonic labyrinthine reflex (TLR), facilitates
sense of ease. Even in normal individuals who are
more significant contractions of the trunk and hip ex
under stress and have increased work levels we are
tensors. Clinically, this often results in a more notice
more cognizant of the increase in work of breathing.
able upright posture and may make the difference be
For a patient that is struggling with every breath and
tween an assisted standing pivot transfer and an
wonders how he or she will get through the day, ven
390
PART III
Breathillg Pattern Termillology

Eupnea-Normal breathing, repeated rhythmic inspiratory-expiratory cycles
Hyperpnea-Increased breathing. usually refers to increased tidal volume with or without increased frequency
Polypnea, tachypnea-Increased frequency of breathing
Hyperventilation-Increased alveolar ventilation in relation to metabolic rate (an increase in alveolar ventilation
seen is a decrease in the arterial Peo2
Hypoventilation-Decreased alveolar ventilation in relation to metabolic rate (a decrease in alveolar ventilation)
seen as an increase in Peo2
Apnea-Cessation of respiration in the resting expiratory position
Dyspnea-The patient's subjective feeling of shortness of breath
Apneusis-Cessation of respiration in the inspiratory position
Apneustic breathing-Apneusis intelTupted periodically by exhalation
Cheyne-Stokes respiration-Cycles of gradually increasing tidal volume followed by gradually decreasing tidal
volume (usually followed by an apneic period)
Biot's respiration-Sequences of uniformly deep gasps and apnea, followed by deep gasps
Adapted from Comroe. J. H . Jr. (1974). Physiology 0/ respiration, (2nd ed). SI. Louis: Mosby.
Indications for Teaching Controlled-Breathing Techniques

Patients with any or t.he following:
Pulmonary dysfunction either pIimary or secondary causes
Pain from surgery, trauma, or disease
Apprehension or nervousness
Bronchospasm or impending bronchospasm in asthma
A irw ay clearance dysfunction
Restriction of inspiration resulting from musculoskeletal dysfunction such as scoliosis. kyphoscoliosis, pectus ex
cavatum, obesity, pregnancy, pulmonary pathology such as fibrosis, scarring from radiation therapy. neurological
weakness such as spinal cord injury. Parkinson's disease, or myasthenia gravis
Congestive heart failure, pulmonary edema, or pulmonary emboli
Rib fractures
Ventilated patients on assist control or intennittent mandatory ventilation (lMV)
Metabolic disturbances that have a compensatory respiratory response
Debilitated or bedridden patients that tend to have constant volume ventilation, retain sel:relions. and are prone to
pneumonia and atelectasis from poor airway clearance
22
them to relax the neck and chest accessory muscles
Goals of Teaching Controlled-Breathing

Techniques
To decretlse the work of breathing
To improve alveolar ventilation
and use more diaphragmatic breathing to reduce the

work of b r eath ing in co mbination with relaxed
pursed-lip breathing on exhalation. Their treatment
programs focus on energy conservation and pacing
activity with breath control.
To improve airway clearance by improving cough
However, with secondary pulmonary dysfunction
To increase strength, coordination. and efficiency
patients, such as spinal cord injury, there is a more
of respil'lltory muscles
restrictive component to inspiration. In this case, they
To teach the patient how to respond to and control
may have accessory muscles intact, but they are not
breathing
To assist in relaxation
To mobilize and maintain mobility of the thorax
To enable patients to feel self-control and confi
391
using them to faciliate deep breathing or coughing.

They may have a strong diaphragmatic breath but the
upper chest collapses on inspiration (paradoxical
breathing, see Chapter 37). In these cases the goal is
dence in managing disease or dysfunction
to teach them to use the accessory muscles to balance

the upper and lower chest. This facilitates an increase
in vital capacity to prevent atelectasis and pneumonia
tilatory strategies and breathing-control techniques
by increasing the volume of ventilation and improv
can be the key to maximizing potential. See the box
ing the cough mechanism.

The choice of appropriate venti latory strategies
above for a list of goals in teaching controlled-breath
depends on the patient's individual problem. The fol
ing techniques.
Breathing control has long been used in yoga to
foclls and promote meditation. This is a key to maxi
lowing questions should be considered when evaluat

ing patients:
mizing rehabilitation. If you can not breathe you can
Does the patient have more difficulty in inspira
not function! It is of primary importance to assess the

patient's breathing at rest and during exercise. We
tion or exhalation?

often hold our breath with exertion, especially with
Is there a normal sequence to inspiration (i.e., ab

dominal wall rises, then mid chest, then upper
new activities. We must assess the cardiopulmonary
chest, with a full inspiration? Or does the chest
and neuromuscular response to each new activity.
sink and the abdomen rise on inspiration?

CONSIDERATIONS FOR TEACHING BREATHING

CONTROL TO PATIENT'S WITH PRIMARY VERSUS
SECONDARY PULMONARY DYSFUNCTION
Does the patient appear to be working hard to

breathe? Is the patient using the accessory muscles
to an extreme?
ing a normal volume and for the normal length of
Patients with primary lung disease, such as emphy

sema, asthma, bronchitis, or cystic fibrosis, present a
much different picture than patients with spinal cord
'
injury, Parkinson's disease, myasthenia gravis, or
Does the patient have trouble coughing or speak

sentences?
Is ventilation the limiting factor in accomplishing

an activity (i.e., transfer, gait, or bed mobility)?
Patients with primary pulmonary disease generally
Guillain-Barre syndrome.
In general, patients with primary lung disease use
benefit from ventilatory strategies that relax the ac
their accessory muscles and greatly increase the work
cessory muscles and facilitate relaxed diaphrag
of breathing secondary to the shortness of breath or
matic breathing.
coughing. They often complain that they have more
On the other hand, patients with secondary pul
difficulty "getting air out," which demonstrates the
monary dysfunction usually benefit from the balanced
decreased expiratory flow rates noted on pulmonary
use of the diaphragm and accessory muscles to in
function tests. The goal with these patients is to teach
crease vital capacity and breath support for activities.
392
PART III
obstructive pulmonary disease (COPD) patients.
Diaphragmatic Facilitation Techniques
Neurologically impaired patients need modifica

tion with their activity levels and capabilities.
I. R elaxation technique
2. Re patterning techniques
Relaxed pursed-lip breathing
POSITIONING CONCERNS
Exhalation, hold, and inhalation
Position of Pelvis
3. Sniffing
The first step in facilitating any breathing pattern is to
4. Diaphragmatic scoop technique
position the patient for respiratory success. The de
5. Lateral costal facilitation technique
tails are discussed in this chapter and Chapter 40.
6. Upper chest inhibiting technique
Often the patient's posture and pelvic position has a

dramatic effect on breathing. In general, a slight, rela
7. Normal timing technique
tive posterior tilt of the pelvis facilitates diaphrag

matic breathing and a relative anterior tilt facilitates
FACILITATING DIAPHRAGMATIC BREATHING

This section is laid out starting with the easiest interven
opening of the anterior chest and upper chest breath

ing. It is helpful to see what difference a slight, rela
tive change in pelvic position will do to the patient's
tion to facilitate diaphragmatic breathing and progress
ability to ventilate. This is especially true with sec
ing to specific inhibition and facilitation techniques.
ondary pulmonary problems related to neurological
See the box above for a summary of methods to
and neuromuscular dysfunction.
facilitate diaphragmatic ventilation patterns.
RELAXATION OF UPPER CHEST AND SHOULDERS

DIAPHRAGMATIC CONTROLLED BREATHING
Diaphragmatic breathing is the normal mode of respi
Jacobsen's progressive relaxation exercises are famil

iar to physical therapists. Jacohsen proposed that a
ration. The diaphragm and intercostals are the normal
maximal muscle contraction would yield a maximal
muscles of quiet inspiration. When evaluating a pa
muscle relaxation. This technique can be applied to
tient's breathing pattern, the use of accessory muscles
the upper chest and shoulders. The therapist places
during quiet breathing should be noted; the patient
his or her hands on the patient's shoulder girdle. The
with primary pulmonary disease should be instructed
patient is asked to shrug his or her shoulders up into
in relaxation of the accessory muscles to decrease the
the therapist's hands and hold it. "Don't let me push
work of breathing. In a patient with a spinal cord in
your shoulders down," is the therapist's command.
jury or other neuromuscular disorders, these muscles
Then, "Let your shoulders relax, let them go." The
may assist in balancing ventilation and may be useful
emphasis is on the relaxation phase. Verbal com
in increasing vital capacity, and improving the ability
mands can be very important with this procedure. A
to cough, improving breath support for speaking, and
strong command to, "Raise your shoulders into my
increasing potential for functional activities.
hands" is followed by a quiet, more relaxed, "Now
In general, controlled diaphragmatic breathing needs
relax and let them go," repeating quietly, "That's it,
to be emphasized in each posture and with all therapeu
let them go, feel them t:elax." Sometimes the relax
tic activities. CatTY-over is not necessarily present. If the
ation activity is all that it takes to resume a more nat
patient is only shown the pattern in supine, it may not
ural pattern of breathing and you can move on to
carry over to sitting or during a sliding-board transfer
other therapeutic activity. If the patient starts to use
when the activity becomes difficult. A helpful sequence
accessory muscles again the technique is repeated.
to use might be teaching the breathing pattern in sidely
The patient learns to feel the difference between ten
ing, supine, sitting, standing, walking, stairs climbing,
sion and relaxation of the shoulders and can self
and other functional activities, especially with chronic
monitor and perform the relaxation independently.
22
REPATTERNING TECHNIQUE
rotation), and
If a patient needs more support to gain control of breath
393
(4) choosing to use a pillow or pillows
under the head. (For details on positioning, see Chap
40.) For each patient, choices will be different (i.e.,
ing and is experiencing shortness of breath, a simple
ter
repatterning technique is very beneficial. An example
the amount of knee flexiol1 or the number of pillows).
might be an asthmatic patient with a high respiratory
Find the right combination of positioning characteris
rate who is feeling panicky. When the patient is asked
tics that best facilitates diaphragmatic movement for
why he or she is breathing so fast the reply will usually
that particular patient. In this manner the therapist sets
be, "I am n ot getting enough air, I can't catch my
up the patient for respiratory success before beginning
breath." The patient is asked to start with exhalation.
the manual or verbal techniques.
"Try to blow out easily with your lips pursed. Don't
Now, begin the techn ique. A s k the patient to
force it just let it come out." By doing this, the respira
place his or her hands on their stomach for increased
tory rate will automatically be decreased. When the pa
proprioceptive feedback and the relative extension,
tient feels some control of this step, then ask him or her
adduction, and internal rotation position of the shoul
to "hold the breath at the top of inspiration just for a sec
ders. In a quiet melodic voice, ask the patient to
ond or two." Make sure the patient does not hold his or
"sniff in 3 times." Note if the patient demonstrates
her breath and bear down as in a Valsalva maneuver.
more abdominal rise and/or lower chest expansion . If
Lastly, ask the patient to take a slow breath in, hold it,
so, draw attention to this fact. During exhalation, tell
and let it go through pursed lips. Patients often learn that
the patient to "let it out slow," which helps to inad
when they are short of breath, this technique will help
vertently slow the respiratory rate
them gain control, making them feel less panicky.
courages some relaxation. Progress the training by
(RR) and often en
asking the patient to "now sniff in twice." Do you

still see greater diaphragmatic excursion and less
Sniffing
upper chest excursion? If so, continue by asking for
If working toward a generalized controlled-breathing
"one long slow sniff." If successful, the therapist
pattern does not improve the patient's ventilatory pat
should follow with: "now do it quieter," then "now
tern adequately, a technique that more specifically
do it slower," "even quieter," and so forth. By this
addresses the n eed to initiate breathing from the di
time, the patient should be demonstrating an easy
aphragm can be attempted. Sniffing is a simple and
onset, slow
effective means of teaching increased diaphragmatic
shoulders.
breathing. Sniffing is primarily diaphragmatic breath
RR, diaphragmatic pattern with relaxed
Clinical experience has shown this technique is
80% of patients who
ing by nature. Use this technique first when attempt
highly successful with about
ing more specific diaphragmatic training with all pa
have primary pulmonary pathologies or neurological
tients who are capable of attempting sniffing because
impairments. The key to success seems to stem from
of its simplicity.
the relaxed tones and words that the therapist uses,
As with all procedures, the most imp0l1ant step is
which decrease anxiety and imply relaxation and not
the first step: position the patient appropriately to in
"effort." Once the pattern has been established, the
crease the likelihood of increased diaphragmatic
patient can easily be instructed to go through the
breathing resulting from musculoskeletal alignmel1t.
training as needed indepen dently. The sequence (in
(I) choosing a gravity
whole or in part) may be appropriate for patients be
eliminated position, such as sidelying, or a gravity-as
fore getting out of bed if they become anxious and
sisted position, such as supported semi-Fowler's sit
demonstrate excessive upper chest breathing during
(2) choosing a relatively

posteriorly tilted pelvis with flexed knees, (3) choos
ing the arms to be down below 90 degrees of flexion
this activity. For other patients, it may be appropriate

viously, the application of this technique will be indi
(in relative shoulder extension, adduction, and internal
vidualized for each patient, depending on the deficits.
This includes the following:
ting (supported spin e),
before or during eating or before climbing stairs. Ob
394
PART III
PROCEDURE FOR TEACHING CONTROLLED

DIAPHRAGMATIC BREATHING (SCOOP TECHNIQUE)
Minimal patient instruction is necessary to facilitate

allows the patient to feel the breathing pattern, then it
is brought to the patient's cognitive awareness. The
breathing pattern.
1. Position the patient for success, generally in a
s i d e l yi n g p o s i t i o n w i t h t h e b e d in s e m i
Fowler's or supine in semi-Fowler's with a
pelvic tilt and relax the abdominal muscles.
)'
The following is a suggested sequence:
bend in the knees to achieve a relative posterior
Y?.
"'.
""f f !
.. '
I! /, J ))
diaphragmatic breathing using the scoop technique. It
patient then learns to self-cue to incorporate the
-::0..
,,/
,
"-
FIGURE 22-4
Therapist's hand placement for diaphragmatic breathing.
2. Place your hand on the patient's abdomen at

the level of the umbilicus. Tell the patient you
perventilate and blow off too much CO2. The fact
want to feel his or her breathing. Follow the pa
that they are breathing more with their diaphragms is
tient's breathing pattern for a few cycles until
the important consideration. Note also the position of
you are in his or her rhythm. Do not invade the
the pelvis and trunk.
patient's breathing pattern rather, at first, fol

low their movement.
When the patient has mastered the breathing pat

tern in sidelying, try supine. Then progress to sitting
3. After the nonnal rate at the end of the patient's
(Figure
22-6), standing (Figure 22-7), walking (Fig

22-8), and finally stairs (Figure 22-9). Each de
exhalation, give a slow stretch and "scoop" your
ure
hand up and under the anterior thorax as shown
velopmental position increases the difficulty in per
in Figure
22-4. The command, "Breathe into my
forming diaphragmatic breathing. In sidelying or
hand," is given as the slow scoop stretch is done.
supine the patient is fully supported. The sidelying
4. As the "scoop stretch" is performed instruct the
position is especially good for initially teaching di
patient to, "breathe into my hand" during the
aphragmatic breathing because the diaphragm is in a
inspiration. Give a scoop at the end of exhala
gravity-eliminated position. In supine the patient
tion with each breath. The verbal command can
must breathe up against gravity. However, as we
be effectively replaced with audible breathing
progress to sitting, the patient must now provide
to facili tate the ventilatory pattern if verbal
trunk support and maintain stability up against grav
cues are ineffective or inappropriate.
ity, as well as relax the shoulders. In standing the en
5. After achieving some success, it is helpful to
tire body must be supported, and when walking or
call the patient's attention to the awareness of
stairs are added, the element of breathing coordina
the breathing pattern. For example, the thera
tion really comes into play.
pist can ask, "Can you feel how your abdomen

rises as you breathe in?"
Coordination of breathing for walking involves

being careful not to allow patients to breath hold. They
6. The patient's hand can be placed on the ab

domen with the therapist's hand on top. Rein
need to keep inspiration and exhalation regular at least

at a ratio of 1'1, preferably exhaling a little longer.
force the breathing pattern, then remove your
In general the preferred pattern for patients with pri
hand and allow the patient to independently
mary pulmonary dysfunction is as follows:
feel the ventilatory pattern (Figure
the base of the stairs to gain controL
22-5).
A few things should be taken into consideration. Try
(I) Pause at
(2) Have the pa
tient take a breath in and move as he or she exhales up
not to have patients take too many deep breaths; they
one stair.
may begin to feel light-headed because they may hy
hales as he or she walks up one stair.
(3) The patient then pauses to inspire and ex

(4) The patient
22
395
FIGURE 22-5
FIGURE 2-6
The patient is encouraged to continue practicing
The patient advances to the sitting position for breathing
diaphragmatic breathing to become aware of his breathing
retraining. Note the relaxed position of the patient's
pattern. this is usually the first position of the
shoulders and hands.
diaphragmatic breathing teaching sequence.
FIGURE 22-7
FIGURE 22-8
The third position in the sequence is standing. Full-length
Walking is the fourth stage of retraining. The patient is
min'ors are helpful at this point.
encouraged to relax, control his breathing, take long steps

and slow down.
396
PART III
C1 0f
-- \y
FIGURE 22-9
FIGURE 22-10
Stairs are important, especially if the patient has them at
Bilateral lower lobe expansion (this also facilitates
home. He is instructed to pause slightly as he breathes in
diaphragmatic movement).
and to exhale as he climbs one to two stairs.
should be encouraged to use the handrail and pace his

or her movement slowly and with breath controL
In general neuromuscular patients with lower-ex
Upper Chest Inhibition

If all other manual facilitation techniques cease to
produce the desired increase in diaphragmatic breath
tremity weakness may benefit from inspiration
ing, then inhibiting the upper chest during inhalation
while ascending stairs and exhalation during de
may be effective.
scent. Going downstairs is an eccentric muscle pat
Again, position the patient appropriately. These
tern and exhalation is a relative eccentric contrac
authors usually choose sidelying or 3/4 supine.
tion of the diaphragm.
Begin by facilitating the diaphragm, usually with the
Refer to the section on ventilation and movement
diaphragm scoop. Slowly bring your other arm
strategies on p. 387 of this chapter to determine appro
across the upper chest at about the level of the ster
priate incorporation of breathing in functional tasks.
nal angle. Leave it there for a couple of respiratory

cycles without applying any pressure to feel the
upper chest's movement.
LATERAL COSTAL BREATHING
After assessing this movement, gently allow your
Lateral costal breathing also facilitates diaphragmatic
arm to follow the upper chest back to its resting posi
excusion. This may be done bilaterally as in Figures
tion when the patient exhales. Now on the patient's
22- I 0, 22-11, 22-12, 22-13, and 22-14 or unilaterally
next inspiratory effort, do not move your arm's posi
as in Figures 22-1S, 22-16, and 22-17. Lower chest
tion. Thus your arm position will apply pressure or
lateral costal expansion facilitates diaphragmatic and
resistance to the expansion of the upper chest. This
intercostal breathing where the mid chest will recruit
gentle pressure will cause postural inhibition to the
primarily intercostal activity.
anterior and superior movement of the upper chest.
22
RGURE22
RGURE22
Bilateral midchest expansion exercise.
Self-assisted bilateral chest expansion exercise. Keep the

patient's shoulders relaxed.
397
----"
,-"I{
FIGURE22-13
FIGURE22-14
Bi lateral posterior chest expansion exercise.
Bilateral posterior chest expansion exercise.
398
PART III
FIGURE 22-16
FIGURE 22-15
Unilateral (segmental) breathing, left
field.
the left lower

shoulder must remain down,
with hands
on ulnar border or palm up in his lap.
FIGURE 22-17
The
either hand on the side of the

by
chest to be
his hand up.
22
399
After each expiratory cycle, add more pressure until
the chest wall to the lower sternum and touches the
the patient subconsciously increases the lower chest
patient with the instructions again to "now breathe

here." Finally, the therapist uses the first hand to
breathing out of necessity.

When you note more diaphragmatic and/or lower
move up to the upper sternum (usually around the
intercostal muscle excursion, verbally note this to the
level of the sternal angle) and asks the patient to
patient. Ask the patient to try to reproduce this pat
"now breathe here." It is impol1ant that the therapist
tern. With your other arm continue to facilitate the
smoothly transitions from one hand to the next to as
desired response, such as with the diaphragm scoop.
sist the patient in developing a smooth motor transi
Slowly, during each of the next series of inhalation,
tion from one area of the chest to the other. The man
release your inhibition as the patient tries to maintain
ual cues provide tactile cuing rather than true motor
the improved lower chest breathing pattern. If the pa
facilitation. Because of this, the normal timing se
tient is only partially successful, the inhibition can be
quence is obviously a more-advanced technique in
partially reapplied to assist the patient. If the patient
tended for use after achieving initial diaphragmatic
becomes anxious because the therapist's inhibition is
training success.
preventing upper chest breathing, then decrease the

inhibition to a comfortable level. This technique
should never cause an increase in anxiety or it will
MOBILIZING THE THORAX
only encourage more upper chest breathing rather
For some patients, controlled breathing alone may
than less.
not alleviate the inefficient ventilatory patterns even

with utilization of good positioning and appropriate
ventilatory strategies. The thorax itself may be inca
Normal Timing
pable of moving freely enough to allow for adequate
During normal quiet inspiration (controlled breath
chest wall excursion necessary for that breathing pat
ing), the diaphragm contracts, which is seen out
tern. For example, a patient with a spinal cord inj ury
wardly as a gentle rise of the abdomen. The second
who is demonstrating an excessive diaphragmatic
movement is seen as lateral costal expansion of the
pattern that is unbalanced by the normal neuromuscu
lower chest and usually to a lesser extent, lower ante
lar support of the intercostal and abdominal muscles
rior chest expansion. Lastly, the upper chest rises
can breathe using minimal chest wall expansion. This
slightly in primarily a superior-anterior plane with
is often noted as belly breathing. It may be necessary
less lateral expansion noted. A normal timing tech
to mobilize individual rib segments to gain the poten
nique adapted from the physical therapy approach of
tial for chest walJ expansion in aIL three planes of
proprioceptive neuromuscular facilitation (PNF) can
ventilation before facilitating a specific breathing pat
help the patient work on this sequence. After the pa
tern. If the potential for movement is not there, then
tient has learned to initiate inspiration with his or her
the breathing pattern cannot change. Likewise, a pa
diaphragm and lower chest wall muscles more con
tient with primary pulmonary dysfunction undergoing
sistently, this technique can help to put the whole se
chest surgery, or a patient suffering from an acute
quence together. The diaphragm continues to be the
chest trauma, may also find the rib cage stiff or sore
primary mover, but the other accessory muscles are
and thus limited in its potential expansion. All three
encouraged to do what they should do, which is to as
of these patients may benefit from the inclusion of rib
sist the diaphragm for better overall ventilation.
cage mobilization in their therapy programs. The rib
Generally, the patient is positioned symmetrically
cage musculoskeletal limitation may be secondary to
in either supine or supported sitting with a neutral
muscular atrophy, spasticity, or pain. Thus patients
pelvic position. The therapist waits until the end of an
with either primary pulmonary dysfunction or sec
expiratory cycle and then, using the hand placement
ondary pulmonary dysfunction can benefit from the
of the diaphragm scoop, asks the patient to breathe in
concept of chest mobilization.
"here." With the other hand, the therapist moves up
It is beyond the scope of this textbook to detail all
400
PART III
her head (shoulder flexion), as far as possible while
Techniques to Mobilize the Thorax
watching his or her hands. Using the appropriate ven
I. Use of towel or pillow rolls to mechanically

open up the anterior or lateral chest wall
2. Use of upper extremity pattern s to facilitate

opening of individual rib segments
tilatory strategy, the patient is also instructed to in

hale during this movement. Because fulJ shoulder
flexion and inspiration both require opening of the in
dividual rib segments, pairing them in this gravity-as
sisted position wiII promote a greater passi ve chest
3. Counterrotation of the trunk

4. Use of ventilatory-movement strategies to facili
tate opening of the entire thorax
5. Specific rib mobilization tu free up an individual

segment
6. Myofascial release techniques to frec up restric

tive connective tissue on and around the thorax
7. Soft tissue release techniques to lengthen indi

vidual tight Illuscles
wall stretch then either technique alone. If straight

flexion is not a viable option, use a buttelily position,
raising the arms up in shoulder flexion, abduction,
and external rotation with elbows bent (like butterfly
wings), again pairing this with voluntary maximal in
spiration and upward eye gaze. Pairing inspiration
and shoulder flexion maximizes the stretch on the
chest and encourages better ventilatory strategies.
In sidelying, ask the patient to bring his or her arm
up in straight flexion to maximize anterior chest ex
the numerous techniques involved in musculoskeletal
pansion or to move the arm into abduction to maxi
mobilization of the thorax, however, some simple
mize the lateral costal expansion. Pair either move
techniques and suggestions for further study are pre
ment with inspiration and upward eye gaze. If upper
sented. See the box above for a summary of mobi
extremity movement is not possible, the therapist can
lization techniques.
passively use countelTotation of the trunk to mobilize
Once again the therapist should note that the initial

step in achieving success begins with positioning
the chest while in the sidelying over the towel or pil

low roll. Continue to ask for active eye gazing.
considerations. Starting in supine, anterior chest wall
The same concepts can be used in upright postures,
mobility can be improved by placing a vertical towel
such as sitting or standing. Use a vertical towel roll
roll down the length of the thoracic spine and allow
again along the thoracic spine either along the back of
ing gravity to pull the shoulders back to the bed. In
a chair (wheelchair) or along the wall. Move the pa
this position, the anterior chest is opened up, placing
tient's arills passively or actively up into the most flex
the intercostal and pectoralis muscles on stretch for
ion or buttert1y ROM possible. The patient will get a
easier facilitation of upper chest expansion.
significantly greater stretch to the anterior chest wall
In sidelying, the lateral aspect of the chest can be
using the towel roll than without it. Precautions apply
passively mobilized with gravity'S assistance by plac
for patients with musculoskeletal problems along the
ing a towel roll(s) or pillow(s) under the lower chest
spine and for patients with impaired skin-tolerance.
(ribs 8 to 10) on the weight-bearing side. To determine
If these general mobilizing techniques do not pro
an appropriate amount of sidebending, make sure that
duce adequate chest wall mobility to allow for freer
the patient's shoulder and pelvis are still in direct con
breathing patterns to occur, then more specific tech
tact with the surface even with the towel roll(s) in
niques need to be considered including the following:
place. This maximizes the stretch on the chest without
(I) specific rib mobilization, (2) myofascial release to
placing the patient in a position that is too advanced
tight connective tissues (e.g., scar tissue secondary to
for his or her present chest wall mobility. Patients vary
surgical or traumatic areas), and/or (3) soft tissue re
from tolerating only a single thin towel roll up to toler
lease of tight muscle groups (neurological patients
ating three pillows under the lower ribs.
often present with tightness in the pectoralis, inter
In both postures, active or passive stretch ing can
costal, and quadratus lumborum muscles groups,
be added after positioning for success. In supine, ask
whereas orthopedic patients tend to have more tight
the patient to bring the arms directly up over his or
ness in the neck and back muscles). Use the position
22
ing and ventilatory strategies previously suggested

(e.g., sidelying over a towel roll) during these spe
Accessory Muscle Facilitation Techniques
cific interventions to maximize the potential gains in
I. Pec to ral i s facilitation
chest wall mobility. It is beyond the scope of this
2. Sternocleidomastoid and scalenes facilitation
textbook to detail all the numerous techniques in

volved in musculoskeletal mobilization and release of
the thorax. These three interventions are intended as
suggestions for further study in outside texts.
401
3. Trapezius facilitation
4. Diaphragm inhibiting technique
Manual inhibition
Postural inhibition
5. Lateral costal facilitation
FACILITATING ACCESSORY
MUSCLES IN VENTILATION
6. Serratus push-up
If the patient is still not demonstrating an optimal

breathing pattern after f acilitating a preferred
muscle breathing, the patient would be put in an ad
breathing pattern through appropriate positioning,
vantageous posture by slightly anteriorly tilting the
appropriate ventilatory strategies, chest wall mobi
pelvis. In supine, this could be as simple as decreas
l ization, and diaphragmatic retraining, then specific
ing the amount of knee flexion that is present or
facilatory or inhibitory techniques should be initi
using a small towel roll under the lumbar spine.
ated to the accessory muscles of ventilation. Spe

cific techniques are discussed here in detail. See the
box above for a summary.
Pectoralis Facilitation
Because the diaphragm normally supplies the bulk
The pectoralis muscle group is a powerful anterior
of the inspired air during quiet breathing, diaphrag
and lateral expander of the upper chest and can sub
matic breathing is the preferred pattern of breathing.
stitute quite effectively for paralyzed intercostal mus
However, after some neurological insults, strictly di
cles in the upper chest when trained to do so. Train
aphragmatic breathing may not be possible or even
ing usually begins in either modified sidelying or
preferred. Unlike pulmonary rehabilitation programs
supine. To increase the use of this muscle during in
for chronic lung or asthmatic patients, where di
spiration, the therapist should place his or her hand in
aphragmatic breathing is almost always encouraged
the same direction as the contracting muscle fibers.
and use of accessory muscles discouraged, restoration
Specific proprioceptive input is very important when
of independent, efficient breathing patterns for the
facilitating a muscle, thus make sure the hand is diag
neurologically impaired patient may require the regu
onally placed on the upper thorax (Figure 22-18).

The heel of the therapist's hand should be near the
lar use of accessory muscles.

Positioning continues to be the single most impor
sternum and the fingers aligned up and out toward the
tant aspect of all ventilatory facilitation techniques. If
shoulder. The patient is then asked to breathe into the
your patient is positioned for success, the probability
therapist's hands while the therapist applies a quick
of a successful response is much more likely. By as
manual stretch (as in repeated contractions PNF) to
sessing the patient's head, upper-extremity, trunk,
the muscle fibers (down and in toward the sternum).
pelvic, and lower-extremity positioning before every
This elicits the quick stretch reflex of the muscle and
activity or technique, the therapist is empowered to
simultaneously provides added sensory input, which
use mechanical positioning and gravity to the pa
facilitates a stronger and more specific muscle con
tient's advantage rather than to a disadvantage. For
traction. To emphasize an increase in lateral expan
example, a slightly posteriorly tilted pelvis tends to
sion, facilitation should gradually be transferred from
facilitate diaphragmatic breathing, whereas a slightly
the sternal arca out toward the therapist's finger tips
anteriorly tilted pelvis tends to facilitate upper chest
by the patient's shoulder. Unlike in the case of facili
breathing. Thus when facilitating more accessory
tating a more diaphragmatic pattern, verbal cues
402
PART III
FIGURE 22-18
Hand placement for facilitation of the pectoralis muscles for upper chest breathing.
should be strong and demanding to elicit a stronger

maximal voluntary effort.
Trapezius Facilitation
The trapezius muscle assists in superior expansion
of the chest. Facilitation can be initiated in supine
Sternocleidomastoid and Scalene Facilitation
or sidelying positions to decrease the resistance

from gravity. It can be progressed to an upright
This same plinciple can be applied to the sternoclei
posture in which the patient would have to work
domastoid and scalene muscles. In supine, therapists
against gravity.
need only change the angle of their hand alignment to
Placing the hands over the tops of the patient's
more specifically facilitate the sternocleidomastoid
shoulders, the therapist quick stretches the trapezius
and scalene muscles. Turning the hands parallel to
in a downward direction to facilitate a stronger eleva
the trunk so that the fingers are pointing up toward
tion response. Repeated contractions e<in be added to
the neck rather than pointing out toward the shoulder,
facilitate the contraction throughout the full ROM.
the therapist applies the same quick stretch and uses
Obviously, the shoulder shrug motion should be
the same verbal cues. The altered hand position now
paired with inhalation and upward eye gaze to maxi
specifically facilitates the sternocleidomastoid and
mize the facilitation response.
scalene muscles and secondarily influences the pec

toralis muscles. The sternocleidomastoid and scalene
muscles primarily expand the chest in a superior and
anterior plane, whereas the pectoralis muscles expand
Inhibition of the Diaphragm

Two techniques are described to inhibit the excessive
the chest in primarily a lateral and anterior plane,
use of the diaphragm during inspiration. Ideally, the
thus accounting for the slight difference in the facili
therapist is venturing to balance the use of accessory
tation positioning.
muscles, especially the intercostal, sternocleidomas
22
403
toid, scalenes, and trapezius muscles with the di
To perform the diaphragm-inhibiting technique,
aphragm's contraction. This is done to prevent para
the patient is positioned supine, semi-sitting or side
doxical movements of the chcst, or worse, to prevent
lying with the top arm positioned overhead or pulled
adverse musculoskeletal changes in the chest wall,
back at the waist to open up the upper chest. If toler
such as a pectus excuvatum that can result from mus
ated, remove pillows from under his or her head, an

teriorly tilt the pelvis and assess patient's airway
cle imbalance.
Inhibiting the diaphragm may be necessary during
safety by checking if he or she can still swallow
breathing retraining for somc patients with spinal
comfortably. The heel of the therapis t's hand is
cord injuries, polio, spina bifida, developmental de
placed lightly on the patient's abdomen at about the
lays, head traumas, and cerebral palsy. The di
level of the umbilicus. No instructions are given to
aphragm may be too weak to produce an adequate
the patient at this point. As the patient begins to ex
tidal volume or vital capacity without the assistance
hale a normal breath of air, the therapist gently al
of accessory muscles. In these cases the diaphragm
lows the heel of his or her hand to move up and in to
inhibiting technique is used to encourage the use of
ward the central tendon of the patient's diaphragm
the accessory muscles to assist in independent volun
(see Figure 22-4, p.
tary ventilation. Patients learn to use their weakened
breath is completed, the therapist strictly maintains
394). When expiration for that
diaphragm muscles in concert with intact accessory
the hand position in that shortened expiratory posi
muscles. Not only does this allow for an increased
tion. During the following inspiratory phase, the di
tidal volume and vital capacity, but it also provides
aphragm will experience some gentle resistance to its
better aeration of all lung segments and better mobi
inferior descent, causing inhibition to its full ROM.
lization of the entire thorax.
On the next expiration, the technique is repeated with
In contrast to the first reason that this technique
the therapist carefully pushing the heel of his or her
may be used, an unusually strong diaphragm, acting
hand further up and in, maintaining greater inhibition
without support from surrounding m u sculature,
during each inspiratory phase. After two or three
specifically the intercostals and abdominal muscles,
ventilatory cycles, a patient usually begins to subcon
may also need to be inhibited. For example, a para
sciously alter his or her breathing pattern to include
plegic or lower level tetraplegic patient with an intact
more upper chest expansion to reconcile the di
diaphragm but absent abdominal and intercostal mus
aphragm's transient inability to produce enough
cles may demonstrate a paradoxical breathing pattern
chest expansion to yield an adequate tidal volume.
(see compensatory breathing patterns, Chapter
The therapist should carefully observe which acces
37). In
this case the accessory muscles must be encouraged
sory muscles the patient spontaneously chooses. Are
to keep the diaphragm in check, attempting to avoid
they used symmetrically? What is the general quality
the development of a pectus excuvatum. The goal of
of the movement? Is the onset harsh or smooth? Does
this breathing retraining method is to stop the para
the patient appear fatigued or uncoordinated?
doxical movements of the upper chest during inspira
It is not until this point that the therapist should
tion by balancing the use of the upper and lower
verbally acknowledge any alteration of the patient's
chest. In some cases, spastic intercostal muscles, like
breathing pattern. Without changing his or her hand
in some spinal cord injury situations, may intercede
position, the therapist tells the patient what it is that
to prevent this paradoxical movement by maintaining
he or she likes about the new breathing pattern (e.g.,
the upper chest's position during inspiration in spite
balance between upper and lower chest expansion or
of the negative pressure within the chest and grav
less paradoxical motion of the sternum). Then the pa
ity's influence on top of the chest. Balancing the
tient is asked if he or she notices any difference from
chest's movements should produce an increase in
before, bringing this breathing pattern to a consciolls
tidal volume and vital capacity potential and mobilize
level. Only after some orientation to this pattern, usu
4 to 6 breathing cycles in the full
a greater portion of the chcst, just as the technique
ally no morc than
does in the first case presented.
inhibiting pattern, should the therapist begin to grad
404
PART III
FIGURE 22-1 9
Diaphragm inhibiting in prone on elbows position.
ually release the pressure being applied.
already been achieved. Extra care must be taken not to
While slowly releasing pressure with each cycle of
initiate any applied pressure quickly because of the
inspiration, the therapist asks the patient to attempt
likelihood of eliciting unwanted abdominal contrac
cognitively to reproduce the desired pattern. It should
tions or spasticity or eliciting a stronger diaphragmatic
take the same number of cycles to release the pres
contraction resulting from the quick stretch reflex. The
sure as it did to apply it. This technique easily allows
technique should never be painful. The therapist must
fo r gradations of i n h ibition, from full inhibition,
keep his or her hand on the abdomen, not the rib cage,
where the patient is forced to use upper accessory
to properly influence the diaphragm. This technique
muscles or risk becoming short of breath, to barely a
can be progressed by c hanging postures, which re
proprioceptive reminder to change his or her breath
quires greater tl1lnk control. Can the patient still main
ing pattern. It also allows for gradation of inhibition
tain the overall pattern? Can the patient breathe with
while the patient is learning to assume control over
out paradoxical movements against gravity?
the new breathing pattern. If during the releasing
The second technique is for the more advanced pa
phasc of this technique the patient begins to lose con
tient and simply presents a physical block to diaphrag
trol over the new pattern, the therapist can gently
matic excursion. The patient is positioned in a prone-on
reapply some pressure during the next expiratory
elbows position (Figure
phase to help the patient regain that control. At that
neurologically impaired patients, the lower chest will be
22-19). With most severely
point, the therapist can release or reapply pressure as
in direct contact with the surface, so lower anterior and
neccssary until the desired pattern is obtained and full
inferior expansion is inhibited and lateral costal expan
release of pressure is completed.
sion is limited. The upper chest is positioned in exten
This technique is particularly effective with patients
sion and the upper extremities are fixated, optimizing the
who are having difficulty cognitively altering their
length-tension relationsh.ip of the anterior and superior
own breathing pattern, such as with small children,
accessory muscles for easy facilitation. In addition, ante
brain-damaged patients, or slow motor learners, be
rior excursion of the upper chest is now in a gravity-as
cause it requires no cognitive effort until success has
sisted posture. Through the use of head and neck pat
22
405
FIGURE 22-20
Static-dynamic upper extremity activities in prone on elbows to encourage upper chest accessory
muscle participalion.
terns, such as in PNF diagonals, or static-dynamic activi
now assisting anterior excursion of the chest and re
ties, such as in weight shifting to one supp0!1ing limb
sisting posterior excursion. To emphasize the serratus
while reaching out with the other extremity, the therapist
anterior muscle's role in posterior expansion, the pa
can readily facilitate greater upper chest breathing (Fig
tient is instructed to perform an upper body push-up
ure 22-20). These are the same patterns the therapist can
(with or without the therapist's assistance). The serra
use to achieve other goals, such as increased head and
tus anterior muscle causes lateral scapular movement
neck control, increased shoulder stability, or increased
thereby facilitating maximal posterior excursion of
upper body balance. Therefore, by helping the patients
the thorax. The patient is instructed to take a deep
to coordinate movement goals with ventilatory patterns,
breath in during the push-up and to exhale the air
it becomes more likely that the patients will incorporate
(passively or forcefully) when returning to the start
these patterns functionally into daily activities. This is
ing position. Forceful exhalation in this activity can
the ultimate goal of any ventilatol)' retraining procedure.
be used as a forerunner to effective cough retraining.
The manual diaphragm-inhibiting technique is
Gentle or controlled exhalation can be used to en
usually less threatening to the patient than the prone
courage greater breath support for vocalization or f6r
on-elbows-inhibition technique. Prone on elbows it
eccentric trunk muscle training.
self can inhibit the diaphragm so completely for neu
Emphasizing posterior chest expansion during in
rological patients lacking spinal extensors that they
halation is the only occasion where inspiration would
become extremely short of breath. Consequently, do
be paired with trunk flexion. In all other inspiratory
not position the patients in this more demanding pos
situations, inspiration is paired with trunk extension,
ture until success appears likely.
and exhalation is paired with trunk flexion.
Serratus Push-up
PATIENTS WITH ASYMMETRICAL DYSFUNCTION
Facilitating greater posterior chest expansion can be
Patients with asymmetrical weakness need a different
achieved in a prone-on-elbows position. Gravity is
approach from the controlled or upper chest breathing
PART III
406
Promoting Symmetrical Ventilatory Function

for Patients With Asymmetrical DefICits
side with his or her arms positioned down below
90
degrees of shoulder flexion, lateral chest expansion

into that side becomes inhibited because of the
I. Use of positioning to achieve more symmetrical
physical batTier. This forces the patient to find an
alignment of the chest and trunk in both reclin
other way to meet his or her ventilatory needs,
ing and upright postures
which indirectly facilitates chest expansion on the
2. Use of postural inhibition to the stronger or unin

volved side to promote greater chest wall expan
sion on the weaker or involved side
3. Timing for emp h asis technique to promote active

symmetrical breathing anywhere in the thorax
opposite side (the uppermost side). The therapist

can then supply sensory and motor input through his
or her hands to the patient's upper, middle, or lower
chest on the involved or weaker side to facilitate in
creased ventilation on that side. Early in the rehabil
itation process or soon after thoracic surgery, the
patient may have difficulty performing lateral chest
expansion against gravity in sidelying (gravity-re
patterns presented previously. These patients need
sisted movement). If so, position the patient in a
facilitation to the weaker side to promote symmetri
3/4-supine position to lessen the workload imposed
cal chest wall expansion in both the upper and lower
by gravity. Gradually, work the patient up to a full
chest. See the box above for a summary of tech
sidelying posture to achieve the greatest strengthen
niques.
ing benefits.
Symmetrical Positioning
Timing for Emphasis
Symmetrical ventilatory patterns may be effortlessly
Another technique to promote symmetrical chest wall
achieved by altering the patient's position in each
movements is performed in numerous postures, such
posture to maximize the chest wall's potential to
as supine, sitting, or standing. The therapist places his
move in a symmetrical pattern. This is especially true
or her hand symmetrically on the lower lateral chest
in an upright position in which asymmetry is gener
wall, on the mid chest, or on the upper anterior chest
ally more pronounced. For example, hemiplegic pa
wall. At the end of exhalation, the therapist gives a
tients may lean toward their involved side in sitting
quick stretch on the muscles being touched to facili
because of weakness or spasticity. Likewise, after
tate a deep inspiratory effort in that area of the chest.
thoracic surgery, a primary pulmonary patient may
Immediately after both sides begin to move into an
lean toward the surgical side to avoid pain caused by
inspiratory pattern, the therapist manually blocks (or
chest movement around the incision. Both situations
inhibits) expansion of the chest on the stronger side
cause asymmetrical breathing patterns and decrease
while giving continued quick stretches on the weaker
ventilation on the involved side. Improving chest
side. This facilitates greater expansion on the weak
wall alignment may alleviate the ventilatory deficit
side by use of an overflow response. This technique,
on the involved side.
adapted from the PNFs timing for emphasis tech

nique, uses the strength of the stronger side to facili
tate movement on the 'Yeaker side. It can be applied
Postural Inhibition
to any area of the chest where symmetrical move
For some patients, more aggressive positioning must
ments should be the norm.
be used to achieve greater chest wall excursion and

ventilation on the involved side. This can be accom
plished by inhibiting the chest wall movements on
REDUCING RESPIRATORY RATES
the uninvolved or stronger side. Usually, the best
In addition to altering breathing patterns through fa
posture in which to achieve this inhibition is sidely
cilitation and inhibition techniques, reducing respira
ing. When the patient lies on his or her uninvolved
tory rates
(RR) may also be necessary before arriving
22
Facilitating Ventilation Pattems and Breathing Strategies
at an efficient breathing pattern for some patients.
407
sisted cough technique. One medical contraindication
See the box below for a summary of techniques.
for this technique is bony instability of the spine be
Many neurological patients with high neuromuscular
cause of its rotary nature.
tone increase their RR to compensate for a decrease
In bed or on a mat, place the patient in sidelying
in their tidal volumes (TV) or because of brain-stem
with knees bent and arms resting comfortably out in
impairments to the respiratory centers. In addition,
front of the head or shoulders. In this technique the
many patients who are anxious, such as asthmatic, or
higher the upper extremities can be placed within a
thopedic, or surgical patients experiencing pain, may
comfort zone, the better the result. Relaxed position
also demonstrate an excessively high RR. Attempting
ing of the patient is essential to the success of this
to restore ventilatory efficiency may require increas
technique, thus position the patient in an open yet
ing TV while concurrently decreasing RR.
comfortable position. Normalizing neuromuscular

tone is the first step in attempting to decrease a high
RR. Patient discomfort is likely to elicit increased
Previous Facilitation Techniques
tone and an increased RR.
The techniques previously described in this chapter
The therapist's own position is also important be
promote an increase in TV by improving the overall
cause it directs the force that is applied to the pa
ventilatory patterns and often cause a secondary reduc
tient's chest. Initially, the therapist needs to stand
tion in RR. See sections on controlled breathing, mobi
behind the patient, perpendicular to his or her trunk.
lizing the thorax, and upper chest breathing facilitation.
If the patient is lying on the left side, the therapist

places his or her left hand on the patient's shoulder
and his or her right hand on the patient's hip. The
Counterrotation
therapist then leaves his or her hands in place and
The technique described next is specifically devel
simply follows the patient's respiratory cycle. This
oped to promote a lower RR. The counterrotation
allows the therapist to assess the patient's subjective
technique reduces high neuromuscular tone and in
rate and rhythm and the patient's overall neuromus
creases thoracic mobility, thus often resulting in an
cular tone. Only after this assessment should the
increase in TV and simultaneous reduction in RR.
clinician begin the active phase of the technique.
These authors have found this technique to be ex
Using a PNF technique called rhythmic initiation,
(I) patients with
the patient is gently log-rolled in a small ROM in
decreased cognitive functioning after a neurological
sidelying. The rolling is gradually increased achiev
tremely effective for the following:
insult or after surgery, (2) very young children be
ing more ROM from sidelying toward prone. This
(3) patients with
progression of movement generally reduces high
high neuromuscular tone. As described in Chapter 21,
tone, which usually makes the second phase of the
it can also be easily adapted as a very effective as-
technique more effective.
cause there are no verbal cues, or
During this phase, the therapist needs to audibly

duplicate the patient's RR. As the patient moves into
greater rolling ROM and begins to slow his or her
Techniques to Reduce High Respiratory Rates
RR, the therapist needs to use the patient's audible

cuing as a facilitator for establishing a slower RR.
I. Previous techniques that increased tidal volume
Thus the therapist begins by having the patient estab
2. Countenotation technique
lish the audible RR and then the therapist slowly
3. Butterfly technique in sitting
Straight planes
Countenotation
takes over. Audible cues can be very strong facilita

tors of ventilatory rhythms.
Phase two requires the therapist to slowly change
4. Relaxed pursed lip breathing with inspiratory

and expiratory pauses
his or her position. Transitioning to a diagonal pos

ture, the therapist now stands or half kneels behind
the patient near his or her hips, turning diagonal to
408
PART III
the patient until
the patient's head at roughly
Assume
more
that the patient is side-
lying on the left At the
removed should be the audible cues. As with the di-
to get
angle, The hand placement
at
biting tech
plying stronger manual input. If the
of the
left hand
cycle, the
patient's shoulder on the

tips, and the
tation can be
hand
to the patient's right
the patient or
back
fossa (the hollow of the
21-6, A,
then
The
can
compress the rib cage in all three
planes of ventilation at the end of exhalation by gen
has an ex-
50 to 60 breaths/min), the facili

every 2 to 3 breaths so as not to
RR
fast
care being taken not to unintentionally use the thumb

or
the therapist can
reestablish control quickly if needed by simply reap
It should be apparent that this technique need not

be used
for
goals but rather
can be
total rehabilita
tion program. It is a natural precursor to active rolling

or it can be used as a vestibular stimulator.
tly pulling the shoulder back and down, while simul

pushing the hip up and forward, This
movement promotes more complete exhalation,
When the patient
the next inspiration, the
therapist switches hand
to capitalize on the
for TV, The therapist's left hand
improved
Butterfly Technique
version of this technique may be appropriate. In un
supported
and the ther
slides back to the patient's
has greater motor control, an
If the
hand slides forward just anterior to the

right iliac crest
21
Figure
stand behind or in front of the pa-
depending on his or her balance
B, p, 376).
or assist his or her arms up to this pos
As the patient inhales, the therapist slowly stretches

volumes (TVs).
the chest to maximize

left hand
The
thorax if the
the scapula (or the
is unstable) up and away from
the spine and the
hand
back and
the
down to maximize all three planes of
re
in greater inspiration. The therapist should use
and ask
to bring his or her arms up into a butter

from a comfortable
that patient,
tient's
ROM position for
to audibly breathe with the pa
RR. When the patient
raise the arms
up into slightly more shoulder flexion. When the pa

tient
lower the arms slightly.
to move in greater and greater increments of range,

all the while
out loud with your
the flat or heel of the hand whenever possible to
Through your audible breathing cues,
avoid unintentional patient discomfort and to maxi
your patient to slow down the
mize the facilitated area.
slower breaths. The use of the followi ng

begins and ends the
Initially, the
cycle according to the patient's
RR.
deeper inhalations
as
tone is relaxed and increased TVs are

through the effects of counterrotation, the
therapist
slows the rate of rotation down,
the
audible breathing cues to also facil
RR. The patient

dates to a slower RR as the therapist
itate a slower
trol over the patient's
tension
more con
and
Thus it becomes
(2) shoulder ex
and
for the pa
tient to increase his or her TV and decrease
RR.
As in the previous technique, the therapist

by
out loud at the

audibly at a
pace, The
pace and transi

more desirable
picks up on this subtle cuing and
subconsciously reduces his or her own
to assist in vol
RR even if
cannot follow verbal commands.

This technique can be modified to encourage more
at the slower rate.
The therapist can progress the
with inspiration and
tension and trunk flexion paired with exhalation.
pattern. With many
cognitively follow commands, he or s h e can be

untarily
and exhalations: ( l ) shoulder flexion and trunk ex
accommo
the results can be marked. If the patient can

alerted to this
to "ask"
RR and take deeper
by de-
the manual input. The last facilitation to be
intercostal and oblique abdominal muscle contrac

tions by using a diagonal rather than a straight
22
FIGURE 22-21
A, butterfly technique facilitating inspiration; B, butterfly technique facilitating exhaltation;
C, butterfly with twnk rotation facilitating inspiration. All threc planes of respiration are stretched
on the patients right side. D, butterfly with twnk rotation facilitating exhaltation. All planes
compressed on the right side.
409
410
PART III
of movement. Have the
look up and over one
and proceeds to force the air back and down the
shoulder as he or she breathes in and brings arms up
throat with a
and behind his or her head. Then have the
ynx, and larynx.
look down and away toward the opposite knee as he
Research has consistently shown that use of this
or she breathes out and brings arms down to the op

knee (Fieure 22-21).
maneuver of the tongue,
with severely
pa
tients can increase pulmonary functions signifi

especially for TV and Vc. If GPB is the only
means of ventilation off of a ventilator or
Relaxed Pursed-lip Breathing
nerve stimulator, mastery of this technique is critical
Use of a relaxed
to a
survival in case of mechanical failure.
ously described under
All
should be made to successfullv teach
breathing pattern," is also a technique to reduce RR.

By
the expiratory
through pursed
the patient secondarily decreases his or her RR.
GPB to this patient population.
SCI while
\"VllllJlilA\V
in front of a train. After he was
medically
GLOSSOPHARYNGEAL BREATHING
to illustrate its use
A clinical example may
fulness. A l4-year-old male sustained a C 1
two phrenic nerve stimulators were

in his chest. The patient had no nonassisted
requires
means of ventilation.
the patient
more than just promoting the use of accessory muscles
had limited use of one
sternocleidomastoid,
A small population of neurological

RR to meet basic
or
last decade, more
needs. In the
SCls (above C4) have sur
vived the initial trauma because of advances in med

the rehabilitation
ical technology.
is then faced with the difficult task of
of life. For these patients, as well as many old polio

breathing
voluntary ventila
technique allows for

tion, which many
to
which was
lost as a result of high neurological
ily believed it could not bear the psychological bur

went home to live.
den placed on them if the

GPB instruction was
and
slowly be
stated that he learned motor skills

the pa
tient learned to breathe without the use of his phrenic

nerve stimulator for 3 to 5 minutes before
this same patient learned to breathe for up to 2 hours
for a way to reduce their de
could actually
air to sustain life without mechanical
To the staff's
he even learned to talk and
mouth,
using the lips, soft
tongue, pharynx, and larynx, a
using GPB
off of his
pendence on the iron lung for ventilation. It was
inhale
wearing
immediate respiratory distress. The fam
and hypoventilating. Within the next I to 2
GPB is a
polio patients
found that
would
slowly. After a painstaking 2-month
some control over their Jives
control over their
and to
out,
cause the
state does improve the
ity of their Jives. This augmented breathing

lows
home
be inevitable because of their fear of his

nerve stimulator malfunctioning or a
quality
mastery of the
and intrinsic neck muscles. The patient and family

feared that
his sip-
GPB. The patient

to his home. This
was then successfully
does not imply that this was the only factor consid
ventilation. Only intact cranial nerves are
ered in his discharge olanning, but it was oerhaos the
This m e t h o d i s s o m e t i m e s referred t o as
most significant.
breathing because it uses the principles of

tion common to the
of
cavity by
Instruction in GPB takes time and concentration. It
The
is best to statt off in small time blocks of 10 to 15 min

However, it is
utes because it can be very
pressure
that internal space,
causing the outside air to rush in. At that

the patient closes off the entrance
lips)
to successful
the patient gets
of the technique that

preferably daily training.
Once the patient has mastered the
22
sessions can be lengthened considerably, and the pa
411
demonstrates to the patient what a stroking maneuver
tient can be taught self-monitoring techniques. Specific
looks like several times to give an idea of the motion
goals of GPB training must be explained to the patient
required. The therapist continues to mimic the pattern
before the beginning of treatment to gain his or her
as the patient attempts to duplicate it. This gives the
support and cooperation. In addition to providing the
patient an active model to mimic and decreases feel
ventilator-or stimulator-dependent patient with a TV
ings of uneasiness surrounding the necessary but
necessary for gaining independence from mechanical
somewhat silly facial grimaces. If the patient is able
assists, GPB has many other b e n e f i t s. F o r the
to breathe independently, his or her ability to breath
tetraplegic patient who has a partially intact diaphragm
hold and to close off the nasal passageway should be
(C3 to C4) or the loss of essential accessory muscles
checked because air leakage is a common cause of
(C5 to C8), GPB can accomplish the following: (1) in
failure. The patient is then instructed to take in a
(2) as
maximal inspiration before attempting the stroking
sist in a longer and stronger phonation effort, and
maneuvers to eliminate the possibility of using other
(3) act as an internal mobilizer of the chest wall.
accessory muscles during the technique.
crease VC to produce a more effective cough,
The muscles used in this technique do not have the
If possible, position the patient in an upright or at
same internal proprioceptive, sensory, or visual feed
least a symmetrical position. Specifically, the patients
back mechanisms as the trunk and limb muscles. Thus
are instructed to bring their jaws down and then for
necessary adjustments in the technique are sometimes
ward as if reaching their bottom lip up for a carrot
difficult to see or feel. The patient cannot see his or
dangling just in front and above the upper lip (Figure
her tongue pushing the air back or truly feel the phar
22-22, A). Slight cervical hyperextension is necessary
ynx swallowing the air into the lungs, so the thera
to allow for maximal temporal mandibular joint
pist's external feedback system is very influential.
(TMJ) excursion. (A contraindication for this tech
Use of a minor can greatly enhance the visual compo
nique is a TMJ disorder.) The lips should be shaped
nent of feedback. Small changes, like adjustments in
as if they were to make the sound "oop." The patient
posture or a suggestion of another sound to imitate,
is then told to close the mouth, reaching the bottom
may be all that is needed for the patient to learn tbe
lip up to the top lip (see Figure
stroking maneuver correctly. Success in GPB can be
and jaw are drawn back toward the throat, with the
22-22, B). The tongue
assessed objectively with a spirometer and a pulse
mouth and tongue formation of the word up or the
oximeter. For those patients incapable of breathing in
sound "ell" (see Figure
dependently, any TV reading will indicate successful
moving in roughly a rectangular pattern. Most pa
22-22, B). The lower jaw is
intake of air. For patients who are not ventilator de
tients learn the stroking maneuvers by making the
pendent, a VC reading that is greater than 5% over the
sounds at first, as they become more proficient, the
baseline indicates successful use of GPB. Lower-level
sounds and excessive head and neck motions dimin
tetraplegics, C5 to C8, have demonstrated increases in
ish. Often, the students (patients) outperform the
VC by as much as 70% to 100%.
teacher (therapist), because through consistent use,
Therapists can monitor their own successes with
they learn all of its finer subtleties.
this technique by taking VC readings with and with
Although this technique can be broken down into
out GPB or by subjective analyses. Maximal inhala
several stages as it has been here for the purpose of de
tion, followed by three or four successful GPB
scription, most of the literature cautions the therapist
strokes, will cause a feeling that the chest will burst if
against it. (Zumwalt, Adkins, Dail, and Affeldt, 1956).
an attempt is made to inhale more air. Likewise, a
Simple, minimal insuuctions seem to accomplish more,
sensation of "needing to cough" is another subjective
perhaps because the continuity of movement is so es
indication of successful GPB. However, a feeling of
sential to the success of the inhalation. Specific instruc
indigestion is usually indicative of swallowed air in
tions can be given later if necessary.
the stomach instead of the lungs.
Common problems encountered with GPB instruc
During the initial treatment session, the therapist
tion are as follows:
(I) an open nasal passage or glot
412
PART III
FIGURE 22-22
Glossopharyngeal breathing; A, mouth opened to draw in air; B, j aw closed to entrap the air; C, air
pushed back with tongue into trachea; D, vocal folds closed to prevent passive air leaks. Entire
maneuver is then repeated.
(2)
a feeling of indi
els begin to fall to the mid 90s and then the low 90s,
gestion indicating that the air is being swallowed into
you can anticipate when they will reach 90%. At that
tis that allows the air to escape,
the esophagus rather than the trachea,
(3)
incorrect
point, end the GPB training and put the patient back
shape of the mouth as the air is bein g drawn in, usu
on the previous ventilatory support system. Oximetery
ally not puckered enough, (4) uncoordinated back
not only allows for accurate monitoring but also pro
ward movement of the tongue, (5) inadequate jaw
vides a means for an objective means for monitoring
mobility, TMJ dysfunction, or decreased cervical
progress over time. In addition, a spirometer objec
ROM, or
(6) incorrect
sounds while performing the
tively measures improvements in VC using GPB. It
technique, such as the word gulp or an "em" sound.
gives the patients concrete indications of success or
A voiding any instruction for the tongue seems to pro
failure with the technique.
duce better results. Concentrate on assisting the pa

tient in learning the external physical movements.
Tolerance to GPB can be increased when mastery
ENHANCING VOCALIZATION SKILLS
of a single stroke becomes consistent. For patients
In contrast to procedures that assist the patient in in
using it as an assist to their own voluntary ventilation,
halation, procedures intended to improve a patient's
to 4 strokes on top of a maximal inspiration is usu
phonation skill must focus on elongating the expira
ally sufficient. Ventilator- or stimulator-dependent pa
tion phase. Coughing is a gross-motor skill that relies
tients may need to use as many as 10 to 14 strokes per
more on force than fine control of the ventilatory
breath. These figures should be used only as rough
muscles for its effectiveness. Conversely, phonation
guidelines. Each patient will use a slightly different
requires precise, fine-motor control of these muscles
technique with a different number of strokes, with the
and the vocal folds to provide a consistent air flow
only important factor being a method that works for
through the larynx. Both are expiration activities and
them. Fatigue with long trials of GPB can be moni
depend on the preceding inspiration for optimal per
tored effectively with an oximeter. The oxygen satura
formance; however, coughing uses concentric con
tion level should stay above 90% to maintain adequate
tractions of the expiratory muscles to force the air
Pa02 levels. For example, if the patient begins the
out, and quiet talking uses primarily eccentric con
GPB session with an oxygen saturation level in the
tractions of the inspiratory muscles to slowly release
upper 90s, fatigue can be monitored and anticipated
the air during expiration. Because of these differ
by watching if the oxygen levels decrease. If the lev
ences, procedures to improve coughing and phona
22
an open anterior chest wall will allow for the greatest
Ellhallcillg Vocalizatioll Skills through
potential for chest wall excursion and thus the largest
ill creased Breath Support
Vc. Use the previously described suggestions for po

sitioning to determine if your particular patient needs
I. Position to achieve a neutral chin tuck and opti

mal vocal fold alignment
positioning to encourage a more diaphragmatic,

upper chest, or unilateral breathing pattern.
2. Manual techniques
Vibration or shaking
Percussion or tapping
413
Manual Techniques
3. Eccentric resistance
Several simple techniques can be used to improve
Agonistic reversal technique
eccentric control of the diaphragm and intercostal
Functional resistance
muscles in preparation for speech. Vibration or shak

ing to the lower chest during expiration assists in a
4. Verbal techniques to refine breath support
Singing and whistling
Games
Wind or brass instruments
Stopping and starting vocalizations
slower, more controlled recoil of the diaphragm.

Why this occurs is not fully understood. It may be
that the sensory and proprioceptive stimulation that
the vibration or shaking provides augments the pa
tient's concentration on those muscles resulting in
longer p h onation. The patient is instructed to
phonate an "ah" or "oh" sound for as long as possi
ble. The therapist simultaneously vibrates the pa
tion will be different in focus. See the box above for
tient's chest with an even and gentle force through
a summary of techniques. Coughing is covered in de
out and slightly beyond the full expiration phase,
tail in Chapter 21.
placing his or her hands on the lateral costal borders
Because the patient's TV and total inspiratory ca
of the thorax, the mid chest, or on the pectoral area,
pacity are the power source for phonation, they be
depending on which area of the chest needs the most
come important concerns in a phonation program.
help in controlling exhalation. This is very different
Generally, a normal TV is adequate for con versa
from the rapid, forceful pressure that is applied to the
tional speech. However, larger volumes of air, thus
patient's chest when promoting a deep cough. Be
greater inspiratory capacities, are required for
certain that the patients understand this important
singing, loud talking, or professional speaking.
difference. The therapist must stress to the patients
Therefore the breathing pattern facilitation techniques
that they should not let air escape before vocalization
described previously in this chapter are ideal before
and that they should try to keep the voice intensity
instructing the patient in better expiration control. For
consistent throughout the procedure. This will pro
example, facilitating diaphragmatic and/or accessory
mote slow eccentric release of the inspiratory mus
muscle breathing techniques, along with the use of
cles during the en tire course of the vocalization.
quick stretches or repeated contractions, can facilitate
Progress can be readily monitored by timing the pa
the desired deeper inhalation.
tient's vocalization, before, during, and after this

technique. About 10 to 12 seconds of vocalization,
or 8 to 10 syllables per breath, is generally consid
Positioning Concerns
ered adequate for functional use in speech.
Consistent with all previous techniques, the first as
For children, this technique can be modified. The
pect of improving breath support for vocalization is
child is asked to say "ah" or "oh" for as long as possi
to optimize the patient's position. The vocal folds
ble while the therapist percusses or taps lightly with his
have an ideal muscle length-tension relationship
or her hands on the child's upper or lower chest so as to
when the head is in a neutral chin tuck. In addition,
produce a series of staccato sounds. Most children
414
PART III
enjoy the new sound that this makes and will try repeat
the arm's descent. The activity can be progressed sev
edly to phonate longer and louder to accentuate the dif
eral ways. The activity can include lifting something
ferent intensities.
heavy off the shelf and controlling it along with the
Therapeutically, this requires them to take a
arm and trunk while lowering the object or weight to a
deeper inhalation before vocalizing, followed by an
table or to the patient's lap. Or the postural demands
elongated expiratory phase, both of which are neces
of the activity can be increased. The patient can still
sary for functional speech. As the child becomes
lift the heavy object or weight but he or she can now
more adept at it, the therapist can apply more pro
be required to do this in standing, which increases the
nounced clapping over the chest, accomplishing a
demands on the musculoskeletal system.
wider range of voice intensities and doubling as a

means of percussion for postural drainage.
Verbal Techniques
Speech activities that do not require a therapist's
Eccentric Resistance Techniques
physical assistance can be done in a group or individ
More specific facilitation can be used to increase
ual setting. Singing, for instance, promotes strong
breath support. Ideally, the patient is positioned sym
and prolonged vocalization with maximal inspiration,
metrically in supine or supported sitting, allowing for
which is a significant goal in a phonation program.
maximal chest wall expansion. The patient is in
Similarly, whistling promotes long, even exhalations
structed to visualize his or her chest being pulled up
but is nonverbal. Both are easily incorporated into a
toward the ceiling and held there. They are then told
group activity on the nursing floor, in therapy or in
to vocalize slowly trying not to let the chest "fall."
the community.
Meanwhile, the therapist is applying consistent pres
Along recreational lines, games that promote con
sure to the patient's chest to try to force a quicker ex
trolled blowing further the refinement of motor con
halation. The patient is told to resist this motion by
trol over the respiratory muscles. This can be accom
trying to control and prolong expiration. Like the an
plished by blowing bubbles, especially large ones,
tagonistic reversal technique described in PNF, the
blowing out candles, especially trick candles, blow
therapist is resisting the patient's attempt to eccentri
ing a ping-pong ball through a maze, or by blowing
cally contract and control the trunk muscles. This
air hockey discs across the table rather than pushing
strengthens the eccentric phase of exhalation and pro
them. Patients with musical inclinations should be
motes greater breath control for vocalization.
encouraged to learn to play wind or brass instruments
The same concept can be applied to functional
where refined breath control is mandatory for suc
tasks. Moving into gravity, that is, coming down to
cess. Obviously, the possibilities for recreational use
sitting from a standing posture, lying down from a sit
are endless, and simply require imagination on the
ting posture, and bringing an ann down from reaching
part of the therapist.
into a higher cabinet, all require eccentric control of
Further refinement of breath control for speech
the muscles involved in that activity to slow the
can be promoted by interrupting the outgoing air
body's descent into gravity's influence. Because quiet
flow. Functional speech is a series of vocal stops and
speech uses a similar muscular contraction, teaching
starts. This procedure is geared toward improving
the patient to count out loud or to otherwise vocalize
functional communication skills. The therapist tells
when performing an overall eccentric activity usually
the patient to take a deep breath and then to count out
improves both activities. For example, the patient can
loud to 100. After a few numbers, the patient is told
be instructed to reach up to a high shelf or cabinet
to "hold it." He or she is then told to start up where
while inhaling. Then, using gravity to provide the ec
he or she left off, with the therapist periodically inter
centric resistance, the patient is asked to bring his or
rupting. Because this activity requires the patient to
her arm back down to his or her lap or side while
stop and start the inhalation and exhalation phases at
slowly counting out loud and controlling the rate of
will in all aspects of the ventilatory cycle, it is more
22
415
advanced and should be used only after some control
more desirable. Some may benefit even more from
of exhalation has been mastered.
techniques to reduce the high RR or to mobilize the

thorax. For a select patient population, instruction
in GPB may be necessary to support breathing off
SUMMARY
of mechanical ventilatory support. Lastly, the ther
In summary, use of appropriate choices in positioning
apist can now choose to use techniques to improve
together with use of an appropriate ventilatory and
the patient in developing adequate breath support
movement strategy for any given task will make the
for vocalization and communication.
success of that task all the more likely. If these sim
It is these authors' hope that the therapist now un
ple, time-efficient methods of facilitation do not pro
derstands how widespread the influence of effective
duce adequate ventilatory changes by themselves, it
ventilation can be on a patient's recovery from dis
is then appropriate to add on the next layer of facilita
ease or trauma. Understanding that facilitating effec
tion-manual facilitation techniques. Specifically,
tive ventilation goes far beyond the old diaphrag
the techniques that are described in this chapter assist
matic exercises, therapists can be empowered to
(1) greater diaphrag
incorporate other techniques and strategies to get
matic breathing patterns (or controlled breathing),
their patients healthier quicker and to assist them in
(2) increased chest wall mobility, (3) greater acces
reaching their greatest rehabilitation potential.
in facilitating the following:
sory muscle breathing patterns (or primarily upper
(4) increased symmetrical breathing

(5) reduction in high
respiratory rates, (6) auxillary techniques GBP, and
(7) improved phonation support. Obviously, not all
chest breathing),
patterns (unilateral disorders),
techniques would be appropriate for any single pa

tient. It is up to the therapist to determine which tech
niques would best address their patients' deficits.
REVIEW QUESTIONS
1. Why would a therapist want to try to change a
patient's breathing pattern?
2. How can ventilatory strategies be incorporated

into a treatment session?
3. When would a therapist not teach diaphragmatic
In conclusion, positioning has everything to do

with increasing ventilation potential and functional
skills. From the beginning of the patient's respira
breathing?
4. What is the role of relaxation in breathing control?

5. When would a therapist consider teaching the pa
tory program, optimizing ventilation and breath
tient to use his upper chest more in breathing?
control through passive and active positioning
6. When would a unilateral breathing pattern be
techniques should be used by all medical disci
taught?
plines, not just physical therapy. As the patients

progress, the clinician can and should, assist them
in developing better and more efficient movement
strategies for higher level activities by coordinating
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Exercise Testing and Training:
Primary Cardiopulmonary Dysfunction
Susan K. Ludwick
KEY TERMS
Arteriovenous-oxygen difference
(a-v02 difference)
Forced vital capacity (FVC)

Minute ventilation (YE)
Cardiac output (Q)
Oxygen consumption ('\102)
Forced expiratory volume in
Stroke volume (SV)

Tidal volume (TV)
I second (FEV)
INTRODUCTION
Shortness of breath, especially with activity, is very
and then be able to devise therapy programs that
common in patients who have cardiopulmonary dis
would keep these individuals active within the limits
eases. Shortness of breath can be quick in onset or
of their disease in order for them to maintain certain
of a chronic nature. One of the results of shortness
levels of independence.
of breath, especially when it is of a chronic nature,

is the vicious cycle of deconditioning it causes in
patients. Eventually, these individuals may become
LUNG DISEASE
deconditioned to the point that activities of daily liv
In individuals without lung disease the cardiovascular
ing usually taken for granted, such as washing up in
system normally limits maximal aerobic exercise.
the morning, may be overwhelmingly fatiguing.
Typically, maximal oxygen consumption (Vo2) may
Physical therapists need to understand the underly
be limited by the heart's inability to increase its cari.i
ing mechanisms of shortness of breath, evaluate
diac output (Q) either by an inability to increase heart
their patients appropriately given their limitations,
rate (HR) or stroke volume (SV) or by an inability to

417
418
PART III
provide adequate oxygen delivery to exerCISing
Impaired Gas Exchange
skeletal muscle represented by the arteriovenous
During exercise, there needs to be a balance of venti
oxygen difference (a-vo2difference). This relation
lation to perfusion (VIQ) in the lungs for adequate
ship of V02 to Q is represented by the Fick equation:

V02
blood oxygenation to occur. In patients with airways

disease, underventilation of the lungs could occur be
Q x a - V02 difference
cause of elastic tissue destruction. Underventilation
However, patients with lung disease may be lim

ited in their exercise capacity for several reasons.
results in V/Q mismatches (low V/Q ratio). Hypox

emia occurs as a result.
They may be limited by altered lung mechanics, im

paired gas exchange, development of pulmonary hy
pertension, or respiratory muscle fatigue. Each of
Pulmonary HypertenSion
these factors make traditional cardiovascular evalua
In normal individuals, there is typically an increase in
tion of exercise capacity inadequate, since these pa
the diameter and in the number of blood vessels with
tients are limited by their breathing and not by their
exercise. However, in patients with lung disease,

there may be a decrease in the number and/or in the
cardiovascular systems.
distensibility of blood vessels. This results in the in

crease of pulmonary vascular resistance. An increase
Altered Lung Mechanics
in the pulmonary vascular resistance contributes to a
One of the characteristics of obstructive lung dis
decrease in left ventricular filling. If there is a de
ease is the destruction of elastic tissue in the lung.
crease in left ventricular filling, then there will be a
The destruction of elastic tissue prevents normal
decrease in cardiac output, which would limit the
recoil of lung tissue on expiration. Therefore it is
ability to do work.
difficult for patients to empty their lungs. This

coupled with the tendency for bronchial walls to
collapse contributes to air trapping. This results in
lung hyperinflation. With exercise, our bodies re
Respiratory Muscle Fatigue

Respiratory muscles in a normal individual con
quire an increase in oxygen uptake to perform
sume little oxygen at rest or with moderately in
more work. Minute ventilation increases in order
creased ventilation during activity. With exercise,
for oxygen u ptake to improve. We know t h a t
oxygen consumption increases greatly. However, a
minute ventilation is t h e product o f tidal volume
patient with lung disease would have an increase in
VE. If respira
ventilatory muscle oxygen consumption up to 40%
tory rate increases as a natural response to an in
of the total body oxygen consumption. The respira
crease in exercise, it may not allow enough time
tory muscles may not be able to keep up with the
and respiratory rate (TV x RR
for lungs to adequately empty and fill again if elas
total demand and would start to fatigue (see Chap
tic tissue is destroyed. Therefore tidal volume can
ter
not adequately increase with increases in exercise
muscle fatigue is the musculoskeletal deformity
25). Another contributing factor in respiratory
intensity. The result is that minute ventilation will
that many of these individuals develop with the dis
not increase in proportion to exercise. If minute
ease processes. Muscle fibers need to be at an opti
ventilation does not increase as required, then oxy
mal length to work efficiently for adequate force
gen consumption and, therefore, amount of work
generation to perform work. However, with muscu
will be effected.
loskeletal deformity, these fibers may be placed at
Patients with restricture lung disease will have
lengths that make it difficult for efficient work to
stiffer lungs that are resistant to expansion on inspira
be done. Eventually, they fatigue because of inade
tion. The patient will have to work harder to maintain
quate force generation needed to support the work
pressures for adequate lung expansion and venti la
of breathing.
tion. Eventually all lung volumes and capacities be

come decreased.
Clinically, patients with obstructive lung disease

show breathing patterns that are slower and deeper at
23
Exercise Testing and Training: Primary Cardiopulmonary Dysfunction
419
rest and with exercise. Specifically, longer expiratory
consumption during exercise above which a sus
cycles are observed because of the extra effort these
tained lactic acidosis occurs, is useful in measuring
patients make to empty their lungs before inspiration.
exercise tolerance in normals. However, it is not par
Patients with restrictive lung disease have a pattern of
ticularly useful with patients, since peak exercise
rapid, shallow breathing in an effort to maintain ade
levels may be below the anaerobic threshold. Some
quate minute ventilation in the face of decreased lung
have looked at the measurements of FEV [ and FVC

to predict exercise capacity. However, the literature
capacities.
has shown that there is no correlation between these

measurements of lung mechanics and exercise ca
HEART DISEASE
pacity. It makes more sense to define exercise capac
Patients with acute or chronic cardiac failure or
ity by evaluating the patient's functional exercise ca
valvular heart disease have elevated pulmonary ve
pacity. This can be done by using timed walking
nous pressures. This develops into intersti tial
distances. The 12-minute walk as defined by Ken
edema. Therefore the lungs are said to be "wet,"
neth Cooper has been adapted by McGavin, Gupta,
their compliance is decreased, and the work of
and McHardy (1976) for use with patients that have

chronic bronchitis. This test is also useful in deter
breathing is elevated.
Clinically, these patients have pulmonary rales on
mining exercise capacity in other patient populations
auscultation. They adopt rapid, shallow breathing
as well. This evaluation is useful because it corre
patterns to minimize respiratory muscle work. These
lates with V02 as measured on the treadmill. How
patients, as with patients with chronic lung disease,
ever, results are reported in terms of distance walked
will have ventilatory responses to exercise, depend
and not in how much oxygen was consumed. There
ing on the severity of the disease.
fore it gives a more functional picture of exercise

tolerance since it uses a familiar activity. If 12 min
utes is too long for some patients, 3- and 6-minute
Assessment
walks are just as useful. These walking tests are sim
Before starting the actual exercise assessment, it is
ple to implement and use simple measurement de
important to get an idea of the patient's activity level
vices. Patients can also use them as methods to mon
and what activities cause shortness of breath. How
itor their own progress.
far can the patient walk before becoming short of
To assess patients using the 12-minute walk, one
breath? Can the patient tolerate walking outside? Is
must simply instruct the patient to walk as far as pos
he or she only able to walk comfortably to get about
sible in 12 minutes. It is not absolutely necessary to
inside a house or apartment? Can the patient walk up
walk without stopping. The patient may slow down
stairs? Does dressing, taking a bath or shower, or
or even stop to take a short rest if needed. The only
combing hair cause shortness of breath? Can the pa
required equipment is a stopwatch and a measured
tient do his or her own grocery shopping? Is the pa
corridor.
tient able to do any heavy housework, such as vacu

uming or bed making? Is the patient able to make his
or her own meals?
If aerobic capacity is limited because of either
UPPER-EXTREMITY VERSUS lOWER-EXTREMITY

ACTIVITY
cardiac or ventilatory limitations, how can we func
Up to this point, we have discussed exercise assess
tionally assess exercise capacity without the use of
ments in reference to lower-extremity activity. How
expensive testing equipment? Traditional methods of
ever, shortness of breath may be of even earlier onset
measuring maximal oxygen uptake, including tread
when perfomling routine activities of daily living in
mill testing, may have limited usefulness because
volving upper extremities (i.e., grooming, lifting, and
oxygen uptake for the pulmonary patient, as ex
carrying). This in fact may be the most frustrating
plained before, is limited by ventilation. Anaerobic
limitation to patients, since these are the types of ac
threshold, which is defined as the highest oxygen
tivities that we normally take for granted in our
420
PART III
everyday Ii ves. When patients begin to have diffi
ing expiration. There are no compressive forces
culty performing these activities, they feel a loss of
working to narrow the airways. However, in patients
control in their lives. It is important to note that the
with airflow limitation, the work of breathing is
exercise responses to these activities are different and
shifted to the muscles of expiration. Therefore expi

ration becomes a more active process, resulting in the
should be assessed separately from walking.

CeJli, Rassulo, and Make
(1986) have reported the
generation of more positive pleural pressures com
appearance of dyssynchronous thoracoabdominal
pressing the airways. Closing off of airways creates
movement when comparing arm activity with leg ac
the feeling of shortness of breath. An impOItant yet
tivity. Early fatigue was observed to occur despite
simple technique that can be taught to patients is the
lower heart rates, minute ventilation, and oxygen up
practice of purse-lipped breathing to control short
take when compared with leg work. It was hypothe
ness of breath. By having the patient expire through
sized that exercise limitation during arm activity was
pursed lips, a back pressure is created in the airways
probably because of a smaller contribution of acces
that helps to keep them from collapsing despite the
sory muscles to the work of breathing, since these
positive pleural pressures down on them. This is a
muscles must contribute to postural support of the
useful technique that can be used at rest and during
upper extremity during activity. Despite these limita
exercise to slow down respiratory rate, increase tidal
tions in upper-extremity exercise tolerance, improve
volume, and increase blood oxygenation.
ments have been demonstrated after an exercise train
When evaluating exercise tolerance with patients,

it is impOItant to assess the work of breathing. Borg
ing program.
Upper-extremity assessments may be considered
(1982) has developed two scales that can help to
two ways. They can be either supported or unsup
quantify dyspnea. In our facility, we have used a sim
ported (Criner and Celli,
1988). Supported assess
ments would be those that may involve the use of an
ple scale of I to
4 to describe shortness of breath (see

421). On our scale, a score of I
boxes below and on p.
upper-extremity ergometer. Unsupported assessments
would represent baseline (comfortable) breathing. A
would include those activities involving reaching.
score of
Since activities of daily living involve combing hair,
vere that one is not able to talk. Since exercise limita
washing, dressing, and reaching at various heights,
tion is more closely related to ventilatory rather than
4 would represent shortness of breath so se
assessments imitating these things would be most

useful. One such test that could be used would in
volve repetitive reaching at a height level to the head.
Reaching up with a light object of approximately I
pound may imitate reaching up to kitchen cupboards
to put away groceries. Counting the number of repeti
tions and timing the activity would give a functional
The 15 Point RPE Scale

6
7
VERY, VERY LIGHT
8
9
VERY LIGHT
10
II
12
13
picture of upper-body activity tolerance.
BREATHING
FAIRL Y LIGHT
SOMEWHAT HARD
14
Patients who have pulmonary diseases have limited
15
ventilatory reserves, which manifests as shortness of
16
breath. The degree of the shortness of breath may de

pend on the severity of the lung disease. Normally,
during quiet breathing, average pleural pressures sur
HARD
17
VERY HARD
18
19
VERY, VERY HARD
20
rounding the large airways are typically negative,

whereas intraluminal pressures are more positive.
Borg, G. (1982). PsychologicaJ Bases of Perceived Exertion, Medi
These positive pressures keep the airways open dur
cine and Science ill Spor/s and Exercise, 14,378.
23
reaching over the head, marching while sitting, knee
The 10 Point RPE Scale

0
0.5
I
2
3
4
5
6
7
8
9
10
421
extension, and stretching hamstrings with the leg
NOTHING AT ALL
being stretched propped on another chair in front. Ex
VERY, VERY WEAK
ercises should be timed with purse-lipped breathing
VERY WEAK
to pace the exercise comfortably and control short
WEAK
ness of breath. An example of this would be:
MODERATE
SOMEWHAT STRONG
Start with your arms stretched forward at shoulder height.
STRONG
Breathe in through your nose while bringing your out

stretched arms out to either side. Blow out through pursed
VERY STRONG
lips while bringing your arms back to the front and crossing
them in a scissoring manner. Repeat 10 times.
VERY, VERY STRONG
Adding scapular retraction exercises to stretch out
MAXIMAL
pectorals (i.e., pinching scapulas together) is helpful
Borg, G. (1982). Psychological Bases of Perceived Exertion, Medi

cine a/ld Science ill SPOI'IS ond Exercise. i 4, 380.
since these patients spend many of their days in for

ward flexion types of postures. These exercises help
with posture and help to increase lung expansion with
inspiration.
cardiovascular limitation, monitoring heart rate is not

an accurate measure of exercise intensity. Asking pa
tients to quantify their dyspnea is much more reliable.
Training Phase
After completing the warm-up exercises, patients
may now start their walks. The patients should prac
tice their purse-lipped breathing during their walking.
EXERCISE GUIDELINES
Walking for 12 minutes at a comfOltable pace to keep
After evaluating your patient's exercise capacity, the
breathing at a level 3 should be the goa\. Rest periods
exercise program can be developed. Structuring the
are acceptable during the 12-minute time. Another
program with the warm-up, training and cool-down
goal could be to minimize rest periods to the points
phases shouId be done.
where a patient could walk for 12 minutes nonstop.
Before starting exercise, purse-lipped breathing
The upper-body exercise session could consist of
should be taught since this should be used throughout
low-resistance, high-repetition exercises combined
the exercise session to control shortness of breath. In
with purse-lipped breathing to help with shortness of
struction for teaching this technique could be as fol
breath. These exercises could consist of PNF patterns
lows: patients should be instructed to take a relaxed
or of ring shifting, for example, at a level just above
breath in through their noses. The breaths should be
the shoulder. Light weights could be added as a pro
relaxed. They should not be forced. Exhalation
gression in addition to adding repetitions.
should be through pursed lips as if to blow out a can

dle. Again, expiration should not be forced.
Cool Down
The cool-down period would consist of repeating the
Warm-up
The exercise program should always start with warm
up exercises. Chair exercises are desirable, since sit
ting up to exercise can help conserve energy that the
patient will need for the training portion. Mixing
warm-up exercises at a pace where breathing would

be brought down to baseline.
Frequency
upper and lower body exercises should be done. Ex
Patients should exercise at least three to four times
amples of these exercises include arm scissoring,
per week.
422
PART III
Interventions
Intensity
more commonly used because walking and running
Patients should exercise so that their breathing
are more natural activities. A
how hard
to reach his or her maximum oxygen consumption
are working. We advocate that
work no higher than a level 3. After the cool-down

breathing should be at baseline.
is more likely
and heart rate. However, ECG recordings tend to

have more artifact and blood pressure
are
more difficult to obtain at high intensities. If tread

mill testing is the
Termination of Exercise Testing or Training

Several
or symptoms will alert the therapist that

This chapter focuses
the session should be
clinical situations not using electrocardio

(ECG) or sophisticated monitoring systems.
response must be watched
closely, such as facial appearance of
in
in addition, blood
creased use of accessory
are
pressure, heart rate, and pulse oximeter
of choice, there are sev
eral different
protocols that use different
combinations of
elevation and belt
type of treadmill test used
The
on the fitness
level of the patient and the reason for doing the test.
For example, certain
protocols may be used
to test initial aerobic fitness levels in

individuals and athletes and then for
fects of their training programs. Another type of
treadmill test may be used to
diagnose cardiac
very important. Exercise should be terminated in any
disease. The two most
of the following situations:
the Bruce and Bakke exercise tests. They have nor
used protocols are
Patient
mative data from which functional aerobic
Chest pain occurs or increases from patient's
ment can be calculated.
normal
Patient appears pale and skin is diaphoretic
Energy Conservation and Work Simplification
elevated or
Blood pressure is
with exercise
with energy conservation and work
Patient complains of leg cramping
fication techniques is an important component of
Oxygen saturation drops below 90%
cardiopulmonary
Patient complains of dizziness
tient's work
Patient's coordination is affected by increased
tion with the goal of achieving increased functional
muscle weakness and
An
of the pa
for modifica
life needs to be stressed. A brief
with prolonged ex
ercise
rices to patients.
TESTING
TRADITIDNAl
Since most individuals have been accustomed to a
without shortness of breath from
For those
faster oaced life. oacing is a basic conceot worth dis-
lung disease or cardiac failure who could tolerate

there are more traditional
exercise
slow down when walking or climbing stairs. Patients
The primary modalities used
will not be as tired and out of breath when reaching
There
their destinations. Rest periods should be planned
are bicycle ergometry and treadmill

are
and
to
it is
that are useful in assess-
to both. ECG
the
If wasting time is a concern while
monitoring and blood pressure readings may be more
taking a break, reading a book or doing some hand
easily obtained if a
work may make this time more worthwhile.
the
is tested on a
to this modality is that
this is not as familiar an activity to some
a cart to carry items is quite helpful.
as
activity while
walking. Therefore maximal heart rates may not be
creases oxygen consumption when
achieved because of leg fatigue. Treadmill testing is
gen consumption is increased,
items in
If oxy
require
23
423
ments also will be increased as described previously.
3. Explain the physiological benefits of exercise
Shortness of breath will increase. If a shopping cart is
training with COPD and the perceived mecha
used, leaning on the cart to take a rest will help to
nisms of improvement.
4. Name the components of a pulmonary rehabilita
keep breathing under control.

Sitting down to work is an energy saver because it
saves the legs the work of standing. Standing in the
bathroom to shave or wash at the sink can be elimi
tion program.
5. Name and discuss techniques of energy conser
vation.
nated by placing a chair in front of the sink or by sit

ting on the toilet-seat lid. Buying a shower chair
helps make washing easier. After coming out of the
References
shower or bath, wrapping up in a terry-cloth robe and
American College of Sports Medicine. (1993). Resource manual
sitting on the toilet-seat lid can help the patient catch
for guidelines for exercise testing and prescription (2nd ed.).
his or her breath while drying off. An ironing board

can be used as an adjustable table. Setting it at low
levels can help with meal preparation while sitting.
Philadelphia: Lea
& Febiger.
Belman, M.1. (1989). Exercise in chronic obstructive pulmonary

disease, in Franklin, B.A., Gordon, S.,
& Timmis,
G.e. (Eds.).
Exercise in modern medicine. Baltimore: Williams a n d
Organizing work areas can help eliminate unnec

essary reaching. Items used most often should be kept
at a level between the shoulders and the hips. Heavy
appliances can be kept out on counter tops or on the
stove so that bending, stooping, and lifting is elimi
nated. Before cooking, filling the sink with soapy
water and putting dirty dishes and utensils in immedi
ately makes clean up easier. A dustpan with a long
handle eliminates bending over when sweeping up.
Understanding the development of shortness of
Wilkins.
Borg, G. (1982). Psychological Bases of Perceived Exertion, Medi
cine and science in sports and exercise, /4,378.
Casey, L.e.,
diopulmonary exercise testing. Philadelphia: WB Saunders.
obstructive pulmonary disease, Chest,

Celli, B.R., Rassulo, J.,
equipment for evaluating and training athletes. In ad

dition to improvements in functional capacity, these
patients may also show some desensitization to their
shortness of breath with an overall improvement in
their sense of well-being.
&
79,
393-398.
Make, B.1. (1986). Dyssynchronous
breathing during arm but not leg exercise in patients with

icine,
testing to sophisticated use of metabolic carts and
Wilson, A.F.
chronic airflow obstruction, The New England Journal of Med

Criner, G.1.,
ing can range from simple, cost-effective in-home
&
(1981). Effects of breathing retraining in patients with chronic
and then evaluating them appropriately for exercise

programs will help these patients improve their func
K.T. (1986) Chronic lung disease and chest
Casciari, R.1., Fairshter, R.D., Morrison, J.T.
breath in individuals with cardiopulmonary disease
tional capacity for activity. Exercise testing and train
& Weber,
wall deformities. In Weber, K.T., Janicki, J.S. (Eds.). Car
314, 1485-1490.
& Celli, B.R.
(1988). Effect of unsupported arm exer
cise of ventilatory muscle recruitment in patients with severe

chronic airflow obstruction, American Review of Respiratory
Disease,
138.
856-861.
&
McGavin, e.R., Gupta, S.P.,
McHardy, G.J.R. (1976). Twelve
minute walking test for assessing disability in chronic bronchi

tis, British Medical Journal,
Reis, A.L., Ellis, B.,
&
I,
822-823.
Hawkins, R.W. (1988). Upper extremity
exercise training in chronic obstructive pulmonary disease,

Chest,
Tangri, S.,
93, 688-692.
& Woolf, e.R.
(1973). The breathing pattern in chronic
obstructive lung disease during the performance of some com
63, 126-127.
& Ross. J.e. (1966f
mon daily activities, Chest,

Thoman, R.L Stroker, G.L.,
REVIEW QUESTIONS
The efficacy of
pursed-lips breathing in patients with chronic obstructive pul
1. Name and explain four limiting factors of exer

cise in the patient with COPD.
monary disease, American Review of Respiratory Disease,

Weber, K.T.,
2. Explain traditional measures of exercise capac

ity. Which ones are useful for measuring exer
93.
100-106.
&
Szidon, J.P.
(J 986)
Exertional dyspnea. In Weber,
K.T., Janicki, J.S. (Eds.): Cardiopulmonary exercise testing.

cise capacity in COPD?
Exercise Testing and Training:

Secondary Cardiopulmonary
Dysfunction
Phyllis G. Krug
KEY TERMS
Exercise blood gases
Respiratory muscle endurance
Nocturnal ventilation
Respiratory muscle fatigue
Oxygen desaturation
Respiratory muscle strength
INTRODUCTION
every system in the body can develop a disorder that
When considering the sensation of shortness of
can have respiratory consequences. It is most effi
breath, one typically pictures someone afflicted with
cient to discuss the more common disorders that pre
a lung disease, such as asthma, bronchitis, emphy
sent themselves clinically. Case studies are presented
sema, or the like. A largely neglected area from the
at the end of the chapter to further elucidate and clar
perspective of physical therapy and rehabilitation is
ify the process clinically.
that population that develops rt:spiratory limitations

secondary to other disease processes.
Secondary respiratory problems are those restric
Psychological Factors
tions arising out of pathology other than primary lung
With respect to shortness of breath, studies related to
disease. Patients falling into this category present
those with the diagnosis of chronic obstructive lung
with a vast atTay of underlying pathologies. Virtually
diseases have shown that people tolerate shorlnt:ss of

425
426
PART III
breath up to 10 years before seeking medical <lttention
review presented here, notes arc included to encour
(Black, 1982). The patient usually attributes the symp
age critical analysis of diagnostic material.
toms to aging and lack of exercise before considering
a medical reason. It has even been documented that

patients will curtail activities, social and recreational,
Pulmonary functions tests (PFTs) are used to evaluate
before seeking medical advice. By the time medical
flow rates and volume capacities of the lung. Detailed
attention is sought, a damaging cycle has been estab
descriptions of these are presented in Chapter 8. Un
lished (Figure 24-1). The results of inactivity con
derlying assumptions in these reports are that a patient
tribute to feelings of inadequacy and poor self image.
(1) has cooperated with the testing procedure, (2) has
The inactivity itself fosters and encourages atrophy,
understood the procedure and, (3) has normal respira
not only in the extremities where it is visibly apparent
tory muscle strength to accomplish the test. Let's try
but also in the respiratory muscles. This fUlther adds
and understand the factors that could blur optimal re
to the debilitating process, creating secondary weak
sults when taking a pulmonary function test. If a result
ness and disabilities that are not necessary and are
is produced that shows the patient has poor lung ca
avoidable. These issues are further addressed in the
pacity, you could walk away thinking. "Wow, that's a
approach to treatment and in the case studies.
really sick person there, most probably there isn't

much I can do to help because he is so restricted in
lung capacity." If you look further and investigate the
EVALUATION
possibilities, you begin to open windows or possibili
The evaluation begins before the patient arrives. It
ties for improvement. If there is weakness of the res
begins with the information collected from the diag
piratory muscles, then the results obtained reflect the
nostic data. Great benefits can be gained from under
patient's breathing capacity based on weak muscles.
standing the information, but it is equally essential to
This leaves open the option of improving the respira
recognize its limitations.
tory muscle strength to see how it may affect the ven

tilatory capacity. Once you begin to think critically,
Critical Usage of Pulmonary Diagnostic Reports
many windows may become apparent that can provide

options for improving the results. For example, if a
The diagnostic criteria for secondary cardiopul
patient with scoliosis has reduced volume capacity, it
monary dysfunction is similar to diagnosis criteria for
is unclear if it is a fixed piece of data or if there is
primary cardiopulmonary dysfunction. In the short
room for improvement from the perspective of posture

and strength. The volume and flow measurements of a
patient with a lot of secretions would be reduced be
cause of the obstructive nature of the mucus. If that
patient was on an aggressive program of postural
THE FOUR Ds
/
Progression
Depression
drainage, would those values improve? Address
Disease
whether the values obtained in the pulmonary function

tests reflect a fixed, irreversible value. The author's
Dyspnea
clinical experience demonstrates that interventions ad

dressing posture, strength, endurance, and optimal
clearance of mucus work to improve values otherwise
Deconditioning
believed to be unchangeable.
X-ray
FIGURE 24-1
Flow of progression of respiratory disability. This
The use of x-ray testing is critical in identifying infil
demonstrates the chronic cyclic pattern that haastens
trates, pneumonias, tumors, and obstructions. Yet it
deterioration and death.
too has its limitations and should not be relied on
24
Exercise Testing and Training: Secondary Cardiopulmonary Dysfunction
427
solely to assess a patient's capabilities. Mr. K had a
stood that patients will be more comfortable and
diagnosis of chronic obstructive lung disease with ex
probably perform better on equipment that mimic
tensive scarring from old tuberculosis. His x-ray was
their present life styles. Although the step test that
opaque. No viable ventilating lung tissue was seen on
has the patient going up and down a step at a given
the left side. Ausculation with a stethoscope revealed
rate is effective in identifying a change in the blood
no breath sounds. Yet after months of breathing re
gases, a patient may feel more comfortable and be
training, thoracolumbar mobilization and soft tissue
able to last longer on either a bicycle or treadmill.
mobilization, this patient established a most definite
Furthermore, during a step test, the patient may fa
improvement in breath sounds on the left side. No
tigue after only a few repetitions. There is more op
improvement was noted in his x-ray. So, our tools are
portunity to evaluate the following: (I) how quickly
helpful to a point, and we should always give our pa
the gases change, (2) if they improve over time, and
(3) the dynam ics of breath ing mechanics when
tient the benefit of the doubt and try.
choosing a modality that the patient may be able to
Auscultation
sustain over a longer period of time.
The stethoscope is effective in identifying many ab

normalities within the lung, such as bronchospasm,
mucous collection, consolidations, and infiltrates. Yet

The foundation of the respiratory system's ability to
it is not uncommon to hear perfectly normal breath
work is the strength and endurance of the respiratory
sounds, and the patient will still report tightness in the
muscles. Strength and endurance form the foundation
chest, wheezing, and even congestion. It is always im
because breathing is an ongoing activity from which
portant to have the patient cough or breathe deeply to
the body cannot take a vacation; it requires the en
increase the flow of air so as to pick up any of these
durance to continue without stopping. There are times
abnormalities. Yet even if this is done and the breath
when the respiratory system requires sudden bursts of
sounds seem normal, always defer to the patient.
increased strength, as is evidenced by the need to

cough. Factors predisposing to fatigue are related to
muscular ability, ventilatory mechanics, reduction of
Arterial blood gases are designed to measure the
energy supply by hypoxemia, reduced cardiac output,
level of oxygen, carbon, dioxide, and pH in the arter
and malnutrition. The measure of respiratory muscle
ial blood (see Chapter 9). It reflects how effectively
strength is done via a gauge that measures inspiratory
the respiratory system is working in supplying the
muscle strength and expiratory muscle strength (PI
body with the fuel to carry on the task of living. It is
max and PE max). A patient unable to generate 60%
quite common to receive an order for physical ther
to 80% of these values reflects respiratory muscle
apy including exercise with the information that the
weakness (Edwards, 1978). A patient who is unable to
blood gases are within normal limits. It is critical to
maintain expected respiratory muscle force with con
identify if the blood gas values were taken at rest or
tinued or repeated contraction demonstrates the level
after exercise. If exercise blood gases are not i n
of respiratory muscle fatigue, which is the precursor
eluded in the report, there is no way of knowing how
of respiratory failure (see box below). A thorough
the patient's oxygenation will be affected by activity

(desaturation). It is possible to have normal resting
blood gases that drop precipitously with activity. This
can be a result of limited ventilatory ability or venti
lation-perfusion mismatch. It is the responsibility of
the therapist of a patient with compromised ventila
Clinical Signs of Respiratory Muscle Fatigue

Hypoventilation
Rapid shallow breathing
tory ability to request exercise blood gases or use an
Paradoxical breathing
oximeter to determine if desaturation is occurring. In
Increased Paco2
discussing exercise blood gases, it should be under
428
PART III
background on a patient includes information on the
100
strength and endurance of the respiratory muscles so

that an effective, practical intervention program can
be planned. An aggressive exercise program cannot be
initiated if a patient is unable to sustain ventilation to
properly oxygenate the body. If a patient is in a state
of respiratory muscle weakness and is then expected
to perform aggressively on a bicycle or treadmill, one
can inadvertently push the patient into respiratory fa
..0
::c
C
75
50
Qi
0...
tigue and possibly failure.
History-Critical Listening
In attaining a history from the patient, it is critical to
27 40
P02
work slowly, so that the patient feels comfortable,

and to encourage what could be deemed as simple
chatter. After discussing a patient's personal inter
ests, family, and home life you will have the informa
tion to recommend an intervention program that will
60
80
mm
100
150
Hg
FIGURE 24-2
Oxyhemoglobin dissociation curve. Demonstrates the point
at which oxygen saturation drops precipitously to between
40 and 60111111 Hg
be beneficial for the patient and that the patient will

actually do. If it is felt that the patient can improve
ally open the perspective of hope for improvement.
his or her endurance to be able to walk a mile and the
Because it is not just one system that becomes sud
patient is only interested in walking a few blocks, the
denly ineffective, physical therapists have the latitude
goals have to be set accordingly. Some therapeutic
to explore the full course of the history and look for
techniques require a quiet passive posture by the pa
the gaps where an intervention can be directed. Has
tient. A more tense individual who is pressed for time
posture changed over time? Has there been progres
will not tolerate that kind of intervention. It is there
sive weakness? Have activity levels diminished?
fore crucial to take the time to get the total picture.

From the perspective of the history of respiratory
Were there frequent respiratory infections? Re

sponses to each of these questions can greatly influ
symptomatology, it is common to hear, "I don't know
ence factors in a rehabilitation program. If a patient's
what happened, I was doing just great until r got that
posture deteriorated over the years, compromising
cold ... then it all fell apart." Pursue the investiga
respiratory ability, a program of stretching and
tion, because undoubtedly the history is much longer.
strengthening of the postural musculature may pro
The difference is that the patient was able to cope and
vide sufficient space in the thoracic wall for im
the presenting situation became excessive. The oxy
proved lung capacity and oxygenation. It takes a
hemoglobin dissociation curve in Figure 24-2 demon
small amount of objective improvement to make a
strates the underlying physiological process (Stoller,
big difference in the quality of life for the individual.
1988). Looking at the S curve, one can see that above
Regardless of the underlying cause, attaining a Pao2
60 mm Hg the curve is fairly flat, and Joss or deple
of at least 60 mm Hg is the primary concern.
tion of oxygen above the level can go undetected
Because the work of breathing becomes very diffi
clinically. However, as the curve demonstrates, there
cult in primary lung diseases or restrictions secondary
is a critical point around the Pao2 of 60 where the
to other disease processes, the symptomatic presenta
person will "suddenly" experience severe shortness
tions can be quite similar. It very closely simulates
of breath. In reality the oxygen level was dropping
the posture of the marathon runner at the end of a
progressively over time but was only critically felt at
run. The runner assumes a bent forward posture,
the drop of the curve. Understanding the progression
leaning on a wall or gaining support by leaning on
of the deterioration with shortness of breath can actu
the knees (Figure 24-3). This position is optimal for
24
Exercise Testing and Tmining: Secondary Cardiopulmonary Dysfunction
FIGURE 24-3
The flexed fOlward posture held when experiencing sho rtne ss of breath. Simi lari t ies between the healthy
marathon runner and the person with chronic respiratory difficulty should be considered in reference to
muscular, skeletal and pressure changes. (Courtesy of David Gorman, The Body Moveahle)
429
430
PART III
enhancing diaphragmatic excursion. After a few mO
baseline exercise test to identify exercise capability.
ments, the runner will get up and walk away. Unfor
It would be premature to begin an exercise training
tunately, the patient experiencing shortness of breath
program. The first step wou Id be to address improve
stays in that bent forward position. A patient may
ment of strength and posture. The goal is directed to
stay that way because it is easier to breath or because
ward improvement in height, lung capacity, and mus
he or she does not realize the precipitating event has
cle strength. The baseline data on the exercise test
passed. The point of emphasis is that any chronic dis
would likely improve. An exercise test subsequent to
ease resulting in shortness of breath will have pos
postural improvement would be a better baseline for
tural effects. Look for limitation in range of motion
an endurance training program.
of the hips and poor mobility of the thorax and the
For the patient with underlying neuromuscular
pelvis. This can be evident in a gait pattern that has
disease, an endurance training program may overfa
minimal rotation of the thorax on the pelvis. The
tigue muscle groups and cause damage. Therefore
stride length will be shortened, with minimal arm
the exercise test, again, is to get a baseline of exer
swing and an overall stiff, nonfluid gait pattern. The
cise ability. The therapeutic intervention would be
gait pattern of those suffering with chronic shortness
directed toward muscle re-education, postural exer
of breath and its associated postural changes can be
cises, and strengthening to help the patient move
described as walking cinder blocks, implying that the
more efficiently and reduce stress on the affected
muscles from the neck to the pelvis are fixed and do
m u s culature. The i m p r ovement in posture and

strength provides a better baseline to sustain an exer
not allow for normal reciprocal movement.
cise test and subsequent training.

A timed-walk test for a patient with severe limita
Exercise Testing
tion would be appropriate. Measure a walkway in
Exercise testing is performed for a variety of reasons.

It is a means of
(1) gaining baseline information of

(2) assessing functional
10-
foot increments and then time the distance walked for

either 6 or
12 minutes. It may be necessary to further

2 minutes.
the patient's activity level,
modify this test into distance walked for
(3) prescribing graded-exercise programs, and

(4) evaluating cardiovascular ability. The choice of
as possible for the timed segment. Record distance
ability,
Instruct the patient to walk as far as possible as fast
exercise testing should reflect the needs of the pa
walked. Monitor the blood pressure, heart rate, respi
tient, the cost-effectiveness of the procedure, and the
ratory rate, ventilatory muscle use, and O2 saturation.
consideration for the need of extensive diagnostic in
A patient at a higher level of function may benefit
formation and its practical application into the pa
from a more aggressive exercise test that allows for a
tient's life. The patient's addressed in this chapter are
more accurate level of cardiovascular response to ex
by and large severely limited in their physical abili
ercise as a basel ine for prescription for endurance
ties because of their underlying disease processes and
training. A baseline level is first obtained from the
their secondary respiratory effects. Typically the
timed-walk test or the patient can walk on the tread
overall presentation is one of atrophy, decondition
mill at 1 to 2 mph, 0% grade for 6 minutes.
ing, and poor mobility that greatly limits the distance
A patient whose exercise ability is limited by respi
walked. The severely limited patient would benefit
ratory factors before the healt rate or blood pressure is
with a simplified exercise test to identify exercise ca
even elevated does not rt;quire a full-graded exercise
pacity. When considering the patient with secondary
test with full ECG, metabolic gas analysis, heart rate,
cardiopulmonary restriction, treatment should be
and blood pressure measures. Interest should be more
aimed at improving the cardiopulmonary status con
directed toward the following:
current to the underlying primary process. A few ex
son walk,
amples can better illustrate this point. The scoliosis
(I) how far can this per

(2) what happens to his breathing pattern and
respiratory rate, and (3) does the oxygen saturation
patient who has progression of the spinal deformity
drop. Based on this, recommendations can be made for
and secondary pulmonary compromise requires a
use of supplemental oxygen and possibly more efficient
24
breathing patterns to allow the patient to persevere

longer. For example, if a patient has a diffusion prob
lem or a ventilation/perfusion mismatch, it would be
helpful to evaluate whether a slower pace would allow
the patient to walk longer. Consider enhancing the time
allowed for diffusion of the oxygen. It may be found
that a slower pace, with attention directed toward deep
effective breathing, may yield different values in oxy
gen saturation and the distance walked. The choice of
testing modality should also take place or location into
consideration. It seems inappropriate to demand that a
severely limited patient being seen in the home undergo
extensive graded-exercise testing before recommending
an exercise program. The choice of exercise testing
should reflect the goals of the patient. If the patient is
ready for an aggressive exercise program, then more
extensive testing is appropriate. Testing can then
progress to stage II. A treadmill stess test begins with a
speed that is comfortable for the patient-usually be
tween 2 to 3 mph. Work is increased every 3 minutes
by either increasing the speed or the incline. It is rec
ommended to increase the speed by 0.5 mph incre
ments, maintain it at a comfortable walking pace, and
progress the incline by 2.5% increments after a com
fortable pace has been established. Measurement of
heart rate and blood pressure should be taken at the end
of each 3-minute stage and Sa02 oxygen saturation
should be monitored throughout and recorded at the be
ginning and end of each stage.
The test is terminated in the following situations:
(I) when the patient reaches 65% to 75% of predicted
maximal heart rate, (2) if oxygen saturation drops
below 90%, (3) if the blood pressure drops with in
creasing activity, or (4) the patient experiences symp
toms of shortness of breath or muscular discomfort.
If a patient is able to reach 65% of predicted
maximum heart rate without cardiop u l monary
symptoms, then the patient is capable of exercise
conditioning. Oxygen saturation should be above
90%. Below this level requires supplemental oxy
gen. If the carbon dioxide (C02) increases more that
10 torr of resting level, the patient will be limited in
exercise potential. Individuals who reach their maxi
mum volume ventilation (MVV) with minimum in
tensity exercise may have difficulty with an en
durance training program.
431
Exercise Training
Design of an exercise prescription must be individu
alized and must be prescribed within both useful and
achievable levels.
Exercise training should not be limited to a mode
of exercise equipment, duration of time, or fre
quency. A person with a chronic condition has
chronic manifestations physically and psychologi
cally. Therapy directed toward the chronic physical
changes, that is, postural and overall movement, can
result in improved endurance. This perspective
should be seriously considered before using preciolls
therapeutic time to put a patient on a treadmill three
times per week to measure a heart rate that does not
elevate because the patient is too short of breath. The
severely limited patient may benefit from general
body movement for a duration of 10 to 15 minutes. It
could include standing and leaning on a chair and
shifting the hips to the rhythm of music. The goal is
initially just to move, create a challenge to the car
diorespiratory system, focus on controlled hrcathing,
and show the patient that he or she can sustai n move
ment for prolonged periods. The therapeutic ball has
proven to be beneficial. The 65-cm ball is a good
size for a patient to sit on (Figure 24-4). It provides
support yet allows for movement. Many severely
limited patients have been able to sit on a ball shift
ing their weight from side to side, working on leg
strengthening, pelvic and spinal mobility, and chal
lenging the cardiorespiratory system. Once a capahle
patient becomes interested in a traditional endurance
training program, the graded-exercise test can pro
vide the necessary information to prescribe one. The
prescription should include intensity, duration, fre
quency, and modality as follows: (I) Intensity is
based on 65% to 80% of the predicted heart rate or a
level where the patient becomes symptomatic or the
oxygen saturation drops to 90O/C . Consider, for exam
ple, an exercise test that is terminated after walking
at a speed of 3 mph, at a 5% elevation, 3 minutes
into lhat level. If the limiting factor was shortness of
breath with a drop in oxygenation, further testing
should be conducted with the use of supplemental
oxygen. If the limiting factor was shortness of breath
without a drop in oxygen, 2.5 mph at 0% elevation
can be used as a 5-minute warm-lip, followed by
432
PART III
training at 3 mph for up to 15 minutes with I minute
Caution is advised in understanding the underly
intervals at 2.5% elevation followed by a cool down
ing pathology that resulted in cardiopulmonary limi
of 2.5 mph, 0% elevation, for 5 minutes. (2) Dura
tations. Post polio syndrome is characterized by
tion of exercise is 15 to 30 minutes per session. Ini
muscles that were weakened during the initial onset
tially this can be broken down into interval training
of the disease and more recently report a recurrence
where short 1- to 2-minute rest periods can be used
of symptoms. Studies have shown that these patients
progressively, lengthening the intervals until the pa
benefit from strengthening and endurance exercise,
tient is able to maintain a c o ntinuous session.
but extreme caution must be directed toward avoid
(3) Frequency of e xercise is three to five times a
ing overuse (Dean, 1991 a; Owen, (985). The patient
week on alternate days. (4) Modality depends on pa
will benefit from a carefully considered, judicious
tient comfort. The target heart rate, or the level be
exercise program.
fore the patient developed symptoms, is used as the

training level. Flexibility exercises or slow walking
are recommended for warm-up before the endurance
exercise program.
SYSTEMATIC APPROACH IN THE

REHABILITATION PROCESS
Nocturnal Ventilation-The Role of Rest
and the Respiratory Muscles
At this point the therapist is equipped with a vast
array of information. The question is how to plan an
effective intervention. Clinical experience has shown
the importance of first directing attention toward the
work of breathing. The literature is filled with discus
sions about the role of resting the respiratory muscles
(Braun, 1983). It is suggested that one of the factors
leading to respiratory failure is the respiratory mus
cles' inability to keep up with the demand of breath
ing. If we consider the patient with severe scoliosis,
the work of breathing is not shared equally by the
respiratory muscles because of distol1ion of the chest
wall. In addition, the curvature will add an additional
load on the energy expenditure of breathing. Like any
muscle in the muscular system, if a load is put on a
muscle, it will train and get stronger. Yet, if this goes
on for an extended period of time the muscle will be
unable to maintain the added work load and the mus
cle fibers themselves will begin to break down. This
process is well understood in the fields of sports med
icine and weight training. It is called overuse atrophy.
This process also occurs in the respiratory system. In
advising a patient in an exercise program, it is clitical
to be aware of how much we are asking our patients
to do. We walk a narrow path between (I) doing
nothing and allowing the patient to accept life with
FIGURE 24-4
Therapeutic ball as part of a program of improving mobility
the shortness of breath and promote further atrophy
and endurance.
and (2) pushing too hard and risking breakdown of
24
Exercise Testing aod Training: Secondary Cardiopulmonary Dysfunction
433
the respiratory system. It is the responsibility of the
for good clinical judgement. Sometimes the patient
therapist to be aware of the diagnostic and clinical
has a bad day and just does not do well, other times
signs of respiratory muscle fatigue.
he or she may be in trouble.
Diagnostic criteria for respiratory muscle fatigue

include the following: (I) increasing pulmonary arte
rial carbon dioxide (Paco2). (2) reduction of high
Managing the patient with clinical
signs of respiratory fatigue
frequency signals (greatcr than 80 Hz) of muscular
If the patient has a prcscription for oxygen, make
activity on electromyography studies (EMG) despite
sure he or she is using it. Get the patient comfortable
continued contraction and dominance of the low
and use your hands to guide the body into shifting the
frequency signals (lcss than 80 Hz), (3) reduction of
work of breathing. This is a very critical factor. In
vital capacity with decrcascs in supine ye t o 50% of
dealing with acute shortncss of breath or muscle fa
sitting Ye, and (4) inspiratory muscle prcssure to
tigue the patient undoubtedly will be in a state of
below 66% of predicted mean.
panic. Panic complicates the situation by increasing
The clinical signs of rcspiratory muscle fatigue in
the respiratory rate and consequently reducing tidal
clude the following: (I) paradoxical breathing, (2) in
volume. The gentle placement of the therapist's
creased respiratory rate, and (3) shallow breathing
hands on the lower rib cage along with a calm, firm,
(see box below). First and foremost, we arc looking
soothing voice can hclp guide the patient into a more
at change from normal. This is where good baseline
calm, efficient breathing pattern. Studies have shown
information is critical. Baseline blood gases, the pa
that tension alone can reduce the expiratory flow rate,
tient's typical breathing patterns, and the baseline for
so the therapist's role in calming the patient is di
dyspnea should be considered. This is a critical area
rectly related to improving the breathing pattern

(Kotses, 1981).
Resting the respiratory muscles

There is increasing interest in the role of resting the
respiratory muscles before it reaches the stage of res
Respiratory Muscle Function Assessment
Pulmonary function test
Respiratory muscle strength
piratory fatigue and failure. This is accomplished

through nocturnal ventilation using positive- or nega
Effort and strength dependent
tive-pressure ventilators (Figures 24-5 and 24-6). The

focus is to increase muscle energy supplies and
stores. Mechanical ventilation will assume the work
PI max-inspiratory pressure
of the respiratory muscles and allow them to rest.
PE max-expiratory pressure
This may allow the time needed to reverse the factors
Respiratory muscle fatigue
that led to fatigue. It substantially reduces the oxygen
60% to 80% PI max
consumption of the respiratory muscles, allowing for
Respiratory muscle enduram:e
more oxygen to reach the other tissues. Studies have
Maximum volume ventilation
shown that after a mean period of approximately 5
Maximum sustainable ventilation
months at home on daily 4- to IO-hour ventilatory

support, there are significant increases in vital capac
80% MVV for 5 minutes or 60% MVV

for 15 minutes
ity, PI max, and PE max (Marino, 1982). It also

showed a reduction in Paco2 along with a reduction
Fatigue: when Ve <minute ventilation)
in hospitalizations and the number of days hospital

ized. The topic of resting the respiratory system adds
NOTE:
Inability to reach
ness or fatigue.
predicted value reflects muscle weak
a different perspective in regard to traditional pul

monary rehabi litation programs promoted. Before
434
PART III
FIGURE 24-5
Positive pressure ventilator used for nocturnal ventilation.
FIGURE 24-6
Negative pressure ventilator used for nocturnal ventilation.
24
435
initiating a progressive exercise program or for that
breath hold. Activities can be divided into two cate
matter, any sort of exercise program, it is important
gories. Static activities and rhythmic activities. Static
to assess the level of respiratory fatigue under which
activities are those that are done once. For instance,
the patient is living. Symptoms, clinical observations,
picking up a shoe. It is done once, until you are ready
or historical findings that are suggestive of further in
for the second shoe. The first rule of thumb is to take
vestigation into the benefit of nocturnal ventilation
a breath in before the activity to supply the body with
include sleep disorder, progressi ve dyspnea, hyper
the oxygen it needs, then exhale with the activity. It
capnia, and dyscoordinate breathing patterns. It has
is simple but it actually helps, and the patient is able
been recommended that a patient be allowed suffi
to perform an activity with less shortness of breath.
cient time to adjust to nocturnal ventilation before ad
The second rule of thumb is to maintain a rhythm
vancing into an active exercise program. This deci
with activity. If the activity is washing dishes, vacu
sion must be made with medical guidance. It is
uming the carpet, or climbing some stairs, the focus
sometimes recommended that a patient rest on this
is to maintain a rhythm. That rhythm will change as
system for a few months to allow the body to reach a
the activity continues, but the idea is to control it
stable level of metabolic rest.
through the purse-lip breathing. For example, climb
BREATHING TRAINING
ficult with each step. Breathe in on step one and ex
ing stairs may begin with ease and become more dif
hale for step two, three, and four. As the activity
Paced Breathing
continues, modify according to the patient's need. It
These techniques are taught regardless of which mus
may progress to breathing in on one step and doing
cles patient uses to breathe. Because breathing is
the fu II exhalation on the second step. The patient
something we do all day lon , it is unfair to expect
may still experience shortness of breath but will have
patients to alter their breathing continuously. There
better control and get further.
fore it is helpful to break down breathing into various

components. Foremost is coordinating breathing with
activity. If a patient is short of breath, he or she needs
to know how to get it back. Pursed-lip breathing is an
Signs of Improvement
The direction toward improved posture and more effi
effective means of helping. Pursed-lip breathing
cient quality of movement is a slower process and
works as the center for controlling the respiratory rate
should be directed in the realm of kinesthetic aware
and maintains more efficient emptying of the lung.
ness. If you are working with a patient and find that in a
Paced breathing and the rule of thumb are handy
certain posture you observed a better breathing pattern
tools that help get through daily activities. Breathing
or that with a certain relaxation technique the patient
has a rhythm of inhale and exhale. Generally, the ex
found relief, you want to harness that sensation. Repeat
hale is longer than the inhale. At rest and with vari
it, use tactile input, have the patient close his or her
ous relaxation techniques, it is possible to greatly ex
eyes and imagine it. If the patient has just learned to
tend the length of the exhale. For example, if at rest
relax the upper thorax and get a good expansion in the
the person inhales for a count of two, the exhalation
lower thorax, he or she will not be able to walk out of
might be for a count of four or five. With deeper re
that session and breathe that way continuously. How is
laxation the length of the exhalation can be extended
this new skill incorporated into a new pattern of breath
to the count of five, six, or even longer. Patients are
ing? It is effective to stop 20 to 30 times per day,

(1) pause, (2) relax the shoulders, (3) focus on the area
to expand, (4) do the breathing technique for a few rep
etitions, and (5) concentrate on it and put it away. The
encouraged to develop and heighten this sense of

awareness and begin to coordinate it with activity.
The concern is that frequently a person will perform
an activity (i.e., bending down to get a shoe, reaching
focus of this exercise is not strength training but rather
to open a door, washing hair, or lifting a package)
kinesthetic awareness. About 2 weeks of this compul
and during the activity actually stop breathing or
sive stopping, sensing. and being aware is enough time
436
PART III
that it becomes the way the patient breathes, becoming
parted slowly, as opposed to thrust or high-velocity
incorporated into the patient's pattern of breathing. This
manipulation. The intent is to regain normal active
obviously will not be successful with someone who
range of motion, thus improving alignment and
mechanically, muscularly, or neurally is incapable of
stress distribution. The improvement in joint func
this parit cular
tion increases a joint's adaptive potential to mechan
panded using the tools of imagery. Too often a patient
ical stress and reduces the possibility of re-injury to
is taught how to brcathc and does so beautifully in the
that joint.
therapy session and then resumes the old pattern after

leaving the office. It is a difficult task to incorporate a
movement performed in a static stationary position and
Soft Tissue Therapies
maintain it during the dynamics of daily life. The
The purpose of soft tissue therapy is to normalize ac
power of suggestion and imagery can be used here.
tivity of the muscle fibers, restore extensibility, and
This scenario becomes a home exercise program of
reduce pain. Soft tissue mobilization includes mas
gaining control of the breathing system. Even if the pa
sage, accupressure, and soft tissue stretching. It uses
tient cannot maintain it through the whole process, it is
low-intensity pressure and should not cause pain. If
a crucial activity in self-control and minimizes the
applied properly, its techniques should result in local
sense of panic that goes along with activities that result
and general relaxation, and reduction in tone. Myofa
in shortness of breath. It is a very beneficial activity
cial release is a method to normalize myofacial activ
that can then be further advanced while working on a
ity, regain tissue extensibility, and reduce pain. It is
bicycle or treadmill. The underlying emphasis is opti
based on neuroreflexive responses that reduce tissue
mizing the patient's efficiency of movement and
tension. With the appropriate application of manual
breathing and reducing the work of breathing.
contact and the determination of the best point of

entry into the musculoskeletal system, a relaxation of
tissue tension and decrease in myofascial tightness
OVERVIEW OF THERAPEUTIC OPTIONS
can be attained.
A myriad of therapeutic techniques exist that are vi
able options in trying to maximize breathing oppor

tunities. It is beyond the scope of this chapter to
elaborate on the technique, rationale, and method of
Neuromuscular Therapy
Proprioceptive neuromuscular facilitation is a method
all the options appropriate for the population. Once
of promoting the response of the neuromuscular
asked by a colleague the appropriate treatments for
mechanisms through stimulation of proprioceptors.
respiratory patients, I replied, "the same as with any
The application of a manual stimulus is used to elicit
disease process." Evaluate the total situation and
efficient neuromuscular responses. Its primary objec
plan an intervention that will reduce stress and in
tive is to develop trunk or proximal stability and con
crease opportunity. If the patient population has de
trol, as well as to coordinate mobility patterns. It can
veloped respiratory problems secondary to an under
be used to help stabilize vertebral motion and im
lying d i s e a s e, p o s ture, muscle l e n g t h , m u s c l e
prove spinal movement control.
strength, and endurance should be considered. The
Muscle energy works under the principle that
manual therapies are excellent vehicles in gaining
muscular activity can be used to restore physiologi

cal joint motion. It uses active muscle contraction
access to improvement.
at varying intensitics from a precisely controlled

position in a specific direction against a distinct
Mobilization: Thorax, Rib Cage, Pelvis,
counterforce. It is used to mobilize joint restric
Sacrum, Hip, Shoulders, and Neck
tions, strengthen weak musculature, stretch tight
Joint mobilization is a nonthrust manipulation. Pres
myofascia, reduce muscle tonus, and improve local
sures may vary from gentle to vigorous but are im
circulation.
24
Positional Release Therapies
437
through a treatment. Get comfortable hand contact
Strain/counterstrain is the passive placement of the
and feel the tissue soften in your hand, then wait.
body in a position of greatest comfort to reduce pain.
Watch what happens to the breathing. Hone in on any
Relief, if achieved by the reduction and arrest of con
changes and help the patient become aware of any
tinuing inappropriate proprioceptive activity, main
changes in the pattern of breathing. The diaphragm
tains the motion dysfunction. The underlying basis is
and thoracic release are also remarkably effective in
that every neuromuscular Clisorder has a palpable
encouraging greater thoracic expansion. These tech
point of tenderness and a position that can be ob
niques alone can be effective in relieving wheezing,
tained for comfort. It is a gentle, nontraumatic type of
improving aeration and even mobilizing secretions.
manipulation that is especially effective when irregu
Take the time to explore options. In reference to
lar neuromuscular activities have maintained and per
the cranial bones, restrictions in the movement of the
petuated abnormal mechanical stress to tissue. A re
temporal bones has been identified in those suffering
turn to normal length is achieved through positional
with shortness of breath, regardless of diagnosis. The
release of abnormal neuroreflexive activities.
temporal wobble therapy, ear pull, and finger in ear

(craniosacral technique) have also becn effective in
easing the work of breathing. The focus of the thera
Craniosacral Therapies
peutic intervention must be to find some relief from
Craniosacral therapy is a gentle hands-on method for
the work of breathing first and then begin a plan of
evaluating and treating problems affecting the cran
enhancement of relief followed by strengthening of
iosacral system. The craniosacral system provides the
those new found movements. Endurance activitics,
environment in which your brain and spinal cord de
that is, treadmills, bicycling or walking, are wonder
velop and function. The palpable parts of the cran
ful adjuncts after these important elements have been
iosacral system are the bones of the skull, sacrum,
addressed.
and coccyx, which attach to the membranes that en

close the cerebrospinal fluid. Treatment involves the
usage of fascial and soft tissue release techniques to
detect subtle biological movements. A 10-step proto
col is used for evaluating and treating the entire body.
CASE STUDIES
Poliomyelitis with Secondary Severe Kyphoscoliosis
Mr. L is a 65-year-old male with history of po
liomyelitis onset at the age of 8 years old. He was left
with a total paralysis of his left arm and a severe scol
Review
iosis secondary to muscle strength imbalance in the
In evaluating the disease process that results in respi
trunk. (Figure
ratory compromise, it is crucial to recognize the long
liomyelitis, his medical history was unremarkable. He
term chronic effects on the total body. It is short
lived independently in a fourth-floor walk-up apart
24-7). After recovery from the po
sighted to limit the focus to the thorax if there is a
ment and worked as a postal clerk until he was admit
respiratory problem. Take a step back and look at the
ted in respiratory failure. At that time his oxygen satu
total picture and look for those windows of improve
ration was 80%, his arterial carbon dioxide (Paco2)
ment. Some specific techniques have cdnsistently
was 61, and his arterial oxygen level (Pao2) was 53.
been helpful in helping ease the work of breathing.
His vital capacity was 1.8 liters-40% of predicted
Both myofacial release techniques and craniosacral
and his ECG showed right ventricular strain sec
therapies focus on the cranium and the sacrum. The
ondary to pulmonary hypertension. Additionally the
mobility of the sacrum and motion of the cranial
myocardium was situated in his right cavity secondary
bones have been shown clinically to be directly re
to pressure gradients that shifted it from its normal po
lated to the ease of breathing. The performance of
sition. His medical management required a tra
traction on the sacrum, a gentle hold, provides a re
cheostomy and respiratory support with a ventilator
lease on the thorax. The key is patience. Do not rush
and oxygen. He stabilized and was sent for an interim
438
PART III
Cal'diopulmonary Physical Therapy Interventions
The physical therapy program was problem

oriented and was modified throughout as the patient's
needs changed.
Problem 1: Shortness of breath

at rest and with activity
Mr. L was instructed in breathing techniques, includ
ing paced breathing, pursed-lip breathing, and relax
ation exercises to help relax the upper respiratory
muscles and encourage deeper, more efficient expan
sion of the thorax.
Problem 2: Paradoxical breathing pattern

Because of the severity of the curve, the thorax
moved in a rotation pattern to the right with the in
hale and to the left with the exhale. It was unclear
how much of this pattern was due to structural factors
or secondary weakness that allowed such severe dis
tortions. A path of exploration was initiated to find
potential areas of movement and to further evaluate if
there was potential to master those movements. Sub
tle movements were evoked in the cervical area and
initiated a treatment plan of soft tissue mobilization,
craniosacral therapy, and strengthening exercises.
The window found was that cervical traction allowed
FIGURE 24-7
Palil:nt with history of poliomyelitis and subsequent
development of severe scoliosis secondary to muscle
imbalances.
Mr. L to increase his head range of motion and he

was able to better relax his sternum and allow for
breathing from lower down. The terminology of
lower down is used because it is mechanically impos
sible for Mr. L to fully use his diaphragm. He was
of rehabilitation. At that facility he was accidentally ex
able to recruit other muscle groups, in addition to
tubated and the tracheal area was Iladly traumatized.
diaphragmatic, to allow for sufficient thoracic ex
The tracheal trauma left the patient comatose for 4 days.

About 2 weeks before the patient's respiratory
pansion relieving the excessive work of his upper

respiratory muscles.
failure, he was at a dinner with friends, and one of the
Aside from the primary paralysis of the left arm,
group videotaped the evening. The tape had invalu
the musculature of the left trunk was also weak and
able information in it. Firstly, in terms of posture, Mr.
kinesthetically deprived. The term kinesthetically de
L's head was totally sunk into the thoracic cavity
prived refers to the convex part of the curve that was
leaving him functionally without a neck. Around the
essentially folded inward in total paradoxical motion.
dinner table his friends were joking and remarking at
Mr. L was totally unaware of that part of his body and
how little he was eating. It is even more noteworthy
had no sense of movement. On soft issue mobilization
that he even dOI.cd during conversation at the table.
and tactile input on the left side, the patient began im
The labored breathing, the excessive use of the upper
mediately to expand on the left side of the thorax. Be
respiratory muscles, the sleepiness, loss of appetite,
cause of the severity of the curve, it would be impos
and lack of energy to eat his meal were all signs of
sible to have normal expansion on the left, but it was
pending respiratory fatigue and fail ure.
unclear if enough force and negative pressure could
24
439
be generated on the left to enable the patient to
with the patient reporting "Oh, I am getting more air!"
(I) shin the myocardium back into the left thoracic
This was easily confirmed; improved aeration was au
cavity, (2) increase his vital capacity enough to reduce
dible with the stethoscope.
his need for oxygen and possibly prevent future respi

ratory complications. Mr. L began a home program
using Theraband, which he looped around his left
shoulder and held across his chest with his right hand
(Figure 24-8). This position allowed him to grade re
sistance to scapular adduction, elevation, and depres
sion. He also used weights in trunk exercises. Therapy
sessions focused on manual techniques to mobilize the
rib cage, stretch the muscles, and release the connec
tive tissue. The technique of the diaphragm and tho
racic release were remarkably effective in opening the
breathing. This method alone was frequently effective
Problem 3: Poor endurance

Mr. L had become so deconditioned and anxious at
the thought of movement that he was unable to walk
even 20 feet. Outdoor ambulation created severe anx
iety for which he was receiving psychological ther
apy. He began a gradual program with walking in
place at 2-minute intervals. It is important to note that
he was extremely motivated and not only followed
his exercise program, but expanded on it (Figure 249). He also used the P-FJex respiratory muscle trainer
attached to his tracheotomy tube beginning on level I
for IS-minute intervals, twice a day.
After I year on the program, Mr. L grew in height
I 114 inches and increased his vital capacity by 700
ml, he no longer required supplementary oxygen, and

his myocardium shifted into the left thoracic cavity
without any signs of right ventricular strain. His ejec
tion fraction was 45%. He still demonstrated para
doxical motion with respiration, but there was a sig
nificant reduction in the amount of sucking in of the
lower rib cage on the left with inhalation. Ausculta
tion was remarkable with excellent breath sounds on
the left and right and some reduced air movement
near the lingula. Mr. L progressed up to walking in
place for 25 minutes with 2-pound weights in both
hands (he is able to clasp a weight with his paralyzed
hand) and attached to both ankles. He gained enough
motion in his neck to allow for full range of motion.
Because the pull of gravity will continually work
on Mr. L to pull him back into dysfunctional patterns,
it is impOltant to keep Mr. L on a program. He is seen
once every 2 months to modify and update his exer
cises and work on his trunk to ensure optimal thoracic
capability. Over this extended time other windows
have been found working on his sacrum and pelvis.
Manual traction, mobilization techniques, and soft tis
sue releases in these areas all provide for improved
thoracic expansion. Hand placement on the sacrum al
lows for a slow release and relaxation of the upper
chest. Manual techniques then followed, encouraging
FIGURE 24-8
Creative use of theraband in strengthening of the thoracic
progressively increasing diaphragmatic excursion. Mr.
musculature.
L is able to cue in to changes in his body and work on
440
PART III
Dystonia With Spasmodic Breathing

Ms. B is a 36-year-old psychologist with the diagno
sis of dystonia. She has a I O-ye ar history of torticollis
that has been treated with Botox. IL is a treatment
aimed at paralyzing selective muscle fibers to allow
for relief of severe spasms. She presented with recent

onset of shortness of breath and inability to get air.
On palpation over the lower rib cage and diaphragm,
it became evident that there was discoordinate move
ment of the thoracic musculature. It was unclear
whether this was merely discoordinate movement or
a function of the dystonia. The technique of diaphrag
matic release as demonstrated in craniosacral therapy
provided immediate release of the symptom of short
ness of breath and reduced the amount of discoordi
nate movement of the chest wall. Ms. B was taught
how to perform the technique on herself and was suc
cessful in the exercise. The P-Flcx was used to give
added resistance to her breathing as a means of ex
trasensory awareness. It gave her an added awareness
of movement of the thoracic wall and a means of
controlling it. The final phase of her therapy was

mild aerobic activity with the focus of coordinating
breathing with movement and increasing overall en
FIGURE 24-9
Respiratory muscle training in p a t ien t with tracheotomy.
durance. She was on a program for 6 months and was

followed once per week. Although her symptoms
persist sporadicalJy, she is able to catch it in time and
gain control of her brcathing. According to medical
opinion, it is likely that she has the rare progression
gaining sensory awareness of the area and aim toward

mastery and control of the movement.
of respiratory muscle dystonia. It is undear at this

time how this situation
will progress, but in the
meantime, she has the means of controlling discoor
Summary of problems
dinate movement and breathing with ease.
Mr. L benefitted from a program that focused on im

proving his total potential. He had the benefit of night
ventilation so that his body was rested. His total en
Postpolio Syndrome
durance capability was based on finding those win
Dr. 0 is a dentist teaching in a dental school and
dows of improvement. The improvement in align
conducting research in a laboratory. He has a his
ment and strengthening of the trunk and respiratory
tory of poliomyelitis with a possible diagnosis of
muscles provided for maximizing his respiratory ca
postpolio syndrome (PPS). Diagnosis is difficult
pabilities, overall endurance, and quality of life. At
because PPS is characterized by progressive weak
this point Mr. L is totally independent. He walks 3
ness and pain in the musculature that survived the
miles per day and goes out with his wife and friends.
original poliovirus. The underlying mechanism is
He has even traveled abroad with a foreign medical
still unclear; it is suggested that the progression is
supply company providing for his ventilatory needs.
resultant to long-term overuse and deterioration of
24
441
surviving muscle fibers. Studies show that the di
primary foundation of rehabilitation potential. Im
rection of therapy is to unload or rest the overused
provement in breathing capacity and overall en
muscles and shift the work of the musculature. It is
durance can be accomplished through techniques to
difficult in the therapeutic setting to identify the
improve posture overall. Endurance training based on
weakness that may be from PPS or weakness from
graded-exercise tests is an important element in the
simple aging and inactivity. Great caution is needed
rehabilitation program but should be placed
in this situation because studies have shown that if
spective to other therapeutic options.
10
per
the PPS muscles are overworked, it can result in

permanent irreversible damage. Dr. 0 presented
with the complaint of cervical pain. On evaluation,
it became evident that the pain was related to the
REVIEWaUESTIONS
1. What laboratory data are needed to determine if
cervical lordosis, resulting from the underlying
a patient is a candidate for endurance training?
muscle loss aggravated by the stooped posture nec
2. What types of treatment can be beneficial, if a
essary for his long hours of work in the laboratory.

Dr. 0 primarily relied on his upper respiratory mus
patient is not a candidate for endurance training?

3. What types of interventions can best help a patient
cles for breathing because of diaphragmatic paraly
enter into a more aggressive exercise program?
sis and extensive intercostal muscle loss. Dr. 0 did
4. Is aerobic training limited to treadmi I I and bicy
not have much time available for home exercise or
cle? Think about the limitations of these modali
for physical therapy sessions. Exercise prescrip
ties and suggest alternatives.
tions that would isolate the weak muscles and then

focus on repetitive exercises to strengthen them
would be problematic because of the threat of tissue
damage to muscles affected by PPS. Dr. 0 was
given one e x ercise to perform twice per day,
rolling, to roll from one end of the room to the
References
Astrand, P.
& Rodahl, K. (1977).
Physical Training. Textbook of
work physiology. New York: McGraw Hill.
Austin, J. (1992). Enhanced respiratory muscular function in nor
adults after lessons
other and back. He was guided in maintaining con
mal
trol of the trunk musculature throughout the activ
cation without exercise. Che,'I, 102,486-490.
ity. This activity was performed semi regularly for a

year with the goal of improving trunk strength and
posture. Over the course of the year, endurance ex
ercises were added using a home stationary bicycle.
In I year, Dr. 0 grew I 1/4 inches. He continued to
rely on the upper respiratory muscles for breathing,
but his overall improved strength and posture left
him pain free.
Basmajian,
Willian,s
in proprioceptive musculoskeletal edu
J. (1993). Rational
& Wilkins.
manu.al Iherapies. Baltimore:
Black, L. (1982), Early diagnosis of chronic obstructive pulmonary

disease, Mayo Clinic Proceeds 57,765-772,
Braun,
N, (1983), When should respiratory muscles be exercised?
Chest, 84,76.
Dean, E. (1991a), Clinical decision making in the management of the

late sequelae of poliomyelitis. Physical Therapy, 71.' 757-761.
Dean, E. (199Ib). Effect of modified aerobic training on move
ment energetics in polio survivor. Orthopedics, 14,1243-1246,
Edwards, R. (1978). Physiological analysis of skeletal muscle
weakness and fatigue, Clinical Science and Molecular Medi
SUMMARY
cine, 54,463.
A multitude of therapeutic options exist for those suf

fering with respiratory limitations. The presentation
of symptomatology of dyspnea is similar in primary
lung disease and in secondary cardiopulmonary
symptoms. It is crucial to understand the underlying
pathology so that the therapeutic intervention and ex
ercise prescription reflect the potential of the patient.
Focusing on issues of respiratory muscle fatigue is a
Feldman, R. (1985). The use of strengthening

polio seq uelae :
methods and results.
exercises in
po s t
Orthopedics, 81.889-891.
Gorman, D. The body moveable. Guelph, Ontario, Canada:Amper

sand Printing Co,
Kotses, H, (1981), "Application of biofeedback to the treatment of
asthma:
critical review, Biofeedback an d Self Regulation,
b,573-593.
Lisboa, C. (1985), Inspiratory muscle function in patients with se
vere kyphoscoliosis, American Review of Respiratory
132,48-51.
Disease,
442
PART III
Marino, W. (1982). Reversal of clinical sequelae of respiratory

muscle fatigue by intermittent mechanical ventilation. Ameri
can
Stoller. J. (1988). Oxygen therapy techniques-Current respiralol),

care. Toronto: BC Della.
Upledger, J. (1992). Craniosacral therapy. Washington: Eastland
Review ofRespiratOlY Disease, 125, 85.
Press.
Owen. R. (1985). Polio residuals clinic: conditioning exercise pro
Weiss, H. (1991). The effect of an exercise program on vital capac
gram. Orthopedics, 8,882-883.

Shneerson, J. ( 1 97 8) . The Cardio respiratory response to exercise
ity and rib mobility in pa tients with idiopathic scoliosis. Spine.
in thoracic scol.iosis. Thorax, 33, 457-463.
16, 88-93.
Respiratory Muscle Weakness

and Training
Maureen Shekleton
Jean K. Berry
Margaret K. Covey
KEY TERMS
Inspiratory muscle trainin g
Respiratory muscle fatigu e
Muscle endurance
Respiratory muscle w eakness
Muscle s tre ngth
Wo rk of breathing
INTRODUCTION
Roussos and Macklem
to ventilatory failure and death. Causes of respiratory
(1982) support the notion of a
pump failure can be grouped into the following two
(I) those in which the respiratory
two-part respiratory system made up of the lungs,
major categories:
which are the gas exchanging organs, and a pump,
drive is decreased or the sensitivity and function of
which ventilates the lungs. The pump is composed of
the respiratory center is altered (i.e., those that affect
the chest wall, the respiratory muscles, and the nerves
the central nervous system control), and
and centers in the nervous system that control the res
which the ventilatory response is decreased through
(2) those in
piratory muscles. The respiratory muscles are ex
impairment of the mechanics of respiration (i.e.,
pected to function continuously throughout life to
those that affect the chest wall or musculature) (Groer
p rovide the appropriate level of ventilation for meet
and Shekleton,
ing the body's metabolic needs.
1989).
The focus of this chapter is on the latter category,
Citing the analogy of the heart as the circulatory
and more specifically, on the role of weakness and fa
pump and the consequences of heart failure, Mack
tigue of the respira tory muscles as a pathophysiologi
(1982) maintains that the respiratory pump can
cal mechanism seen in many clinical conditions. The
fail, leading to a condition characterized by hypoven
view of respiratory muscle fatigue as a cause of venti
tilation and hypercapnia that may ultimately progress
latory failure is an idea becoming more widely ac
lem
443
444
PART III
cepted among pulmonary clinicians (Sharp, 1984).
of origin: central fatigue, transmission fatigue, or
Respiratory muscle fatigue is postulated to be the final
contractile fatigue. Central fatigue is due to a de
common pathway to respiratory failure in all condi
crease in neural drive, which reduces the number of
tions in which the respiratory musculature is affected
firing frequency of motor units. The resulting force
(Cohen, Zagelbaum, Gross, Roussos, and Macklem,
generated by voluntary effort is less than that which
1982; Grassino, Gross, Macklem, Roussos, and Zagel
can be achieved by electrical stimulation of the motor
baum, (1979); Derenne, Macklem, and Roussos,
nerves. If electrical stimulation can restore contractile
1978; Roussos and Macklem, 1982).
force or if stimulation and force decline in parallel,
Although both the inspiratory and expiratory res
central fatigue is present. Transmission fatigue results
piratory muscles are susceptible to fatigue, clinically,
from an impairment in the transmission of impulses
concern centers on the inspiratory muscles. The di
along the nerves or across the neuromuscular junc
aphragm is of particular interest. Under normal con
tions. Contractile fatigue results from impairment in
ditions, the inspiratory muscles including the di
the contractile response to neural impulses within an
aphragm, the external intercostals in the parasternal
overloaded muscle. Both transmission fatigue and
region, and the scalene muscles are responsible for
contractile fatigue are classified as peripheral fatigue.
the active process of breathing, and expiration is a
Peripheral fatigue is present if force is decreased but
passive process. An analysis of the phenomenon of
electrical stimulation is constant. All three types of
inspiratory muscle fatigue is presented initially in this
fatigue are reversible (Mador, 1991).
chapter. This is followed by a discussion of the iden
Peripheral fatigue can be further categorized ac
tification and management of inspiratory muscle fa
cording to the selective loss of contractile force that
tigue and its possible prevention through training of
occurs at varying stimulation frequencies. High-fre
the inspiratory muscles.
quency fatigue is a selective loss of contractile force

at high-stimulation frequencies; low-frequency fa
THE CONCEPT Of INSPIRATORY MUSCLE fATIGUE
tigue is the selective loss of force at low-stimulation

frequencies. High-frequency fatigue is thought to be
It is important to differentiate between muscle weak
the result of impaired neuromuscular transmission
ness and muscle fatigue, although both may lead to
and/or propagation of the muscle action potential.
hypoventilation (Bryant, Edwards, Faulkner, Hughes,
This type of fatigue is seen in myasthenia gravis, dur
and Roussos, 1979). Muscle weakness refers to a loss
ing ischemic exercise, with muscle cooling, and with
in the capacity of a rested muscle to generate force
partial curarization. It is reversible in minutes. The
that is chronic situation. Muscle fatigue refers to a
mechanism underlying low-frequency fatigue is
loss in the capacity of a muscle under load to develop
thought to be impaired excitation-contraction cou
force or velocity that is reversible by rest (NHLBI
pling. Recovery from this type of fatigue may take
Workshop Summary, 1990). Fatigue is an acute loss
hours to days and possibly longer. Intense dynamic
of contractile force wherein, despite constancy of
and static muscular activity can lead to low-fre
stimulation, force declines from the initial value. If
quency fatigue (Edwards, 1983; Moxham, 1990).
fatigue is the inability of a muscle to continue to gen

erate a required force, then in the respiratory system,
fatigue will be manifested by the inability of the in
spiratory muscles to continue to generate the force re
Mechanisms and Etiology of fatigue

The major mechanisms thought to be responsible for
quired to maintain the necessary level of alveolar
inspiratory muscle fatigue include an imbalance be
ventilation to meet the body's metabolic needs. Inspi
tween energy supply and demand and impaired exci
ratory muscle fatigue occurs when inspiratory effort
tation-activation. Edwards (1983) has proposed a
exceeds the capacity of the inspiratory muscles to
model that accounts for the interaction of both mech
sustain that effort (Rochester, 1982).
anisms in the development of muscle fatigue. He has
Physiologically, fatigue has been characterized as
also proposed the idea that fatigue serves a protective
one of the following three types, depending on its list
function in that serious irreparable damage may be
25
Respiratory Muscle Weakness and Training
Possible
fatigue mechanism
Psyche
Brain
Impaired motivation
i.e. neural motor
drive and motor
unit recruitment
SP'''' Co ,d
)
p",p"r ""'"
I mpaired reAex
drive
Impaired neuro
muscular transmission
Muscle sarcolemma
Impaired action
potential
K*, Na*, H20
Transverse
,"bO',
'!
'y"eo"
imbalance
Impaired excitation
Ca**
Impaired activation
Impaired energy supply
Actin-myosin
interaction
CN" b'''g'
r1
"o"' + heat
Thermal damage
Sarcomere damage
Force power
OUlput
FIGURE 25-1
Chain of command for muscular contraction and the possible mechanisms underlying fatigue.
(From Edwards, R.A.T. (1983). Biochemical basis of fatigue in exercise petformance: Catasptrophe
theory of muscular fatigue. In Knuttgen, H., Vogel, J., Poortmans, 1. (Eds.). Biochemistry of
exercise. Champaign, Ill. Human Kinetics Publishers.).
445
446
PART III
prevented if the muscle is unable to continue per
pattern of fiber distribution is most pronounced in
forming beyond a critical point. The central nervous
the premature infant. This condition exists in infants
system may exert a protective mechanism to avoid
for up to a year after birth.
these adverse effects. This idea has persisted and the
The energy supply to the muscles depends on an
term central wisdom is used to describe the phenome
intact oxygen transport system, adequate oxygen-car
non (Moxham, 1990) (Figure 25- I, p. 445).

The energy demands of the inspiratory muscles
rying capacity of the blood, blood tlow, substrate

stores and availability, and the efficiency of oxygen
are determined by the work of breathing, the strength
uptake and uti lization by the muscles. The energy
and endurance of the respiratory muscles, and the ef
supply to the inspiratory muscles is compromised
ficiency of the muscles. The work of breathing is the
when cardiac output is reduced, the hemoglobin con
total amount of effort required to expand and contract
tent of the blood is low, blood flow to the muscles is
the lungs. It is determined by the degree of compli
decreased, or energy substrates are lacking.
ance of the lung tissue and the chest wall, the resis
tance of the
Excitation-activation depends on intact, function
airways, the presence of active expira
ing, neuromuscular pathways. Impaired excitation-ac
tion (normally a passive process), and use of the
tivation is probably the primary mechanism underlying
accessory muscles of respiration. The work of breath
respiratory muscle weakness and fatigue in the patient
ing is increased by decreased pulmonary compliance,
with a neuromuscular disorder (Edwards, 1979). Dis
increased airway resistance, active expiration, and
ruption of excitation-activation can occur at any point
use of the accessory muscles.
along this pathway, which Edwards (1983) refers to as
Strength and endurance are the fundamental prop
a chain of command for muscular contraction. Pre
erties of muscle. Strength is defined as the maximal
sented in Figure 25-1 is a list of the possible mecha
force that a muscle can develop with maximal stimu
nisms that may lead to fatigue by disrupting the neuro
lation. Contractile force is governed by the force
muscular pathway. Impaired excitation of the muscle
length (length-tension), force-velocity, and force-fre
membrane is probably interrelated with energy metab
quency relationships. Contractile force diminishes in
olism. For example, if the ATP supply to the Na+ - K+
conditions characterized by increased lung volume
pump is compromised, an alteration in the Na+ and K+
(hyperinflation), since the muscles are stretched be
concentrations in the transverse tubular system may re
yond the optimal length to generate maximal force.
sult in impaired excitation-contraction coupling.
This stretching of the muscle fibers produces a less
Although it is difficult to demonstrate the precise
desirable length-tension relationship and causes a
mechanisms causing respiratory muscle fatigue in pa
loss of the zone of apposition, with resulting decrease
tients, support is found for the concept that central
in strength generation. Strength is also determined by
nervous system output is modified to avoid overt fa
the number and size of individual fibers in a muscle.
tigue. With extremely high loads imposed on respira
Strength is adversely affected in conditions in which
tory muscles, patients adopt a rapid shallow pattern
the size of the fibers is reduced (atrophy) or the num
of breathing that reduces the work of breathing and
ber of fibers is reduced (e.g., in malnutrition).

Endurance is defined as the ability to maintain a
contraction against a given load and is determined
can be sustained. Eventually, this pattern of rapid

shallow breathing will lead to hypercapnia and acido
sis (Moxham, 1990).
by muscle fiber type, blood supply, and the force
In summary, those patients who are at risk for the
and duration of the contraction. Normally, the inspi
development of inspiratory muscle fatigue are those
ratory muscles are fatigue resistant. Approximately
in whom energy demands are increased, energy sup
75% of the muscle fibers in the adult diaphragm are
plies are compromised, or whose neuromuscular
of the high oxidative, fatigue resistant type (type I
chain of command has been disrupted at some point.
and type IIA). In contrast the diaphragm of the
Patients at highest risk for the development of inspi
neonate contains a relative paucity of type I fibers
ratory muscle fatigue are those in whom the work of
that have the greatest endurance capacity, and this
breathing is increased, thus increasing the demands
25
447
for energy, and those who are experiencing hypox
power spectrum, which is indicative of muscle fa
emia, acidosis, low cardiac output, or any other con
tigue in normal subjects exercised to fatigue, in pa
dition in which the blood supply to the muscle is di
tients experiencing difficulty being weaned from me
minished, thus reducing oxygen supply. Patients
chanical ventilation, and in animals in whom fatigue
whose nutritional status is poor or who are experienc
was experimentally induced. When fatigue is present,
ing a catabolic state, such as stress or fever, will have
the ratio of high-to-low frequency power, which can
reduced energy stores and may experience muscle fa
be detected by EMG, shifts as low-frequency power
tigue during times of high need.
increases and high-frequency power decreases. The

difficulty in obtaining an EMG at the bedside and in
analyzing the results makes its use in most clinical
Assessment of Fatigue
situations unrealistic at this time.
The clinician will most often have to rely on physi
In summary, rapid shallow breathing is the initial
cal signs exhibited by the patient to recognize inspi
sign of inspiratory muscle fatigue (Yang and Tobin,
ratory muscle fatigue. Other laboratory methods that
1991). The physical signs previously described are
would yield more objective evidence of inspiratory
reliable and can be used in a clinical situation to de
muscle fatigue include power spectral analysis of the
termine whether the patient is experiencing inspira
electromyelogram (EMG), measurement of the max
tory muscle fatigue.
imal relaxation rate, and examination of twitch oc

clusion pressure.
The following signs are indicative of inspiratory
Treatment of Fatigue
muscle fatigue and are listed in their characteristic
The goals of treating inspiratory fatigue are as fol
order of appearance:
lows:
(I) restore the balance between energy supply

(2) improve diaphragmatic contractility,
and (3) increase the strength and endurance of the in
I. Tachypnea
2. Decreased tidal volume
3. Increased PC02 (which is a late sign)
and demand,
spiratory muscles. The last goal is obviously a more
4. Bradypnea and decreased minute ventilation
long-term preventive approach, whereas the first two
Formerly, development of a discoordinated respi
goals apply in the more acute situation when inspira
ratory pattern characterized by inward abdominal
tory muscle fatigue is present.
ab
Energy demands in the patient experiencing fa
dominal paradox) and alternating abdominal and tho

racic respiratory patterns (a sign referred to as respi
ratory alternans) were t h o u gh t to result f r o m
tigue can be decreased by reducing the work of

breathing through activities intended to promote
respiratory muscle fatigue. Presently, these changes
wall and airways, and promote normal lung volumes
in breathing patterns are thought to result from in
and pressures. Energy supplies can be enhanced by
movement on inspiration (a sign referred to as
compliance, decrease resistance in the lung, chest
creases in respiratory load rather than muscle fatigue
ensuring maximal oxygen transpOit to the tissues and
(Mador,
1991; Tobin, Perez, Guenther, Lodato, and

Dantzker, 1987). However, discoordinated respira
the availability of adequate amounts of oxygen and
tory patterns are important clinical signs of respira
hanced by promoting adequate cardiac output, blood
tory distress and, although they are not specific in
flow to the tissues, and oxygen-carrying capacity of
their etiology, they are sensitive indicators of impor
the blood. Various forms of respiratory therapy are
tant declining respiratory function.
other energy substrates. Oxygen transport is en
available to supplement oxygen supplies. Losses of
In animals in whom inspiratory muscle fatigue has
organic and inorganic energy in substrates must be
been experimentally induced the fall in respiratory
replenished and adequate levels maintained. Nutri
rate and minute ventilation immediately precedes res
tional supplementation and administration of elec
piratory arrest and death. This sequence of events has
trolytes and inorganic phosphate may be necessary to
been observed after an initial change in the EMG
augment energy supplies. Rest therapy with mechani
448
PART III
cal ventilation may be required to allow the fatigued
plished by training the inspiratory muscles in much
muscle to recover and to bring energy supplies and
the same way that athletes train and condition their
demand into balance.
muscles. Inspiratory muscle training may represent a
Much current research is being done in the area of
useful clinical approach to prevent the development
pharmacological interventions to improve diaphrag
of inspiratory muscle fatigue in those patients who
matic contractility. Aminophylline w as initially
are at risk.
thought to increase the contractile force of the di

aphragm at any given level of activation, but further
research indicates that this drug increases muscle en
INSPIRATORY MUSCLE TRAINING
ergy consumption and potentiates fatigue (Janssens,
Inspiratory muscle training (lMT) is currently used in
1988). Other drugs with
pulmonary rehabilitation to increase the strength and
Reid, Jiang, and Decrarner,
inotropic properties are the beta-agonists. Clinical in
endurance of the inspiratory muscles. Patients with
vestigation of the potential usefulness and application
chronic obstructive lung disease experience func
of these pharmacological agents in inspiratory muscle
tional weakness of the respiratory muscles, which can
fatigue is ongoing.
contribute to dyspnea and functional impairment.
The last goal, that of increasing the strength and
Theoretically, IMT should reduce dyspnea by im
endurance of the inspiratory muscles, can be accom
proving respiratory muscle function and exercise tOI-
RespiralOn' muslle Ir,lillillg
i Sirengill
,tlld cndurancc of respiralon' llluscies
I
Delay lhe onsel of
respiralory llluscle faligut'
IllllJrOl'e
I
I
Prel'em/dcler I hc Ollsel of
Illlpn)IT lissuc o"ygemllio)l
1'espi1';lIOl} insuUiciell(Y allcl
faliguc
cog"niliol1
pcn:cplion
pS)Tilo-lllOI01' hlllCiioll
ImpnJl'
1m p1'Ol'c
signs anc! "mplOms
\\ell-being.
Improl't'
IlllprOl'c
tlaih liling
life
FIGURE 25-2
Conceptual framework for respiratory muscle training. (From Kim M: Respiratory muscle training:
Implications for patient care .
Hearl and Lung. 13(4):333-40).
25
erance. These effects have yet to be demonstrated in

large, controlled studies (Smith, Cook, Guyatt, Mad
havan, and Oxman, 1992).
General principles of skeletal muscle training that
must be considered when designing and evaluating an
IMT program for respiratory patients include over
load, specificity, and reversibility. To train a muscle
to improve its functional ability, the muscle must be
subjected to a stress greater than its usual load (over
load), the training must be directed at developing spe
cific functional attributes (e.g., strength or endurance)
of the muscle (specificity), and the training must be
maintained or function will revert back to pretraining
levels (reversibility) (Kim, 1984; Sharp, 1985).
The effects of strength training on the respiratory
muscles may include an increase in the size (hypertro
phy) and number of the muscle fibers by an increase
in protein synthesis by the muscle fibers and a de
crease in degradation. Endurance training of the inspi
ratory muscles is thought to promote an increase in
the proportion of fatigue-resistant fibers in the di
aphragm, an increase in the metabolic capability of
the muscle, and a reduction in the susceptibility of
muscle fibers to the deleterious effects of exercise
(Leith and Bradley, 1976). Newer evidence suggests
an improvement in neuromuscular coordination and
efficiency resulting from training (McComas, 1994).
Strength training to increase the size and number of
myofibrils requires a high load and a slow rate of rep
etition. Endurance training to increase the metabolic
capability of the muscle requires exercise of a suffi
cient load, speed, and duration, such that cellular con
centrations of energy producing substrates drop to
minimal levels (Kim, 1984). Endurance training of
skeletal muscle has been found to be most effective
when brief periods of fatiguing exercise are alternated
with periods of rest (Aldrich, 1985) and this concept
may be applied to inspiratory muscle training regimes.
Improvement in the strength and endurance of the
inspiratory muscles through training has the twofold
effect of enhancing the resistance to inspiratory mus
cle fatigue and improving ventilatory function. The
work of breathing is reduced and respiratory reserves
are increased. Because the clinical signs and symp
toms are diminished, the ultimate outcome for the pa
tient is an improved quality of life. Kim (1984) has
449
developed a model that outlines the relationship be

tween the effects of a respiratory muscle training and
potential patient outcomes (Figure 25-2).
Inspiratory muscle training has been used to suc
cessfully increase muscle strength and endurance in
healthy volunteers and in patients with chronic air
flow limitation (Belman and Mittman, 1980; Larson,
Kim, Sharp, and Larson, 1988), cystic fibrosis
(Keens, Krastens, et ai, 1977). Early Duchenne mus
cular dystrophy (Wanke et aI, 1994), and in those
who are quadriplegic (Gross, et ai, 1980).
Theoretically IMT in patients experiencing acute
respiratory failure should promote improved function
of the muscles, and fatigue resistance should facili
tate the process of weaning these patients from me
chanical ventilation. In conditions requiring full ven
tilatory support, the respiratory muscles may contract
at minimal levels for a period of time, possibly lead
ing to the development of disuse atrophy. As their
strength and endurance decrease, the inspiratory mus
cles will be more prone to fatigue because of the in
teraction of disuse, the underlying pathophysiological
state, and catabolic effects of stress. The ultimate ef
fect of these interacting processes will be difficulty in
weaning the patient from the ventilator. An EMG pat
tern of fatigue has been documented in the ventila
tory muscles of neonates who experienced difficulty
in weaning (Muller, Gulston, and G ade, 1979).
Grassino et al. (1979) found an EMG fatigue pattern
in a patient being weaned from mechanical ventila
tion. Cohen et al. (1982) found an EMG pattern of fa
tigue in 7 of 12 patients who experienced difficulty
during discontinuation of mechanical ventilation.
Resolution of the fatigue pattern was observed in
those neonates who recovered and in adult patients
who were successfully weaned (Andersen, Kann,
Rasmussen, Howardy, Mitchell, 1978). There is some
evidence that respiratory muscle training may prove
to be an important adjunct therapy to facilitate wean
ing in the patient who requires mechanical ventilation
of acute respiratory failure (Aldrich and Karpel,
1985; Aldrich et ai, 1989; Shekleton, 1991). How
ever, controlled studies have not been conducted in
this patient population.
Two techniques have been used for inspiratory
muscle training: isocapnic hyperventilation (also
450
PART III
called isocapnic hyperpnea) and inspiratory resistive

or resistance breathing. Isocapnic hyperventilation is
dynamic and is used to increase the endurance of the
inspiratory muscles. Expiratory muscles will benefit
as well with this technique. Patients are asked to
breathe at the highest rate they can manage for 15 to
30 minutes. A rebreathing circuit or the addition of
CO2 to the inspired air must be used with this tech
nique to prevent hypocapnia (Belman, 1981; Belman,
and Mittman, 1980). Because of this requirement, the
usefulness or this technique will be limited until
portable, inexpensive, easy-to-use equipment for
home use is developed.
I nspi r a t o r y r e s i s t i v e b r e a t h i n g a l l o w s b o t h
strength and endurance training, since i t incorporates
both isometric and isotonic exercises. There are two
devices available for this purpose, a nonlinear device
and a threshold JMT device (Figure 25-3). The non
linear device has been noted to produce unreliable
training loads if the rate of inspiratory flow is not
controlled (Guyatt, Keller, Singer, Halcrow, and
Newhouse, 1992). With a controJI.ed rate of breath
ing, patients inspire through a narrow tube that offers
a nonlinear airway resistance for one to three daily
periods of 15 to 30 minutes. The size of the orifice
through which the patient inspires is adjusted to pro
vide a level of resistance that the patient can tolerate
without becoming immediately exhausted. In addi
tion, this device is not well suited for stronger pa
FIGURE 25-3
Handheld resistive breathing training devices. A, Threshold;
resistance level is altered by tightening screw to increase
tension on the spring. B, P-Flcx; resistance level is altered
by changing settings on dial.
tients, since they have difficulty achieving a satisfac

tory tidal volume with the extremely small orifice at
Potential outcomes of a training program geared
higher loads. With the tllreshold device, a reliable in
toward increasing inspiratory muscle strength and
spiratory pressure load is provided regardless of air
endurance might include any of the following, de
flow rate. The load is adjusted by a nurse therapist,
pending on the individual patient's conditions and
or patient according to a desired percentage of the
goals of treatment: (I) prevention of acute deteriora
patient's maximal inspiratory pressure (PImax). Usu
tion of respiratory status and ventilatory failure,
ally, the patient begins training at a low load, equal
(2) improvement of ventilatory function and de
to about one third of the PImax and progresses slowly
crease in the work of breathing, which may lead to
in small increments adjusting a screw to alter the ten
an increase in general exercise tolerance and an im
sion until the training load reaches 60% of the cur
proved quality of life as tissue oxygenation improves
rent PImax. The threshold device delivers a reliable
and signs and symptoms are attenuated (Pardy,
tension because the poppet valve at the end of the de
Pardy, Rivington, Despas, and Macklem, 1981a;
vice will not open and allow inspiration unless the
1981b), (3) extension of time before onset of respira
patient generates the designated negative pressure.
tory muscle fatigue, and (4) facilitation of the wean
Both types of devices are hand held and pOltable and
ing process in acute respiratory failure patients who
are easily used and maintained by patients.
are being mechanically ventilated.
25
451
SUMMARY
Edwards, RAT (1979). The diaphragm as a muscle: Mechanisms
Inspiratory muscle training and conditioning is a newer

area of research and treatment for the respiratory pa
tient. As such, further validation of its efficacy and tar
geting of specific patient populations at greatest risk
for loss of inspiratory muscl
strength will define its
use in pulmonary rehabilitation programs. At this time,

inspiratory muscle training looks promising as a means
of offering the respiratory patient one possible method
of control over disease processes that are most often
very debilitating and unrelenting in their course.
underlying fatigue. American Review of Respiratory [iseases.
fJ9, (2 pt 2),81-84.
Edwards, RAT (19 83). Biochemislry of Exercise. Champaign, lL,
Human Kinetics Publishers.
Grassino,
A.,
Gross, D., Macklem, P., Roussos,
c., &
Zagelbaum, C.
(1979). Inspiratory muscle fatigue as a factor limiting ex.ercise.

Bullelin European de Physiopalhogie Re.lpiraloire, 15, 105-111.
Groer, M.,
&
Shekleton, M. (1989). Basic palhophysiology: A
holistic approach. (ed. 3).
Gross, D.,
St. Louis,
Mosby.
et al. (1 980) . The effect of training on strength and en
durance of the diaphragm in quadriplegia. American Journal of

Medicine. 68, 27-35.
Guyatt, G., Keller, J., Singer, J., Halcrow, S., Newhouse, M.
(1992). Controlled trial of respiratory muscle t raining in
REVIEW QUESTIONS
chronic airtlow limitation. Thorax, 47, 598-602.
I. What are three types of respiratory muscle fatigue?

2. Name two major mechanisms thought to be re
sponsible for inspiratory muscle fatigue.
&
Decrame r. (1988).
Jardim, J., et al. (1982). Inspiratory muscle conditioning training in

chronic obstructive pulmonary disease (COPD) patients. Amer
ican Review ofRespiralory Diseases, 125. (pt 2 of 2), 132.
Keens, T., et al. (1977). Ventilatory muscle endurance training in
3. What factors determine the work of breathing?

4.
Janssens, Reid Jiang,
What is the initial physical sign of inspiratory

muscle fatigue?
S. What rehabilitation techniques should be used to

increase the strength and endurance of the inspi
normal subjects and patients with cystic fibrosi s . American Re

view ifRespiralory Diseas'es, 116, 853-860.
Kim, M.J. (1984). Respiratory muscle training:
I mplic at io ns
for
patient care. Hearl and Lung, 13, (4),333-340.

Larson, M., Kim, MJ. (1984). Respiratory muscle training with the
incentive spirometer resistive breathing device. Hearl (lnd
ratory muscles?
Lung, 13. (4),341-345.

Leith, D., Bradley, M. (1976). Ventilato ry muscle strength and en
References
traini ng. Journal of Applied Physiology, 41, 508-516.

& Roussos, C. (1977). Respiratory muscle fatigue: A
cause of respiratory failure1 Clin Sci Mol Med, 53, 419-422.
Macklem, P.T (1982) The diaphragm in health and diseas e. Jour
durance
Macklem, P.
Aldrich, T (1985). The application of muscle endurance training
teChniques to the respiratory muscles in COPD. Lung, 163, 15-22.
Aldrich, T (1984). Inspiratory muscle resistive training in respira
Aldrich, TK., Karpel, J.P., Uhrlass, R.M., Sparapani. M.A., Erami,
D.,
Fenanti. R. (1989). Weaning from mechanical ventilation:
&
tern. Chesl, 100, 430-435.

Martin,
L. (1984).
Respiratory
musc l e
function: A clinical study.
Hearl and Lung. /3,346-348.
Adjunctive use of inspiratory muscle resistive traini.ng.
J.,
ncd ojLaborolory and Clinical Medicine. 99. 601-610.

Mador, JJ. (1991). Respiratory muscle fatigue and breathing pat
lory failure. CheSl. 86(2), 302.
Mitchell,
McComas, A. (1994). Human neuromuscular adaptations that ac
J. (1978). Respiratory thoracoabdominal coordination and mus
company changes in activity, Medicine and Science in Sporls
Andcrsen,
Kann, T, Rasmussen. J.P. , Howardy, P.
cle faligue in acute respiratory failure. American Review of
Respimlorv Dis('(I.I'es, 117 (2),89.
and Exercise, 26, 1498-1509.

Muller, N., Gulston, G., Cade,
0.,
et al. (1979). Diaphragmatic
Belman, M. (1981). Respiratol)' failure treated by ventilatory mus
muscle fatigue in the newborn. Journal of Applied Physiology,
c a se s. European Journal of Respi

62, 391-395.
Edwards, R., Faulkner, .I., Hughes, R.L., & Roussos, C.
Moxham, J. (1990). Respiratory muscle fatigue: mechanisms, eval
et al. (1986). Respiratory muscle failure: Fatigue or weakness.
National Heart Lung Blood Institute Workshop Summary (1990).
cle training: A report of two
ralorv Di.l'eoses,
Bryant, S.,
Chesl, 89. (1),116-124.

Cohen,
c.,
Zagei bau 111, G., Gross, D.,
Clinical mani
Medicine, 72, 308-316.
J.,
uation and therapy. Brilish Journal ofAnaeslhesia, 65, 43-53.

Respiratory muscle fatigue: report of the respiratory muscle fa
et al. (1982).
festations or inspiratory muscle fatigue. American Journal of

Derenne,
46, 688-695.
American Review ofResfliralOry Diseases. 118. 581-60 I.
ea se,
142,474-480.
Pardy, R.L., Rivington, R.N., Oespas, PJ.,
Macklem, P., Roussos, C. (1978). The respiratory
muscles: Mechanics, control, and pathophysiology, Part
tigue workshop group. American Review of Respiralory Dis
III.
&
Macklem, P.T.
(l981a). The effects of inspiratory muscle training on exercise

performance in chronic airtlow limitation. American Review of
Respiralory Diseases, 123. 26-433.
Patient Education
Alexandra J. Sciaky
KEY TERMS
Education
Methods
Effectiveness
Needs assessment
Health behaviors
Resources
Learning theory
INTRODUCTION
in their care. Unless effective patient education is im
In cardiopulmonary physical therapy, sound treat
plemented this opportunity will be lost.
ment is based on the physiological assessment of the
The overall objective of this chapter* is to provide
patient. Similarly, effective patient education is based
the clinician with an understanding of the principles
on the learning needs assessment of the patient
and practice of effective patient education. To meet
(Rankin & Stallings, 1990). Cardiopulmonary patient
this objective, patient education is defined and perti
education poses a significant challenge because the
nent learning theories with examples of how they re
physical therapist's duties can range from teaching a
late to cardiopulmonary patient education are pre
hospitalized cardiac patient to do a self pulse check to
sented. The learning needs assessment of the patient
designing a series of community-based exercise
is explained, followed by a description of patient edu
classes for senior citizens with emphysema. Meeting
cation methods and materials. Because the effective
this challenge is important because the benefits of pa
ness of patient education efforts are important to
tient education include reduced health-care costs, re
evaluate, ways to determine this are addressed. Fi
duced patient anxiety, increased patient knowledge,

satisfaction with care, and incrcased quality of life. In
addition, physical therapists share the responsibility
thank Jennifer L. Wai ters, D. Min. and

expertise in education and assistanc e
man uscri pt
'The author wishes to
with other health-care providers of ensUling that pa
Patricia Wren, MPH for their
tients have the opportunity to make informed choices
in preparing this
453
454
PART III
nally, interdisciplinary considerations and educa

tional resources are discussed.
Patient Education Objectives

I. Enhanced patient-clinician rapport
2. I n creased
DEFINING PATIENT EDUCATION

Physical therapists believe that patient education is an
i m p o r t a n t part of
p a t i ent
knowledge
of
he alth
disorder/condition
t r e a t m e n t (C h a s e ,
3. Increased adherence to physical therapy treat-
E l k i ns,
ment plant
Readinger, and Shepard, 1993). The teaching role of
4. Decreased health-care costs
the physical therapist has been reported as highly val
5. Increased patient self-efficacy
ued by patients as well (Grannis, 1981). According to
6. Increased ability to make informed health-care
Bartlett (1985), patient education is "a planned learn
choices
ing experience using a combination of methods such

as teaching, counseling, and behavior modification
techniques which influence a patient's knowledge
and health behavior."
patient education program, and finally evaluating its
Several factors make patient education unique

when compared with other types of teaching. The pa
effectiveness. Specific examples of patient education

learning objectives are listed in the box above.
tient may have limited or no access to the teaching
Achieving these objectives will lead to the enjoy
because of financial and/or geographical barriers to
ment of a host of documented benefits of patient edu
health care. The student may lack a sense of well
cation. These include reduced length of hospital stay
being because of signs and symptoms of an acute ill
(Devine & Cook, 1983), reduced patient anxiety
ness, making learning more difficult. The relationship
(O'Rourke, Lewin, Whitcross, and Pacey, 1990), im
between the teacher and the learner in patient educa
proved health-related knowledge (Rowland, Dickin
tion may be perceived as hierarchical-a medical au
son, Newman, and Ebrahim, 1994), increased quality
thority figure instructing a lay person. The student's
of life (Manzetti, Hoffman, Sereika, Sciurba, and Grif
emotional status may be fearful or anxious, depend
fith, 1994), and improved response to and adherence
ing on the medical situation. There may be superim
with medical treatment (Mazzuca, 1982). Patient edu
posed time constraints, such as length of hospital stay
cation has also been shown to empower patients to
or clinic appointment, which have a direct impact on
take more active roles in their health care (Smith,
patient education. All of these factors may pose barri
1987). Patients who are educated partners in their care
ers to learning. As in other types of teaching, how
are able to be smart consumers in the health-care sys
ever, patient education is information shared in the
tem and adapt more readily to changes in their life
hope that it will not only be understood but applied in
styles resulting from illness.
ways that produce the desired changes in health

related behavior.
Learning Theory: Concepts Pertinent to

Cardiopulmonary Patient Education
Objectives
The American Physical Therapy Association's Com
The overall objective of patient education is to affect

a durable cognitive improvement that results in a pos
mission on Accreditation of Physical Therapy Educa

'
tion (1990) requires that the graduate physical thera
itive change in an individual's or group's health be
pist be able to "... apply concepts of teaching and
havior. In many cases the physical therapist must em
learning theories in designing, implementing and
bark on a process to meet this objective in the course
evaluating learning experiences used in the education
of treatment. This process consists of assessing the
of patients." Twentieth century behavioral scientists
learning needs of the patient, identifying measurable,
have developed a variety of learning theories and
realistic objectives, planning and implementing the
models attempting to explain the complexities of
26
human behavior. Subsequent models have
455
Patient Education
pm,, r'(7pf1
address health behavior. Although a
that
discllssion of these models is

a list of references for fur
the scope of this
on energy
receives
ther reading may be found at the end of this
conservation techniques from the staff (verbal persua
The discussion of the three theoretical
sion), and notes that oxygen saturation measured 95%
to
which follows is
the clinician
before
with a rationale for patient education practice in

terms of its basis in learning
The concepts are
theory, the health-belief
and
the behavior-modification approach,

The
theory as
by Ban
in the early
are likely t o take a
1950s, theorizes that

health action in the
Iieve
that human behavior can be ex-
dura (1986)
state).
The health-belief model,

situations:
are at risk of illness;
the disease poses
be-
(I)
they believe that
serious threat to their lives should
they contract it;
they desire to avoid illncss and
believe that certain actions will prevent or reduce the

of the
a myocardial infarction
value in following the exercise pro
will attempt to exercise
This
gram
if he or she believes his or her current
life
and
believe that taking

than the illness it
the health action is less
self (Roenstock, 1974). This model was originally de

veloped in an attempt to understand why
num
care or
bers of people failed to accept
poses a threat to health. The
tests for early disease detection. Subse
lieves exercise will reduce that threat (outcome ex
quent studies have used the model to
pectation) and that he or she
ance with
personally
of
betes
the exercise program

Outcome and
compli
asthma, and dia
for
, 1985).
re
The health-belief model conveys that in the con
late to patients' beliefs about their capabilities and
text of health behavior some stimulus or "cue to ac
the
of their behaviors to successful out
comes, In essence
behavior is i nfluenced by
that create expectations for similar out

comes over time.
environment
a belief in one's ability to attain a certain

level of
Bandura terms this
se(refficacy
He argues that percei ved sel f

efficacy influences all aspects of behavior including
new skills and inhibiting or
behaviors,
current
has the
mary determinants:
(I)
cough) or external
structural,
of
Once the behavior

UUHV,",''''Ull
and social elements are

the behavior. In
may limit or
unpleasant side
barriers
prevent undertaking the recommended behavior.

has its roots
The behavior-modification
four pri
refers to
a productive
instructional video tape on
commences, it is understood that many
theory and consists of

environmental rewards and
performance accomplish
ments, the strongest
ments in relationship to a specified behavior

man, 1993). The theme of this approach
the desired behavior and mastery over the

in increased
that an in
dividual's behavior can gradually be
involves learning
comes;
necessary to initiate the
pulmonary hygiene
To function competently in a
others,
tion"
process. These cues can be internal
a set
Iy those with
(3) verbal
ical state as it relates to
rewarding out-
and (4) one's physiolog-
program increases a
(1
frequently follows a
plan: "identify the problem; describe the
ability to perform a
task. For example, a pulmonary rehabilitation
t o Becker
behavior-modification
in behavioral terms; select a

that is
when he or
behavior
identify the antecedents and conset behavioral
456
PART III
Health Care Contract

Date:
_ _ _ _ _ __ __
Contract Goal: (Specific outcome to be attained)

I. (client's name), agree to (detailed descriptioll of required behaviors, time and frequency limitations)
in retun! for (positive reinforcements contingent upon completion of required behaviors: timing and mode of delivery
of reinforcements)
I. (provider's name), agrees to (detailed description of required behaviors, time and frequency limitations)
(Optional) I, (significant other's name), agree to (detailed description of required behaviors, time and frequency
limitations)
(Optional) Aversive consequences: (Negative reinforcements for failure to meet Illinium contract requirements).
We will review the terms of this agreement, and will make my desired modifications. on (date). We hereby agree to
abide by the terms of the contract describe above.
Signed: (Client)
_
__ _
_
_
_
__ _ __ _ __ _ _ __ _ ___ _ _ _
_ _ __ _
Signed: (Significant other. if relevant).

Signed: (provider)
____ ________ ______ ______

_
_
___________________ ________ ____
Contract effective from (Date)
to (Date)
_
_______ ____
(From Janz NK, Becker MH, Harlman PE: Parienr Educ COUllS 5(4): 165-178, 1984).
devise and implemellt a behavior change program;
to facilitate the desired behaviors in the patient. Ide
and evaluate the program." This plan is very similar
ally, once the contract expires, the patient feels com
to the approach the physical therapist takes on being
petent and is able to continue the desired behaviors
referred to evaluate and treat a patient. The physical
without the external reinforcements.
therapist identifies the patient's deficits, describes

the problem(s) in functional terms, sets short-term
and long-term functional goals, designs a treatment
plan to meet those goals, implements the treatment
NEEDS-BASED APPROACH TO PATIENT EDUCATION

The most important aspect of planning for patient ed
plan and reevaluates the patient. These similarities
ucation is assessing the learners (Kopper, 1987). The
may facilitate the use of the behavioral-modification
process of patient education requires assessment of
approach by physical therapists.
the total patient, including an understanding of the
Health-care contracts can be useful in implement
psychosocial, socioeconomic, educational, vocational,
ing the behavior-modification approach. An example
and cultural qualities of the person (Verstraete and
of such a contract may be seen in the box above. The
Meier, 1973). Assessing educational needs of the pa
contract should be realistic, measurable, and renew
tient allows the physical therapist to determine what
able (Herje, 1980). Specific goals, time frames, be
the patient needs to know to meet the desired cogni
haviors, and contingencies are written in the contract.
tive and behavioral teaching objectives. This assess
The clinician and patient discuss, then sign the con
ment also increases patient-teacher rapport and pre
tract. Positive and negative reinforcements are used
vents needless repetition of already familiar material.
26
LEARNING NEEDS ASSESSMENT
Patient Education
457
Learning Needs Assessment Areas
Tools
Perceptual
Learning needs can be assessed in a variety of ways.

These include patient and family interviews, ques
tionnaires and surveys, written tests, and observation
of patient performance (Haggard,
1989). Interviews
allow the physical therapist to ask questions directed

at determining the patient's view of the illness, in
cluding associated beliefs and attitudes. Question
naires and surveys can be used in conjunction with
Ability
to receive input (vision, hearing, and touch)
Comprehension of symbols (figures, numbers,

words, and pictures)
Cognitive
Knowledge and analytical skills
Memory
Motor
the interview to document the patient's responses to
Fine- and gross-motor skills
specific questions about his or her condition. Open
Physical adaptations and responses to illness or
ended questions such as "What are the major prob

lems your illness has caused for you and your fam
ily?" elicit more information than a multiple-choice
format. Written tests can be helpful in determining
what patients already know when the tests are given
before any teaching. These tests can also identify
problems with reading and comprehension skills. Ob
serving patients as they perform a skill, such as di
aphragmatic breathing, reveals whether or not the pa
tient can demonstrate the correct technique. The
physical therapist can also pose questions to the pa
tient during the demonstration to determine whether
stimuli
Affective
Attitudes
Value-belief system
Motivation (readiness to learn)
Environmental
Personal and societal resources
Amount of instructor contact and setting
Cultural influences (language. traditions, roles,
religion. and life style)
or not the patient knows the rationale for the exercise.

The cognitive area addresses the learner's knowl
Areas to Assess
edge and problem-solving skills. The instructor needs
The learning needs assessment encompasses the fol
to know how much the learner already knows and
(2) cognitive,
what needs to be learned. The instructor also needs to
(3) motor, (4) affective, and (5) environmental (see
know if the learner has any problems with memory.
the box at right). By addressing these five areas, the
Short- or long-term memory deficits may require that
lowing five major areas: (I) perceptual,
physical therapist will obtain an accurate picture of
the instructor integrate a prompting system into the
the patient's learning abilities, knowledge level, per
education plan.
The patient's fine- and gross-motor skills and func
formance skills, attitudes, and cultural influences.

The perceptual area encompasses the learner's
tional mobility are covered in the motor area. The in
ability to receive information via the senses. If the
structor needs to be aware of the physiological
learner's sight, hearing, or sensc of touch is impaired,
changes in the patient that affect abilities to perform
the instructor may need to makc modifications so that
activities necessary for a given education program.
the information can be received by the learner. The
For example, if a support group is being held in a
comprehension of symbols. such as numbers, words,
room that is not wheelchair accessible, patients who
or pictures. also needs to be assessed in the percep
are wheelchair users will not be able to readily attend.
tual area. The instructor nceds to know what meaning
The affective area comprises the learner's attitudes,
the learner attributes to the symbols that will be used
beliefs. and readiness to learn. Identifying the learner's
in the education program to ensure clarity.
value-belief system will assist the instructor in deter
458
PART III
Learning Needs Assessment Survey

Your physical therapist would like to help you learn what you need to know to function as independently as possible
and manage your illness/disability. Please answer the following questions to identify your own needs.
Part I.
Name:
Your illness and/or disabi Iity is:
J.
Do you have any problems seeing
2.
Do yu have any body areas which are numb (can't feel)?
or
hearing?
3.
How long have you had this illness/disability?
4.
What problems has it caused you?
5.
Are you able to care for yourself at home?
6.
Are you responsible for the care of any others at home?
7.
Do you have someone at home to help you? If so, whom?
8.
What questions or concerns do you have?
9.
Do you practice a religion? If so, which?
10. The language you understand best is?

I I. How much education/schooling have you had?
Part II. There are many different ways to learn. Please read the list of ways to learn below and circle the ones which
help you learn best.
Group discussion
Reading materials
Lectures (listening)
By myself
Demonstrations watching)
Games
Videos
Computer programs
Audiotapes (cassettes)
Seminars
Practice/Stimulation (doing)
Role playing
Written tests
Other
Part III I would like to know more about: (Check all that apply to you.)
How to clear mucus from my lungs
What causes heart disease
How to avoid shortness of breath
What I should eat
Exercise
My medications
Monitoring myself
Planning my social life
What to do if I have chest pain
Planning for sexual intimacy
What causes lung disease
Coping with my feelings
Other things J would like to know:

The three most important things I need to know are:
26
Patient Education
459
mining what is important to the learner and facilitate
learning activities. By identifying the patient's needs
motivation. What the instructor feels is important to
the physical therapist can then make informed
learn may not be what the patient feels is important to
choices in the course of planning and implementing
learn. Identifying what the patient values early will
each patient education experience.
prevent instructor (and patient) frustration later.

Cultural influences and personal and societal re
sources are included in the environmental area. Being
aware of the patient's life style, religion, traditions,
Formulation and Prioritization of Goals

As physical therapists set treatment goals for their pa
roles, and primary language are important for the in
tients, they should also set educational goals. Treat
structor to assess to individualize the patient's learn
ment goals usually describe functional outcomes
ing experience. Presence or absence of the patient's
(e.g., the patient will perform a stand and pivot trans
resources may affect consistency in and access to pa
fer from bed to chair, i ndependently) and they are
tient education.
written in behavioral terms. Educational goals should
All five of these areas can be addressed with the
also be written in behavioral terms. For example,
use of a learning needs assessment survey. See Figure
"Mr. J will safely perform percussion and postural
26-2 for an example. By using a survey in combina
drainage to Mrs. J's right lower lobe." The stated be
tion with the physical therapy patient evaluation, the
havior needs to be measurable in some way. Motor
therapist can gather all the necessary information to
skills can be observed, knowledge skills can be
create an optimal patient education experience. The
tested, and safety can be documented.
survey in the box on p. 458 consists of three parts,
Prioritizing the patient's educational goals in con
which can be adapted to any patient-care setting. In
junction with treatment goals enhances the therapist's
the pediatric setting, some of the questions could be
efficiency. Referring again to the learning needs as
asked of the parent(s) or rephrased to address elemen
sessment survey (see the box on p. 458) to determine
tary-school-aged children. Part I primarily assesses
what is important knowledge to the patient will guide
the patient's perception of the illness or disability and
the therapist in creating the most appropriate prioriti
its impact on the patient's life. Part II lists a wide va
zation of goals. Simplicity is usually best. Over
riety of teaching methods and asks the patient to indi
whelming patients with a huge list of items to be ac
cate which methods are most useful personally. Part
complished may discourage them before they even
III identifies specific topics about which the patient
start. If the patient's learning needs are very great,
would like to know more. This part is also helpful in
start by breaking down the list of goals into smaller
alerting the therapist that referrals to other members
groups. Choose the most important goals and try to
of the interdisciplinary health-care team may need to
accomplish them first. If you run into a series of fail
be made. For example, if the patient checked off
ures, tackle the next group. Build on each success the
"what I should eat," the therapist should make a re
patient experiences.
ferral to the dietician.
EDUCATIONAL METHODS
Interpretation of Findings
Method Selection
The next important step after gathering information
Using the learning needs assessment survey (see the
with the learning needs assessment survey is to inter
box on p. 458) will allow the clinician to choose edu
pret the findings. The physical therapist must look at
cation methods that will facilitate optimal learning in
the answer to each item on the survey and use that in
a given patient or group. The patient(s) can self-select
formation in the process of designing the content and
the available learning methods that have the greatest
method for teaching that patient. Interpretation of the
learning potential. A combination of methods may be
survey findings means applying the patient's current
necessary to achieve the educational goals that have
health concerns and knowledge deficits to future
been set. If a patient is not sure which methods to in
460
PART III
dicate, the therapist can base the choice on the other
therapist in determining the settings and populations
information provided in the survey (e.g., sensory
in which the methods will be most useful. This is not
deficits, level of schooling, or type of information de
a comprehensive list. In fact, some health-education
sired). Surveys generally require regular updates to
challenges require truly innovative approaches.
ensure that all of the offered methods are listed and

the discontinued methods are removed from the list.
In 1988, for example, community health-care

providers in Boston were faced with a dilemma. The
incidence of acquired immune deficiency syndrome
(AIDS) among women of color was increasing and
Advantages and Disadvantages
Latino, African-American, and Haitian women were
Each education method has its own advantages and
not receiving vital information about how to prevent
disadvantages. Table 26-1 shows 13 education meth
the transmission of the human immunodeficiency
ods listed with their key advantages and disadvan
virus (HIV). These communities were largely dis
tages. The table is designed to assist the physical
trustful of the health-care establishment and were not
TABLE 26-1
Comparison Chart for Education Methods (Adult'i and children unless otherwise noted)
TYPE
ADVANTAGES
DISADVANTAGES
Reading
Patient can refer back to material.
Requires instlUctor follow-up for comprehension.
Low effort for instructor.

Lecture
Time-efficient for instructor. Cost-efficient.
Low interaction. May pacify rather than engage.
Demonstration
Adds sensory data to learning. Allows for
Instructor needs proficiency in skill to be
problem solving and modification.

Video
Access to restricted areas. Portrays events that are

infrequent, costly, and difficult to reproduce.
Portable.
demonstrated.
Noninteractive. May pacify rather than
engage. Costly, requiring electronic
equipment. Difficult to control quality.
Audiotape
Portable. Useful for sight-impaired learner.
Requires electronic equipment.
Group discussion
Effective use of instructor time. Enlarges pool
Not as much individual attention given. Group
Clubs, camps,
and retreats
Individual
instlUction
Games and directed
activities
of real-life experiences. Nonthreatening to
may be hard to control (e.g., too talkative,
some learners. Mutual support possible.
shy,hostile). Strong facilitator skills needed.
Draws on community and individual resources.

Needs less professional input and time.
Instructor can tailor learning to student's
needs and desires. More one-on-one time.
Helpful for children. Reduccs anxiety. Uses
Same as above. Some risk of perpetuating

myths and false information.
Inefficient use of instructor time. Limited pool
of experience on which to draw.
Scheduling space. Finding participants.
repetition. Fun. Unexpected experiences

can lead to new understandings or insights.
Computer programs
Interactive, self-paced. Large information

capacity. Time-cfficient for instructor.
Seminars and
workshops
Diversity of instructors and formats. Pool
Expensive. Special equipment and space

needed. May require expert help.
Expense, scheduling, and space.
of expel1s and community resources. Can

tailor content broadly or narrowly.
Role-playing
Trial runs, problem-solving, simulated
Threatening to some. Can be time-consuming.

Instructor needs to be skilled in techniques and
experiences.
dealing with effects on participants.

Oral and written
tests
Can provide instructor with evidence of what

learner needs to be taught and what has been
learned.
Literacy and supplies required, if written. May

be time-consuming.
26
mobilized to stop the spread of HIV. How could they

be reached? The Boston Women's AIDS Information
Project (BWAIP) trained lay women to educate other
women in the places where they congregate, such as
beauty salons. Informational brochures, condoms,
and posters were distributed in a number of beauty
salons in communities where women were at highest
risk for contracting HIV. Lay and professional educa
Patient Education
Cardiopulmonary Patient Education Content

Smoking cessation
Risk-factor modification
Benefits and effects of exercise
Resumption of sexual activity
Normal cardiopulmonary anatomy and physiology
tors would give presentations, show videos, and an
Cardiopulmonary disease process
swer questions of the staff and patrons of these estab
Airway clearance techniques and suctioning
lishments to empower them to disann myths about
Energy conservation and pacing techniques
AIDS, encourage other women to make appropriate

behavior changes, and to make referrals to neighbor
hood health centers for testing and evaluation.
Teaching young children about their bodies and
health may also require unique approaches. In 1993,
members of the interdisciplinary team caring for chil
461
Stress management
Cardiopulmonary resuscitation (CPR)-basic life
support
Hemt rate, blooo pressure, and dyspnea self-monitoring
Nutrition
dren with cystic fibrosis (CF) at Texas Children's Hos
Medications (schedules. actions, and side effects)
pital, Houston, held a CF Education Day for the chil
Use of oxygen and other respiratory equipment
dren and their parents. The children ranged in age from
Medical procedures (e.g., cardiac catheterization or
7 to .1 I years old. To teach them about anatomy, a spe
cial anatomy apron was fabricated. The apron had life

sized removable "organs" made of stuffed fabric. The
children took turns wearing the apron and learned to
bronchoscopy)
Community resources
Emergency procedures
identify and locate the organs by removing and replac

ing the apron's heart, lungs, intestines, and pancreas.
By evaluating the advantages and disadvantages of
available education methods, the physical therapist
can choose the methods that are most effective and
education experience. Although the physical thera
use them to their best advantage. Consideration must
pist may not be responsible for teaching on all these
be given for cost, equipment, scheduling, labor, time,
topics, she or he should be familiar with them as
site, flexibility, and reusability. For example, video
they are taught by others on the health-care team.
taped presentations may be easy for the instructor to
Educational materials on all of these topics have al
schedule, present, and reuse but they can be costly to
ready been developed by a variety of health-care
purchase and require expensive equipment to view.
providers, educators, and organizations and may be

available for physical therapists' use (see "Interdis
ciplinary Considerations and Resources").
Content
The specific content of patient education materials
and programs should be determined by the needs of
DETERMINATION OF EFFECTIVENESS
the individual or group being taught. However, there
Determining the effectiveness of patient education ef
are topics common to many cardiopulmonary educa
forts involves evaluating not only what the patient
tion efforts. These topics are listed in the box above.
learned but also how the teacher taught. Sometimes
The physical therapist can use the topics listed in
patients learn in spite of educational efforts. As phys
the table as a checklist to explore the content cov
ical therapists, we need to examine how effective we
ered (or to be covered) in a given cardiopulmonary
are at teaching and strive to improve our teaching
462
PART III
skills just as we strive to improve our treatment
sition the woman without disturbing the many tubes
skills. Being able to communicate ideas and receive
and lines that were present. Later the woman ex
feedback from patients from diverse racial, ethnic,
pressed that she did not want to have two physical
vocational, religious, and generational backgrounds is
therapy clinicians working with her at the same time.
crucial for physical therapists. We develop rapport
She confided to the nurse that it was because she felt
with our patients by communicating to them that we
it was too much like the Jewish ritual washing of the
have an understanding of their illnesses or disabili
body after death, which is traditionally pelformed by
ties, as they perceive them, and that we plan to inte
two people. This interpretation of the therapy sur
grate their goals or priorities into the treatment plans.
prised the physical therapy staff members who

treated the woman because they were also Jewish and
the thought never occurred to them. The next time tl1e
Teacher-Learner Relationship
clinicians went to see the woman, they explained why
According to Locke (1986), the primary step to under
it was necessary for both of them to be present during
standing others, is an awareness of one's self. Ac
the treatment. They also encouraged the woman to
knowledging one's own personal values, interests, and
have other supportive people present and to play her
biases will significantly increase one's sensitivity to
favorite recorded music during the therapy session.
ward others. The skilled teacher is aware of her or his

own communication style and its limitations and can
convey the desire to help despite those limitations.
The teacher-learner relationship that develops be
Patient Adherence
The effectiveness of physical therapy treatment, or
tween physical therapist and patient largely is due to
of any medical treatment, depends on the patient
communication between the two in the context of
following the health-care provider's recommenda
culture. Communication is a two-way process con
tions (adherence.) Unfortunately there is often a gap
sisting of verbal and nonverbal messages. The inter
between what the patient is asked to do and what the
pretation of these messages depends on the cultural
patient actually does. This gap, or nonadherence,
cues operating in the educational setting. Fairchild
has an incidence rate estimated between 50% to
(1970) defines culture as all social behavior, such as
80% (Meichenbaum and Turk, 1987). Factors af
customs, techniques, beliefs, organizations, and re
fecting patient adherence include knowledge of and
gard for material objects, including behaviors trans
course of the illness, complexity of the recommen
mitted by way of symbols. "The primary mode of
dations, convenience, availability of support system,
transmission of culture is language, which enables
and the patient's beliefs.
people to learn, experience, and share their traditions
Patient education can improve adherence when the
and customs" (Locke, 1992). In addition, culture can
information given includes what behaviors are ex
be expressed or experienced via economic and politi
pected, when they should be performed and what to
cal practices, art, and religion. Health care and medi
do should problems mise. Plans for patient education
cine have their own cultures. To meet the needs of
sessions should strive to remove or avoid barriers to
culturally diverse populations and engage in positive,
patient adherence. These efforts include simplifying
productive relationships, physical therapists need to
and individualizing treatment regimens, fostering col
operate from a framework of cross-cultural under
laborative teacher-learner relationships, enlisting
standing. This understanding and knowledge can then
family support, making use of interdisciplinary and
be reflected in patient education efforts.
community resources, and providing continuity of
For example, in a large, urban, acute-care hospital
care (Meichenbaum and Turk, 1987). By using an ap
two physical therapy staff members were working to
proach that integrates these efforts, the physical ther
gether to treat an elderly Jewish woman who was
apist can optimize patient adherence to the prescribed
critically ill. The clinicians worked carefully to repo
physical therapy program.
26
INTERDISCIPLINARY CONSIDERATIONS
AND RESOURCES
Patient Education
463
Health-related organizations can also be rich re

sources for patient education information. The Amer
The interdisciplinary health-care team has evolved as
ican Heart Association and the American Lung Asso
the complexity and amount of available medical
ciation, for example, have many cardiopulmonary
treatments and information has grown. Physical ther
materials available to health-care providers for little
apists are trained to function as part of an interdisci
or no cost. State public health and local community
plinary team and are respohsible for learning the
service agencies may also be sources for printed or
areas of responsibility and expertise covered by each
audiovisual materials. The Health and Human Ser
member of their team. The team often consists of li
vices Department of the Federal government has nu
censed and nonlicensed health-care providers and
merous divisions addressing health education. Cata
may include any or all of the following:
logs listing these publications can be obtained from
Physician
the Federal Consumer Information Center, Pueblo,
Nurse
Colorado
Physical therapist
81009.
Community organizations such as YMCA, YWCA,
Occupational therapist
and the American Red Cross offer a wealth of health
Exercise physiologist
education materials and classes. Many of these agen
Dietician
cies also have catalogs of their educational offerings,
Laboratory technologist
which can be obtained by telephoning their local of
Pharmacist
fices. Local public, medical, and hospital libraries are
Social worker
also useful for seeking out available health-education
Chaplain or pastoral care associate
materials. Many Chambers of Commerce keep lists of
Clinical psychologist
local support groups or clubs, such as Breather's Club
Speech therapist
or Heartbeats. Regional state colleges or universities
Vocational rehabilitation counselor
have departments dedicated to health education and
Home-care personnel
may have cardiopulmonary materials to share.
All of the above providers may not be present on

every team, but their services should be available for
patients who need them. By understanding what ser
SUMMARY
vices and patient education material are provided by
This chapter defined patient education and described
each discipline, the physical therapist can reinforce
selected learning theories as they relate to cardiopul
previously presented concepts and avoid giving con
monary patient education. The evaluation of the pa
flicting information. This also allows the physical
tient's learning needs was emphasized and the advan
therapist to make referrals to the appropriate disci
tages and disadvantages of a variety of educational
pline when other knowledge deficits are identified.
methods were discussed. The role of the teacher-learner
Interdisciplinary team members can also provide
relationship and patient adherence were explained in
the physical therapist with important patient feedback
reference to the determination of patient education and
and information. Teaching methods found to be suc
treatment effectiveness. Finally, interdisciplinary
cessful with a given patient by the nurse, for exam
health-care team interactions and resources for patient
ple, could be communicated to the physical therapist.
education materials were considered.
The therapist can then use similar methods with that

patient for physical therapy education objectives.
Communication between team members is enhanced
REVIEW QUESTIONS
by regular team meetings or rounds and by having a
I. Discuss the benefits of patient education, includ
central location to document completed patient edu
ing impact on health care costs and patient's re
cation experiences (i.e., the medical record).
sponse to treatment.
464
PART III
2. Define the overall obj ective of patient education
Liedekerken, P.e., Jonkers,
ways to minimize them.

3. Explain the rationale for patient education using
concepts of adult learning theories or models.
R.,
DcHaes. W.F., Kok, G.1., & Saan,
J. (Eds.) (1990). Effecti veness of healrh education: review alld
and discuss the potential barriers to learning and
analysis. Assen, Netherlands: Van GorcllJn.

Locke, D.e. (1992). Increasing multicultural IJIlderstandillg: a
comp rehensive lIIodel. Newberry Park: Sage Publications.
Locke, D.C. (1986). Cross-cultural counseling issues. In A.J.
Palmo & W.J. Weikel et al (Eds.), Foundations of Ille II ta I
4. Describe the most important aspect of planning
health counseling. Springfield, IL: Charles
for patient education.

S. Discuss the components of a learning needs as
e.
Thomas.
Manzelli, J.D., Hoffman, L.A., Sereika, S.M., Sciurba, F.e., &

Griffith, B.P. (1994). Exercise, education, and quality of life in
sessment survey and ways to modify it for spe
lung transplant candidates. Journal of Heart and Lung Trans
cific patient populations.
plantation. 13(2),297-305.
Mazzuca, S. (1982). Does patient education in chronic disease have
therapeutic value.
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10
PART
IV
Guidelines for the Delivery

of Cardiopulmonary
Physical Therapy: Acute
Cardiopulmonary Conditions
Acute Medical Conditions
Elizabeth Dean
Willy E. Hammon
Lyn Hobson
KEY TERMS
Acute exacerbations of chronic
Cystic fibrosis
airflow limitation
Hypertension
Alveolar proteinosis
Alveolitis
Pneumonia
Asthma
Stable angina
Atelectasis
Stable myocardial infarction
Bronchiolitis
Tuberculosis
Bronchitis
INTRODUCTION
circulation to effect cardiac output and tissue perfu
The purpose of this chapter is to review the manage
sion (Dantzker, 1983; Dantzker, 1988; Scharf and
ment of primary cardiopulmonary dysfunction sec
Cassidy, 1989; Wasserman and Whipp, 1975). Thus
ondary to other medical conditions. Several types of
impairment of one organ inevitably has implications
medical conditions are presented to illustrate the prin
for the function of the other organ. In addition, threat
ciples and basis for cardiopulmonary physical therapy
to or impairment of oxygen transport has implications
in their management. These principles serve as a
for all other organ systems, thus a multisystem ap
guide to problem solving when the practitioner is con
proach is essential (see Chapters I and 5). The pri
fronted with pathologies that are not presented. Al
mary pulmonary conditions that are presented include
though conditions are usually classified as either pri
atelectasis, pneumonia, bronchitis, bronchiolitis, alve
mary lung disease or primary cardiovascular disease,
olitis, alveolar proteinosis, acute exacerbations of
the heart and lungs work synergistically to effect gas
chronic airflow limitation, asthma, cystic fibrosis, in
exchange and in series with the peripheral vascular
terstitial pulmonary fibrosis, and tuberculosis. For fur

469
470
PART IV
Guidelines for the Delivery or Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions
ther epidemiological and pathophysiological detail on
have reduced lung volumes and are prone to breath
these conditions refer to Bates (1989), the Epidemio
ing at low lung volumes and microalelectasis, requir
logical Standardization Project of the American Tho
ing prophylactic measures to avoid significant effects
racic Society (1989), Luce (1986), Murray and Nadel
of atelectasis on oxygen transport and gas exchange.
(I 988a), Murray and Nadel (1988b), and West (1987).
When the conditions for normal lung inflation are re
The primary cardiovascular conditions presented in
moved, alveolar collapse occurs instantaneously.
clude hypertension, medically stable angina, and un
Microatelectasis is associated with reduced lung
complicated myocardial infarction. For further details
compliance because of reduced lung expansion. Me
on these condi tions refer to Goldberger (1990),
chanically ventilated patients are prone to microat
Sokolow, McIlroy, and Cheitlin (1990), and Under
electasis because the normal mechanics of breathing
hill, Woods, Froelicher, and Halpenny (1989).
are violated. In part, this may be explained by re
Treatment principles are presented that are not in
stricted mobility, recumbency, and reduced arousal,
tended to be a treatment prescription for a particular
in addition to reduced functional residual capacity
patient. The treatment priorities are presented based
(FRC). Positive end-expiratory pressure (PEEP) is
on the underlying pathology. However, without dis
routinely added to minimize these effects. High ven
cussion of a specific patient and knowledge of other
tilator system pressure is required to counter reduced
significant factors (i.e., the effects of restricted mobil
lung compliance, which indicates that atelectatic lung
ity, recumbency, and the effects of extrinsic and in
tissue it not readily reexpandible.
trinsic factors) (Chapter 16), the specific parameters
Microatelectasis is not detected readily with chest
of the treatment prescription cannot be established.
x-ray but is on the basis of clinical findings. Nonethe
Integration of this information is essential for treat
less, microatelectasis can be anticipated in every ill
ment to be specific and maximally efficacious. For
and hospitalized patient whose normal respiratory me
specific examples of patient treatment prescriptions
chanics are disrupted, and particularly, in recumbent,
refer to the companion text Clinical case studies in
relatively immobile patients. These effects are further
cardiopulmonary physical therapy.
exacerbated in older patients, patients who are over

weight, have abdominal masses, spinal deformities, or
chest wall asymmetry, smokers, and sedated patients.
Atelectasis
Pathophysiology and medical management
Commensurate with its distribution, atelectasis

presents with reduced chest wall movement and re
A t e l e c t a s i s refers to p a r tial collapse of lung
duced breath sounds over the involved area. A chest
parenchyma. The pathophysiological mechanisms
x-ray shows increased density over the involved areas
contributing to atelectasis are multiple (see box on
with a shift of the trachea and mediastinum toward
p. 471). These mechanisms include physical compres
the collapsed lung tissue. The patient may be tachyp
sion of the lung tissue (e.g., resulting from increased
neic and cyanotic because of shunting. Segmental at
pleural fluid, pus, pneumothorax, or adjacent areas of
electasis results from significant progression of mi
lung collapse) or from an obstructed airway (e.g., se
croatelectasis and by obstruction of airways with
cretions or tumor) with subsequent reabsorption of
resorption of gas in the distal lung units of a bron
oxygen from the trapped air by the pulmonary capil
chopulmonary segment or lobe.
laries resulting in a collapse of the lung tissue distal to

the obstruction (i.e., reabsorption atelectasis).
The ventilator-dependent patient is predisposed to

developing atelectasis because of an unnatural, mo
There are two primary forms of atelectasis-mi
notonous breathing pattern, restricted movement, and
croatelectasis and segmental and lobar atelectasis.
abnormal and prolonged recumbent body positions.
Microatelectasis is characterized by a diffuse area of
These factors contribute to reduced mucociliary trans
lung units that are perfused but not ventilated, hence,
port, abnormal distribution of pulmonary mucus, and
right-to-Ieft shunt. III and hospitalized patients who
the accumulation of mucus in the dependent lung
are deprived of being regularly upright and moving
fields. Furthermore, production of mucus may be in
Pathophysiological Mechanisms Contributing to Atelectasis

Central Mechanisms
Breathing at low lung volumes (e.g., when in pain or after certain medications)
Inability to gcnerate adeljuate inspiratory pressure and volume
Central disruption of breathing centers controlling normal periodic and rhythmic breathing pattern
Extramural Mechanisms
Chest wall deformity
Asymmetry of intrathoracic ,tructures
Respiratory muscle weakness (e.g., neuromuscular disease)
Phrenic nerve inhibition (e.g., secondary to upper abdominal or cardiovascular thoracic surgery)
Compression of lung parenchyma secondary to pleural tluid accumulation, blood, plasma. and pus
Compression of lung parenchyma during surgery

Reduced lung expansion secondary to reduced movement
Compression of lung parenchyma secondary to static body positioning
Compression of lung parenchyma secondary to prolonged static body positioning
Mechanical ventilation
Increased alveolar surface tension
Mural Mechanisms
Airway narrowing seconuary to increased bronchial smooth muscle tone
Calcification or altered anatomical integrity of airways
Edema of the bronchial wall and epithelium
Intramural Mechanisms
Impaired mucocilial'Y transport
Increased pulmonary secretions
Inspissated pulmonary secretions
Altereu distribution of pulmonary secretions
Mucolls plug
Space.Occupying Lesions
Exuuative and transudative tluid in the lung parenchyma
Foreign-bouy aspiration
Intlammation
Other Factors
Increased compliance and dynamic airway compression secondary to age-related changes to the lung
Increaseu timc constants because of increased airway resistance. reduced compliance. or both
Splinting or casting of chest wall restricting normal three-dimensional chest wall movement
Pain anu altered breathing pattern
Medications including narcotics, sedatives, and relaxants
Oxygen
472
PART IV
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions
creased due to tracheostomy or the presence of an
these interventions distributes ventilation more uni
endotracheal tube. Mucociliary clearance is further
formly rather than directing gas to already open alve
compromised by reduced ciliary activity resulting
oli, which will overdistend these units. The distribu
from high concentrations of oxygen, medication,
tion of ventilation is primarily altered by body
and loss of an effective cough because of an artifi
positioning and not by deep breathing (Roussos, Fix
cial airway.
ley, Geriest, Cosio, Kelly, Martin, and Engely, 1977).
The effect of atelectasis on oxygen transport re
Sustained maximal inspiratory efforts may augment
flects its type and distribution. Hypoxemia, right to
alveolar ventilation, however, the parameters for such
left shunt, reduced lung compliance, and increased
efforts to be maximally therapeutic have not been
work of breathing are common clinical manifesta
studied in detail.
tions. An increased temperature reflects an inflamma

tory or infective process and not atelectasis per se.
Principles of physical therapy management

Because it can develop instantaneously when respira
tory mechanics are disrupted, microatelectasis should
If impaired mucociliary transport or excessive secre

tions are obstl1lcting airways and contributing to atelec
tasis, mobilization of pulmonary secretions is the goal
that may be affected by mobilization and a "stir-up reg
1941; Ross and Dean,

1989). In addition, postural drainage coordinated with
imen" (Dripps and Waters,
be anticipated and prevented. Those factors that con
breathing control and coughing maneuvers can facili
tribute to atelectasis for a given patient are countered
tate airway clearance. The addition of modified manual
accordingly with aggressive prophylactic manage
techniques may be indicated in some patients.
ment (see the box on p.
471).
Once developed, however, atelectasis is treated

aggressively. Treatment is primarily directed at re
versing the underlying contributing mechanisms
whenever possible (Don, Craig, Wahba, and Couture,
1971; Glaister, 1967; Leblanc Ruff, and Milic-Emili,

1970; Lewis, 1980; Ray, Yost, Moallem, Sanoudos,
Villamena, and Paredes, 1974; Remolina, Khan, San
tiago, and Edelman, 1981). For example, atelectasis
Pneumonia
Pneumonia is a common cause of morbidity and mor
tality in the hospitalized patient, particularly in very
young and very old patients (Bartelett and Gorbach,
1976). Comparable wi th other systemic infections,

pneumonia results when the normal defense mecha
resulting from restricted mobility is remediated with
nisms of the respiratory system fail to adequately
mobilization. Atelectasis resulting from prolonged
protect the lungs from infection.
static positioning and monotonous tidal ventilation is
Air inspired through the nasal passages is cleansed
managed with mobilization, manipulating body posi
of particulate matter by filtration (cilia sweep it to the
tion to increase alveolar volume of the atelectatic
nasopharynx); impaction (irregular contour of the
area, manipulating body position to optimize alveolar
chamber causes particles to rain out); swelling of hy
ventilation, or some combination of these interven
groscopic droplet nuclei, which are either filtered or
tions. Atelectasis arising from reduced arousal is
become impacted; and defense factors located in the
managed by reducing the causative factors contribut
mucous blanket, such as immunoglobulins (IgA),
ing to reduced arousal coupled with frequent sessions
Iysozymes, polymorphonuclear leukocytes, and spe
of mobilization and the upright position to increase
cific antibodies. Particles that escape one of these de
arousal, promote greater tidal volumes and alveolar
fense mechanisms in the nasopharynx may be pre
ventilation, increase zone 2 (area of optimal ventila
vented from entering the lower airways of the larynx.
tion and perfusion matching), increase FRC, and min
The mucosa of the larynx is sensitive to chemical irri
imize closing volume.
tation or mechanical deformation and responds to this
Breathing control and coughing maneuvers aug
stimuli by producing a cough. The high velocities
ment the cardiopulmonary physiological effects of
created by the cough are sufficient to clear several
mobilization and body positioning. Coordinating
branches of the tracheobronchial tree of particulate
27
473
matter. The cough reflex is frequently absent or de
common cold. The ciliated cells of the respiratory
pressed in hosts who are unconscious from drug
tract are the most frequent site of infection. They be
overdose, epilepsy, alcohol ingestion, or head injury.
come paralyzed and degenerate with areas of necrosis
Patients with artificial airways are more susceptible
and desquamation. The mucociliary blanket becomes
to infection because all the previously mentioned de
interrupted because destruction of the cilia leaves a
fense mechanisms are bypassed, causing organisms
thin layer of nonciliated basal replacement cells. In
to be deposited directly in the lower airways. In the
flammatory responses cause exudation of fluid and
lower airways the cough mechanism is rendered inef
erythrocytes in both the alveolar septae and airways.
fective by endotracheal tubes, which prevent approxi
Congestion and edema become predominant with the
mation of the vocal cords, and by tracheostomy
formation of intraalveolar hyaline membranes. These
tubes, which cause air to bypass the cords altogether.

The trachea and the tracheobronchial tree to the
changes in the normal mucosal structure and cilia

make involved areas of the lung susceptible to super
level of the respiratory bronchioles are protected by
imposed bacterial infections. This is the most com
the cough reflex, filtration (again by cilia which
mon complication seen in viral infections and is usu
transport particles to the pharynx), impaction, and
ally responsible for the fatalities that occur.
chemical factors (IgA). Below the level of the respi
The patient with viral pneumonia presents with
ratory bronchioles, the cough reflex is ineffective,
fever, dyspnea, loss of appetite, and a persistent non
and filtration and transportation of particles by cilia
productive cough. On auscultation, normal breath
cannot occur because cilia are absent. The alveolar
sounds are heard throughout both lung fields with
macrophages play an important role in protecting
scattered inspiratory crackles. X-ray changes range
these airways from particulate matter. Macrophages
from minor infiltrates to severe bilateral involvement.
ingest organisms and transport them to the lymphatic
Consolidation and pleural effusions occur less fre
system or higher in the tracheobronchial tree to
quently. Secondary bacterial infections occur fre
where cilia can sweep them to the pharynx. This
quently, causing patients to develop productive
process of phagocytosis can be slowed or stopped by
coughs.
hypoxia, alcohol ingestion, air pollutants, corticos
Influenza may lead to viral pneumonia in I % to
teroids, immunosuppressant agents, starvation, ciga
5% of cases. Influenza includes acute viral respira
rette smoke, and oxygen. Particulate matter may also
tory tract infection, characterized by a sudden onset
be removed from the airways below the level of the
of headache, myalgia, and fever. The route of infec
respiratory bronchioles by postural drainage.
tion is by inhalation of airborne particles from an in
Routes of Infection
hours.
A host who has impaired or ineffective defense
tory epithelium with necrosis and hemorrhage. At the
fected person. The incubation period is 24 to 72

Pulmonary lesions include edema of the respira
mechanisms of the respiratory tract becomes suscep
alveolar level, interstitial edema, proliferation of type
tible to a variety of organisms. The major routes of
I cells, hemorrhage, and an increased number of
infection include airborne organisms, circulation,
macrophages are seen. In patients with pneumonia,
contiguous infection, and aspiration.
secondary bacterial infections are frequent and are

the cause of most fatalities.
Medical treatment of viral infections is supportive
CLASSIFICATION OF PNEUMONIA
Viral Pneumonias
and preventative. Patients should receive vaccines
Most respiratory viral infections are contracted by
cific viruses. Once the patient has contracted the or
droplets from the respiratory tracts of infected per
ganism, treatment becomes supportive, with rest, sali
whenever possible to buildup antibodies against spe
sons. These viruses are responsible for interstitial
c y lale s , and high f luid intake b e i n g the m a i n
pneumonias, tracheobronchitis, bronchiolitis, and the
treatment priorities. Patients w h o become more
474
PART IV
acutely ill with viral pneumonia should be on a vigor
illness characterized by fever, tachypnea, dyspnea, hy
ous preventative program to lessen the possibility of
poxemia, tachycardia, and a cough producing bloody
bacterial infection.
or purulent sputum. The clinical findings depend on
Recovery also depends on good nutrition, hydra
the organism involved and the extent of the pneumo

nia in the lungs. The infective process may cease with
tion, sleep, rest, and reduced stress.

Patients may respond to mobilization coordinated
the use of chemotherapeutic agents, aerosols, and

physical therapy, or it may spread to contiguous areas,
causing pleural effusions and empyemas.
with breathing control exercises and positional rota
Bacterial pneumonias can occur as either primary
tion for enhancing alveolar ventilation, mucociliary
or secondary infections. Primary pneumonias arise in
transport, and gas exchange overall (Orlava, 1959).
otherwise healthy individuals and are usually pneumo
Extreme body positions may enhance alveolar volume
coccal in origin. Secondary pneumonias occur when
and ventilation and ventilation and perfusion match
the patient's defense system becomes ineffective.
ing (Dean, 1985; Douglas, Rehder, Beynen, Sessler,
Pneumococcal pneumonia is caused by pneumo
and Marsh, 1977; Grimby, 1974; Piehl and Brown,
coccal bacteria, a gram-positive organism. It occurs
1976). Vigorous treatment should be initiated at the
most frequently in the winter months among adults
first sign of a superimposed bacterial infection, which
between 15 and 40 years of age with a predilection for
is often accompanied by a productive cough. At this
males. Patients present clinically with an abrupt onset
time, the appropriate devices should be prescribed
of illness characterized by fever, cough, purulent or
(e.g., ultrasonic or medication nebulizers to loosen se
rust-colored sputum, and pleuritic chest pain over the
cretions). Postural drainage may be indicated in addi
affected lung field. Physical examination may reveal
tion to mobilization for airway clearance. Treatments,
decreased expansion of the chest over the affected
particularly mobilization, need to be paced to mini
area and muscle splinting. On auscultation, there may
mize unduly tiring the patient or increasing oxygen
be bronchial breath sounds (indicating consolidation),
demand beyond the patient's capacity to adequately
decreased or absent breath sounds, and wheezes or
deliver oxygen. Increasing oxygen demands exces
crackles over the affected lung. Chest x-rays may
sively may compromise the patient's gas exchange.
show infiltrates, consolidation, or atelectasis.
Patient education is also fundamental to the treatment
There are four stages associated with bacterial in
that is to be instituted between treatments (i.e., mobi
fection of lung tissue-engorgement, red hepatiza
lization and positional rotation coordinated with
tion, gray hepatization, and resolution. The engorge
breathing control and coughing maneuvers).
ment stage occurs within the first few days of
The focus of cardiopulmonary physical therapy in
infection and is characterized by vascular engorge
the management of viral pneumonia is to augment
ment, serous exudation, and evidence of bacteria col
alveolar ventilation, increase perfusion, increase dif
onization. Red hepatization occurs within 2 to 4 days
fusion, and improve ventilation and perfusion match
as a result of diapedesis of the red blood cells. The
ing, thereby reducing the threat to oxygen transport
alveoli are full of polymorphonuclear leukocytes, fib
and gas exchange. Treatments are prescribed to opti
rin, and red blood cells. The organism continues to
mize oxygen transport and gas exchange and to mini
mUltiply within the fluid exudate. Areas of consolida

tion become evident. Gr<!y hepatization occurs within
mize fatigue and lethargy.
4 to 8 days and is characterized by evidence of abun

dant fibrin, decreased polymorphonuclear leukocytes,
Bacterial Pneumonia
and dead bacteria. Consolidation continues to be a
Bacterial pneumonia causes the largest number of
problem in this stage. Resolution occurs after 8 days
deaths per year by an infective agent and is the fifth
as areas of consolidation begin to resolve. Many
most common cause of all deaths in North America.
macrophages are seen and evidence of enzymatic di
The patient presents with an abrupt onset of a severe
gestion of exudate is present. The affected tissue be
27
comes softer with large amounts of grayish-red fluid
475
is the same as that for pneumococcal pneumonia.
present within the alveol i. This process continues for
Hemo philus inJluenzae pneumonia is caused by a
2 to 3 weeks with the lung gradually assuming a
gram-negative organism and occurs primarily in chil
more normal appearance.
dren as bronchiolitis and in adults who have chronic
Pleural involvement occurs frequently, with the
bronchitis. The clinical picture is the same as for the
pleural spaces filling with the same type of fluid
other bacterial pneumonias, with numerous areas of
seen within the alveoli. Resolution is much slower
infiltration evident on x-ray. On auscultation, breath
because there are few surfaces available for phago
sounds are generally good, with crackles heard at the
cytosis. Complications that may occur in patients
end of inspiration. Treatment of this pneumonia in
with pneumococcal involvement include empyema,
cludes chemotherapeutic agents (ampicill in), oxygen,
superinfections (occur when large numbers of new
ultrasonic nebulization, and physical therapy.
organisms invade the lung), abscesses, atelectasis,
Other gram-negative organisms causing pneumo
and delayed resolution (defined as taking more than
nia include Esch erichia co li and Pseudomo n as
aeruginosa. They are seen most frequently in patients
4 weeks to resolve).
Treatment of pneumococcal pneumonia involves
with underlying disease, especially pulmonary dis
the use of chemotherapeutic agents, with penicillin
ease, or in those who are debilitated. They are fre
being the antibiotic of choice. If the patient is allergic
q uently the cause of superinfections in individuals
to penicillin, erythromycin or lincomycin is used.
who have received massive doses of broad-spectrum
Thoracentesis is performed when pleural fluid is pre
antibiotics. Clinically these patients present with
sent. The patient should also receive ultrasonic nebu
cough, fever, and dyspnea. On auscultation, crackles,
lization and physical therapy. Supplemental oxygen
bronchial breathing, and diminished
therapy may be indicated.
sounds can be noted. X-ray changes frequently show
Staphlococcal pneumonia is caused by a gram
or
absent breath
bibasilar infiltrates, with the amount of involvement
positive organism. It rarely occurs in the healthy
being widely variable. As for other bacterial pneumo
adult but is a frequent cause of pneumonia in chil
nias, treatment includes chemotherapeutic agents, ul
dren, infants, and patients with chronic lung diseases,
trasonic nebulization, and physical therapy.
especially carcinoma, tuberculosis, and cystic fibro

sis. Clinically, the patient presents with the same pic
ture as the patient with pneumococcal pneumonia.

The goals of management of bacterial pneumonia in
There are some differences in the chest x-ray (e.g.,
clude reversing alveolar hypoventilation, increasing
patchy areas of infiltrate). Consolidation occurs infre
perfusion, reducing right-to-Ieft shunt, increasing
quently in this type of pneumonia. Pleural effusions,
ventilation and perfusion matching, minimizing the
empyema, abscesses, bronchopleural fistulas, and
effects of increased mucous production, and optimiz
pneumatoceles (subpleural cyst-like structures) occur
ing lymphatic drainage. Bacterial pneumonia is fre
frequently. Treatment includes chemotherapeutic
quently associated with increased mucous produc
agents, rest, increased fluid intake, ultrasonic nebu
tion. With respect to airway clearance, management
lization or medication nebulizers, and aggressive
focuses on augmenting mucociliary clearance overall,
physical therapy.
reducing excess mucous accumulation, and reducing
Streptococcal pneumonia is caused by a gram-posi
mucous stasis. Patients are often mobile and should
tive organism, Streptococcus pyogenes. It occurs most
be encouraged to be so to promote mucociliary trans
frequently in very young, very old, and debilitated pa
port and enhance lymphatic drainage (Dean and
tients. The clinical picture is very similar to that of
Ross, I 992a; Orlava, 1959; Wolff, Dolovich, Obmin
staphlococcal pneumonia. Again consolidation is rare
ski, and Newhouse, 1977). However, the oxygen de
and chest x-rays usually show one or more areas of
mands of mobilization and exercise should be well
patchy infiltrates. Complications are rare but empyema
within the patient's capacity to delivery oxygen.
does occasionally occur. Treatment for this organism
These interventions should be prescribed to avoid
476
PART IV
jeopardizing this balance and unduly fatiguing the pa
term, the bone marrow produces more red blood
tient (Dean and Ross, I992b). Deep breathing and ef
cells, leading to polycythemia. The work of the heart
fective coughing are singularly important maneuvers
is increased due to increased blood viscosity. Long
for clearing airways with special attention to the avoid
term hypoxemia leads to increased pulmonary artery
ance of airway closure (Bennett et aI., 1990). Prescrip
pressure and right ventricular hypertrophy.
tive body positioning can be used to optimize ventila
Patients with chronic bronchitis have tenacious,
tion and perfusion matching (Clauss, Scalabrini, Ray
purulent sputum that is difficult to expectorate. In an
and Reed, 1968; Douglas et aI., 1977; Hietpas, Roth
exacerbation, usually because of inflammation, infec
and Jensen, 1974; Hasani, Pavia, Agnew, and Clarke,
tion, or both, they produce even more sputum, which
199 I; Ross and Dean, 1992; Ross, Dean, and Abboud,
tends to be retained and stagnate. Retained secretions
I992b; Zack, Pontoppidan, and Kazemi, 1974).
obstruct airways and thus air flow, and reduce alveo

lar volume. The resulting venti lation and perfusion
inequality increases hypoxemia, CO2 retention, ac
Acute Exacerbation of Chronic Bronchitis

cessory muscle use, melabolic demand, and breathing

rate. Pao2 is further reduced and Paco2 tends to in
Chronic bronchitis is a disease characterized by a
crease. Hypoxemia and acidemia increase pulmonary
cough producing sputum for at least 3 months and for
vasoconstriction, which increases pulmonary artery
2 consecutive years. Pathological changes include an
pressure and predisposes the patient to right heart
increase in the size of the tracheobronchial mucous
failure (cor pulmonale) over time.
glands (increased Reid index) and goblet cell hyper
A patient having an acute exacerbation of chronic
plasia. Mucous cell metaplasia of bronchial epithe
bronchitis tends to have the following characteristics:
lium results in a decreased number of cilia. Ciliary
(I) The patient is often stocky in build and dusky in
dysfunction and disruption of the continuity of the
color. (2) The patient exhibits significant use of acces
mucous blanket are common. In the peripheral air
sory muscles of respiration and has audible wheezing
ways, bronchiolitis, bronchiolar narrowing, and in
or wheezing that is audible on auscultation. (3) Inter
creased amounts of mucus are observed.
costal or sternal retraction of the chest wall may be
Chronic bronchitis results from long-term irrita
noted. (4) Edema in the extremities, particularly
tion of the tracheobronchial tree. The most common
around the ankles, and neck vein distention reflect de
cause of irritation is cigarette smoking. Inhaled
compensated right heart failure.
smoke stimulates the goblet cells and mucous glands
report that breathing difficulty began with increased
(5) The patient may
to secrete excessive mucus. Smoke also inhibits cil
amounts of secretions (with a change in their normal
iary action. The hypersecretion of mucus and ciliary
color), which is often difficult to expectorate, and in
damage and dyskinesis lead to impaired mucous
creased cough productivity. (6) Pao2 is reduced, Paco2
transport and a chronic productive cough. The fact
increased, and pH reduced.
that smokers secrete an abnormal amount of mucus
Pulmonary function tests indicate reduced vital
increases the risk of respiratory infections and in
capacity, FEY!, maximum voluntary ventilation,
creases the length of the recovery time from these in
and diffusing capacity and increased FRC and resid
fections. Although smoking is the most common
ual volume.
cause of chronic bronchitis, other factors that have

been implicated are air pollution, certain occupational
environments, and recurrent bronchial infections.

During an exacerbation requiring hospitalization,
Patients with chronic bronchitis have been referred
these patients are usually treated with intravenous
to as blue bloaters because of a tendency to have a
fluids, antibiotics, bronchodilators, and low-flow
dusky appearance and be stocky in build. Although
oxygen. Diuretics and digitalis are often given to treat
many patients have a high Pac02, the pH is normal
right heart failure. Airway clearance interventions are
ized by renal retention of bicarbonate. Over the long
selected (i.e., mobilization, body positioning, and
27
477
postural drainage). These interventions are coordi
thickened basement membrane. The obstruction as
nated with breathing control and coughing maneuvers
sociated with bronchiolitis leads to ventilation and
to facilitate secretion removal and optimize coughing
perfusion abnormalities and diffusion defect. Clini
and expectoration, while minimizing dynamic airway
cally, the patient presents with a productive cough.
compression and alveolar collapse. During recovery,
Obliterative bronchiolitis has been reported to be
exercise with supplemental oxygen may also benefit
the most significant long-term complication o f
the patient. It is important for these patients to avoid
heart-l u n g t r a n s p l a n t a t i o n (B u r k e , Gla n v i lle,
bronchial irritants (e.g., cigarette smoking, second
Theodore, and Robin, 1987).
hand smoke, and air pollutants), and to be adequately
Medical management is directed at inflammation
hydrated to thin secretions to facilitate mucociliary
control with pharmacological agents, fluid manage
transport and expectoration.
ment, and oxygen administration if necessary. Pre
Patients with chronic bronchitis can benefit from

a comprehensive rehabilitation program designed
specifically for patients with chronic pulmonary
vention of infection is a priority.
disease (Murray, 1993; Oldenburg, Dolovich,
The principal pathophysiological defects include ven
Montgomery, and Newhouse, 1979). Specific de
tilation and pelfusion inequality and diffusion defect.
tails of exercise prescription in the management of
These defects result from secretions produced by in
chronic lung disease and of a comprehensive pul
flammation and increased mucous production and
monary rehabilitation program are described in
from atelectasis of adjacent alveoli. Physical therapy

treatment should promote mucociliary transpol1 and
Chapter 23.
the removal of secretions and mucus to central air

ways, promote alveolar expansion and ventilation,
Bronchiolitis
optimize ventilation and pelfusion matching and gas
exchange, and reduce the risk of infection.
Bronchiolitis results from peripheral airway inflam
Bronchiol i tis is primari Iy, al though not exclu
mation. In severe cases the exudate in the peripheral
sively, a childhood condition. The effects of inflam
airways becomes organized into a connective tissue
mation and obstruction in small children are always
plug extending into the peripheral airway. The in
serious because the anatomical and physiological
flammatory process resembles that in other tissues
components of the cardiopulmonary s ystem are
(i.e., an inflammatory stage followed by a prolifera
smaller, respiratory muscle tone is less well devel
tive healing stage). Such inflammation is associated
oped, the anatomical configuration of the chest wall
with vascular congestion, increased vascular perme
is cylindrical, breathing is less efficient until after the
ability, formation of exudate, mucous hypersecre
age of 2, spontaneous movement and body position
tion, and shedding of the epithelium. Fluid is exu
ing are more restricted (infants in particular spend
dated o u t of the circulation onto the alveola r
more time in nonupright positions), and children are
surfaces replacing the surfactant. This in turn in
at greater risk of infection (see Chapter 35).
creases the surface tension and promotes airway clo

sure. The secretion production associated with air
way irritants and inflammation results from the
excess mucous production in combination with the
inflammatory exudate consisting of fluid protein
Alveolitis
Bronchioalveolitis is another inflammatory disorder
and cells of the exudate. Airway obstruction results
of the peripheral airways that is often associated
if these substances are not removed. The airway ep
with an extrinsic allergic reaction. Comparable with
ithelium has the capacity to repair and reline the
bronchiolitis, alveolitis is prevalent in young chil
lumen. A rapid turnover of cells may contribute to
dren. In adults, chronic alveolitis may be a precursor
cell sloughing and further airway obstruction and a
to interstitial pulmonary fibrosis. Acute bouts of
478
PART
IV
alveolitis are reversible, however, chronic inflam
position with the lung to be lavaged downward. The
mation can produce airway narrowing secondary to
Carlen's tube enables the patient to be ventilated by
fibrosis in the alveolar wall and complete obstruc
the uppermost lung while the lower lung is care
tion of the airway by organization of the exudate.
fully filled with saline to FRC. Then an additional
Chronic inflammation can lead to permanent irre
300 to 500 ml of saline is alternately allowed to run
versible parenchymal changes and chronic restric
into and out of the lung by gravitational flow. As
tive lung disease.
the saline flows out, manual percussion over the af
fected lung being lavaged has been reported to in

c r e a s e t h e a m o u n t of p r o t e i n a c e o u s m a t e r i a l
The principles of physical therapy management are
washed f r o m t h e lung (see Figure
comparable with that for the management of bronchi
(Hammon,
4-11, p . 86).
1987).
olitis. Principles of the management of cardiopul

monary dysfunction in children are presented in
Chapter
35. Because children and infants in particular
are physically immature, the principles of manage

ment are different from those for adults.
Acute Exacerbation of Chronic Airflow limitation

PathophYSiology and medical management
Emphysema. There are two principal types of em
physema-centrilobular and panlobular. BOlh types
may coexist, however, centrilobular emphysema is
Alveolar Proteinosis
20 times more common than panlobular emphy

sema. Centrilobular is characterized by destruction
4-1, p. 73), as
Alveolar proteinosis is a condition of unknown etiol
of respiratory bronchioles (see Figure
ogy, characterized by alveoli filled with lipid-rich
well as edema, inflammation, and thickened bron
proteinaceous material and no abnormalities in the
chiolar walls. These changes are more common and
alveolar wall, interstitial spaces, conducting airways,
more marked in the upper portions of the lungs.
or pleural surfaces. Most often it is found in men be
This form of emphysema is found more often in
tween 30 and 50 years of age, although it has been re
men than in women, is rare in nonsmokers, and is
ported in both men and women of all ages.
common among patients with chronic bronchitis.
The most common symptoms are progressive dys
Panlobular emphysema is characterized by destruc
pnea and weight loss, with cough, hemoptysis, and
tive enlargement of the alveoli distal to the terminal
chest pain reported less frequently. Chest x-rays re
bronchioles (see Figure
veal diffuse bilateral (commonly perihilar) opacities
physema is also found in patients who have an antit
4-10, p. 86). Physical findings include
rypsin deficiency. Airway obstruction in these indi
fine inspiratory crackles, dullness to percussion and,
viduals is caused by loss of elastic recoil or radial
(see Figure
4-1, p. 73). This type of em
in the later stages, cyanosis and clubbing. Pulmonary
traction on the bronchioles. When individuals with
function studies usually show decreased vital capac
normal lungs inhale, the airways are stretched open
ity, FRC, and diffusing capacity. Arterial blood gases
by the enlarging elastic lung, and during exhalation
indicate a low P02, especially during exercise, with
the airways are narrowed due to the decreasing
often nonnal Pe02 and pH.
stretch of the lung. However, the lungs of patients
with panlobular emphysema have decreased elastic

ity because of disruption and destruction of sur
One treatment for patients with moderate-to-severe
rounding alveolar walls. This in turn leaves the
dyspnea on exertion from alveolar proteinosis is
bronchioles unsupported and vulnerable to collapse
bronchopulmonary lavage. The patient is taken to
during exhalation. This form of emphysema can be
the operating room. After general anesthesia and
local or diffuse. Lesions are more common in the
placement of a Carlen's tube (which isolates each
bases than the apices and tend to be more prevalent
lung), the patient is turned in the lateral decubitus
in older people.
27
than I cm in
emphysematous spaces
4-2, p.
prolonged. On expiration, the

neoLlsly
may be found in patients with

It is thought that
develop
from an obstruction of the conducting airways that

permits the flow of air into the alveoli
479
may sponta
a pursed-lip
pattern, which is
believed to augment alveolar
and
collateral ventilation and gas exchange in the

by
positive back pressures
tion but does not allow air to flow out again
and
1970). In addition, the
expiration. This causes the alveoli to become
tively
to compensate for the loss of the passive
inflated and eventually leads to destruction of the
elastic recoil that normally
inspira
air space in
alveolar walls with a resultant
the lung parenchyma. These bullae can be more than

10 em in diameter
intervention to
4-3, p. 75). If this happens,
creased. As the
rel-shaped and
bar
Loss of the normal
of the
chest and bucket and pump handle motions further

mechanics and
efficient
Dempsey, and
of
one of these bullae.
1976).
The emphysema patient's most common com
Both types of
can lead to chronic
chest wall
The loss of elastic recoil of the

disturbs the balance between the
norma.!
become more chronically
the chest wall becomes
remove the buJla is often necessary. Pneumothorax, a

serious complication, can result from the
the lungs at end
tidal volume. Overall the work of breathing is in
compression. can compro
mise the function of the remaining lung tissue (Figure
Petty,
may ac
recoil pul
the chest wall in and the
is dyspnea.
these patients appear
thin and have an increased anteroposterior chest wall

d iameter.
breathe
on disease
, they
the accessory muscles of inspiration
natural tendency of the chest wall to spring out. This
(Chapter
These patients may be observed leaning
balance is essential in maintaining norma.! FRC
forward,
their forearms on their knees, or sit-
the air in the
at the end of normal end tidal ex
with their arms extended at their sides,
piration). Because the residual volume of the lungs is
down against the bed or chair to elevate their shoul
FRC is correspondingly increased. This in
ders and improve the effectiveness of the accessory
H"'vU
VU,
crease is not functional,
because it reflects
are still prone to
muscles of
be-
have been referred to as pink

puffers because of the increased respiratory work
cause of the loss of the normal elastic recoil of the
they must do to maintain relatively normal blood
(i,e., increased
gases. On auscultation, decreased breath sounds can
increased dead space, These

dynamic airway
lung
and airway closure
This
contributes to uneven distribution of ventilation and
be noted throughout most or all of the
decreased diffusing
diologically, the
The pressure volume
lungs, flattened hemidiaphragms, and a small, elon
curve is shifted and ventilation is less efficient.
gated heart
With loss of elastic recoil and the normal

them patent, the chest wall
to the
outward, thereby
tends to
fields. Ra
patient has overinflated

Figure
p.
Pulmonary func
tion tests show a decreased vital capacity, FEY I,

maximum voluntary
and a
hyperinflated chest associated with the patient with
duced diffusing
chronic airflow limitation. The alveolar units are
increased and the residual volume and FRC are even
less uniform and the distribution of venti
The total
is
more increased. Arterial blood gases reflect a mildly

lowered
lation becomes even less homogeneous.
or
and expiratory times of the alveolar units also be
raised PaC02, and a normal pH. Emphysema pa
heterogeneous. The alveoli require
unlike patients with chronic bronchitis, tend to
filling times
For this reason, the
long time conwith chronic air
flow limitation adopts a characteristic breathing

tern in which
and expiration tend to be
a normal or slightly
with
cardiac
of the
condition,
to failure at the end stage of the
disease (see
4-5, p. 77). At this stage, cardiac
hypertrophy may be evident.
480
PART IV
Hypoxemia leads to hypoxic pulmonary vasocon
patients with a FEY1 less than 0.75 L. However, if
striction, which shunts blood from underventilated to
these flow rates are found in patients with complica
better-ventilated areas of the lung. The afterload
tions of resting tachycardia, chronic hypercapnia, and a
against which the right heart has to pump is in
severely impaired diffusing capacity, the survival rates
creased. This elevates the pulmonary artery blood
should be reduced by 25%. Other factors that have
pressure (i.e., pulmonary hypertension). Over the
been associated with a poor prognosis are cor pul
long term, the right heart hypertrophies to work
monale, weight loss, radiological evidence of emphy
against this increased resistance and eventually may
sema, a dyspneic onset, polycythemia, and Hoover's
fail (cor pulmonale). Heart enlargement secondary to
sign (inward movement of the ribs on inspiration).
any cause alters the electrical conduction pattern ef
The most frequent causes of death in patients with
fecting electromechanical coupling and cardiac out
airflow limitation are congestive heart failure (sec
put. The altered size and heart position within the
ondary to cor pulmonale), respiratory failure, pneu
chest wal.l can be detected by ECG changes.
monia, bronchiolitis, and pulmonary embolism.
Treatment of emphysema that requires hospitaliza
As emphysema becomes chronic, the hemidi
tion often includes intravenous fluids, antibiotics, and
aphragms become more horizontally positioned, plac
low-flow oxygen (Geddes, 1984; Make, 1983). Some
ing the muscle fibers at a less efficient position on
patients require bronchodilators, diuretics, and digi
their length tension curve (Druz and Sharp, 1982).
talis. Patients with chronic airflow limitation adapt to
Breathing when the muscle fibers of respiration are
high Paco2 levels, thus becoming dependent on their
mechanicall y disadvantaged increases the work of
hypoxic drives to breathe. Therefore, low flow oxy
breathing and therefore energy demands and oxygen
gen is administered to these patients to avoid abolish
cost. Respiratory muscle weakness and fatigue are se
ing their drive to breathe.
rious complications of chronic lung disease that pre
The etiology of emphysema is uncertain. The inci

dence of emphysema increases with age. It is most
dispose the patient to respiratory muscle failure

(Rochester and Arora, 1983) (Chapter 4 and 32).
often found in patients with chronic bronchitis and is
The net effect of these pathological changes on
significantly more prevalent in smokers than non
gas exchange is hypoxemia, hypercapnia, and re
smokers. There appears to be a hereditary factor. Se
duced pH consistent with respiratory acidosis. Long
vere panlobular emphysema can develop in patients
term respiratory insufficiency leads to chronically
with an alpha-antitrypsin deficiency relatively early
impaired oxygen transport and gas exchange. To
in life even though they never smoked. Repeated
compensate for hypercapnia, production of bicarbon
lower respiratory tract infections may also play a role
ate is increased to buffer retained CO2 (i.e., compen
in the pathology of emphysema. However, the inter
sated respiratory acidosis). Red blood cell production
relationship of these and other factors in producing
(i.e., polycythemia) is increased to increase the oxy
the condition is still not well understood.
gen-carrying capacity of the blood. The negative ef
Chronic bronchitis and emphysema are marked by a
fect of polycythemia, however, is increased viscosity
progressive loss of lung function and corresponding
of the blood, leading to increased risk of circulatory
cardiac dysfunction. At the end of 5 years, patients
stasis, thromboses, and increased work of the heart.
with chronic airflow limitation have a death rate four

to five times greater than the normal expected value.
Death rates reported by various studies depend on the
The patient with emphysema is prone to pulmonary
methods of selection of patients, types of diagnostic
infections and respiratory insufficiency. The clinical
tests, and other criteria. In general the death rates 5
picture is hallmarked by alveolar collapse and de
years after diagnosis are 20% to 55%. The 5-year sur
struction, ventilation and perfusion mismatching, and
vival rates based on FEY I have been reported as fol
diffusion defect. These defects result in impaired or
lows: 80% in patients with a FEY I greater than 1.2 L,
threatened oxygen transport if the physiological com
60% in patients with a FEY L close to 1 L, and 40% for
pensations are unable to maintain adequate blood
27
gases. Shortness of breath is exacerbated and breath
481
the chest wall by the viscera falling against the un
ing is labored. Increased work of breathing reflects
derside of the diaphragm in this position (i.e., vis
airway obstruction and inefficiency of respiratory
cerodiaphragmatic breathing) (Barach, 1974). The
mechanics and the respiratory muscles. Because of
muscle fibers of the diaphragm are mechanically
long-term airway disease, mucociliary transport is
placed in a more favorable position with respect to
disrupted. Therefore, in the presence of a pulmonary
their length-tension characteristics. This effect may
infection and increased production of pulmonary se
further be augmented in the head-down position in
cretions, secretion removal can be a significant prob
some patients (Barach and Beck, 1954). Other pa
lem for the patient.
tients, however, cannot tolerate recumbent posi
Specific treatments are prescribed for the patient
tions; in fact, respiratory distress may be increased.
based on the specific clinical findings (i.e., the type
If optimal treatment outcome has not been achieved
and severity of the cardiopulmonary dysfunction
with mobilization and body positioning coordinated
and the presence of infection). Therefore treatments
with breathing control and coughing maneuvers,
include mobilization coordinated with breathing
conventional physical therapy procedures may offer
control and coughing maneuvers, which are effec
additional benefit in some patients (e.g., postural
tive in enhancing alveolar ventilation, mobilizing
drainage and manual techniques).
secretions, and in ventilation and perfusion match
Because of the tendency toward dynamic airway
ing. Body positioning can be prescribed to alter the
compression resulting from the highly compliant air
distribution of ventilation, to aid mucociliary trans
ways of emphysema patients, open-glottis coughing
port, and to remove pulmonary secretions. Although
maneuvers are indicated. Specific outcome measures
"pure" emphysema is t y p i c a l l y dry, p o s t u r a l
are recorded before, during, and after treatment to as
drainage positions can facilitate the removal o f pul
sess short- and long-term treatment effects. In addi
monary secretions from specific bronchopulmonary
tion, between-treatment treatments are central to
segments if indicated. In any given body position,
maximizing overall treatment efficacy. Thus convey
alveolar volume is augmented in the uppermost lung
ing information effectively and specifically to the pa
fields and alveolar ventilation is augmented in the
tient, nursing staff, and possibly family members is
lowermost lung fields. The type and extent of
crucial to achieve an optimal treatment outcome.
pathology will determine the degree of benefit these
Comparable with the chronic bronchitis patient, an
physiological effects will have on oxygen transport.
exercise program for these patients should be pre
In addition, body positioning is essential to optimize
scribed to maximize oxygen transport capacity. Such
respiratory mechanics and enhance pulmonary gas
conditioning may reduce the frequency and severity
exchange, thereby reducing the work of breathing
of subsequent acute exacerbations. In addition, the
and the work of the heart. The assessment will de
patient may benefit from other components of a com
fine the parameters of the treatment prescription that
prehensive pulmonary rehabilitation program.
will be effective in relieving the work of breathing

and the work of the heart. This information is essen
tial not only for prescribing beneficial positions but
also for avoiding deleterious positions. A sitting
Acute Exacerbation of Asthma

lean-forward position will assist ventilation sec
Asthma is a condition characterized by an increased
ondary to the gravitational effects of the upright po
responsiveness of bronchial smooth muscle to vari
sition on cardiopulmonary function. If the arms are
ous stimuli and is manifested by widespread narrow
supported, this position stabilizes the upper chest
ing of the airways that changes in severity either
wall and rib cage, thereby facilitating inspiration.
spontaneously or as a result of treatment (Hogg,
Some patients with horizontal diaphragms and sig
1984; Rees, 1984). During an asthma attack, the
nificant respiratory distress benefit from recumbent
lumen of the airways is narrowed or occluded by a
positions in which the diaphragm is elevated within
combination of bronchial smooth muscle spasm, in
482
PART
IV
flammation of the mucosa and an overproduction of
Factors That Precipitate Asthmatic Symptoms
viscous, tenacious mucus.

Asthma is a widespread disorder affecting I % of
the population. It is common in children under
years of age; its prevalence is estimated to be
Allergic or Extrinsic Asthma
15
Pollen (especially ragweed)
5% to
Animals
15%. It is estimated that 80% of asthmatic children

do not have symptoms after the age of 10 years.
Asthma that begins in patients under the age of 35
Feathers
Molds
is usually allergic or extrinsic. These asthma attacks
Household dust
are precipitated when an individual comes into con
Food
tact with a given substance to which he or she is sen
Nonallergic or Intrinsic Asthma
sitive, such as pollens or household dust (see the box

at right). Often asthmatic patients can be allergic to a
Inhaled irrita1lts
number of substances rather than to one or two.
Cigarette smoke
lf a patient's first asthma attack occurs after the

age of
35, often there is evidence of chronic airway
Dust
obstruction with intermittent episodes of acute bron
Pollution
chospasm. These individuals, whose attacks are not
Chemicals
triggered by specific substances, are referred to as

having nonallergic or intrinsic asthma (see box at
Weather
right). Chronic bronchitis is commonly found in this
High humidity
group, and this is the type of asthma seen in the hos
Cold air
pital setting.
The asthmatic patient presents wi th the follow
Respiratory i1lfectiOlls
ing picture during an attack. Lung volumes and ex
Common cold
piratory flow rates are reduced, and the distribution
Bacterial bronchitis
of ventilation is less homogeneous (Ross et aI.,

1992a). The patient has a rapid rate of breathing
Drugs
and uses the accessory respiratory muscles (Figure
Aspirin
4-6, p.
78). The expiratory phase of breathing is

Emotio1ls
prolonged with audible wheezing. The patient may

cough frequently, although un prod ucti vely, and
Stress
may complain of tightness in the chest. Radiologi
Excitement
cally, the lungs may appear hyperinflated or show
Exercise
small atelectatic areas (reabsorption atelectasis).

Early in the attack, arterial blood gases reflect
slight hypoxemia and a low PaCo2 (from hyperven
tilation). lf the attack progresses, the P02 continues
to fall as the Peo2 increases above normal. As ob
tack more effectively, and also provides a means of
struction becomes severe, deterioration of the pa
helping to reduce subsequent attacks. Airway clear
tient is evidenced by a high CO2, a low Po2, and a
ance procedures may have a role should the cough
pH of less than
become productive. Patients should avoid bronchial
7.3.
Hospitalized asthmatic patients are treated with in

travenous fluids, bronchodilators, supplemental oxy
irritants and substances that worsen or induce signifi

cant bronchospasm or an attack.
gen, and corticosteroids. Breathing control in the
An asthmatic attack that persists for several hours
acute attack relaxes the patient, helps manage the at-
and is unresponsive to medical management is re
27
483
ferred to as status asthmaticus. This condition consti
bronchial lumen, further contributing to the stasis of
tutes a medical emergency, necessitating admission
secretions. Thus optimizing the mobilization of secre
to the intensive care unit (see Chapter
32).
tions and their removal is a priority even in tile pres

ence of scant secretions. Interventions that optimize
mucociliary transport are selected to minimize exac
The hallmark of an acute exacerbation of asthma is
erbating bronchospasm and further increases in air
an increased responsiveness of airway smooth muscle
way resistance.
to various stimuli (bronchospasm) (i.e., reversible air
The primary goals in the management of asthma
way obstruction). Although bronchospasm can be a
include reducing airway narrowing, improving alveo
feature of chronic bronchitis and emphysema, the pri
lar ventilation, reducing the work and energy cost of
mary cause of airway obstruction in these conditions
breathing, reducing hypoxemia or minimizing its
results from anatomical and physiological changes
threat, and optimizing lung compliance.

Treatment outcome is assessed with indices of
that are not usually reversible.

Physical therapy is directed at improving gas ex
oxygen transport overall and of the function of the in
change without aggravating bronchospasm and other
dividual steps in the pathway (Epstein and Henning,
symptoms and reversing these when possible. Thus
1993). Bedside spirometry, including peak expiratory
promoting more effective and efficient breathing with
flow rate, is a sensitive indicator of ensuing compro
relaxed controlled breathing maneuvers and con
mise in oxygen transport. Some patients use a peak
trolled unforced coughing maneuvers in optimal body
expiratory flow rate meter at home to detect such
positions is a priority. Overall oxygen demand, in
changes and as an early indicator of the need for
cluding that associated with an increased work of
medical attention.
breathing, needs to be reduced during an exacerba

tion of asthma. This may require reduced activity,
body positioning that improves breathing efficiency,
judicious rest and sleep periods, altered diet or re
stricted diet, adequate hydration, maintaining a ther
Acute Exacerbation of Cystic Fibrosis

Cystic fibrosis (CF) is a complex multisystem disor
moneutral environment, rest, reduced arousal, re
der transmitted by an autosomal-recessive gene that
duced social interaction and excitement, and reduced
affects the exocrine glands (Landau,
environmental stimulation. Although general relax
volves all of the major organ systems in the body
1973). CF in
ation does not directly relax bronchial smooth mus
and is characterized by increased sweat electrolyte
cle, relaxation will assist breathing control, reduce
content, chronic airflow limitation, ventilation inho
arousal and metabolic demands, and promote more
mogeneity, and pancreatic insufficiency. Definitive
efficient breath ing.
diagnosis of CF includes positive family history,
Airway narrowing and obstruction is a hallmark of
clinical symptoms of poor digestion, growth or re
this condition secondary to increased bronchial
current pulmonary infection, and, most importantly,
smooth muscle tone and airway edema. Even small
a positive sweat chloride test. Survival has increased
amounts of pulmonary secretions can obstruct the
paired gas exchange, and reduced P aoz. Thus mu
1940 when survival was reported

1980, patients
survival was estimated to be 20 years of age and in
creasing (Hunt and Geddes, 1985). Thus although
cociliary transport is a priority. Mucous clearance can
CF is congenital and manifests in childhood, this
lumen of narrowed airways, which leads to reabsorp

tion atelectasis distal to the site of obstruction, im
dramatically since
to be approximately 2 years of age. In
be further impclled by the addition of serous fluid to
condition has now become an adult disorder. Adult
pulmonary mucus, resulting from airway irritation
patients with CF often have an upper lobe infiltrate,
and inflammation. Cilia are less effective at clearing
with evidence of atelectasis and bronchiectasis, and
mucoserous fluid compared with mucus alone. In ad
chronic staphlococcal infections. The beat fre
dition, sheets of ciliated epithelium are shed into the
quency of the cilia is often slowed to approximately
484
PART IV
Guidelines for the Delivery of Cardiopulmonary Physical Thel'apy: Acute Cardiopulmonary Conditions
3 mm/min, compared w i t h 20 m m/min in age
The clinical deficits related to oxygen transport in
matched healthy control subjects (Wood, Wanner,
clude impaired mucociliary transport, increased mu
Hirsch, and Farrell, 1975). Patients can be catego
cous production, increased difficulty clearing mucus,
rized into three general groups-those with no sig
impaired ventilation and perfusion matching, right
nificant pulmonary signs, those with pulmonary
to-left shunt, a diffusion defect, respiratory muscle
signs and occasional cough and sputum, and those
weakness or fatigue, and reduced cardiopulmonary
with pulmonary signs and constant cough and spu
conditioning (Chatham, Berrow, Beeson, Griffiths,
tum. Those patients in the last group tend to have
Brough, and Musa, 1994). The incrcased production
significantly impaired pulmonary function test re
of mucus and the difficulty removing mucus in
sults, reduced diffusing capacity, and increased he
creases the risk of bacterial colonization and chronic
moptysis, particularly in the presence of an abnor
respiratory infections. These manifestations of CF are
m a l che s t x - r a y a n d h y p e r i n f la ti o n . A i r w a y
worsened with recumbency. Significant postural hy
hyperreactivity appears t o b e variable.
poxemia has been reported in CF patients when mov
The A-a gradient for nitrogen reflects lung regions
ing from sitting to a supine position (Stokes, Wohl,
with low ventilation and perfusion ratios. Peripheral
Khaw, and Strieder, 1985). Thus the object of treat
airways are often abnormal either anatomically or
ment is to optimize oxygen transport and pulmonary
functionally because of mucous plugging. The lungs
gas exchange. Given the pathophysiological deficits
of patients with CF may be excessively stiff at maxi
in an acute exacerbation of CF, the specific goals are
mal lung capacity, with a loss of elastic recoil at low
to enhance mucociliary transport, promote airway
lung volumes (Mansell, Dubrawsky, Levison, Bryan,
clearance, optimize alveolar ventilation and therefore
and Crozier, 1974). Regional ventilation is nonuni
gas exchange, maximize the efficiency of oxygen
form contributing to ventilation and perfusion mis
transport overall, and prevent and minimize infection.
match and hypoxemia (Cotton, Graham, Mink, and

Habbick, 1985; Ross et aI., 1992a).
Although the degree to which patients with chronic

lung conditions, and in palticular CF, can respond to
The chronic pulmonary limitation in CF is related
aerobic training may be limited, it is essential that
to increased secretion of abnormally viscous mucus,
their capacity to transport oxygen overall is optimized
impaired mucociliary transport resulting in airway ob
to compensate for deficits in specific steps of the oxy
struction, bronchiectasis, hyperint1ation, infection, and
gen transport pathway (Cystic Fibrosis and Physical
impaired regional ventilatory function, leading to im
Activity, International Journal of Sports Medicine,
paired ventilation and perfusion matching and gas ex
1988; Dean and Ross, 1989). Deconditioning severely
change. Radiologically, changes are most pronounced
impairs oxygen transport. Improved aerobic capacity
in the upper lobes, especially the right upper lobe.

Prophylactic cardiopulmonary physical therapy, in
and cardiopulmonary conditioning is central in the

management of CF. Prescriptive aerobic exercise en
hances the efficiency of oxygen transport overall by
reducing airway resistance by mobilizing secretions,
cluding facilitation of mucociliary transport and max
improving the homogeneity of ventilation in the lungs
imizing alveolar ventilation, in conjunction with the
and therefore ventilation and perfusion matching, op
judicious use of antibiotics provides effective mea
timizing oxygen extraction at the tissue level, and in
sures for controlling or s l o w i n g the effects of
creasing respiratory muscle endurance (Keens,
bronchial and bronchiolar obstruction. Involvement
Krastins, Wannamaker, Levison, Crozier, and Bryan,
of the patient and caregivers in chronic care in the
1977; Zach et aI., 1992). If optimal conditioning is
long term is particularly important. Understanding of
maintained, oxygen transport is not as compromised
the pathology and course of CF is essential to modify
during acute exacerbations given the improved effi
treatment prescription during exacerbations and re
ciency of oxygen transport overall. These effects will
missions of the disease.
be lost, however, as the patient deconditions with re
27
465
stricted mobility and recumbency
the acute
sure, because of the concomitant increase in intratho
episode. Thus it is important that
is mlnl
racic pressure and strain on the heart and lungs. Pa
maJly restricted during an exacerbation (based on the
tients with CF have severe paroxysms of
clinical assessment and morbidity) and that exercise
This
conditioning is a
which in turn
of
between
clearance in these patients, the untoward
importance for CF
Shepard,
cardiac effects need to be minimized.
1991). This may minimize
and
venous return and cardiac out
put. Although coughing is an essential mechanism for
exacerbations. An important additional effect of

which has
increases intrathoracic pressure,
other interventions aimed at
Over the past
the risk of infection and perhaps minimize the
secretion clearance in the treatment of CF have in
of an infection once acquired.
cluded
the use of the positive ex-
In severe exacerbations the patient is

has a
stressed
oxygen
1993; Webber and Pryor, 1
increased
and is prone to
is shifted along the airways
the selection of treatment
j.Jv,,,.-..tu'-"
at low lung volumes is believed to loosen
tions are selected based on the assessment and the pa

to tolerate the treatment and derive
body
enhance mu
clearance and maxi
cociliary transport and
This is fol
secretions from the walls of the

at mid
lowed
volumes, which
breathing at
lung volumes is believed to
centralize and facilitate the removal of the secretions

Thus
with
may enhance
manipulat
mize t he efficiency of t h e s t e p s i n t h e o x y gen

transport pathway. Postural
can offer addi
tional benefit in these patients if further clearance i s

The addition o f manual
indicated, however,
ing
monitoring must be car
the
and Maz
Murray, 1979;
therapist
and deliber
the
who gauges
the patient's ventilatory effort and work with the

chest. The patient is not
,,,,..; to breathe below
volume
"'''''An"
'
... ..
and expiratory techniques can
contribute to airway
whereas
and is encouraged to suppress coughing until the ex
and
other forms of modified
(i.e., the phase

is breathing at high
tis minimize
which the patient
volumes),
may be a useful adjunct for fa
tive in removing secretions that have accumulated
cilitating airway clearance in
centrally without compromising ventilation and gas
procedure that
1974; Nunn,
Sa
and Laws, 1965). Forceful

closes, contributes to
with CF. It is a
may use independently and can
relatively unobtrusively. It
be
the patient's
tial for
efforts and minimizes the poten

airway closure in these
The PEP mask and flutter valve are believed to re
airway closure and thus should be avoided,

lady in
is coached by
breathe
at the volumes set

hands around the
1982).
Forced
and wastc
of energy. The
ful
(Kirilloff,
volumes and flow rates and controlling
coughing to avoid unproductive
may be
ried out given their potential deleterious effects on

gas
be
lieved to help localize and collect the secretions. Fi
benefit. Gradual, paced low-intensity mobi

lization and
at low
volumes, then at mid and high lung volumes,
monitoring. These patients become

and distressed readily, Treatment interven
tient's
and
tient initially breathes
interventions and their parameters in conjunction

with
altering the
volume at which the patient breathes. The pa
arterial desaturation. Thus minimizing undue oxygen

demand and
that the equal pres
is based on the
in part because of the increased
work of breathing and for the
mask, and the flutter valve
pressure
with elevated pulmonary artery pres
duce airway closure and thereby
alveolar
486
PART IV
ventilation and enhance mucociliary clearance in pa
als exposed to plastics being heated at high tempera
tients with CF.
tures are also exposed to gases that are toxic to the

respiratory system. Chronic pathological changes and
Acute Exacerbation of Interstitial Pulmonary Fibrosis

Interstitial lung disease has been associated with var
impaired gas exchange can result.

Medical management is directed at reducing in
flammation, reducing pulmonary hypertension, and
increasing arterial oxygenation. Pharmacological
ious occupations and the inhalation of inorganic and
management may include corticosteroids for inflam
organic dusts. Conditions associated with the inhala
mation, immunosuppressive agents, and oxygen
tion of inorganic dusts include silicosis, asbestosis,
therapy. Removing the patient from the work envi
talc coal dusts, and beryllium. These conditions are
ronment contributing to interstitial pulmonary fibro
most often seen in miners, welders, and construction
sis is essential in managing the disease and its long
workers. Workers exposed to organic material, such
term consequences.
as fungal spores and plant fibers, may develop a seri
PrinCiples of physical therapy management
ous pulmonary reaction known as extrinsic allergic

alveolitis. Generally, interstitial lung disease is char
The primary clinical manifestations of an acute exac
acterized by inflammation of the lung parenchyma,
erbation of interstitial pulmonary fibrosis reflect an
which may resolve completely or progress to fibro
acute on chronic problem usually resulting from an
sis. Interstitial pulmonary fibrosis results from the
inflammatory episode, pulmonary infection, or both.
deposition of connective tissue after repeated bouts
The mechanisms responsible include reduced alveo

lar ventilation, an inflammatory process and its mani
of infection.
The pathophysiological deficits are commensu
festations, potential airway obstruction, and increased
rate with morphological changes of interstitial infil
work of breathing and of the heart in severe cases.
tration and fibrosis, intraalveolar exudate and alveo
These patients are prone to desaturation during exer
lar replacement (Chung and Dean, 1989) (see Figure
cise and thus need to be monitored closely.
4-12, p. 88). Lung compliance and lung volumes are
In mild cases, mobilization increases the homo
reduced, expiratory flow at mid lung volume is in
geneity of ventilation, and ventilation and perfusion
creased (stiff, inelastic lungs), diffusing capacity is
matching (Jernudd-Wilhelmsson et aI., 1986). Be
reduced, and hypoxemia can be present in the ab
tween treatments and in the management of the se
sence of hypercapnia (Chung and Dean; 1989; Jer
verely affected patient, body positioning is used to re
nudd-Wilhelmsson, Hornblad, and Hedenstierna,
duce the work of breathing and arousal, maximize
1986). The chest x-ray of a patient with interstitial
alveolar ventilation, maximize ventilation and perfu
pulmonary fibr osis secondary to sarcoidosis is
sion matching, and optimize coughing.
shown in Figure 4-12, p. 88. Other changes include
Patients with moderate-to-severe interstitial lung
increased resting heart rate, pulmonary hyperten
disease may desaturate during sleep (Perez-Padilla,
sion, impaired gas exchange, and shortness of breath
West, and Lertzman, 1985) and readily desaturate on
during exercise and, in some cases, at rest. Symp
physical exertion (Arita, Nishida, and Hiramoto,
toms can be reversed by removing the worker from
1981), thus warranting close monitoring during and
the exposure by a change of employment, by modi
between treatments. Increased pulmonary vascular re
fying the materials handling process, or by using
sistance secondary to hypoxic vasoconstriction con
protective clothing and masks. Repeated exposure to
tributes to increased work of the right heart and po
these organic dusts may result in irreversible inter
tential cardiac insufficiency.

General debility and deconditioning warrant a
stitial fibrosis.
Reaction to fumes and gases can also lead to
modified exercise program that can optimize the
chronic restrictive patterns of lung disease. Individu
function of all of the steps in the oxygen transport
27
pathway (Arita et aI., 1981; Chung and Dean, 1989).
487
in milder cases. If fibrosis has occurred, lung compli

ance will be correspondingly reduced. Airflow resis
tance may be increased from narrowing or distortion
Tuberculosis
of the bronchioles because of fibrosis. Pleural in
volvement may result in effusions, empyema, pleural
Although the incidence of tuberculosis, a life-long
fibrosis, and spontaneous pneumothorax. Unlike
disease, has declined significantly over the past sev
parenchymal damage, small amounts of pleural re
eral decades, this disease has been experiencing a
striction can produce significant changes in pul
resurgence in the industrialized world in recent
monary function. Clinically, patients with significant
decades. This may reflect declining sanitation and
pleural involvement have significant restrictive dis
health standards in some segments of the population
ease and correspondingly low lung volumes. The
and immigration patterns.
work and energy cost of breathing are markedly in
Most infections result from inhalation of airborne
creased. Shortness of breath is a common complaint.
tubercle bacilli, which triggers an inflammatory re
Comparable with an interstitial pulmonary fibrosis
sponse (luce, 1986). This response includes flooding
patient, the patient adopts a rapid shallow breathing
of the affected area with fluid leukocytes, and later
pattern to reduce the high cost of elastic work of
macrophages. The area becomes consolidated and
breathing. Thus the dead space tends to be hyperven
pathologically the condition is considered a tubercu
tilated and alveolar hypoventilation results.
lous pneumonia. The infiltrating macrophages be
In addition to alveolar hypoventilation, lung tissue
come localized and fused, resulting in the characteris
and pulmonary vascular damage impairs ventilation
tic tubercle. Within 2 to 4 weeks, the central part of
and perfUSion matching and diffusing capacity. In se
the lesion necroses. Tuberculosis is associated pri
vere cases, hypoxemia and hypercapnia are present.
marily with pulmonary infection that is comparable
Chronic adaptation includes polycythemia and hyper
with other infectious pneumonias. Tuberculosis, how
volemia. Right heart failure may ensue.
ever, is distinct in that it may affect other parts of the
The lungs become shrunken and geometrically
body. Symptoms include fatigue, fever, reduced ap
distorted because of fibrotic changes in the lungs.
petite, weight loss, night sweats, hemoptysis, and a
These changes can lead to kinking and obstruction of
cough with small amounts of nonpurulent sputum
the pulmonary blood vessels and maldistribution of
with pulmonary involvement. The course of the dis
pulmonary blood flow, which further compromises
ease is variable. Some lesions heal promptly, whereas
ventilation and perfusion matching.
other patients experience progression and ensui ng
Tuberculosis may be associated with an obstruc
death. Other systems that can be involved include
tive component. An increase in airflow resistance
brain and meninges, kidney, reproductive system, and
comparable with emphysema can be present. This ob
bone. In some individuals the disease appears to
struction results from chronic infection, mucosal
remit, whereas in others tuberculosis progresses to af
edema, retained secretions, and bronchospasm.
fect other organ systems or previously dormant foci

can be reactivated.
Antibiotics can be effective in managing the dis

ease such that hospitalization is avoided. If detected
The effects of tuberculosis on pulmonary function
early, the prognosis is favorable, provided the patient
are variable, depending on the extent and type of le
adheres to the medication schedule and the bacilli do
sions. lesions may involve the lung parenchyma, the
not become resistant to the medications. Surgery may
bronchi, the pleurae, and chest wall. Parenchymal i n
be indicated to resect lung segments that are chroni
volvement can reduce lung volumes, leading to hy
cally involved. The extent and seveJ;ty of the disease
poventilation of pelfused lung units. Significant dis
determines the course of recovery.
ease leads to impaired artcrial blood gases, whereas
The maintenance of good general health is particu
areas of unaffected lung may adequately compensate
larly important in the management, control, and pre
488
PART IV
vention of tuberculosis (e.g., sanitation, balanced

diet, sleep, regular exercise, and stress control).
whether the patient is being treated for osteoarthritis,

stroke, or cardiopulmonary dysfunction, treatment is
modified accordingly. An exercise prescription in
cludes generalized aerobic exercise at an intensity
Although the acute presentation of tuberculosis is com
that is optimally therapeutic and not associated with
parable with acute pneumonia (refer to pneumonia sec
any excessive or untoward hemodynamic responses
tion), there are some important differences with respect
(Blair, Painter, Pate, Smith, and Taylor, 1988).
to physical therapy management. First, tuberculosis is
Labile hypertensive patients are the most difficult
particularly infectious, thus special precautions should
patients to prescribe an exercise program for because
be taken by the physical therapist to prevent its spread
of the irregularity of their blood pressure responses.
during its infectious stage. Second, patients are prone to
The intensity is modified at each session to accom
excessive fatigue; treatments should be selected to pro
modate these variations. Because beta-blockers and
mote improved oxygen transport without exceeding the
other medications blunt heart rate responses to exer
patient's capacity to deliver oxygen and without con
cise, the exercise prescription parameters are defined
tributing to excessive fatigue. Stimulation of the oxy
on the basis of some other objective hemodynamic
gen transport system with exercise is necessary to avoid
response or on subjective responses (e.g., the Borg
the deleterious effects of deconditioning and further
scale of perceived exertion).
compromise of oxygen transport. The patient therefore

warrants being monitored closely.
The benefits of a modified aerobic exercise pre

scription include elimination of medication, reduction
of medication, and improved pbarmacological control
on the same dose of medication. In addition, the pa
Hypertension
Essential hypertension is the most common type of
tient derives all the other multisystem health benefits

of exercise. A program of aerobic exercise should be
carried out in conjunction with other life-style changes
hypeltension (90% of all reported cases) (i.e., of un
associated with blood pressure control (e.g., nutrition,
known etiology). Generally, hypertension is classified
weight control, stress reduction, and smoking cessation
as mild, moderate, or severe. Hypertension is man
program). Medications should be monitored by the
aged pharmacologically with vasodilators (i.e., after
physician during the training program. In addition to
load reducers), diuretics (i.e., volume reducers), and
exercise having a direct effect on controlling hyperten
beta-blocking agents (i.e., inotrophic agents). Hyper
sion, the effect of exercise on overall metabolism may
tension is a significant health-care concern in that this
alter the absorption and degradation of the medica
condition is frequently associated with heart disease
tions, which in turn can reduce the prescriptive re
and stroke. Thus its consequences can be dire.
quirements of that medication. Those types of exercise
that are associated with a disproportionate hemody

namic challenge (e.g., static movements and stabilizing
Physical therapists treat patients with hypertension as
postures) are not usually indicated. Rather, aerobic ex
a primary or secondary condition. A prescription of
ercise that is rhythmic, involves the large muscles of
regular aerobic exercise may control hypertension
the legs and possibly the arms, and is performed fre
(Froelicher, 1987; Goldberger, 1990). The prescrip
quently is indicated (Blail: et aI., 1988).
tion is based on a consideration of the patient's coex

istent problems and general health status. If obesity is
a concurrent problem, an exercise program is pre
scribed to address both concerns.
Angina
More frequently, physical therapists treat patients
Angina refers to pain resulting from ischemia of the
whose hypertension is a secondary condition. Thus,
myocardium and often precedes myocardial infarction.
27
489
Coronary cutery disease is the primary cause of myocar
propriately? Is the prescription current? Are
dial infcu'ction and is among the leading causes of death
there other medications that may influence the
in the Western world. Life-style factors including rugh
patient's cardiopulmonary status and response to
fat diet, stress, and low activity levels contribute to ath
treatment? What are they? Does the patient have
erosclerosis and fat deposition within the coronary
the antianginaJ medication present at all times?
blood vessels. When these deposits narrow or totally

occlude the vessel lumen, blood flow is restricted or to
5. What physiological parameters should be moni

tored before, during, and after treatment?
tally obstl11cted. As the hecut continues to demand oxy
6. What is the patient's knowledge about his or
gen and nutrients to work, blood supply needs to be in
her condition? Can the patient clearly identify
creased. If one or more of the myocardial blood vessels
what triggers the angina and what makes it
is stenosed, insufficient blood reaches the working my
worse and better? What life-style changes have
ocardial fibers, and ischerrua and pain result. Although
been made? What should be reinforced and
the classic description of anginal pain is retrosternal

vice-like, gripping pain radiating to the left side and
down the
what education is needed?

A key consideration in the management of any pa
and up into the neck, anginal pain may
tient with cardiovascular dysfunction is minimizing
occur bilaterally anywhere above the umbilicus. Fur
myocardial strain (Sokolow et aI., 1990). Thus mobi
arm
thermore, patients vary considerably with respect to the
lization and exercise prescription needs to incorpo
degree to which the severity of the pain correlates with
rate an appropriate warm-up, steady-rate, cool-down,
the degree of myocardial ischemia and infarction. Thus
and recovery phases, and the type of exercise should
even apparently minimal chest pain may be associated
be rhythmic and involve the legs (i.e., areas of large
with significant ischemia and should not be rrunirruzed
muscle mass) and possibly the arms as well. Initially,
with respect to its clinical significance.
low-intensity activity that restricts the heart rate to no

more than 20 beats above resting heart rate may be
indicated to minimize the work of the heart without
The management of patients with healt disease who
immobilizing the patient completely. Ejection frac
are hemodynamically unstable and require intensive
tion is not necessarily a good indicator of exercise
monitoring to assess and to monitor physical therapy
tolerance because these vruiables are not well corre
treatment is described in Chapter 32. This chapter ad
lated (Dean, 1993). Upper-extremity work alone is
dresses the management of the cardiac medical patient
more hemodynamically demanding than lower ex
who is stable and uncomplicated. Physical therapists
tremity work and thus is prescribed cautiously if at
must be knowledgeable and proficient in the manage
all, at least in the early stage. Exercise or physical ac
ment of the cardiac patient because these patients are
tivity, involving sustained static postures and isomet
referred with cardiac disease as a primary or secondary
ric muscle contraction, are contraindicated. Breathing
problem. Because physical therapy invariably involves
should be coordinated with activity such that breath
physically stressing a patient either with therapeutic
holding and straining are avoided.
exercise or with the application of a therapeutic modal
A patient with a history of angina, regardless of
ity, the physical therapist must address the following
whether that individual is taking antianginal medica
questions when managing a patient with heart disease:

I. Does the patient's cardiac status preclude treat
ment? Why?
tions, must be hemodynamically monitored (i.e.,

heart rate, blood pressure, rate pressure product, and
subjective responses).
2. Is additional information on the patient needed
Patients prone to angina may exhibit symptoms in
before physical therapy assessment and treat
certain body positions (L ange, Katz, McBrid e ,

Moore, a n d Hillis, 1988; Langou, Wolfson, Olson,
ment? What information?

3. How should treatment be modified? Why?
and Cohen, 1977; Prakash, Parmley, Dikshit, For
4. Is the patient using antianginal medication ap
rester, and Swan, 1973). Usually, this reflects an in
490
PART IV
creased workload and increased work of the heart.

Recumbent positions increase the mechanical work
of the heart by increasing central blood volume
(Kaneko, Milic-Emili, Dolovich, Dawson, and Bates,
1966). These patients are not encouraged to lie flat,
instead the head of bed is elevated 10 to 15 degrees.
Sidelying positions, particularly left sidelying, in
crease the work of the heart by compressing the heart
and impeding ventricular filling and ejection. Patients
with impaired oxygen transport and without prior car
diac disease may exhibit myocardial stress and is
chemia in these body positions. Thus patients with
impaired or threatened oxygenation must be moni
tored closely, particularly during turning and activi
ties in which oxygen demand is increased and oxygen
delivery needs to increase cOITespondingly.
Uncompliicated Myocardial Infarction
Myocardial infarction commonly referred to as a

heart attack refers to insufficient myocardial pelfu
sion resulting in a macroscopic area of damage and

necrosis of the heart. Infarction results most fre
quently from narrowing and occlusion of the coro
nary blood vessels secondary to atherosclerosis.
Other causes include occlusion secondary to a throm
bus or embolus, reduced blood pressure, or coronary
vasospasm. Angina, or ischemic chest pai n, often
precedes or accompanies a myocardial infarction. In
farctions vary in severity from being silent (i.e., hav
ing no characteristic signs and symptoms) and thus
going undetected to being fatal. Most infarctions
when detected require some hospitalization and mon
itoring to ensure that the infarction is not evolving
further and that the patient is medically stable and in
no danger. Chapter 32 describes the management of
patients with myocardial infarctions who are admit
ted to a coronary care unit. This section focuses on
the patient with mild heart disease, the medical car
diac patient who is discharged from hospital, the pa
tient who has a history of ischemic heart disease, and
the patient who is hospitalized for a condition other
than heart disease but develops and is being managed
for myocardial ischemia. Judicious movement and
body positioning are essential elements in the man
agement of the myocardial infarction patient (Harri

son, 1944). Because these interventions can place sig
nificant demands on cardiopulmonary function and
oxygen transport, they must be prescribed specifi
cally by physical therapists with considerable knowl
edge and expertise in the area.
Physical therapy stresses patients hemodynamically

(Dean, Murphy, Parrent, and Rousseau, 1995). Thus
the adequacy of their cardiopulmonary system to ef
fect oxygen transport during and between treatments
is essential to establish. The optimal treatment pre
scription is based on the patient's overall signs and
symptoms of coronary insufficiency and hemody
namic instability. The physical therapist must be
knowledgeable in detecting inadequate myocardial
tissue perfusion and in reducing and preventing my
ocardial tissue damage. In addition, acute or chronic
impaired heart pump function leads to reduced car
diac output and systemic tissue perfusion. Clinical
manifestations include reduced mentation, reduced
renal function, fatigue, malaise, and moist, cool, and
cyanotic skin.
Regardless of whether the patient i s being
treated in hospital, either on the ward or in the de
partment, or in the private physical therapy clinic,
the patient must be hemodynamically monitored.
Minimall y, heart rate and blood pressure must be
taken before, during, and after treatment, along
with a subjective rating of anginal chest pain. ECG
monitoring is usually continuous in the early stages
of the infarction. The object of treatment is to have
the patient remain below his or her anginal thresh
old so that anginal pain is avoided. Breathlessness
or rating of perceived exertion may also be used.
The rate pressure product (RPP) (i.e., the product
of heart rate and systolic blood pressure) is highly
correlated with myocardial oxygen uptake and
work. Previous stress tests will establish the RPP
at which angina occurs and the intensity of the ex
ercise dose should be set at 65% to 80% of this
threshold. Patients on beta-blockers have a blunted
hemodynamic response to exercise, particularly
heart rate responses. Use of ratings of perceived
exertion to define the upper and lower limits of an
27
491
acceptable mobilization stimulus may be indicated
they can undertake. Thus performing physical activ
in these patients.
ity and exercise while monitored and under the su
In some cases, patients have labile angina (i.e., the
pervision of a physical therapist is often reassuring
onset of angina does not occur reliably at a given
and gives the patient confidence for performing ac
RPP). This patient and the patient who reports angina
tivity when unsupervised.
at rest are at higher risk and appropriate precautions
The quality and quantity of the patient's sleep and
must be taken. First, the patient must be assessed to
a profile of sleep-wake periods should be reviewed to
establish that treatment is not precluded (see pertinent
ensure he or she is deriving maximal benefit. REM
questions to be answered before treating a patient
sleep with bursts of sympathetic activity during the
with angina). Second, monitoring is essential and
early hours of the morning may constitute a period of
may include ECG monitoring. Third, treatments are
increased risk for the cardiac patient.
prescribed below symptom threshold, which is usu
Appropriate safety precautions must be taken in
ally consistent with a low exercise intensity in these
all settings where physical therapists practice, given
patients. Comparable with any patient experiencing
that most physical therapy interventions physically
low functional work capacity, exercise prescribed on
stress patients and that coronary symptoms can occur
an interval schedule enables the patient to achieve a
regardless of whether the patient has a known under
greater volume of work.
lying heart disease. In addition, because the popula
Similar to the patient with angina, body positions
tion is aging, physical therapists are treating a grow
are selected for the patient with a myocardial infarc
ing number of older persons who are known to have a
tion that will minimize the work of breathing and of
higher prevalence of cardiovascular disease.
1968).
Good life-style habits are central to maximizing
Significant central fluid shifts are minimized by en
recovery and improving the long-term prognosis
the heart (Sonnenblick, Ross, and Bruanwald,
couraging the upright position as much as possible to
(e.g., good nutrition and hydration, good sleep habits,
reduce the work of the heart (Levine and Lown,
stress management, and regular physical exercise that
1952) and by maintaining the head of bed up to 10 to

15 degrees when the patient is recumbent. Patients
is prescribed by the physical therapist) (Underhill et

aI.,
1989).
with elevated intracardiac pressures are less suscepti

ble to orthostatism (Chapter
18).
Comparable with the management of the patient
SUMMARY
who has a history of angina, body positions, static
The primary acute cardiopulmonary medical condi
postures, activities, and respiratory maneuvers associ
tions that are treated by physical therapists include
ated with increased hemodynamic strain (e.g., breath
primary lung dysfunction (i.e., atelectasis, pneumo
holding) are avoided.
nia, bronchitis, bronchiolitis, alveolitis, alveolar pro
Relaxation is central in the management of the
teinosis, and acute exacerbations of chronic airflow
cardiac patient who is prone to being anxious and
limitation, asthma, cystic fibrosis, interstitial pul
apprehensive. Relaxation interventions include auto
monary fibrosis, and tuberculosis) and primary car
genic relaxation, progressive relaxation, Benson's
diac disease including hypenension, uncomplicated
relaxation response procedures. biofeedback, and
angina, and myocardial infarction. This chapter fo
1989). Also, the patient
cuses on the pathophysiology underlying these disor
meditation (Underhill et aI.,
needs to identify and minimize stress triggers and ef
ders and the mechanisms by which they threaten or
fective individual-specific nonpharmacological re
impair heart-lung interaction and oxygen transport.
laxants. Relaxation training with or without pharma
Thus the basis for the principles of cardiopulmonary
cological support can be integrated into treatment
physical therapy are described rather than specific
1989; Webber and Pryor, 1994).
treatment prescriptions. Treatment prescription is
(Underhill et aI.,
Patients with heart disease are often apprehensive
based on the effects of restricted mobility, recum
and anxious about the intensity of physical activity
bency, and extrinsic and intrinsic factors in addition
PART IV
492
Guidelines fOl" the Delivery of Cardiopulmonary Physical Therapy: Acute Cardiopulmonary Conditions
is directed
Bennett, W.o., Foster, W.M., & Chapman, W.E (1990). Cough
at the underlying pathophysiological mechanisms re
enhanced mucus clearance in the normal lung. Journal of Ap
to the underlying
sulting from these four factors wherever
and
to symptom reduction. To prioritize treat
plie d Physiology,
(1988). Resource maaual for guidelines for exercise leslillg
interventions are ex
ments, the most
ploited foremost because these address multiple
and prescriplioll. Philadelphia: Lea
are instituted after the most physio
Lung immunogenicity, rejection, and obliterative bronchiolitis.

Chesl, 92,547549.
Chatham, K, Ben'ow, S .. Beeson. C, Griffiths, L., Brough. D" &

Musa, L (1994). Inspiratory pressures in adult
interventions have been exploited or in con

junction with these. The challenge of clinical
lem
is
spect to oxygen transport with the least risk in the
fibrosis,
Physiorherap)" 80, 748-752,
Chung, F, & Dean, E. (1989). Pathophysiology and cardiorespira

tory consequences of mterstitial lung diseasc:--review and clin
the optimal treatment
prescription that will effect the best results with re
& Febiger.
Burke, CM., Glanville. AR , Theodore, l, & Robin. E.D. (1987).
in the oxygen transport pathway. Less physiological

, conventional
69, I 67()-1675,
Blair, S.N.. Painter, P., Pate, R,R., Smith, LX, & Taylor, CB.
ical implications. Phvsical Therap>", 69, 956-966

Clauss,R.H., Scalabrini, BY,Ray.R.F, & Reed, G.E. (1968), Ef
fects of changing body posilion upon improved venliiation-per
shortest period of time.
fusion relationships. Circulalioll, 37 (SuppI4), 214-117.

Cotton, D1.. Graham, BL. Mink. JT, & Habbick. B.t'. (1985).
Reduction of the single breath diffusing capacity in cystic fibro
REVIEW QUESTIONS
sis. Europ ean Journal of Resp ira to ry Diseases, 66, 173-180.
I. Describe the primary cardiopulmonary patho
physiology of acute
pneumonia,
bronchitis, bronchiolitis,
alveolar pro-
acute exacerbations of chronic airflow
Cystic fibrosis and physical activity. (1988), illiemaliollul jouma!

of SporlS Medicille,
xchange. Clinics in Chest Medicine,
lOry Care,
limitation, asthma, cystic fibrosis, interstitial

and stable myocardial infarction.
2. Relate cardiopulmonary
ology of each of the above acute conditions and
Therapy,
Canada,
4/, 46-47.
Dean, E., &Ross, J. (1992a). Oxygen transport. The basis for con
temporary cardiopulmonary physical therapy and
optimiza
tion with body positioning and mobilization. Physical Therapy
I, 34-44.
Dean, E. & Ross, 1. (I 992b). Mobilization and exercise condition
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lOry Disease, 63, 188-201.
Acute Surgical Conditions
Elizabeth Dean
Maureen Fogel Perlstein
Mary Mathews
KEY TERMS
Sedation
Anesthesia
Cardiovascular surgery
Surgery
Risk factors
Thoracic surgery
INTRODUCTION
The four categories of factors contributing to or
The purpose of this chapter is to review the manage
threatening oxygen transport are described in Chapter
ment of cardiopulmonary dysfunction secondary to
16. Specifically, these factors include the underlying
acute surgical conditions. The cardiopulmonary ef
pathology, restricted mobility, and recumbency, ex
fects of surgery are described. The two types of
trinsic factors related to the patient's care and intrin
surgery that have the greatest impact on cardiopul
sic factors related to the patient. This chapter exam
monary function, namely, thoracic and cardiovascular
ines in detail the extrinsic factors related to surgery
surgery, are then presented. These surgeries are par
and anesthesia and the impact of underlying disease,
ticularly invasive and lengthy, require heavy and pro
restricted mobility, recumbency, and intrinsic factors
longed anesthesia and sedation, and are associated
on the effects of surgery and anesthesia.
with increased risk, thus warranting intensive periop

erative physical therapy.
Treatment principles are presented. These are not

intended to be a treatment prescription for a particular
495
496
PART IV
patient. The effects of surgery and anesthesia need to
Surgical Factors That Contribute to

Perioperative Cardiopulmonary Dysfunction
be considered in addition to the underlying pathology,

the effects of restricted mobility, body position, and
intrinsic and extrinsic factors (see Chapter 28). All of
Type of surgery
these factors must be considered and integrated in the
Surgical procedures
treatment prescription and in defining the precise pa
Anesthetics (general, with or without intubation. or
rameters of the prescription. Such integration is es
regional) and sedation
sential for treatment to be specific and maximally ef
Muscle-relaxant agents and neuromuscular blockade
ficacious. For specific examples of patient treatment
Supplemental oxygen and humidification
prescriptions refer to the companion text Clinical
Static body position assumed
case studies in cardiopulmonary physical therapy.
Duration of surgery and static body positioning
PERIOPERATIVE COURSE
Incisions
Surgery and its Cardiopulmonary Consequences
Use of the cardiopulmonary bypass machine (CBM)

Use of the extracorporeal membrane exchanger
Many factors contribute to perioperative cardiopul
(ECMO)
monary dysfunction (see the box at right). Anesthesia
Dressings and binders
and tissue dissection contribute to major changes in
Splints and fixation devices
lung volume, mechanics, and gas exchange. The ex
Lines and leads
tent and duration of these changes increase with the

magnitude of the operative procedure and degree of
Monitoring devices
anesthesia required. Anesthesia results in depression
Chest tubes placement and number
of breathing. Thoracic respiratory excursion is signifi
Catheters
cantly reduced. The tone and pattern of contraction of
Perioperative pain
the respiratory muscles, particularly the diaphragm
Perioperative pain control management
and the intercostal muscles, change, which contributes
Peri operative fluid balance management
to many of the secondary cardiopulmonary effects ob
Perioperative blood and plasma transfusions
served after surgery (Muller, Volgyesi, B e cker,

Bryan, and Bryan, 1979). The loss of end-expiratory
diaphragmatic tone causes the diaphragm to ascend
into the chest by 2 cm during anesthesia with or with
out paralysis (Froese and Bryan, 1974). Reductions in
The consequences of reduced FRC with anesthesia
functional residual capacity (FRC) are correlated with
and surgery have significant implications for postop
this change and with altered chest wall configuration
erative complications and the course of recovery. Air
and increased thoracic blood volume (Hedenstierna et
way closure occurs with anesthesia and this likely
aI.,
1985; H e d e n s t i e r n a , Tokics, Strandberg,

Lundquist, and Brismar, 1986). One of the most per
contributes to intrapulmonary shunting. Compression
vasive and predictable clinical effects observed in the
surgery. In addition, compression atelectasis occurs
atelectasis of the dependent lung fields occurs during
postoperative period is alveolar collapse. Total lung
when lung tissue and sur ounding structures are being
capacity, FRC, and residual volume are significantly
physically manipulated. Although reduced airway
decreased. The FRC is reduced by approximately I L
caliber in areas of low lung volume can be offset by
in supine compared with the erect sitting position
the airway-dilating effect of many inhaled anesthet
(Behrakis, Baydur, Jaeger, and Milic-Emili, 1983;
ics, airway resistance is increased by obstruction of
Nunn, 1989) and is further reduced with the induction
the breathing circuits, valves, and tracheal tubes. The
of anesthesia. Anesthesia, however, fails to reduce
airways may also be obstructed with foreign matter,
FRC in the sitting position (Nunn, 1989).
such as blood and secretions, or from bronchospasm
28
497
because of irritation of the airways. Because of the
fect is indicated. Patient controlled analgesia (PCA)
decrease in FRC, compliance is decreased and the
is an effective means of having the patient regulate
work of breathing is increased. Hypoxemia secondary
the amount of analgesia he or she is receiving. Intra
to transpulmonary shunting is usually maximal
venous administration prolongs the peak-effect time
within 72 hours after surgery and often is not com
of analgesics and therefore helps the patient tolerate
pletely resolved for several days. Persistent reduction
longer, more intense treatments. Transcutaneous elec
in FRC after surgery delays .the restoration of the nor
trical nerve stimulation (TENS) can be a useful ad
mal alveolar-arterial oxygen gradient (Alexander,
junct in the management of postoperative pain in
Spence, Parikh, and Stuart,
1973).
some patients. Pain control with TENS may enable
A complication of thoracic and upper abdominal
the patient to participate more fully in mobilization,
surgery, (e.g., cholecystectomy) is irritation or com
deep breathing, coughing, and bed mobility. Research
pression trauma of the phrenic nerve. This complica
is needed, however, to evaluate this technique in the
tion may be more common than expected. Inhibition
management of acute pain and define the prescription
of the phrenic nerve impairs the contraction of the af
parameters needed to produce an optimal therapeutic
fected hemidiaphragm, causing it to ascend into the
effect. A nonpharmacological, noninvasive means of
thorax and contribute to atelectasis on that side. This
managing acute pain would be of considerable bene
inhibition may last for several days (Dureuil, Viires,

and Cantineau,
1986; Ford and Guenter, 1984).
fit to patients and would enable them to participate

more fully in physical therapy treatments in the ab
The FIo2 depends on the mode of 100% oxygen

administration. Low-flow nasal oxygen reduces hy
sence of untoward side effects often associated with

drug administration.
poxemia in the absence of hypercapnia and marked
Although sedatives or tranquilizers are prescribed
transpulmonary shunting in the postoperative patient.
to make the patient more comfortable and to reduce
Low oxygen flows and low FI02S tend to be delivered
suffering, sedatives, in particular, reduce the patient's
via nasal cannulae, whereas higher flows can deliver
arousal and often the ability to cooperate actively
higher FIo2s via oxygen masks and masks with reser
with treatment. Thus these medications must be pre
voir bags. FIo2 and the body position of the patient at
scribed judiciously to ensure the patient is able to co
the time the blood sample was taken must always be
operate with physical therapy and other components
considered when interpreting arterial blood gases. The
of care. Oversedation must be avoided if the patient
FIo2 is selected to provide adequate oxygenation with
is to derive maximal benefit from cardiopulmonary
the lowest oxygen concentration possible.
physical therapy treatments.
After surgery the normal pattern of breathing is
Special attention in the postoperative period is
disrupted. Shallow, monotonous tidal ventilation
given to the prevention or management of cardiopul
without normal occasional, spontaneous deep breaths
monary complications associated with reduced arousal,
1989).
surgical pain, and restriction of lung capacity and sec
causes alveolar collapse within an hour (Nunn,
Unless resolved, atelectasis becomes increasingly re
ondary to dressings, binders, and diminished ability to
sistant to reinflation within a few hours. This compli
cooperate, move spontaneously, and hyperventilate the
cation is exacerbated in patients receiving narcotics.
lungs periodically. Patients are prone to aspiration in
Tachypnea and tachycardia are commonly ob
the immediate postoperative period, particularly while
served with gross atelectasis secondary to hypoventi
the sedation and anesthetic agents are wearing off.
lalion. Breath sounds are decreased at the bases, and
This risk is further increased if an airway is required or
the coarse wheezes associated with mucus obstruct
if an airway and mechanical ventilation is instituted.
ing airflow are heard on auscultation. Large areas of
Postextubation atelectasis must be anticipated and
atelectasis are present. Left lower lobe atelectasis is
avoided. To minimize this risk, patients are requested
common after cardiac surgery.
not to cat or drink fluids the day before surgery.
If narcotics impair the patient's ability to partici
Endotracheal intubation and mechanical ventila
pate in treatment, analgesia with a less systemic ef
tion are indicated if blood gases fail to improve with
498
PART IV
conservative management. See Chapter 32 for treat
tively, he or she will be better oriented and capable
ment priorities for a patient during ventilation and the
of cooperating when waking from anesthetic.
course of weaning from the mechanical ventilator.
The patient's position is changed frequently in the
The importance of a thorough preoperative as
initial postoperative period. The patient is usually en
sessment and teaching by the physical therapist can
couraged to change his or her body position fre
not be overstated. The components of preoperative
quently, transfer, sit in a chair, and ambulate as soon
teaching are summarized in the box below. In cases
as possible after surgery. The importance of frequent
of elective surgery, preoperative teaching includes a
postural changes and early ambulation in the initial
general description of the surgery to be performed,
postoperati ve period are stressed (Dull and Dull,
the effect of anesthesia and surgery on cardiopul
1983). Early ambulation is a priority in the manage
monary function, and the systemic effects of re
ment of all surgical patients unless contraindicated.
stricted mobility and recumbency. The lines, leads,
After surgery, the patient is detained in the recovery
and catheters usually associated with the surgery are
room until the vital signs have stabilized, there is no
explained. The patient i s instructed in breathing
apparent internal or external bleeding, and the patient
control maneuvers, supported coughing, chest wall
is responding to his or her name. Patients recovering
mobility exercises, mobility exercises for the limbs
from minor surgery are usually transferred to a ward
(e.g., hip and knee and foot and ankle exercises),
once discharged from the recovery room. A patient is
turning in bed, sitting up, transferring, chair sitting,
transferred to the ICU after surgery if complications
and walking erect postoperatively.
arise during surgery, if the patient cannot be readily
In addition, the
patient is taught methods of maximizing comfort
stabilized and requires close monitoring, or if the pa
with body positioning and supporting the surgical
tient has had more serious surgery such as cranial, car
incision. If the bed has controls the patient can ma
diovascular thoracic, or emergency surgery, such as
nipulate, she or he is taught how to make bed adjust
that resulting from mUltiple trauma (Chapter
34).
P a tients considered for elective surgery are
ments as required. The postoperative course is ex

plained in general terms so the patient can anticipate
screened regarding their risks for postoperative
this period. If the patient is well informed preopera
complications. The physical therapist is often con-
Objectives of the Preoperative Physical Therapy Assessment and Teaching

Develop rapport with patient
Assess the patient and estimate degree of surgical risk (e.g .. age, smoking. previous cardiopulmonary dysfullction,
neuromuscular dysfunction. musculoskeletal deformity, obesity. substance abuse, pregnancy. nutritional status,
and hydration status)
Describe the general preoperative, intraoperative, and postoperative course
Review specific surgical procedures relevant to physical therapy (e.g., anesthesia. type of surgery. body position dur
ing surgery, airway, mechanical ventilation, duration, incisions, infusions. drainage systems, chest tubes. and re
covery room)
Provide the rationale for, describe, demonstrate, and have the patient practice and provide feedback on the following
breathing control maneuvers: maximal inspiratory hold, supported coughing maneuvers, relaxation, bed mobility
and positioning, transfers, and mobilization
For patients at risk of postoperative cardiopulmonary dysfunction and complications. review the use of the incelltive
spirometer and conventional airway clearance interventions (e.g
postural drainage and manual techniques if indicated)
Ask for any questions
28
499
su lted by the surgeon to help make a poor-risk pa
ing suboptimal, suprathreshold physiological states.
tient into a relatively better-risk patient. Patients
Suprathreshold states are associated with an inappro
wit h upper-respiratory tract infections before
priate balance between oxygen delivery and demand
surgery may have their surgeries postponed, de
such that the patient becomes compromised (e.g., he
pending on the type and extent of surgery to be per
modynamically unstable), cardiopulmonary distress
formed, levcl of anesthesia indicated, and other
is precipitated, or botb).
medical conditions, including cardiopulmonary dis

ease, age, and smoking history. Patients with lower
respiratory tract infections preoperatively constitute
a greater operative risk, hence these patients often
Preparation for Surgery

To minimize risk and reduce perioperative morbidity
have their surgeries postponed until the infection
and mortality, patients need to be in the best medical
has resolved. Patients with chronic cardiopulmonary
and physical condition before anesthesia and surgery.
diseases require a prolonged period of preoperative
In the case of elective surgery, some patients are pre
physical therapy in preparation for surgery. Elective
scribed modified aerobic training, smoking cessation,
surgery is not usually considered during an exacer
and weight control programs before surgery.
bation of chronic lung disease. Even minor surgery
Preoperative teaching is a central component of
may be potentially hazardous for the patient with
physical therapy management of the surgical patient.
previous lung disease. The adverse effects of total
Such teaching establishes rapport with the physical
anesthesia on these patients is magnified because of
therapist who informs the patient about what to ex
their reduced pulmonary reserve capacity. Smoking
pect before and after surgery. In addition to review
should be discontinued for as long as possible be
ing the surgical procedures, the physical therapist re
fore surgery. The patient is placed on an exercise
views, and has the patient perform, deep breathing
conditioning program, a regimen of bronchial hy
and supported coughing maneuvers, relaxation, bed
giene, oxygen if necessary, and prophylactic antibi
mobility, positioning, transfers, and mobilization.
otics. Even patients with extremely low functional
Preoperative teaching reduces the patient's anxiety
work capacity can enhance the efficiency of the
and encourages the patient to be as active as possible
steps in the oxygen transport pathway (Chapter 17)
in her or his recovery. Preoperative teaching reduces
with a modified aerobic exercise conditioning pro
postoperative complications and the length of the
gram. This preoperative preparation may take one to
hospital stay.
several weeks, depending on the patient and the in
There are no strict guidelines ahout which patients

should receive peri operative physical therapy. Al
dications for surgery.

Rest during the postoperative period is prescribed
though nonthoracic surgeries are generally associated
judiciously as treatment because rest is the time for
with fewer cardiopulmonary complications (e.g.,
healing, repair, and restoration. Sleep deprivation im
surgery of the extremities or lower abdomen), patients
pairs recovery and healing. Sleep at night is biologi
with preexisting cardiopulmonary, hematological or
cally more restorative than daytime sleep. Thus day
neuromuscular pathology, or musculoskeletal pathol
time and nighttime cues are given to restore the
ogy of the chest wall are at greater risk even in these
patient's circadian rhythms. Although injudicious and
relative low-risk types of surgeries. In addition, pa
excessive recumbency, bedrest, and prolonged peri
tients are at additional risk if they are older or
ods in any given body position are deleterious, spe
younger, smoke, or are overweight or pregnant. Thus
cial attention is given to maximizing the amount of
each surgical patient needs to be assessed individually
quality rest and sleep periods and minimizing disrup
to establish the degree of relative risk during surgery
tion of nighttime sleep. Rest needs to be prescribed
and the need for perioperative physical therapy. In this
both within and between treatments. Appropriate rest
way, perioperative complications can be anticipated
periods are interspersed witbin eacb treatment ses
and avoided or reduced, which is preferable to manag
sion, according to the patient's needs to avoid reacb
ing complications once they have developed.
500
PART IV
Guidelines for the Delivery of Cat'diopulmonary Physical Thet'apy: Acute Cardiopulmonary Conditions
MAJOR TYPES OF SURGERY
Factors Determining the Effect of Surgery

A p atient's response to surgery and the cardiopul
Thoracic Surgery
monary complications that may develop depend on
Thoracic surgery refers to surgery necessitating
496). The type of
opening of the chest wall. By convention, this gen
many factors (see the box on p.
surgery determines the degree of invasiveness, the
eral term usually excludes specialized cardiovascular
type or types of anesthetics and sedatives, whether
surgery (i.e., surgery of the heart and great vessels).
the patient needs to be intubated, the static body posi
Thoracic surgery is commonly performed for lung
tion assumed during surgery, the approximate dura
resections secondary to cancer (e.g., pneumonec
tion of the surgery and period of anesthesia, the inci
tomy, lobectomy, segmentectomy, and wedge resec
sions that are required, the dressings, the lines, leads,
tion). In addition, thoracic surgery is performed to
catheters, and monitoring devices needed, the chest
remove an irreversibly damaged area of lung tissue
tubes, the type and degree of pain, and the need for
secondary to bronchiectasis, benign tumors, fungal
pain control after surgery.
infections, and tuberculosis.

The most common incisions are posterolateral tho
racotomy and median sternotomy. The posterolateral
Pathophysiology
thoracotomy procedure requires the patient to assume
The type and severity of underlying cardiopulmonary
the sidelying position with the involved side upper
dysfunction increases a patient's risk of compromised
most for the duration of the surgery. The uppermost
oxygen transport and gas exchange perioperatively.
arm is fully flexed anteriorly. The incision is made

through an intercostal space, corresponding to the lo
cation of the lesion to be excised. The muscles in
Restricted Mobility and Recumbency
cised include latissimus dorsi, serratus anterior, exter
Surgery imposes two nonphysiological states on the
nal and internal intercostals laterally, and trapezius
patient that impact significantly on oxygen transport.
and rhomboid posterioriy.

At the conclusion of the surgery, chest tubes are
These conditions include the following:

I. Restricted mobility
placed to evacuate air and fluid from the pleural space
2. Recumbency, specifically a prolonged period
by means of an underwater chest tube drainage sys
of static positioning with the patient breathing
tem. The chest tube and drainage system resolve the
at monotonous tidal volumes
pneumothorax created by reestablishing negative pres

sure in the pleural space and help to reinflate the re
maining atelectatic lung tissue. After thoracic surgery,
Extrinsic Factors
two chest tubes are usually inserted, one at the apex of
496 are
the lung to evacuate air and one at the base of the lung
the p rimary extrinsic factors contributing to cardiopul
Surgery including the factors in the box on p.
to drain serosanguinous fluid. The therapist should be
monary dysfunction in the perioperative period.
come familiar with the various drainage systems, how

drainage can be facilitated with mobilization and body
positioning coordinated with breathing control and
Intrinsic Factors
supported coughing malleuvers, and certain precau
Intrinsic factors that contribute to cardiopulmonary
tions that need to be observed to avoid impairing
dysfunction in the surgical patient include a patient's
drainage or disconnecting the tubing.
premorbid status (e.g., preexisting cardiopulmonary,
Provided the chest tubes are not kinked, there is
renal, endocrine, and hematologic pathology). In ad
no contraindication to lying on the side of the chest
dition, life-style factors are significant (i.e., preopera
tubes. Lying on this side, which is usually the side
tive conditioning level, nutrition, hydration, stress
of the surgery and incision, is typically avoided by
levels, weight, and smoking history).
the patient. Consistent with the adage, "down with
28
the good lung," a patient prefers to lie on the non

surgical side. However, prolonged periods in any
position, and particularly, lying on the unaffected
side, places these lung fields at risk. To minimize
the risk of positional complications and hypoxemia,
the patient is encouraged to turn to both sides
(Leaver, Conway, and Holgate, 1994; Seaton, Lapp,
and Morgan, 1979; Sutton, Pavia, Bateman, and
Clarke, 1982). The specific positions and the dura
tion of time spent within each, however, is based on
a comprehensive assessment of the patient's condi
tion and the indications and contraindications for
each body position.
Patients may appear to splint themselves, thereby
restricting chest wall motion, to avoid including pain

when moving and deep breathing. They also may re
sist maximal inspiratory efforts when coughing. Al
though pain likely contributes to breathing at low
lung volumes and ineffective coughing, phrenic nerve
inhibition in patients with thoracic and upper abdomi
nal surgeries is likely a more important factor re
stricting lung expansion than is fully appreciated in
many patients (Ford and Guenter, 1984).
Postoperative complaints of pain are both muscu
loskeletal and pleural in origin. The large number of
muscles incised, particularly in the posterolateral tho
racotomy incision, combined with the operative posi
tion, contributes to the patient's complaints of chest
wall pain, shoulder soreness, and restricted move
ment. Deep breathing and coughing maneuvers may
be associated with considerable discomfort after
surgery. Pain is accentuated by apprehension and
anxiety. Therefore treatments are coordinated with
relaxation, noninvasive pain control modalities, and
pain medication schedules to elicit the full coopera

tion of the patient.
Cardiovascular Surgery
Cardiovascular surgery is specialized thoracic
surgery involving the heart and great vessels. Be
cause the flow of blood through the cardiopulmonary
system is interrupted, the patient is placed on a car
diopulmonary bypass machine or on a machine called
an extracorporeal membrane oxygenator. Cardiovas
cular surgery is most commonly performed for coro
501
nary artery bypass grafting, valve replacements, and

aneurysm repairs. Bypass patients, in whom the
saphenous vein is excised for graft material, have the
added complication of surgery and wound healing in
one leg. Mobility exercises on that leg are often re
stricted until there is no risk of bleeding or interfer
ence with healing. Comparable with the thoracic sur
gical patient, a cardiovascular patient leaves the
operating room with various monitoring Jines and
leads, intravenous fluid infusions, possible blood or
plasma infusions, a Swan-Ganz catheter (Chapter
15), a central venous pressure line, an arterial line, a
Foley catheter, and oxygen cannulae.
The preoperative preparation and teaching and
the postoperative physical therapy management is
intensive. Because of the invasiveness of cardiovas
cular surgery, patients are usually treated postopera
tively in a specialized intensive care unit (Chapter
31). The preoperati ve and postoperative physical
therapy management of patients in the intensive care
unit is a specialized area and is described in Chapter
34. Providing the patient with information about
what to expect during the perioperative course re
lieves fear and anxiety. In addition, relaxation pro
cedures can be useful. Patients need to be reassured
that their incisions and suture lines will not be dis
rupted with movement and physical therapy and that
supported coughing and supporting themselves
when moving will maximize comfort. Until the pa
tient has stabilized, the patient's mobility is re
stricted to low-intensity mobilization to promote its
benefits on gas exchange and reduce metabolic de
mands and body positioning to optimize alveolar
ventilation coordinated with deep breathing and
supported coughing maneuvers. Conventional air
way clearance interve n tio ns (e.g., postural drainage
and manual techniques) may be prescribed in the
presence of excessive secretions, difficulty in mobi
lizing secretions, and in the event of productive hy
drostatic pneumonia.
Patients undergoing cardiovascular surgery are
transferred from the cardiovascular intensive care
unit to the ward as quickly as possible. From the
ward, these patients should be referred to a physical
therapist and a cardiac rehabilitation program in the
community for continuity of care and to maximize
502
PART IV
the functional gains resulting from the surgery. Exer

cise is prescribed progressively to maximize oxygen
transport at each step of the rehabilitation period (i.e.,
Goals of Postoperative Physical Therapy

Related to Oxygen Transport
acute, before and immediately after discharge, and
Maximize arousal
long term). The conditioning effects of exercise en
Maximize alveolar volume
able the patient to resume various activities of daily

living commensurate with an increasing capacity of
the patient's oxygen transport system to meet the de
mands of these activities. Activities involving strain
ing and isometric contractions are avoided. Weight
lifting may be introduced in a long-term rehabilita
Optimize alveolar ventilation

Optimize perfusion
Maximize lung volumes and capacities, especially
functional residual capacity
Minimize closing volume
tion program, but the weights are not sufficient to
Minimize intrapulmonary shunting
cause strain. Patients with median sternotomy inci
Optimize lung compliance
sions are usually prohibited from using their anns to
Optimize mucociliary transport
support themselves when sitting or driving and dur

ing activities that may strain the incision site for sev
eral weeks or more.
Optimize mucous clearance

Optimize ventilation and perfusion matching and
gas exchange
Maximize expiratory flow rates
PREOPERATIVE PHYSICAL THERAPY:
Maximize chest tube drainage
PRINCIPLES OF MANAGEMENT
Optimize fluid balance systemically (renal function)
Preoperative management includes assessment and
Optimize lung water balance and distribution
preoperative education; the primary components are
Promote optimal lymphatic draining
shown in the box on p. 498. During this time the phys

ical therapist has an opportunity to develop rapport
with the patient. The assessment establishes the risk of
cardiopulmonary complications and prolonged hospi
Minimize third spacing and collection of fluid

Minimize the risk of aspiration
Minimize undue work of breathing
tal stay and the type and extent of perioperative physi
Minimize undue work of the heart
cal therapy required. The assessment establishes what
Maximize chest wall mobility and movement in
the postoperative priorities will be; however, these are

modified based on the postoperative assessment. The
surgical procedures are described and the effects of
three planes
Optimize body and posture alignment when sitting,
standing. walking, and recumbent
surgery and anesthesia and sedation on gas exchange
Optimize circulatory status and tissue perfusion
are reviewed so that the patient understands the im
Optimize peripheral blood flow and velocity
portance of being actively involved in physical ther

apy, both dUling and between treatments after surgery.
Optimize muscle pump actioll

Minimize effects of central fluid shifts with recum
bency
POSTOPERATIVE PHYSICAL THERAPY:
Maintain t1uid-volume regulating mechanisms
PRINCIPLES OF MANAGEMENT
Minimize pain nonphal1nacologically and coordinate
The goals of postoperative physical therapy manage

ment related to oxygen transport appear in the box at
with the patient's pain medications if indicated

Maximize cardiopulmonary endurance
right. It is essential that these goals are addressed be
Optimize relaxation
tween and during treatments. Thus the patient is in
Provide instruction to patient on "between-treat
structed in mobilization and body positioning coordi

nated with deep breathing and supported coughing
ment" treatment
28
maneuvers between treatment sessions, and these in
503
going thoracic or cardiovascular surgery, are usually
terventions should be performed hourly during wak
extubated before leaving the operating room or re
ing hours (Bennett, Foster, and Chapman, 1990;
covery area. Provided no complications develop,
Blomqvist and Stone, 1983; Bourn and Jenkins,
most other patients do not require an airway. Patients
1992; Hasani, Pavia, Agnew, and Clarke, 1991; Hiet
undergoing major thoracic surgery or cardiovascular
pas, Roth, and Jensen, 1974; Orlava, 1959). Pain
surgery remain intubated and mechanically ventilated
medications are coordinated as needed with treat
from several to 24 hours after surgery to minimize
ments to maximize treatment efficacy.
the work of breathing and hence the work of the heart
In addition to goals related to oxygen transport, other

important postoperative goals include the following:
to meet the metabolical demands of respiration.

These patients are informed that artificial airway and
I. Maximize joint range of motion
mechanical ventilation enables them to breathe more
2. Maximize muscle length and ligament integrity
efficiently initially. A patient is also informed that he
with range of motion exercises
or she will not be able to speak while the airway is in
3. Maximize patient's ability to perform activities

of daily living
place and may have a sore throat after its removal.

Patients are usually aroused and repositioned be
4. Maintain or increase general muscle strength

and endurance
fore leaving the operating room, although this is sel

dom remembered by patients. Not recalling the im
5. Maintain normal cognitive function to avoid
mediate postoperative course is common. Patients are
disorientation and hospital-related psychoses.
likely to be receiving some form of pharmacological
These goals are achieved with the prescription of
analgesia (e.g., morphine). If blood was required in
general mobility exercise, including hip and knee
traoperatively, whole blood, packed cells, or plasma
flexion and extension exercises and foot and ankle
may still be infused in the immediate postoperative
exercises. These exercises are performed hourly re
period or longer. Saline or other solutions are also in
gardless of whether the patient is sitting in the chair
fused for regulation of fluid balance until the patient
or resting in bed.
is able to drink and eat normally. Once vital signs
Finally, there are important preventative goals
have stabilized, wounds are stable and not draining,
(e.g., minimizing the effects of restricted mobility and
and the patient reasonably alert, the patient is trans
recumbency on all organ systems) (Chapters 17 and
ferred to the ward. The patient is retained in the re
l8). Of particular concern in the surgical patient is the
covery area should further monitoring be required. If
risk of thromboemboli and pulmonary emboli and the
complications develop and oxygen transport and gas
risk of pressure points and skin breakdown. Thus mo
exchange threatened, the patient may be transferred
bilization and regular activation of the muscle pumps
to the intensive care unit.
to minimize circulatory stasis and frequent body-posi
The physical therapist may be consulted to assess
tion changes are essential to reduce risks, which can
and treat the patient as soon as he or she leaves the
have serious consequences for the patient's recovery.
operating room or while in the recovery room. Most
Compression stockings are often put on the patient
frequently the physical therapist sees the patient once
after surgery. These are not removed other than for
he or she has been transferred to the ward and has
cleaning and redistributing pressure until the patient is
been settled. The first 24 hours are critical.
consistently up and about. These stockings facilitate
The risk of cardiopulmonary complications is
venous return and increase blood flow and velocity,
greatest during the perioperative period and dimin
thereby minimizing the risk of thrombus formation.
ishes as the patient becomes increasingly upright and
Should thrombus formation be suspected, an intermit
mobile. Atelectasis and aspiration after extubation are
tent compression device may need to be attached to
significant risks for the patient who has been intu
the legs to simulate muscle pump action.
bated. The goal immediately after extubation is to
Not all patients who have surgery are intubated.
promote optimal alveolar ventilation, maximize lung
Those that are, with the exception of patients under
volumes and capacities (especially FRC), minimize
504
PART IV
closing volumes, and maximize expiratory flow rates
There are several factors that are particulary im
and hence cough effectiveness. Areas most suscepti
portant in surgical patients that can affect their sensi
ble to atelectasis are those that may have been physi
tivity to narcotic analgesics, such as morphine
cally compressed during surgery (e.g., the left lower
(Gilman, Goodman, and Gilman, 1990: Malamed,

1989). First, there is considerable intersubject re
lobe of the cardiovascular surgical patient and areas

adjacent to a lobectomy or segmentectomy).
Surgery constitutes a significant insult to the body.
sponse variability to these agents. Second, older pa

tients can be expected to be more sensitive to nar
After the trauma of surgery, anesthesia, sedation,
cotics. Three, diverse multisystem pathology has a
fluid loss, incisions, and the significant energy re
significant effect on the degradation, absorption, bio
quirements for healing and repair, patients can be ex
transformation, and excretion of morphine. Four, ex
pected to be lethargic and difficult to arouse. The re
aggerated effects of morphine have been reported
laxed state induced by anesthesia, sedation, and
when administered in conjunction with other agents,
narcotics increases the risk of aspiration. This risk is
such as other narcotic analgesics, phenothiazines,
exacerbated further in some patients by nausea and
tranquilizers, or sedative-hypnotics; in addition, such
vomiting associated with anesthesia and narcotics.
exaggerated effects have been reported in patients
Moving and positioning the patient upright whenever
with respiratory depression, hypotension, and seda
possible and interacting with the patient stimulates
tion and in patients who are unconscious. These situ
the reticular activating system making the patient
ations in which exaggerated drug effects have been
more responsi ve and aroused. The increased meta
reported are commonly encountered in the intensive
bolic demands that this requires, along with increased
care setting and can result in unpredictable responses.
catecholamine release, helps overcome the residual
Finally, the physical dependence and abuse potential
effects of anesthesia, sedation, and muscle relaxants
of these agents cannot be ignored.
and their threat to oxygen transport, provided the de
The physical therapist must be familiar with the
mands are not beyond the capacity of the oxygen
patient's medications and the medication's indica
transport system to deliver oxygen.
tions, side effects, and contraindications. The physi
Alternatively, some patients are restless and agi
cal therapist can determine to what extent oxygen
tated after the effects of anesthesia have worn off.
transport may be compromised by medication effects,
Hypoxemia can lead to restlessness and agitation.
whether some recommendation needs to be made to
Thus it is important that these patients are not inap
minimize untoward drug effects on arousal or some
propriately sedated. This compounds their need for
other factor that negatively affects oxygen transport
treatment while making them less able to cooperate
and gas exchange. For example, although narcotics
with treatment simultaneously (Dripps and Waters,
are excellent analgesics, they have widespread sys
1941; Ross and Dean, \989).
temic effects including cardiopulmonary depressant
At the outset of any treatment, the patient must be
effects, gastrointestinal depressant effects, and mus
aroused as much as possible to cooperate fully and
cle relaxant effects-all of which compromise oxy
derive the maximal benefit from treatment. The phys
gen transport. Thus consideration needs to be given
ical therapist interacts continuously with the patient
regarding whether other forms of analgesia can be
to arouse the patient fully, maintain arousal, stimulate
used. Have nonpharmacological means of analgesia
normal cognitive function and orientation, and elicit
been exploited? If pharmacological analgesia is indi
feedback from the patient to assess the response to
cated, can analgesics other than narcotics be used? Or
treatment. Narcotics depress respiratory status and
at least, can the dose of narcotic be reduced so that
arousal, and these effects are accentuated in patients
satisfactory pain control can be achieved in combina
whose metabolic states have been disrupted with ill
tion with nonpharmacological interventions?
ness and in older persons. Thus the physical therapist
Mobilization in the upright position coordinated
must be vigilant in detecting untoward residual ef
with breathing control and supported coughing ma
fects of narcotics in the surgical patient.
neuvers is encouraged immediately after the patient is
28
505
first aroused after surgery, unless contraindicated, to
cilitate frequent turning. Cycle pedals can be adapted
help reverse and mitigate reduced arousal, atelectasis,
to chairs and recumbent exercise in bed if necessary.
FRC, and impaired mucociliary transport associated
Patients whose positioning is restricted with fixation
with surgery. Mobilization augments cardiopul
and traction devices require hand, wrist, or ankle
monary function (see Chapter 1 7) particularly when
weights, and possibly pulleys and other devices, to
the patient is upright (Levine and Lown, 1952;
maintain muscle strength and power. Movements per
Lewis, J 980). These beneficial effects are enhanced
formed with moderately heavy weights for multiple
by improved three-dimensional chest wall motion,
sets (e.g., three sets of 10 repetitions) develop muscle
improved gut motility, and reduced intraabdominal
strength. Movements performed with lighter weight
pressure. Extremity movement during ambulation in
for multiple sets (e.g., 5 to 10 sets of 10 repetitions)
creases alveolar ventilation, enhances ventilation and
tend to develop endurance and aerobic capacity. Be
perfusion matching by increasing zone 2 of the lungs,
cause of the restrictions imposed by these devices,
and optimizes diffusing capacity. The upright posi
maintaining joint range is essential (i.e., of the neck,
tion is essential such that the spine is erect, upper
spinal column, and chest wall, as well as the extremi
body musculature relaxed, and the chest wall sym
ties). The rotation component of joint movement is
metrical. Slouching and leaning particularly to the af
readily compromised, thus this needs to be an integral
fected side reduces alveolar ventilation and con
component of joint range of motion exercises. Propri
tributes to uneven distribution of ventilation and
oceptive neuromuscular facilitation (PNF) move
areas of atelectasis (Bake, Dempsey, and Grimby,
ments of the extremities can be beneficial. PNF
1976; Don, Craig, Wahba, and Couture, 1971; Glais
movements of the chest wall can be coordinated with
ter, 1967). In addition, if this abnormal posture is
breathing control and supported coughing maneuvers.
maintained, mucociliary transport of the area is im
Upper body and trunk mobility and strengthening are
paired and mucus collects and stagnates, increasing
important goals particularly in the patient with chest
the risk of bacterial colonization and infection. Sym
wall incisions. The prescription is progressed gradu
metrical posture is monitored at a] I times (i.e., during
ally in the patient with a chest wall incision, particu
ambulation, sitting at bedside, bed mobility exercises,
larly in the patient with a median sternotomy who is
sitting up in bed, and lying in bed). Slouching and fa
usually restricted to unresisted, upper-extremity mo
voring the affected side will lead to cardiopulmonary
bility exercises in the first several weeks.
complications and possibly musculoskeletal compli

cations in the short and long term.
Prescription of body positioning is essential in the

management of the surgical patient for two reasons.
Mobilization and active exercise in upright pos
First, without direction, the patient will tend to as
tures whenever possible are prescribed based on the
sume a deleterious body position (i.e., maintaining a
need to enhance multiple steps in the oxygen trans
restricted number of body positions that favor the af
port pathway (Dean and Ross, 1992; Ray et aI.,
fected side for prolonged periods of time with mini
1974). The priority is to perform as much activity as
mal movement and "stirring up"). Thus once the ef
possible out of bed ancl upright (i.e., ambulation,
fects of mobilization have been exploited in a given
transferring, sitting upright in a chair, and chair exer
treatment session, body positions are prescribed for
cises with or without hand weights or exercise
"between-treatment" times that continue to enhance
bands). When in bed, similar devices can be used, in
oxygen transport for a given patient and discourage
cluding a monkey bar to facilitate moving in bed for
excessive time in deleterious body positions. When
patients other than cardiovascular thoracic patients
not ambulating, patients are encouraged to assume a
(e.g., the orthopedic patient with extremity fractures
wide range of body positions (e.g., semi-prone) be
and traction). In addition, the use of the monkey bar
tween treatments, as frequently as possible, (i.e., at
to perform repetitive bouts of exercise to maintain
least every I to 2 hours) (Dean, 1985; Douglas, Re
upper-extremity strength and some general endurance
hder, Beynen, Sessler, and Marsh, 1977; Piehl and
capacity, to relieve pressure and stiffness, and to fa
Brown, 1976; Remolina, Khan, Santiago, and Edel
506
PART IV
FIGURE 28-1
Incentive spirometers.
28
man, 19S I; Ross and Dean, 1992; Zack, Pontoppidan,
507
mizing FRC, reducing closing volume, maximizing

expiratory flow rates, promoting mucociliary trans
and Kazemi, 1974).

Alveoli are likely to remain patent for I hour after
port, promoting airway clearance, optimizing lym
reinflation. Thus to sustain alveolar inflation and nor
phatic drainage, minimizing the effects of increased
mal FRC, mobilization and body positioning coordi
thoracic blood volume, maintaining fluid-volume
nated with breathing control and supported coughing
regulating mechanisms, and minimizing the work of
must be carried out frequently (i.e., every I to 2
breathing and of the heart. Sustained maximal inspi
hours) to maintain optimal alveolar volume and dis
ration is one intervention that promotes alveolar ex
tribution of ventilation. Maximal inspiratory maneu
pansion. Each deep breath is performed to maximal
vers are coordinated with mobilization and body po
inspiration to total lung capacity with a 3- to 5-sec
sitioning at \east every hour as tolerated. Maximal
ond breath hold. This maneuver may reduce pul
inspiratory maneuvers alone, however, are unlikely to
monary complications by promoting alveolar infla
be effective because the inspiratory pressure may be
tion and gas exchange. The patient is encouraged to
insufficient to inflate atelectatic alveoli. Rather patent
repeat this maneuver several times hourly, and fre
alveol i will tend to be overexpanded. Mobilization
quently during mobilization, and before, during, and
and body positioning will directly alter the in
after body-position changes.
trapleural pressure gradient and thereby optimize

alveolar expansion (Roussos et at. 1977).
Incentive spirometry can be useful in patients who

are resistant or unable to cooperate fully with maxi
Normal passive expiratory efforts to end tidal
mal inspiratory efforts (Figure 2S-I ). Postoperative
volume are encouraged and maximal or forced expi
hypoxemia may be reduced with this technique,
ratory efforts are usually avoided to prevent airway
which uses the principle of sustained inspiration
closure and potential increase of atelectasis (Has ani
using a feedback device (either flow or volume feed
et aI., 1991; Hietpas et aI., 1974; Nunn, Coleman,
back) to achieve maximal inflating pressure in the
Sachithanandan, Bergman, and Laws, 1965). Huff
alveoli and maximal inhaled volume. The incentive
ing (glottis open) rather than coughing (glottis
spirometer can be used independently by the patient.
closed) also minimizes airway closure. There is less
This technique ensures that each inspiration is physi
risk of bronchospasm than with coughing in which
ologically optimal and is reproduced precisely from
the glottis is closed, transpulmonary pressure is in
one inspiration to the next. Patients who are surgical
creased, and a compressive phase is involved. If in
risks can benefit from being taught the use of the in
dicated, coughing maneuvers are most effective in
centive spirometer during preoperative teaching by
the sitting or slightly lean-forward position in which
the physical therapist to promote better inflation of
lung volumes and forced expiratory flow are maxi
the lungs with incentive spirometry postoperatively.
mized and the respiratory muscles are mechanically
The patient continues with a regimen of breathing
advantaged with respect to the length-tension char
control and coughing maneuvers until full mobility
acteristics of the muscle fibers. Airway closure is
and activities of daily living are resumed.
position-dependent (Chapter IS); therefore the de
The application of intermittent positive pressure
gree of expiration encouraged by the physical thera
breathing (IPPB) appears to be less effective for the
pist should be based on the patient's body position.
postoperative patient than previously believed. The
Airway closure is potentiated in patients who are
details of this modality are described in Chapter 41.
older, smoke, or are obese and in patients who are in

horizontal as opposed to upright body positions.
M obilization and body posi tioning coordinated
SUMMARY
with breathing control and supported coughing ma
This chapter reviews the management of cardiopul
neuvers offer the greatest benefit to oxygen transport
monary dysfunction secondary to acute surgical con
in the postoperative patient. Specific benefits are de
ditions. Surgery and its physiological effects are de
scribed in Chapters 17 and IS. They include maxi
scribed. Special reference is made to two specialized
508
PART IV
types of surgery that have the greatest impact on car

diopulmonary function, namely, thoracic and cardio
vascular surgery.
The four categories of factors contributing to or
threatening oxygen transport are described in Chapter
16. These factors include pathology, restricted mobil
ity and recumbency, extrinsic factors related to the
patient's care, and intrinsic factors related to the pa
tient. This chapter examines in detail those extrinsic
factors related to surgery and anesthesia, and the im
pact of underlying disease, restricted mobility, re
cumbency and intrinsic factors on the effects of
surgery and anesthesia.
In this chapter, treatment principles are pre
sented rather than treatment prescriptions for partic
ular patients. For specific examples of patient treat
ment prescriptions refer
to
the companion
workbook Clinical case studies i n cardiopulmonary

physical therapy.
Bennett, W.D., Foster, W.M.,
&
Chapman, W.F. (1990). Cough
enhanced mucus clearance in the normal lung. journal of Ap

plied Physiology.
&
Blomqvist, e.G.,
69,
1670-1675.
Stone, H.L. (1983).
Cardiovascular adjust
ments /0 graviratiollal stress. Handbook ofphysi()lo y (Vol. 2).

Washington, DC: American Physiological Society.
&
Bourn, J.,
Jenkins, S. (1992). Post-operative respiratory physio
78,
therapy. Indications for treatment. Physiotherapy,

Dean, E.
(1985).
Physical Therapy,
Dean, E.,
&
80-85.
Effect of body position on pulmonary function.
65,
613-618.
Ross, J. (1989). Integrating current literature in the
management of cystic fibrosis: a rejoinder. Physiotherapy

Canad{1,
Dean,
E., &
4/, 46-47.
Ross, J. (1992).
Mobilization
and
exercise condition
ing. In e.e. Zadai (Ed.), Puhllo/1ary management in physical

therapy. New York: Churchill Livingstone.
Don. H.F., Craig, D.B., Wahba, W.M"
&
Couture, J.G. (1971). The
measurement of gas trapped in the lungs at functional residual

capacity and the effects of posture. Anesthesiology,
K.,
Douglas, W.W., Rehder.
35,
582-590.
Beynen, F.M .. Sessler, A., D.,
&

acute respiratory failure: the prone position. American Review
oJ Respiratol),
Dripps. RD.,
&
Disease,
//5,559-566.
Waters, R.M. (1941). Nursing care of the surgical
4/, 53-34.
& Dull, W.L. (1983). Are maximal inspiratory breathing ex
patient. I. The "stir-up." American .lournal of Nursing,
REVIEW QUESTIONS
Dull,1. L.,
1. Describe the physiological effects of surgery in

cluding the specific surgical procedure, the type,
depth and duration of anesthesia, sedation, types
of respiratory support, static body positioned as
sumed during surgery, length of surgery, number
and type of invasive periooperative procedures,
and incisions.
ercises or incentive spiromeny betler than early mobilization after

cardiopulmonary bypass surgely? Physical Therapy,
Dureuil, B., (Viires, N.,
&
contractility after upper abdominal surgery. journal oJ Applied
6/, /775-1780.
& Guenter. e.A. (1984).
Physiology,
Ford, G.T.,
3. Relate cardiopulmonary physical therapy treat

ment interventions to the underlying pathophysiol
ogy associated with surgery and those factors
listed in Question 1 and provide the rationale for
your choice.
Toward
prevention of postop
erative complications. American Review of Respiratol)' Dis

eases,
/30,
4-5.
& Bryan, A.e.

paralysis on diaphragmatic
4/,242-255.
Froese, A.B. ,
2. Describe surgical risk factors.
63, 655-659.
Cantineau, J.P. (1986). Diaphragmatic
(1974).
ErI'eCls
of anesthesia and
mechanics in man. Anesthesiology,
Glaister, D.H. (1967). The effect of posture on the distribution of

ventilation and blood flow in the normal lung. Clinical Science,
33,
391-398
Gilman, A.G., Goodman, L.S.,

and
Gilnwn's th e
&
Gilman, A. (1990). Goodman
plwrmacological basis of therapeutics (8th
ed.). New York: Macmillan Publishing.

Hasani, A., Pavia, D., Agnew, J.E.,
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Alexander, J.L., Spence, A.A., Parikh, R.K.,
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Stuart, B. (1973).
The role of airway closure in postoperative hypoxaemia.

British journal ofAnaeslhesiology,
Bake, B., Dempsey, J.,
(1991). The ef
fect of unproductive coughinglFET on regional mucus move
&
59, 1070- 1 079.
85, 23-26.
Hedenstierna, G., Standberg, A.; Brismar, B., Lundquist, H., Sven

son, L.,
&
Tokics, L. (1985). Functional residual capacity, Iho
racoabdominal dimensions and central blood volume during
Grimby, G. (1976). Effects of shape
on distribution of inspired gas. Amer

icall Review of Respira/ory Disease, //4, 1113-/120.
Behrakis, P.K., Baydur, A., Jaeger, M.J., & Milic-Emili, J. (1983).
changes of the chest wall
general anesthesia with muscle paralysis and mechanical venti
lation.
Anesthesiology,
62, 247-254.
Hedenstierna, G., Tokics, L., Strandberg, A., Lundquist, H.,
&
Brismar, B. (1986). Correlation of gas exchange impairment to
Lung mechanics in sitting and horizontal body positions. Ches/,
development of atelectasis during anaesthesia and muscle
83,
paralysis. Acta Anaesthesiologica Scal1dinavica,
643-646.
30, 183-191.
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Hietpas, B,G" Roth, RD, & Jensen. W,M. (1974), Huff coughing
and
patency, Respiratory Care, 24,

The incidence
of post-operative hypoxaemia following

a
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pulmonary
Khan, A.U"
Santiago, T.V"
& Edelman, N.H,
(1981), Positional hypoxemia il) unilateral lung disease, New

England Journal of Medicine.
Levine, S,A" & Lown, B, (1952), 'Armchair' treatment of acute
of Surge ry, 109,
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P., & Paredes, R.M. (1974), Immobility, hypoxemia, and
Leaver, H" Conway. JR, & Holgate, S,T, (

monectomy:
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523-525,
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Lewis, F.R. (1980), Management of atelectasis and pneumonia,

Malamed, S,F, ([989), Sedation, A g uide
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P u lmo ll ary mana gement in physical Iherapy, N e w York:
Surgical Clinics of North America, 60, 1391-1401,

palielll manag ement
(2nd ed,) 51. Louis: Mosby,
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I/O, 149-153,
PAR T

of Cardiopulmonary
Physical Therapy: Chronic
Cardiopulmonary
Conditions
Chronic Primary Cardiopulmonary

Dysfunction
Elizabeth Dean
Donna Frownfelter
KEY TERMS
Angina
Hypertension
Asthma
Bronchiectasis
Lung cancer
Chronic airflow limitation
Cystic fibrosis
Diabetes
Val vula heart disease
INTRODUCTION
there is no clear line between obstructive and restric
The purpose of this chapter is to review the pathophys
tive patterns of lung disease, pathology can be gener
iology, medical management, and physical therapy
ally defined based on the primary underlying patho
management of chronic, primary, cardiopulmonary
physiological problems. Thus the primary conditions
pathology. Because the heart and lungs are interdepen
that are presented include obstructive lung disease
dent and function as a single unit, primary lung or
(i.e., chronic airflow limitation, asthma, bronchiecta
heart disease must be considered with respect to the
sis, and cystic fibrosis) and restrictive lung disease
other organ and in the context of oxygen transport
(i.e., interstitial pulmonary fibrosis). Lung cancer,
overall (Dantzker, 1983; Ross and Dean, 1989; Scharf
which has the characteristics of both obstructive and
and Cassidy, 1989; Wasserman and Whipp, 1975).
restrictive patterns of patho.logy, is also presented.
The long-term cardiopulmonary management of
The long-term cardiopulmonary management of
chronic lung diseases is presented first. Although
heart disease is then presented with special attention

513
514
PART V
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions
to angina, myocardial infarction, and valvular heart
breathing re s ponse to vertilatioll-perfusion imbalance
disease. Chronic vascular diseases, including periph
and hypoxemia, and tissue defenses against elastase.

Decline in pulmonary function and rate of devel
eral vascular disease, hypertension, and diabetes, are
opment of the syndrome depend on the combination
also presented.
The principles of management of the various
of causative factors and individual responses to them.
chronic primary cardiopulmonary conditions are pre

sented rather than treatment prescriptions, which can
not be discussed without consideration of a specific
Chronic Bronchitis
patient. (For specific examples of patient treatment

prescriptions refer to the companion test Clinical case
Chronic bronchitis is usually associated with a his
studies in cardiopulmonGl)1 physical therapy.) In this
tory of smoking and is defined as mucous hyper
context the goals of long-term management of each
secretion and cough producing sputum for three
condition are presented, followed by the essential
months or more over a two-year period (Murray and
monitoring required, and the primary interventions for
Nadel, 1988a). Over the first few years of smoking,
maximizing cardiopulmonary function and oxygen
reversible airways changes occur. Over 10 to 15
transport. The selection of interventions for any given
years of smoking, mucous hypersecretion and chronic
patient is based on the physiological hierarchy. The
bronchitis become apparent. After 25 to 35 years of
most physiological interventions are exploited first
smoking, irreversible airway damage and chronic dis
followed by less physiological interventions and those

whose efficacy is less well documented (Chapter
16).
ability occur. Smoking is the major cause of lung

cancer. The pathophysiology of chronic bronchitis is
reviewed in detail in Chapter 29.
The patient is prone to infection and repeated peri
PRIMARY PULMONARY DISEASE
ods of morbidity. Deterioration of aerobic capacity
OBSTRUCTIVE PATTERNS
and functional capacity is related to the severity of

the condition. Nutrition and hydration may be im
Chronic Airflow Limitation
paired particularly in severe cases because of neglect
Chronic airflow limitation is a descriptive term that
and the excessive energy cost of activities of daily
refers to those disorders that previously have been
living. Sleep may be irregular, thus the patient's
termed chronic obstructive pulmonary disease (e.g.,
symptoms are worsened (e.g., reduced endurance, fa
chronic bronchitis, emphysema, bronchiectasis, and
tigue, and lethargy) because of lack of normal physi
cystic fibrosis). Although there may be a reversible
ological restoration from sleep.
component, airflow obstruction associated with these
The natural history of chronic bronchitis related to
disorders is largely irreversible. The pathophysiology
smoking includes mucous hypersecretion, reduction in
of these conditions is reviewed in detail in Chapter 29.
forced expiratory volume (FEV), and increased hetero
Bates (1989) described the syndrome of chroruc air
geneity of the distributions of ventilation, perfusion,
flow limitation as being caused by four external fac
ventilation-perfusion matching, and diffusion (West,
tors, mediated by four primary tissue responses, and
1987). General debility and deconditioning ensue.
modified by four physiological responses. The princi
Smoking contributes to increased mucous produc
pal external causative factors include inhaled irritants,
tion in the small airways, increased mucus in the large
allergens, infectious, and climate. The four principal
airways, respiratory bronchiolitis, reduced elastic re
tissue responses include large airway changes, small
coil, increased airway reactivity, and vascular changes
airway changes, airway hyperreactivity, bronchiolar
(Bates, 1989). These changes, lead to nonuniformity
damage, and alveolar destruction. The principal physi
of time constants in the lung, with consequent inho
ological responses include a reversible increased air
mogeneous distribution of inspired gas and premature
way reactivity component, pulmonary vascular re
small airway closure, and to nonuniformity of ventila
sponse to alveolar hypoventilation, control of
tion, perfusion, and diffusion distributions. Although
29
Chronic Primary Cardiopulmonary Dysfunction
515
vaJiable among smokers, pulmonary function changes
crease the demand on the left heart to maintain cardiac
generaHy corrcspond to the amount smoked and dura
output. Similar to right-sided failure, the left heart
tion of the smoking history. Over time, the pulmonary
may become hypertrophied, and over time, may fail.
function profile becomes increasingly consistent with
The significantly increased intrathoracic prcssures
chronic airflow limitation (i.e., reduced FEY, and re
generated during chronic coughing reduce venous re
duced FEY,IFYC), however, these are late indicators
turn, cardiac output, and coronary perfusion and in
of pulmonary changes. Signs of uneven distribution of
crease blood pressure. These effects exert additional
ventilation and increased closing volumes, indicative
myocardial strain, lead to arterial desaturation, and
of small airway involvement, are early pulmonary
increase the potential for cardiac dysrhythmias.
function changes in smokers. Exercise diffusing ca
The complications of chronic bronchitis are exacer
pacity is reduced which explains in part the reduced
bated by cardiopulmonary deconditioning. Despite the
maximal Y02 of smokers. Dynamic compliance with
pathology, the efficiency of oxygen transport along the
breathing frequency is also reduced. Residual volume
steps in the pathway is suboptimal. This reduced effi
is increased as a percent of total lung capacity. Tra
ciency increases the oxygen demands of the patient
cheal mucous velocity is reduced and secretion clear
overall who is unable to adequately supply oxygen.
ance is impaired. Any patient with a smoking history,
Pharmacological support in the tong-term manage
regardless of a diagnosis, has some degrcc of chronic
ment of chronic bronchitis includes bronchodilators
airflow limitation, which must be considered when
(e.g., oral, metered-dose inhalant, inhaled powdered, or
these patients are receiving medical or surgical care.
aerosol), corticosteroids (e.g., oral or inhaled), expecto
The cardiac manifestations of chronic bronchitis
rants, antibiotics, inotropic agents (e.g., digitalis), beta
stem from airway obstruction, secretion accumulation
blockers, antidysrhythmic agents, and diuretics. Patients
and reduced capacity to effectively expectorate, poly
with chronic lung disease must be monitored closely
cythemia, low arterial oxygen tensions, and cardiopul
during exercise given the potential cardiac effects of
monary deconditioning. Increased airway resistance
disease and medications (e.g., beta-blocker agents atten
secondary to obstruction increases oxygen demand
uate the normal hemodynamic responses to exercise and
and hence the work of breathing. This increased de
bronchodilators, such as ventolin, elicit tachycardia).
mand is superimposed on an oxygen transport system

that is already compromised. The cardiovascular sys
tem attempts to compensate for chronically reduced
The goals of long-term management for the patient
arterial oxygen tension by increasing cardiac output
with chronic bronchitis include the following:
(i.e., stroke volume and heart rate). As blood gases de
(i.e., polycythcmia) to enhance the oxygen-carrying

capacity of the blood. However, polycythemia in
Maximize the patient's quality of life, general

health, and well-being and hence physiological
teriorate, the production of red blood cells increases
reserve capacity
Educate about chronic bronchitis, self-manage
creases the viscosity of the blood, and in turn, the
ment, effects of smoking, nutrition, weight con
work of the heart to pump blood to the pulmonary and
trol, smoking reduction or cessation, other life
systemic circulations. Furthermore, viscous blood is
style factors, medications, infection control, and
prone to circulatory stasis and clotting.
role of a rehabilitation program
Low arterial oxygen tensions lead to hypoxic pul

monary vasoconstriction and increased pulmonary
vascular resistance (i.e., pulmonary hypertension).
Facilitate mucociliary transport
Optimize secretion clearance
This also increases the work of the right heart in eject
Optimize lung volumes a n d capacities a n d
ing blood to the lungs. Chronic overwork of the right
flow rates
ventricle leads to hypertrophy, insufficiency, and
eventual failure of the right heart (cor pulmonale).

Chronically reduced arterial oxygen levels can in
Optimize ventilation and perfusion matching

and gas exchange
Reduce the work of breathing
516
PART V
Reduce the work of the heart
health practices (e.g., smoking reduction and cessation,
Maximize aerobic capacity and efficiency of
cold and flu prevention, flu shots, aerobic exercise,
oxygen transport
strengthening exercises, nutrition, weight control, hy
Optimize physical endurance and exercise ca
dration, pacing of activities, energy conservation, re
pacity
laxation, and stress management). Chronic bronchitis
Optimize general muscle strength and thereby
and emphysema are often associated with sleep distur

bances. Obstructive sleep apnea is increasingly preva
peripheral oxygen extraction

Patient monitoring includes dyspnea, respiratory
lent with disease severity. Thus activity and sleep pat
distress, breathing pattern (depth and frequency), ar
tems need to be assessed to ensure sleep is maximally
terial saturation, cyanosis (delayed sign of desatura
restorative and is not contributing to the patient's
tion), heart rate, blood pressure, and rate pressure
symptoms. Integral to an exercise prescription is the
product. Patients with cardiac dysfunction or low
time of day. Exercise is prescribed when the patient is
arteral oxygen tensions require ECG monitoring, par
least fatigued, most energetic, and when performing
ticularly during exercise. If supplemental oxygen is
such a program is most convenient.
used, the FIo2 administered is recorded. Subjectively,
Aerobic exercise is an essential component of the
breathlessness is assessed using a modified version of
long-term management of the patient with chronic

bronchitis to optimize the efficiency of oxygen trans
the Borg scale of perceived exertion.

Medication that is needed to maximize treatment
POit overall and mobilize and remove secretions (Old
response is administered before treatment (e.g., bron
enburg, Dolovich, Montgomery, and Newhouse, 1979).
chodilators). Knowledge of the type of medication,

its administration route, and time to and duration of
peak efficacy is essential if treatment is to be maxi
mally efficacious.
Emphysema
The primary interventions for maximizing car
Emphysema is associated with a prolonged history
diopulmonary function and oxygen transport in pa
of smoking and chronic bronchitis and indicates sig
tients with chronic bronchitis include some combina
nificant irreversible lung damage. A less common
tion of education, aerobic exercise, strengthening
type of emphysema not associated with smoking is
exercises, chest wall mobility exercises, range of mo
alpha-antitrypsin deficiency. Antitrypsin is essential
tion, body positioning, breathing control and coughing
in balancing elastin production and degradation and
maneuvers, airway clearance techniques, relaxation,
in preserving optimal lung parenchymal compliance.
activity pacing, and energy conservation. An er
A deficiency of antitrypsin reduces lung elasticity
gonomic assessment of the patient's work and home
and contributes to the characteristic increase in lung
environments may be indicated to minimize oxygen
compliance that is the hallmark of emphysema. The
demand and energy expenditure in these settings.
pathophysiology of emphysema is presented in detail
The use of supplemental oxygen depends on the
in Chapter 4. The principal pathophys iological
severity of the disease. Some patients have no need for
deficits include irreversible alveolar damage result
supplemental oxygen, some need it only during exer
ing from loss of elastic recoil and the normal tether
cise, and some patients require continuous oxygen with
i n g of
proportionately more delivered during activity and ex
parenchyma excessively compliant and floppy. Ex
ercise compared with rest. Supplemental oxygen is not
cessi ve distension and' dil atation of the termi nal
usually required until lung damage becomes extreme
bronchioles and destruction of alveoli reduces the
t h e a l v e o l i,
w h i c h renders t h e lung
(i.e., the morphological changes are consistent with the
surface area for gas exchange. Hence diffusing ca
irreversible changes associated with emphysema).
pacity is correspondingly reduced. The dead space in
Education is a principal focus of the long-term
the lungs and total lung capacity increase s ignifi
management of the patient with chronic bronchitis. Ed
cantly. Breathing at normal tidal volume, the pa
ucation includes the reinforcement of preventative
tient's airways close beyond that which normally oc
29
517
curs with aging, which contributes to ventilation and
poxic vasoconstriction in the lungs. Over time, the
perfusion mismatch and hypoxemia. Time constants
heart becomes enlarged and pumps even less effi
are altered such that alveolar units are not being
ciently. In the long-term management of the patient
evenly ventilated. In its nonacute, chronic stages the
with emphysema, alveolar ventilation, gas exchange,
primary problems include inadequate and inefficient
reduced oxygen transport efficiency, and the work of
gas exchange resulting from the structural damage to
breathing and of the heart are the primary pathophys
the lungs and altered respiratory mechanics of the
iological problems. Unlike chronic bronchitis, secre
lungs, chest wall, and their interaction. The lungs are -
tion accumulation may be less problematic in emphy
hyperinflated, the chest wall becomes rigidly fixed in
sema patients during nonacute periods. Nonetheless,
a hyperinflated position, the normal bucket handle
optimizing mucociliary transport is an ongoing con
and pump handle motions of the chest wall are im
cern in that the consequences of mucous retention
paired, the hemidiaphragms are flattened, the medi
and infection can be devastating.
astinal structures are shifted, and the heart is dis

placed and rotated, making its function inefficient
(Bake, Dempsey, and Grimby, 1974; Geddes, 1984;
The goals for long-term management of the patient
Murray and Nadel, 1988a). The normal mucociliary
with emphysema include the following:
transport system is ineffective because years of
smoking destroy the cilia, reduce their number, and
reserve capacity
alter their configuration and orientation; thus their

function is correspondingly obliterated or impaired.

In addition, these patients are unable to generate
Educate about emphysema, self-management,

smoking reduction and cessation, medications,
high transpulmonary pressures and forced expiratory
nutrition, weight control, infection control, and
flow rates because of altered respiratory mechanics.
the role of a rehabilitation program
Consequently, coughing maneuvers are weak and in
effective. The administration of supplemental oxy

Optimize lung volumes and capacities and flow
rates
gen is limited because these patients rely on their hy

poxic drive to breathe. This life-preserving drive can
be attenuated with even moderate levels of oxygen.
Thus oxygen administration is limited to low flows.
The respiratory muscles are often weak, if not fa
transport system and the capacity of other steps in

the pathway to compensate.

There are several physiological compensations

pacity
sema, tend to be inactive and deconditioned, which

further compromises the efficiency of the oxygen

oxygen transport
tigued (Rochester, and Arora, 1983). Overall, pa

tients with emphysema, particularly severe emphy
Optimize respiratory muscle strength and en

durance and overall respiratory muscle efficiency
that occur in response to chronic hypoxemia. Stroke
Education focuses on teaching the patient about
volume and cardiac output are increased. The red
emphysema, self-management of the disease, the effect
blood cell count increases (polycythemia), however,
of smoking and smoking cessation. nutrition, weight
the blood becomes more viscous and requires more
control, hydration, relaxation, sleep and rest, stress
work to eject and distribute throughout the body.
management, activity pacing, energy conservation, and
Thus the stroke work of the heart is further increased.
prevention (e.g., cold and flu prevention, flu shots, aer
This load on the heart is additional to the increased
obic exercise, diet, sleep, and stress management).
afterload on the right ventricle because of an increase
Comparable with the patient with chronic bronchi
in pulmonary vascular resistance secondary to hy
tis, sleep disturbances are common in the emphysema
518
PART V
patient. Activity and sleep patterns are assessed to en
anaerobic capacity, improved ventilatory muscle
sure sleep is maximally restorative. If obstructive
strength and endurance, and increased motivation (Bel
sleep apnea is disturbing the patient's sleep, medical
man and Kengregan, 1981; Belman and Wasserman,
1981; Dean, 1993). Exercise intensity is prescribed
intervention is required.
based on rating of breathlessness (mod ified Borg
scale) (Chapter 17), in conjunction with objective and
terial saturation, lightheadedness, discoordination,
other subjective responses from the exercise test.
heart rate, blood pressure, and rate pressure product.
Patients with chronic airflow limitation alter their
Patients with cardiac dysfunction or low arterial oxy
breathing patterns so that they are breathing on the
gen tensions require ECG monitoring particularly
most metabolically efficient portion of the pressure
during exercise. Subjectively, breathlessness is as
relaxation curve (Chapter 4 and 29). These patients
sessed using a modified version of the Borg scale of
tend to breathe with prolonged expiratory phases to
perceived exertion.
maximize gas transfer and mixing in the lungs to
minimize the effects of altered ventilatory time con
stants. To facilitate such a breathing pattern, the pa
chodilator). Knowledge of the type of medication, its
tient tends to breathe through pursed lips, which may
administration route, and time to and duration of peak
create back pressure to maintain the patency of the
efficacy is essential if treatment is to be maximally
airways (Muller, Petty, and Filley, 1970). The meta
efficacious. When patients are on multiple medica
bolical efficiency of the patient's breathing pattern
tions, the interactions and implications on treatment
may be improved further by altering breathing me
response must be identified.
chanics rather than imposing a different breathing
pattern that may be suboptimal. Altering breathing
mechanics involves manipulating the patient's body
tients with emphysema include some combination of
position to promote alveolar ventilation, perfusion,
education, aerobic exercise, strengthening exercise,
and ventilation and perfusion matching.
ventilatory muscle training (strength and endurance)
The increased intrathoracic pressures generated
or ventilatory muscle rest, low flow oxygen, mechan
during chronic coughing limit venous return, cardiac
ical ventilatory support for home use, chest wall mo
output, and coronary perfusion. Blood pressure is
bility exercises, range of motion exercises, body posi
also increased. These effects exert additional myocar
tioning, breathing control and coughing maneuvers,
dial strain, lead to arterial desaturation, and increase
airway-clearance techniques, relaxation, activity pac
the potential for cardiac dysrhythmias. Breathing
ing, and energy conservation. An ergonomic assess
control and coughing maneuvers coupled with body
ment of work and home environments may be indi
positioning and exercise are instructed such that the
cated to minimize oxygen demands in these settings.

The benefits of aerobic and strengthening exercise
work of breathing is minimized (i.e., alveolar ventila

tion and gas transfer is as efficient as possible), and
in the long-term management of airflow limitation to
coughing is also as efficient as possible (i.e., maxi-
optimize oxygen transport in patients with compro
mally productive with the least energy expenditure).
mised oxygen delivery is well established (Dean,
Physical therapy is one component of a compre
1 9 9 3 ; Niederman et aI., 1 9 91 ; R i e s , Ellis, and
hensive rehabilitation program in the long-term man
Hawkins, 1988; ZuWallack, Patel, Reardon, Clark, and
agement of emphysema. Such a program also needs to
Normandin, 1991). Patients with severe limitations are
include information on health promotion and mainte
often unable to exercise at a sufficient intensity to ef
nance, ongoing review and log of medications, respi
fect aerobic adaptations to the exercise stimulus. Bene
ratory support (e.g., oxygen aerosol therapy, and me
fits of exercise in these patients may be explained by
chanical ventilatory support), occupational therapy,
desensitization of dyspnea, improved movement effi
sexual rehabilitation, psychosocial rehabilitation, and
ciency and hence movement economy, improved
vocational rehabilitation (Dean, 1993; Murray, 1993).
29
Asthma
Patients with cardiac dysfunction or low arterial oxy
Asthma is a common respiratory condition that is
gen tensions require ECG monitoring particularly dur
hypersensitivity of the airways to
various
and bronchial edema
struction (i.e.,
1984; M urray a n d Nadel, I

(Chapter
exercise.
ob
in reversible
519
heart rate, blood pressure, and rate pressure product.

characterized
breathlessness is assessed
a modified version of the Borg scale of per

ceived exeltion.
In mild cases, no treatment
other than prophylaxis may be needed. In severe
chodilators and antiinflammatories). Knowledge of
cases, asthma can be life
the type of medication, its administration route, and
Once af
the
fected by the
narrow, increas
time to and duration of
efficacy is essential if
treatment is to be maximally efficacious. When panarrowed
Breathing
con-
tributes to wheezing, reduced alveolar ventilation,

rapid shallow
shortness of breath, in
their interactions
tients are on multiple
must be known.
for
and the
c reased work of brea t h i n g , des a t u r a t i o n , a n d
diopulmonary function and oxygen
cyanosis. Increased inhomogeneity o f the distribu
tients with asthma include education, aerobic exer
tion of ventilation is present in some nonacute

asthmatic patients
boud, I
in pa
chest wall
Dean, and Ab
Although some
may
ing, and stress management.
mucous hypersecretion, even normal amounts of

pulmonary secretions can obstruct narrowed air
E ducation is c e n t r a l to
is
asthma. The
t of
the basic pathophysiol
Other central top
ways leading to atelectasis. Asthma that has welI
ogy of the disease and its
defined triggers is easier to manage than cases
ics including preventative health practices are also
where the triggers are less specific.
taught
cold and flu
t'f1J1CllJrt8S of physical therapy management
flu
control,
The goals of long-term management of the patient
reduction and
with asthma include the following:
agement, and the benefits of an
quality of
Maximize the
life-long
mention needs to be made regarding the
reserve capacity
relaxation and stress man

rehabilitation program).
and hence
and
med
use of medications and inhalers. These are frequently
Educate about asthma, self-management, nutri
used
tion,
with the basic pharmacokinetics of the medications
control,
reduction and ces
sation, medications and their uses,
of
used and thus are not
and infection control
asthmatic
Maximize aerobic
(i.e., the patient is unfamiliar

ef
In addition, inhalers are often used improperly;

therefore the patient does not derive the full benefit
and
of
oxygen transport
of the medication. The instructions provided
the
supplier of the inhalers should be strictly followed.
physical endurance and exercise ca
There are numerous types of

ent applications.
pacity
muscle
pe-
ripheral oxygen extraction
the
time and effort is wasted
haler ineffectively, the
Patient monitoring includes dyspnea,
all with differ
not adhering to the instructions,

the in
does not derive the full
benefit of the medication, an excessive amount of in
,,,.,,,, ",,'", breathing pattern (depth and frequency), alter

of desaturation),
haler may be used to
for ineffective ap
plication, there may be increased exposure of the pa
520
PART V
tient to the side effects of the
and there is
The patient with bronchiectasis has
considerable economic waste.
impaired respiratory
of the
of increased
sensitivity enables the
pattern, reduced
to exert control over
bronchospastic attacks, The patient is taught to record
cretions, reduced aerobic caDacitv. and is

debilitated.
the freauencv of bronchospastic attacks and
The increased intrathoracic pressures
and what relieves them. In this way, the
bouts of chronic coughing limit venous return,
learns to avoid or minimize their frequency,
caridac output, and coronary perfusion, Blood pres
severity, and duration and minimizes the amount of

medication
benefits.
These are
sure is also increased. These effects exert additional

myocardial
The ex ercise prescription parameters are set
lead to arterial desaturation, and
increase the potential for cardiac dysrhythmias and
below the bronchospasm threshold, which is estab
17 and 23).
lished based on an exercise test
Principles of physical therapy manal,emrenl
tests are performed in a pul

monary function laboratory with appropriate med
to
ical support. Exercise training enables the
The goals of
management of the patient
with bronchiectasis include the
determine the balance between optimal aerobic ca
Maximize the patient's
and medication and the optimal physical en
and well-being and hence
vironment for exercise. Temperature and humidity
reserve capacity and function
can have significant effects on work outout in asth
matic n.,tipntc
Educate about
nutrition,
control,
cessation, medications and their use, and infec

tion control
Bronchiectasis

Bronchiectasis is characterized by dilatation and
anatomical distortion of the airways and obliteration
of t h e
b r o n c h i a l t r e e (West,
Bronchiectasis is often the

chronic
secretion clearance
1987).
of
ventilation and
infection. The associated inflammation
leads to occlusion of the airways, which results in
atelactasis of the
tion of central
and
dilata

In addition,

to further dilatation. Fibrotic, connec
"'''''''!,'''::>
mechan
Optimize ohvsical endurance and exercise ca

Optimize general muscle
and thereby
Patient monitoring includes dyspnea,

breathing
distortion. These anatomical
adversely affect normal
of
oxygen extraction
tive tissue changes in the wall contribute further to

dilatation and
Maximize aerobic
pacity
chronic inflammation weakens the walls of the air

ways,
Reduce the work of

oxygen
by increased traction on the
peribronchial sheath (Bates, I
and flow
Optimize lung volumes and

rates
terial saturation,
(depth and
(a delayed
ics and hence pressure volume characteristics of the
tion), heart rate,
lung. The chest wall becomes hyperinflated and as
product. Patients with cardiac dysfunction or low ar
sumes the barrel shape associated with chronic air
terial oxygen tensions
flow limitation. The overall
ticularly during exercise.
of bronchiectasis
on the number of lung segments involved.

There is often some reversible airflow limitation as
pressure, and rate pressure

ECG monitoring par
breathlessness
is assessed using a modified version of the Borg scale

of
exertion.
sociated with bronchiectasis.
29
521
response is administered before treatment. Knowl
Between exacerbations, the medical priorities are
edge of the type of medication, its administration
to reduce the risk of infection and morbidity and pro
route, and time to and duration of peak efficacy is es
mote optimal health, growth, and development.
sential if treatment is to be maximally efficacious.

tients with bronchiectasis include some combination
with cystic fibrosis include the following:
of education, aerobic exercise, strengthening exer
and physiological reserve capacity
exercises, body positioning, breathing control and

coughing maneuvers, airway clearance interventions,

health and well-being, growth and development,
cise, chest wall mobility exercises, range of motion
Educate the patient and family about cystic fibro
optimizing rest and sleep, relaxation, pacing, and en
sis, self-management, nutrition, prevention of acute
ergy conservation. An ergonomic assessment of the
exacerbations of the disease, infection control, and
patient's work and home environments may be indi
medication's uses, modes of adi

m nistration,
cated to maximize function in these settings.
macokinetics and times to peak efficacies.
Education is a central component of the patient's

long-term self-management rehabilitation program.
Preventative health practices are taught (e.g., cold and
flu prevention, flu shots, smoking cessation, sleep,
benefits of an integrative, rehabilitation program).
Cystic Fibrosis

rates
aerobic exercise, nutrition, weight control, and hydra

tion, relaxation, stress management, and the long-term

Reduce the work of and strain on the heart
oxygen transp0l1
significant systemic effects (Landau and Phelan,

1973; Murray and Nadel, 1988b). The diesase is con

pacity
Cystic fibrosis is a complex exocrine disease that has


genital and is hallmarked by nutritional deficits con
tributing to impaired growth and development. Pul
monary function shows progressive decline with
terial saturation, cyanosis (a delayed sign of desatura
commensurate reductions in homogeneity of ventila
tion and inspiratory pressures (Chatham et aI., 1994;
product. Patients with cardiac dysfunction or low ar
Cotton, Graham, Mink, and Habbick, 1985; Ross et
terial oxygen tensions require ECG monitoring, par
aI., 1989). Cardiopulmonary involvement can be clas
ticularly during exercise. Subjectively, breathlessness
sified into three groups, namely, no physical signs in
the chest, occasional cough and sputum, and constant
of perceived exertion.
cough, sputum, and other signs. Patients in each clas
sification can benefit from physical therapy with re
spect to enhancing oxygen transport. Moderate and
severe disease is characterized by significant airflow
obstruction secondary to copious, tenacious secre
tions. In addition, pulmonary hypertension and right
heart insufficiency may be manifested and eventual
diopulmonary function and oxygen transport in
failure may ensue.
patients with cystic fibrosis include some combina
522
PART V
tion of education, aerobic exercise, strengthening ex
drainage can be integrated into breathing control.
ercise, ventilatory muscle training (strength and en
This procedure focuses on eliciting coughing when
durance), ventilatory muscle rest, supplemental oxy
it will be most productive, thereby minimizing less
gen, mechanical ventilation for home use, chest wall
productive, exhaustive coughing. Patients with cys
mobility exercises, range of motion exercises, body
tic fibrosis often cough so violently and uncontrol
positioning, breathing control and coughing maneu
lably that it leads to significant arterial desaturation,
vers, airway clearance interventions, relaxation, pac
vomi ting, and exhaustion and impedes venous re
ing, and energy conservation.
turn and cardiac output.
Education focuses on teaching preventative health
Ventilatory devices such as the positive expiratory
practices and infection control (e.g., cold and flu, flu
pressure (PEP) mask and the flutter valve have
shots, aerobic exercise, nutrition, hydration, relax
shown benefit in some patients with CF with respect
ation, stress management, activity pacing, and energy
to reducing airway closure, clearing secretions, and
conservation).
enhancing gas exchange (Pryor, 1993; Webber and
Physical activity and aerobic exercise need to be
Pryor, 1994). Such aids may be useful adjuncts in
integrated early into the life style of the child with
some patients, however, they do not replace the mul
cystic fibrosis (Cystic Fibrosis and Physical Activ
tiple benefits of physical activity and exercise on op
ity, International 10urnal of Sports Medicine, 1988;
timizing oxygen transport including mobilizing and
Keens, Krastins, Wannamaker, Levison, Crozier,
removing secretions.
and Bryan, 1977; Zach, Oberwaldner, and Hausler,
1992). As much as possible, the child is integrated

into activities of his or her peer group. A prescribed
aerobic exercise program is designed to optimize
the efficiency of oxygen transport at all steps in the
RESTRICTIVE PATIERNS
Interstitial Lung Disease
pathway and thereby enhance functional capacity
The pathophysiology of restrictive lung disorders
overall. Physical activity and aerobic exercise en
and interstitial lung disease (ILD) in particular is
hances mucociliary transport and mucociliary clear
described in Chapter 4. This clasification of lung
ance, maximizes alveolar ventilation and ventila
disease is associated with various occupations and
tion and perfusion matching, increases ventilatory
the i n h a l a t i o n of i n o r g a n i c and organic dust
muscle strength and endurance and airway diame
(Chung and Dean, 1989). As the disease pro
ter, and stimulates a productive effective cough.
gresses, total lung capacity (TLC) and vital capac
Furthermore, physical activity and exercise have
ity (VC) are reduced. Residual volume often re
been associated with improved immunity and re
mains the same. Maximal flow rates tend to be
duced risks of infection (Pyne, 1994; Shephard,
increased as compliance is reduced. The drive to
Verde, Thomas, and Shek, 1991). These are signifi
breathe, breathing frequency, and the ratio of tidal
cant outcomes for patients with cystic fibrosis who
volume to total lung capacity are increased. Glan
have thick copious secretions.
dular hyperplasia may be present, leading to mu
In addition, breathing control and coughing ma
cous hypersecretion in some patients. Diffusing ca
neuvers are included as a component of a long-term
pacity may be reduced but may only be apparent
self-management rehabilitation program. Postural
during exercise (i.e., art.erial desaturation and dys
drainage and manual techniques have been the
pnea). Exercise-induced desaturation and reduction
mainstay of airway clearance in the past. Exercise,
in Pa02 may also reflect shunt and ventilation and
however, has a primary role in secretion mobiliza
perfusion mismatch (Jernudd-Wilhelmsson, Horn
tion and as an airway clearance intervention (Dean
blad, and Hedenstierna, 1986).
and Ross, 1989). Breathing control and coughing
Hemodynamic changes may be present (e.g., in
stategies are coupled with exercise to facilitate se
creased pulmonary artery pressure). Chronically in
cretion clearance. The principles of autogenic
creased pulmonary artery pressures and hence in
29
vascular
Chronic Primary Cardiopllinl10nal
Dysfunction
523
lead to in
maneuvel'S, relax
hypertrophy,
and energy conservation. An er

exercise
"Hv
assessment of work and home environ
ments may be indicated to maximize f u nction In

these

of
The
with interstitial
-'.""'MC'
Education is a central component of a
disease include the following:
sive rehabilitation program for the management of in

terstitiallung disease. Education includes information
quality of life, general

and hence physiological
on preventative health
removal from
the causative
vention shots,
cessation, nutrition,
tion, medications and their uses, prevention,

health promotion, and infection control
with interstitial
During aerobic
lung disease are prone to arterial desaturation (Arita,
ation, activity
volumes and capacities
Nishida, and
ventilation and perfusion matching
198
Patients who desatu
rate during
and
oxygen
1985) require
The intensity of the exercise

arterial

and efficiency of
endurance and exercise ca
and thereby
muscle
oxygen extraction
heart, in
with other
Pathophysiology and 1lIt:UI(;,(l1 management

incidence is
ar
responses.
lung Cancer
Lung cancer is a
includes
is defined by
breathlessness, and work of the
cause of death for men and

for women. Once
80% of
cancer is
terial
heart rate, blood pressure, and rate
correlated with a
and exposure to
pressure
Patients with cardiac
coal tars, asbestos, and radioactive dusts. The
(depth and
low arterial oxygen tensions

particularly
exercise,
ness is assessed
scale of
or
ECG monitoring,
breathless
a modified version of the Borg

exertion,

of
its administration
efficacy is es
sential if treatment is to be
The
efficacious,
located and thus con
tribute to bronchial
monia. Pathophysiologically,

of the
ity of primary malignant tumors are bronchogenic

carcinomas. They are
and pneu
cancer has features
of both obstructive and restrictive lung disease. The

patient presents with
obstruction, dyspnea,
cough, and hemoptysis (MlIITaY and
Treatment is limited to surgery, if metastasis has been

mled out, or conservative management with radiation
interventions for maximizing car
and chemotherapy.
Bronchogenic carcinomas metastasize
tients with interstitial lung disease include some
through the circulation and
c o m b i n a t i o n o f e d u c a t i o n, a e r o b i c e x e r c i s e,
other organs including
chest wall mobility exer
and adrenal glands.
channels to
524
PART V
If detected early, thoracic surgery may be per
diac dysfunction or low arterial oxygen tensions re
fonned to excise the cancerous tumor (Chapter 28). If
quire ECG monitoring. Subjectively, breathlessness
inoperable, or in the case of metastases, a patient may
be managed at home or in a hospice. Patients are de
bilitated, often undernourished, fatigued, short of
breath, lethargic, depressed, and in pain (Saunders
response is administered before treatment (e.g., anal
and McCorkle, 1985). Although these patients are
gesics or bronchodilators). Knowledge of the type of
often extremely ill, there is a growing trend to man
medication, its administration route, and time to and
age these patients in the community whenever possi
duration of peak efficacy is essential if treatment is to
ble. As the disease progresses, maintaining function
be maximally efficacious.
and reducing the rate of deterioration become pri

mary goals.
tients with lung cancer include some combination of

education, mobilization, strengthening exercises,
The goals of long-term management of the medical
chest wall mobility exercises, body positioning, sup
patient with lung cancer include the following:
plemental oxygen, mechanical respiratory support,

reserve capacity
Educate the patient and family about the bene

fits of a palliative program
Provide supportive care
Optimize pain control
Optimize scretion clearance
mobilization and physical activity (Calabrese, 1990).

The prescriptive parameters are adjusted each session
given the rapid changes in these patients' conditions.
Patients with lung cancer often cough up and ex
Optimize ventilation and pelfusion matching

oxygen transpolt

pacity
tients' peak times during the day.

logical effects, as well as oxygen transport effects of
rates
tivity pacing, and energy conservation. Treatments

are timed whenever possible to coincide with the pa
Patients with cancer may benefit frol11 the immuno
Promote self-determination
breathing control and coughing maneuvers, airway

clearance interventions, sleep and rest, relaxation, ac
Otimize general muscle strength and thereby pe

Optimize the benefits of sleep and rest
Minimize the effects of restricted mobility and

recumbency
pectorate blood in their sputum. The airways need to

be as clear as possible to avoid obstruction, atelecta
sis, risk of infection, and pneumonia. Although air
way clearance is an important goal, treatments should
avoid contributing significantly to bleeding and blood
loss if possible. This blood loss may contribute to
anemia and fatigue.
Manual airway clearance interventions may be in
dicated in some patients. Postural drainage may be
coupled with percussion and manual vibration. The
impact of manual interventions, however, may con
tribute to bleeding; thus the patient requires stringent
monitoring. Metastases to the thoracic cavity and the
ribs in particular may preclude percussion in favor of
manual vibration being petformed over nonaffected
areas. Treatment duration may be limited by the pa
terial saturation, cyanosis (a delayed sign of desatura
tient's tolerance. Tolerance may be improved by
modifying body position or by shortening treatments
product. Patients who can be mobilized but have car-
but increasing their frequency.
29
pist should examine the medication before treatment
PRIMARY CARDIOVASCULAR
and
to ensure that the expiratory date has not
Angina
to take responsibility for
the medication
near the patient for access to it should the patient de
from reduced
refers to pain
treatment.
blood flow to the myocardium. Even though

elicited during
525

include the following:
with
angina may be
stress or, in severe cases, may occur at rest. Atheroscle
rosis of one or more of the coronary arteries is the prin
health, and
cipal cause. Coronary vasospasm is a less common
serve
cause of
Educate about heart disease,
The pathophysiology of
is de
and hence
scribed in detail in Chapter 4. A history of

cessitates further examination to establish the
of the coronary
medica
occlusion. If severe, the patient is
scheduled for coronary
surgery
28) to
restore normal coronary blood flow. The acute and

long-term management of the
presented in
tions and their use,

activity, and exercise
Maximize aerobic capacity and efficiency of oxy

gen transport of all steps in the
cardiac
is
endurance and exercise
28. In less severe cases,
is
general muscle strength and thereby pe
with medications (e.g., sublin
managed
and physical
has stabilized, a 2TElaea-Exer
'J
H1
oxygen extraction
Patient monitoring includes hemodynamic moni
toring (i.e., heart rate, blood pressure, rate pressure
else tolerance test may be conducted under supervision
product, and
in a cardiac stress testing facility where l2-lead ECG
ment, particularly exercise, should also be recorded
monitoring can be performed. The exercise
(e.g.,
which the
chest
exhibits
(i.e., the
and serve as the basis for
activity and exercise.

is important in patients with heart disease. Positions
to the central circulation. This in
creases venous return and the work of the heart. Thus
body positions are selected for these patients
to minimize cardiac work during exercise and when
resting after exercise
Levine and
Wolfson,
and
Patients may be referred to

lem.
care and
or as a
need to be monitored.
(i.e., a
is not an
symptom under any circurmstance. Should it occur,

treatment is immediately
and
emergency measures instituted. Treatments will be

safer and more
EeG
prescribed with continous

treat
Without ECG
ments need to be conservative. If there is any doubt at

of a
any time about the
should be referred to a general practitioner or

cardiologist for clearance before being treated.
therapy with a
prob
angina is managed with the same
of the
of medication, its administration
route, time to as well as duration of
given it can be a
condition. A patient for whom antianginal medication

is prescribed must have the medication present. The
medication must not have expired and must be within
visible access during treatment. The
dizzi
and her or his ability to tolerate treatment safely, the
1952).
PrinCiples 01 physical therapy management

history of angina as a
Signs of
n e s s, dis orientation, dis c oordination, cyanosis,
increase the volume of fluid shifted
Cohen,
rating of
dyspnea,
coughing, and chest sound
The body position in which exercise is performed

of
responses to treat
efficacy is
essential if treatment is to be maximally efficacious.

For the long-term
of angina, interven
tions include some combination of education, aerobic
thera
chest wall
526
PART V
and energy con
activity
Injured myocar
jury and cell death
servation. Education includes information about heart
dial cells either recover or die
disease and risk factors
period. Thus minimizing further damage and maxi-
weight,
smoking, diet, stress,
and being
active in
hot environments) and
preventative strate
smoking reduction and
low-fat
reduced alcohol comsumption, exercise, relax

ation, activity pacing, and stress management).
are at risk of
Patients with
infarctions can range from
silent and unnoticed by the patient to

threatening.
can occur
life
in the my
ocardium but occur primarily in the ventricles. The

the greater the risk of ventricu
acute
monitor-
or frank myocardial
are needed to detect
during this 6-week period is crit
the
ical.
an in-
and
the healing
edema, and left
ventricular failure. Because myocardial ischemia
infarction. These patients are potentially hemody
and infarction impair the pumping action of the
namically unstable; thus their
heart and thus cardiac output, patients tend to be
sponses
re
and in need of oxygen. Even after the oxy
during, and after treatment,
larly aerobic and
should be
has
gen has been discontinued and the
monitored and recorded. Minimally, heart rate,
healed, the patient may continue to be vulnerable
blood pressure, and rate pressure product should be
hemodynamically.
taken alonll with the
some
the myocardium will have
that will affect both the electrical ex
citability and the mechanical function of the heart.

may continue to have low
the
In
normal arterial blood gases. Hypoxemia is lethal in

that it
and predisposes tissues
to
activity and aerobic exer
namic response.
must be avoided. Post
myocardial infarction
are usually dis-
home on several medications (e.g., nitro
heart rate or per
cise are prescribed at a
ceived exertion ranges that are below the anginal
glycerin, calcium antagonists, beta-blockers, and di
threshold based on a
uretics).
,f'V"""""'"
tolerance text
Peak exercise tests in cardiac
of
on the
one or more of
usually continue to
that may elicit angina o r
these medications over the long term. The need for
are performed i n a cardiac stress
oxygen is usually short term and restricted to the
laboratory under the supervision of a
s hospital stay.
The body position in which aerobic exercise is

IS
with heart disease.
Important in
Positions of
increase the volume of tluid

from hospital, many post myocardial
After
shifted from the periphery to the central circulation.
infarction patients see a physical therapist either pri
This increases venous return and the work of the
vately or through a cardiac rehabilitation program.
heart. Thus
positions are selected for

exer
these patients to minimize cardiac work
cise and during rest after exercise (Lanllou et

1977; Levine and Lown, 1952).
The majority of
an exercise program
for 6 to 12 months.
therapy in
Regardless of the setting,

cludes education,
for
vised
Myocardial Infarction
frequently
will remain on
rehabilitation program
frank myocardial is
confidence
support, and a super

safely and
physical exertion. In addition, an
exercise program is specifica!Jy prescribed for the pa

tient to enhance oxygen transport
chemia and infarction. Myocardial ischemia is re

whereas infarction denotes mvoeardial in
and utilization at the tissue level)

the metabolic demand on the heart.
up-
29
527
A GXTT is conducted before leaving the hospital
or when the patient is enrolled in an exercise pro
toring (i.e., healt rate, blood pressure, and rate pres
gram. The time between the exercise test and the ex
sure product). Subjective responses to treatment, par
ercise prescription and implementation of the exer
ticularly exercise, should also be recorded (e.g.,
cise program should be minimal. Peak (formerly
Borg's rating of perceived exeI1ion). Angina is not an
referred to as maximal) exercise tests are conducted
acceptable symptom under any circumstance. Should
in the presence of a cardiologist and provide the opti
it occur, however, treatment is immediately discontin
mal basis for an exercise prescription. Submaximal
ued and emergency measures instituted. Treatments
exercise tests can be conducted by the physical thera
will be safer and more precisely presclibed with con
pist. These can provide the basis for an exercise pro
tinuous ECG monitoring. Without ECG monitoring,
gram, however, the prescription is conservative com
treatments need to be conservative. If there is any
pared with that based on a peak exercise test. The
doubt at any time about the hemodynamic stability of
principles and practice of exercise testing are de
a patient and her or his ability to tolerate treatment
scribed in Chapter 17, 23 and 24. Such testing is an
safely, the patient should be referred to a general prac
art and an exacting science and should be carried out
titioner for clearance before being treated.
in a rigidly standardized manner to ensure the test re

response is administered before treatment (e.g., an
sults are maximally valid, reliable, and useful.

Comparable with the angina patient and not overt
tiarrhythic agents). Knowledge of the type of medica
infarction, the following caution must be adhered to
tion, its administration route, and time to and dura
with the patient who has a history of myocardial in
tion of peak efficacy is essential if treatment is to be
farction. A patient jar whom antianginal medication
maximally efficacious.
is prescribed must have the medication present. The
medication must not have expired and must be within
visible access during treatment. The physical thera
tients with myocardial infarction include some combi
pist should examine the medication before treatment
nation of education, aerobic exercise, strengthening
to ensure that the expiratory date has not passed and
exercises, chest wall mobility exercises, body position
to take responsibility for positioning the medication
ing, breathing control and coughing maneuvers, relax
near the patient for access to it should the patient de
ation, activity pacing, and energy conservation. An er

gonomic assessment of b o th work a n d h ome
velop angina during treatment.

dial strain.
with myocardial infarction include the following:
environments may be indicated to minimize myocar
Education focuses on the teaching the basic patho
physiology of heart disease, its risk factors, and pre
reserve capacity
vention. Health promotion practices are advocated
Educate about myocardial infarction, self-man
(e.g., smoking reduction and cessation, good nutrition,
agement, nutrition, weight control, smoking re
weight control, hydration, quality rest, and sleep peri
duction and cessation, risk factors, disease pre
ods). In addition, types of physical activity that im
vention, medications, life style, activities of
pose undue myocardial strain, increase intrathoracic
daily living, and avoiding static exercise, strain
pressure, and restrict venous return and cardiac out
ing, and the Valsalva maneuver
put, such as heaving lifting, straining, or the Val salva
maneuver, are avoided. The patient is taught to moni
oxygen transpOlt
tor and practice vigilance in monitoling his or her own
condition (e.g., new signs of infarction). These pa
tients are potentially hemodynamically unstable and
pacity
thus their hemodynamic responses before, dUling, and
after treatments, particularly exercise, should be mon
itored and recorded (i.e., heart rate, blood pressure,
528
PART V
and rate pressure product should be taken, along with

their subjective responses to treatment).
Prophylactic antibiotics against endocarditis are

administered to most patients with significant valvu
Peak exercise tests in cardiac patients that may

elicit angina or ST -segment changes are performed in
a cardiac stress testing laboratory under the supervi
sion of a cardiologist. The parameters of the exercise
lar involvement and in mild disease before proce

dures such as dental work.
prescription are set based on a peak exercise test. In
tensity is set within a heart rate, oxygen consumption,
with valvular heart disease include the following:
and exertion range (e.g., 70% to 85%, of the anginal
threshold) (Chapter 17).

Aerobic exercise of large muscle groups rather
reserve capacity
than small muscle groups (e.g., arm ergometry) is se
Educate about cardiac valvular disease, self
lected to minimize the increased hemodynamic de
management, nutrition, weight control, smoking
mand and strain and the increased work of the heart
reduction and cessation, cardiac risk factors, dis
associated with this type of work. Hot and humid con
ease prevention, medications, life style, activities
ditions also place additional stress on the heart, thus
of daily living, and avoiding static exercise, strain
exercising under these conditions should be avoided.
ing, and the Valsalva maneuver
performed is important in patients with heart disease.

Positions of recumbency increase the volume of tliud

oxygen transport

pacity
heart. Thus upright body positions are selected for
these patients to minimize cardiac work during exer

cise and during rest after exercise (Langou et aI.,
Physical therapists are involved with the manage
1977; Levine and Lown, 1952; Prakash, Parmley, Dik
ment of patients with valve defects medically, either
shit, Forrester, and Swan, 1 973).
as a primary or secondary problem, and surgically.

After surgery, these patients progress well; the princi
ples of their management are presented in Chapter
Valvular Disease
28. With respect to the medical management of valve

defects, the goal is to optimize oxygen transport in
Valve dysfunction is either congential or acquired and
the patient for whom surgery is not indicated either
may require treatment as a primary condition or is pre
because the defect is not sufficiently severe or be
sent as a secondary condition. Any of the heart and
cause the patient cannot or refuses to undergo
pulmonary valves may be affected. Rheumatic fever
surgery. Although the mechanical defect cannot be
was a common cause of rheumatic heatt disease and in
improved, oxygen transport may be improved with
particular mitral valve insufficiency (Goldberger,
judicious exercise prescription in some patients. The
1990). Interconnecting lymphatic vessels between the
parameters of the exercise prescription are usually
tonsils and the heart are thought to be responsible. Cal
moderate in that inapprop'riate exercise doses can fur
cification of valves that impairs opening and closing is
ther disrupt the inappropriate balance between oxy
another example of an acquired valve dysfunction.
gen demand and supply and thus further exacerbate
Clinically, patients may present with exertional
symptoms. In addition, there is the potential for fur
dyspnea, excessive fatigue, palpitations, fluid reten
ther valvular dysfunction if the myocardium is me
tion, and orthopnea (Sokolow, McIlroy, and CheitJin,
chanically strained.
1990). These sypmtoms are often relieved when exer

tion is discontinued.
The goal of the aerobic exercise prescription is to

identify the exercise dose that will optimize the effi
29
529
ciency of other steps in the oxygen transport pathway
pain, lightheadedness, dizziness, disorientation, dis
such that the available oxygen delivered to the pe
c o o r d i n a tion, c y a n o s i s , c ou g h i n g , chest s o u n d
ripheral tissues is maximally used without constitut
changes (i.e., a gallop) need t o b e monitored. Treat
ing a significant mechanical strain on the heart. Max
ments will be safer and more precisely prescribed
imizing work output over time is the goal. Thus the
with continuous ECG monitoring. Without ECG
severely compromised patient will perform a signifi
monitoring, treatments need to be conservative. If
cantly greater volume of functional work over time
there is any doubt about the hemodynamic stability of
with short, frequent sessions of exercise rather than
a patient and her or his ability to tolerate treatment
longer, less-frequent sessions.
safely, the patient should be referred to their general
If the valve defect is a secondary problem, the
practitioner for clearance before being treated.
physical therapist must assess the severity of the de
fect and its functional consequences. The following
questions must be addressed:
tients with cardiac defects include some combination
I. Does the defect preclude treatment?
of education, aerobic exercise, strengthening exercises,
2. Does the defect require that treatment be modi
chest wall mobility exercises, body p ositioning,

breathing control, coughing maneuvers, relaxation, ac
fied, if so, how?

3. What special precautions should be taken?
tivity pacing, and energy conservation. An ergonomic
4. What signs and symptoms would indicate the
assessment of both work and home environments may

be indicated to minimize myocardial strain.
patient is distressed?
Exercise prescription for patients with valvular heat1
5. What parameters should be monitored?

6. Is the patient taking medications as prescribed?
disease is modified to ensure that the energy demand is
How might these medications alter the patient's
commensurate with oxygen supply. Otherwise, exces
response to treatment?
sive oxygen demand will worsen the patient's response
7. Is there any evidence of heart failure? If so,

what will the effects of exercise be?
to physical activity, lead to further distress, and possi

bly reduced functional capacity. Aerobic exercise of
8. If there is no evidence of heart failure at rest,
large muscle groups rather than small muscle groups
what is the chance that insufficiency will de
(e.g., arm ergometry) is selected to minimize the in
velop with exercise?
creased hemodynamic demand and strain and the in
Comparable with the management of the patient with
creased work of the heat1 associated with this type of
a history of angina with or without a history of my
work. As for other types of cardiac conditions, exercis
ocardial infarction, body positions, activities, and res
ing in hot and humid conditions shoud be avoided.
piratory maneuvers that are associated with increased

hemodynamic strain are avoided.

performed is important in patients with heart disease.
Positions of recumbency increase the volume of fluid
heart. Thus upright body positions are selected for
these patients to minimize cardiac work during exer
These patients are potentially hemodynamically

unstable; thus their hemodynamic responses before,
cise and during rest after exercise (Langou et aI.,
1977; Levine and Lown, 1952).
during, and after treatments, particularly exercise,

should be monitored and recorded. Monitoring in
cludes hemodynamic monitoring (i.e., heart rate,
blood pressure, and rate prcssure product). Subjective
Peripheral Vascular Disease

Patholphysiology and medical management
responses to treatment (e.g., rating of perceived exer
Peripheral vascular disease results primarily from ather
tion) should also be recorded. Signs of dyspnea, chest
osclerosis and occlusion of the peripheral arteries (e.g.,
530
PART V
thoracic aorta, femoral artery, and popliteal artery)
Educate about atherosclerosis, self-management,
1980). Diabetes mel
nutrition, weight control, smoking reduction and
litus, which can result in microangiopathy and auto
cessation, risk factors, disease prevention, medica
nomic polyneuropathy, is another contributing factor to
tions, life style, activities of daily living, and
(Juergens, Spittell, and Fairbairn,
peripheral vascular disease in the lower extremjties.
avoiding static exercise, straining, and the Valsalva
Al1erial occlusion results in reduced blood flow to

the extremities and hence reduced segmental blood
maneuver
pressure distal to the occlusion. In mild cases of arter

ial stenosis the patient may be asymptomatic because
considerable stenosis has to occur before significant
reduction in peripheral blood flow. Furthermore, if

atheroslerosis develops gradually, collateral circula
Maximize arobic capacity and efficiency of oxy

gen transport
Optimize the work of the heart
pacity

tion may develop sufficiently to offset progressive

vessel narrowing. Clinically, the patient presents with
complaints of limb pain on exercise, coldness in the
with peripheral vascular disease secondary to dia
1987).
betes mellitus must incorporate both the principles
The characteristic limb pain results from ischemia and
for the managment of the patient with peripheral vas
affected leg, and possibly numbness (Dean,
is referred to as intermittent claudication. Mild to
cular disease secondary to atherosclerosis and sec
moderately severe cases are managed conservatively.
ondary to diabetes mellitus.
Pain at rest is suggestive of severe stenosis and signif
icant reduction of blood flow to the limb. Signifi
toring (i.e., heart rate, blood pressure, and rate pres
cantly reduced blood flow leads to ischemia color
sure product). Subjective responses to treatment,
changes, skin breakdown, ulceration, and eventually
particularly exercise, should also be recorded (e.g.,
gangrene. Bypass surgery is carried to revascularize a
pain scale and Borg's rating of perceived exertion).
threatened limb or in severe cases where gangrene has
These patients have an increased risk of angina.
developed, amputation of the limb is indicated.
Angina is not an acceptable symptom under any cir
Intermittent claudication secondary to mild-to
cumstance. Thus patients should be cleared by their
moderate arterial stenosis can benefit from aerobic
physicians or cardiologists before undertaking a
exercise, which may stimulate the development of
therapeutic exercise program. Diabetic patients are
collateral blood vessels around the stenosed vessel.
potentially hemodynamically unstable; thus their he
This condition can severely restrict mobility, which
modynamic responses before, during, and after
reduces function in addition to aerobic capacity and
treatment, particularly exercise, should be moni
efficient oxygen transport overall.
tored and recorded (i.e., heart rate, blood pressure,
Patients with pelipheral vascular disease from dif
and rate pressure product should be taken) along
fuse systemic atherosclerosis can be expected to have
with their subjective responses to exercise (e.g.,
stenosis of the coronary arteries even though they
pain and perceived exertion). If there is any doubt at
may be asymptomatic. These patients are monitored
any time about the hemodynamic stability of a pa
as stringently as cardiac patients.
tient and her or his ability to tolerate treatment

with peripheral vascular disease secondary to athero
sclerosis include the following:
safely, the patient shou. l d be referred to a general

practitioner for clearance before being treated or
continuation of treatment.
reserve capacity
29
531
The body position in which aerobic exercise is per
diopulmonary function and oxygen transport in patients
formed is important in patients with peripheral vascu
with pe[ipheral vascular di:;ease secondary to athero
lar disease. Positions of recumbency eliminate the
sclerosis include some combination of education, aero
vertical gravitational gradient. This gradient increases
bic exercise, strengthenjng exercises, relaxation, activ
blood pressure significantly to the lower extremeites.
ity pacing, and energy conservation. An ergonomic
Therefore the claudication threshold is lowered in re
assessment of both work and home environments may
cumbent positions. Recumbent positions also increase
be indicated to minimize myocardial strain.
venous return and the work of the heart. Thus upright
Education focuses on teaching the basic patho
body positions are selected for these patients to maxi
physiology of atherosclerosis, its risk factors, and
mize blood pressure in the lower extremities and to
prevention. Health promotion practices are advocated
minimize cardiac work during exercise and during rest
(e.g., smoking reduction and cessation, nutrition,
after exercise (Langou et aI., 1977).
weight control, hydration, quality rest, and sleep peri

ods). In addition, types of physical activity that im
pose undue myocardial strain, increase intrathoracic
pressure, and restict venous return and cardiac output,
Hypertension
such as heaving lifting, straining, or the Valsalva ma
Hypertension or high blood pressure is a serious
neuver, are avoided. The patient is taught to monitor
condition. Most patients experience no symptoms;
and practice vigilance in monitoring signs and symp
thus adherence to medication regimens is often
toms of vascular insufficiency in the affected limb
poor. Approximately 90% of hypertension is termed
and intermittent claudication. Any sign of skin red
essential hypertension (i.e., no known etiology).
ness in the feet should be monitored closely. In the
Hypertension predisposes a patient to stroke, my
diabetic patient, any threat of skin breakdown re
ocardial infarction, hemorrhage, and infarction of
quires medical attention and discontinuation of exer
other vital organs (Sokolow, McIlroy, and Cheitlin,
cise until medical clearance has been obtained. Pa
1990). Blood pressure tends to increase with age.
tients with peripheral artery disease are taught to take
With the aging of the population, the incidence of
care of their feet particularly before and after exer
hypertension is increasing. Increased blood pressure
cise. The feet and footwear should be kept clean. The
results from increased peripheral vascular resis
inner surfaces of shoes and socks should be smooth.

During peak exercise tests, patients with periph
eral vascular disease secondary to atherosclerosis
tance; therefore medications are prescribed that re

duce myocardial afterload and peripheral vascular
resistance (Goldberger, 1990).
have an increased risk of angina or ST-segment
Patients with existing cardiovascular disease (i.e.,
changes. Such tests therefore should be performed in
hypertension) are at risk for other manifestations. In
a peripheral vascular laboratory or cardiac stress test
addition, this population tends to be older and older
ing laboratory under the supervision of a peripheral
populations are known to have a higher prevalence of
vascular specialist or cardiologist. The parameters of
cardiac dysrhythmias. Thus knowledge of cardiac sta
the exercise prescription are based on a peak exercise
tus, including ECG history, should be obtained.
test. Walking is the activity/exercise of choice be

cause this activity is most severely limited by inter
mittent claudication, which has significant implica
Physical therapy contributes to increased metabolical
tions for function. Intensity of the training stimulus is
demands and therefore imposes a hemodynamic load
based on pain rating in conjunction wi th hemody
resulting in increased heart rate and blood pressure.
namic and other subjective responses. The patient
The assessment should document the history of hy
walks at a comfortable, even cadence within her or
pertension, its medical management, and the patient's
his pain tolerance (objectively defined on the pain
response. Regardless of the condition being treated,
scale) so that limping and gait deviation is avoided.
the hypertensive patient's blood pressure must be
532
PART V
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Chl"Onic Cardiopulmonary Conditions
monitored and treatment modified accordingly. How
sure product). Subjective responses to treatment, par
ever, blood pressure medications are known to atten
ticularly exercise, should also be recorded. Signs of
uate hemodynamic responses to exercise (Chapter
dyspnea, headache, lighheadedness, dizziness, disori
; thus the limitations of blood pressure measure
entation, discoordi nation, cyanosis, coughing, and
43)
ment must be considered.
chest sound changes (i.e., a gallop) need to be moni
A program of aerobic exercise can effectively re
tored. Blood pressure responses that fail to increase
duce high blood pressure in some patients (Blair,
with increasing work load and power output may be
Painter, Pate, Smith, and Taylor,
1988; Sannerstedt,
1987). The parameters of the exercise prescription
indicative of congestive healt failure.
needed to control hypertension include an aerobic
scribed with contiuous ECG monitoring. Without ECG
type of exercise that is rhythmic and involves large
monitoring, treatments need to be conservative. If there
muscle groups, an intensity of
Treatments will be safer and more precisely pre
is any doubt about the hemodynamic stability of a pa
60% to 75% of the pa

tient's age predicted maximal heart rate, 60 to 90 min
utes in duration, performed 5 to 7 times weekly, for 3
the patient should be referred to a general practitioner
months to achieve an optimal effect. The exercise in
or cardiologist for clearance before being treated.
tensity should be equivalent to a perceived exertion

rating of
tient and her or his ability to tolerate treatment safely,
3 to 5 on the Borg scale (the patient is able to
response is administered before treatment (i.e., hyper
speak while exercising without gasping) provided that
tension medications). Knowledge of the type of med
blood pressure has not increased excessively. Only
ication, its administration route, and time to and dura
modest exercise intensities are prescribed if the pa
tion of peak efficacy is essential if treatment is to be
tient has extremely high resting blood pressure to en
maximally efficacious.
sure that the blood pressure does not rise excessively
The primary interventions in the long-term man
and is not maintained at a high pressure for a pro
agement of hypertension include education, aerobic
longed period. If the patient's hypertension responds
exercise, general body strengthening, range of motion,
to the exercise regimen, exercise needs to be included
body mechanics, relaxation, stress management, pac
into the patient's life style in order for the effects to be
ing, and energy conservation. The patient is instructed
maintained. In addition to exercise, many patients lose
in self-monitoring blood pressure, recording her or his
weight, adopt healthier life-style habits, and learn
blood pressure and those factors that associated with
stress management and coping skills concurrently.
both high and low pressures, and blood pressure
changes after having had medication. Such monitoring

enables the patient to self-manage his or her hyperten
with hypertension include the following:

sion and thereby reduces the need for medication, if
health, and well-being and hence physiological re
not, eliminate it entirely. Patients, however, should
serve capacity
only alter their medications with their physicians' ap
Educate about hypertension, self-management, nu
proval. Physical therapists work closely with both hy
trition, weight control, smoking reduction and ces
pertensive patients and physicians.
sation, risk factors, life-style factors, disease pre
Systemic blood pressure responses to dynamic ex
vention, medications and their applications and
ercise are greater for upper-extremity than for lower
side effects
extremity work (Dean and Ross,
cise prescription includes aerobic exercise of the
1992). Thus exer
gen transport
large muscle groups to avoid small muscle group
Optimize physical endurance and exercise capacity
work and increasing peripheral vascular resistance
Optimize general muscle strength and thereby pe
and hence hemodynamic work, and the increased ex
ertion, strain, and work of the heart experienced with
upper-extremity work. Exercise is also performed in
toring (i.e., heart rate, blood pressure, and rate pres
erect and upright rather than recumbent positions to
29
minimize the increased work of the heart secondary
533
can be tolerated over the short term. However, these
to central fluid shifts when the patient is Lying in re
factors may result in a critical situation for the dia
cumbent positions.
betic patient.

Diabetes Mellitus
Diabetic patients may be referred to a physical thera
pist for several reasons. First, a newly diagnosed dia
Diabetes mellitus is a condition associated with im
betic patient may be referred so that the physical ther
paired insulin metabolism that can result in serious
apist can expose the patient to a quantified exercise
long-term multisystem consequences (Guyton, L991).
stimulus under supervised conditions and thereby
The disease. is classified as insulin-d ependent
help refine the prescription of insulin. Second a pa
(100M) and non-insuLin-dependent diabetes mellitus
tient may be referred for an exercise prescription to
(NIODM). Insulin is the carrier responsible for trans
help minimize the insulin dose or avoid insulin ad
porting glucose into the cells to undergo oxidation.
ministration entirely, depending the disease type and
Juvenile-onset diabetes is frequently the insulin
severity and the patient's response. Third but most
dependent type, whereas adult onset diabetes often is
frequently, patients are seen by a physical therapist
non-insulin-dependent. The underlying pathophysiol
for the treatment of some other condition and also re
ogy of juvenile and adult-onset diabetes, however, is
port diabetes in their histories. A history of diabetes
distinct. Juvenile-onset diabetes results from an inad
must be considered in the treatment of a patient who
equate number of islets of Langerhan in the pancreas,
is referred for any reason to either improve or at least
which are responsible for insulin production. Adult
not contribute to abnormal blood glucose levels and
onset diabetes, on the other hand, results from re
late complications.
duced insulin sensitivity. In Western industrialized
Diabetic patients are treated cautiously. Exercise
countries, adult-onset diabetes is associated with obe
increases metabolical demand commensurate with
sity, inactivity, diet, and stress. In addition, medica
intensity and hence cellular demand for glucose
tions can contribute to blood sugar disturbances. The
(Amercan College of Sports Medicine, 1995; Blair
sequelae of diabetes mellitus that frequently result
et aI., 1988). Usually, insulin administration is in
from poor regulation and management of the disease
creased in preparation for exercise. Many acti ve di
include angiopathy, peripheral neuropathy, autonomi
abetic patients are closely attuned to their dietary
caL neuropathy, gastrointestinal paresis, visual distur
and insulin needs, which permits them to be as
bance, and renal dysfunction (Bannister, L988; Ewing
physically active as nondiabetic individuals. How
and Clarke, L986).
ever, the diabetic patients seen by physical thera
Patients with diabetes mellitus have an accelerated
pists are often labile and less well managed. Thus a
rate of atherosclerotic changes in the vasculature
readily available sugar source must be nearby for
compared with age- and gender-matched nondiabet
insulin reguLation when a diabetic patient exercises
ics. These patients are also prone to peripheral vascu
or when exercising a diabetic patient on a ergome
lar disease secondary to microangiopathy, macroan
ter after anterior cruciate ligament repair in a pri
giopathy, and autonomical neuropathy. Diabetic
vate clinic.
patients constitute a significant proportion of patients
In addition, diabetic patients may have hemody
with peripheral vascular disease who require surgical
namic disturbances because of a autonomic neuropa
amputation of affected limbs.
thy and may exhibit impaired fluid-volume regulation
Abnormalities of blood sugar metabolism may be
during exercise (Bannister, 1988). Patients may expe
observed also in nondiabetic patients. Diabetogenic
rience postural hypotension and become dizzy and
factors, such as restricted mobility and stress, lead to
Iightheaded. In addition, diabetic patients may re
glucose intolerance and insulin oversecretion (Lip
quire a longer cool-down period to adjust hemody
man, 1972). In the nondiabetic patient, these effects
namically after exercise.
534
PART V
Hypoglycemia or low blood sugar is one of the
lant in monitoring signs and symptoms of vascular in
most common complications of diabetes mellitus.
sufficiency in the affected limb. Any sign of skin red
This condition results from excess administration of
ness in the feet should be monitored closely. In dia
insulin or oral hypoglycemic agent, insufficient food
betic patients, any threat of skin breakdown requires
in relation to insulin dose, or an abnormal increase in
medical attention and discontinuation of exercise until
physical activity or exercise. Hyperglycemia is com
medical clearance has been obtained. Healing is con
mon in obese patients with adult-onset diabetes. High
siderably delayed in the diabetic foot. Without appro
insulin levels are associated with a higher risk of
priate attention, infection and potential necrosis can
coronary artery disease. Myocardial infarction and
ensue. Patients with peripheral neuropathy are taught
stroke are common causes of death. Another compli
to monitor their footwear and socks diligently, to en
cation is cardiac hypertrophy secondary to hyperten
sure the inner surfaces are clean and smooth before
sion and cardiomyopathy, which predisposes the pa
each exercise session, and to check for areas of red
tient to congesti ve heart failure. The incidence of
ness or abrasion of their feet after exercise.
peripheral vascular disease is also increased in dia

betic patients.
The goals of the long-term management of dia
betes mellitus include the following:

response is administered before treatment (e.g., in
sulin or oral hypoglycemic agents). Knowledge of the
type of medication, its administration route, and time
to and duration of peak efficacy is essential if treat
health and well-being, and hence physiological re
ment is to be maximally efficacious.
serve capacity

The primary interventions in the long-term man
Educate about diabetes mellitus, self-management,
agement of diabetes mellitus include education,
nutrition, weight control, blood sugar regulation
maintainance of a log of diet and insulin regimens,
and its managment (i.e., the balance between nu
activity and exercise, aerobic exercise, strengthening
trition, diet, exercise, stress and insulin require
exercises, relaxation, stress management, activity
ments), medications, smoking reduction or cessa
pacing, and energy conservation.
tion, relaxation, stress management, foot care,
Generally, there are no contraindications to patients
hygiene, and infection control
with diabetes mellitus being physically active and par
ticipating in an exercise program. Daily exercise is ad
gen transport
vocated for insulin-dependent and non-insulin-depen
Optimize physical endurance and exercise capacity
dent diabetic patients to optimize glucose control. The
Optimize general muscle strength and thereby pe
exercise prescription parameters are set at 40% to 85%
of peak functional work capacity (American College
Patient monitoring includes signs and symptoms of
of Sports Medicine, 1991). If the patient is exercising
hypoglycemia (e.g., lightheadedness, weakness, fa
daily, the exercise parameters are set at the lower end
tigue, disorientation, and glucose tolerance test) or hy
of this range. If the exercise sessions are less frequent
perglycemia (e.g., glucose tolerance test). Hemody
(e.g., in the case of a non-insulin-dependent diabetic
namic responses (i.e., heart rate, blood pressure, and
patient whose blood glucose is well maintained and
rate pressure product) provide an index of the inten
whose weight is acceptable) the exercise intensity is
sity of an exercise stimulus, however, these responses
set at the higher end of this range.
may be attentuated in the diabetic patient because of
The risk of hypoglycemia can be reduced by observ
the autonomic neuropathy; both parasympathetic and
ing the following precautions: frequently monitor blood
sympathetic neuropathies.
glucose, decrease the insulin dose (in consulting with
Subjective responses to exercise, including the rat
the physician) or increase carbohydrate intake before
ing of perceived exertion, may be more valid indica
exercise, avoid injecting insulin into areas that are ac
tors of exercise intensity than hemodynamic responses
tive during exercise, avoid exercise during peak insulin
in the diabetic patient. The patient is taught to be vigi
activity, consume carbohydrates before, during, and
29
2, Relate
aerobic
and symptoms of
ican
Chronic Primary
of Sports Medicine,
un'l'u"mu",,,, J Dysfunction
535
physical therapy treat
1991).
ology of
each of the above chronic conditions

rationale for your choice.
and provide the
SUMMARY
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view of RespiratolY Disease, 120, 739-745.
Chronic Secondary Cardiopulmonary

Dysfunction
Elizabeth Dean
Donna Frownfelter
KEY TERMS
Muscular dystrophy
Cerebral palsy
Osteoporosis
Chronic renal insufficiency
Parkinson's disease
Hemiplegia
Rheumatoid arthritis
Kyphoscoliosis
Scleroderma
Late sequelae of poliomyelitis
Spinal cord injury
Multiple sclerosis
Systemic lupus erythematosus
INTRODUCTION
injury, and the late sequelae of poliomyelitis. The
The purpose of this chapter is to review the patho
musculoskeletal conditions that are presented include
physiology, medical management, and physical ther
kyphoscoliosis and osteoporosis. The collagen vascu
apy management of chronic, secondary cardiopul
lar/connective tissue conditions that are presented in
monary pathology. Specif ically, this chapter
clude systemic lupus erythematosus, scleroderma,
addresses chronic cardiopulmonary dysfunction sec
ankylosing spondylitis, and rheumatoid arthritis. Fi
ondary to neuromuscular, musculoskeletal, collagen
nally, management of the patient with chronic renal
vascular/connective tissue, and renal dysfunction.
insufficiency is presented. The principle.<> of manage
The neuromuscular conditions that are presented in
ment are presented rather than treatment prescrip
clude muscular dystrophy, hemiplegia, Parkinson's
tions, which cannot be given without consideration of
disease, multiple sclerosis, cerebral palsy, spinal cord
a specific patient. (For specific examples of patient

537
538
PART V
treatment prescriptions refer to the companion text
abnormal ventricular wall motion. Fatty and fibrous
Clinical case studies in cardiopulmonary physical
tissue infiltrate the myocardium and conduction sys
therapy.) In this context the goals of long-term man
tem and electrical conduction is slowed. Thus sub
agement of each condition are presented, followed by
clinical cardiac involvement is prevalent in patients
the essential monitoring required and the primary in
with muscular dystrophy and may explain sudden
terventions for maximizing cardiopulmonary function
death in this patient population.
and oxygen transport. The selection of interventions
Chronic respiratory muscle weakness is character
for any given patient is based on the physiological hi
istic of muscular dystrophy and other neuromuscular
erarchy. The most physiological interventions are ex
disorders. Because the cardiopulmonary system is sel
ploited followed by less physiological interventions
dom stressed due to musculoskeletal dysfunction in
and those whose efficacy is less well documented
these patients, respiratory muscle weakness is seldom
(Chapter 16).
detected. Such weakness is significant, however, in

that it contributes to several other serious problems,
including thoracic mechanical abnormalities, diffuse
NEUROMUSCULAR CONDITIONS
microatelectasis, reduced lung compliance, a weak
Muscular Dystrophy
Degenerative neurological and muscular diseases, in
cough with impaired mucociliary transport and secre

tion accumulation, ventilation and perfusion imbal
ance, and noctural hypoxemia (Smith, Calverley, Ed
cluding Duchenne's muscular dystrophy, lead to res
wards, Evans, and Campbell, 1987; Smith, Edwards,
piratory muscle weakness and alveolar hypoventila
and Calverley, 1989). Progressive respiratory muscle
tion (Black and Hyatt, 1971; Braun, Arora, and
weakness increases the risk of respiratory muscle fa
Rochester, 1983; Inkley, Alderberg, and Vignos,
tigue and failure (Macklem and Roussos, 1977).
1974). Vital capacity, forced expiratory volume, air
The severity of disease is not consistently corre
flow rates, and maximum inspiratory and expiratory
lated with compromised pulmonary function; thus
pressures are reduced. These patients are at risk for
cardiopulmonary function must be assessed individu
the development of atelectasis, impaired mucociliary
ally in each patient (Hapke, Meek, and Jacobs, 1972).
transport, and pneumonia. In addition, long-term gen
Patients with mild-to-moderate involvement of pe
eralized muscular weakness, particularly of the tho
ripheral muscles may exhibit disproportionate respi
racic cavity and abdomen, as well as restricted mobil
ratory compromise (Kilbull1, Eagan, Sieker, and Hey
ity and confinement to a wheelchair, predispose the
man, 1959). This may be explained by differential
patient to thoracic deformities (e.g., scoliosis and
changes in the degree of involvement of the di
dropping of the ribs, and further muscle disuse). Pa
aphragm and the abdominal and intercostal muscles
tients with Duchenne' s muscular dystrophy are sus
(Nakano, Bass, Tyler, and Carmel, 1976). Over time,
ceptible to dysphagia and upper airway obstruction
musculoskeletal changes of the chest wall lead to
secondary to gag reflex depression and hypotonia of
spinal deformity and stiffness with loss of its elastic
the pharyngeal structures (Murray and Nadel, 1988a).
recoil. Chronic alveolar hypoventilation leads to res
These factors further compromise or threaten car
piratory insufficiency and the need for ventilatory as
diopulmonary function and oxygen transport.
sistance. With progressive respiratory insufficiency,
Cardiac dysfunction has also been reported in pro
noctural hypoventilation with hypercapnia and hy
gressive muscular dystrophy (Moorman et aI., 1985;
poxemia develop (Bach, O'Brien, Krotenberg, and
Perioff, de Leon, and O'Doherty, 1966). Although
Alba, 1987). Nocturnal respiratory support should be
the majority of patients have no clinical evidence of
considered early to postpone the need for intubation
cardiac dysfunction, a high proportion have abnormal
and mechanical ventilation, which is associated with
E CGs at rest or during exercise and a b n o r m a l
a poor prognostic outcome in patients who have
echocardiography and radionuclide ventriculography
chronically reduced vital capacities and weak cough.
showing reduced left ventricular ejection fraction and
Clinically, patients with muscular dystrophy pre
30
sent with low functional
commensurate
Chronic Secondary Cardiopulmonary Dysfunction
with the extent of muscle weakness and
cardiopulmonary function, including alveolar
Facilitate mucociliary
on re-
transport, difficulty
orthopnea (shortness of
impaired
and increased work of breath-
clearing
provides an index
Abdominal muscle
539
oxygen transport
of pulmonary function in that it is correlated with

and expiratory flow rates
vital
aI., 1
The
general muscle strength and thereby
et
progressive functional
with Duchenne's muscular dystro
loss
susceptibility to the se-
phy increases the
and reduced
oxygen transport, circulatory
of desatura-
Lion), heart rate, blood pressure, and rate pressure
muscular weak
product. Patients with cardiac dysfunction need to be

cleared
ness, and bone loss.

of the complica
medical
(depth and frequency), ar
breathing
terial
of restricted mobility, including

monary
respiratory
Patient monitoring includes

LI,,,'""''''',
before
a rehabilita
when it involves a mobi
tion program,
tions of myopathies has significantly increased the
lization or exercise program, to refine the prescriptive
life expectancy of p atients, such as those with
of the program. If supplemental oxygen is
Duchenne's muscular
20
over the
age, further complications will
years. With
administered is recorded.
breathlessness is assessed
arise from
the
function (Dean, 1994;
nighttime and
Thus in the years ahead an
needed because
of patients with myopathies will be
car
of long-term management for the patient
p at i e n t s with
of the
of medication, its administration
route, and time to and duration of
efficacy is es
sential if treatment is to be maximally efficacious .
health, and well-being and hence
in
with muscular dystrophy include the
reserve
rPt'r'lII'"tl,nl
n o c turnal h y p o x e m i a
with
Duchenne's muscular dystrophy,
diopulmonary management and prophylaxis.
The
a modified version of
scale of
The
interventions for
--t"--" J
car
in pa
Educate about cardiopulmonary manifestations
tients with muscular
of muscle
nation of education, mobilization, primarily in the
medica
reduc
tion and cessation,
protection, infection
include some combi
form of functional activities,

primarily in the form of functional activities
ventila
control, the role of a rehabilitation program, and
maintain strength or reduce rate of
the eventual need for mechanical
tory muscle training, postural correction exercises,
support
chest wall mobility
cises,
volumes and
rates
control and coughing maneuvers,

ance
ventilation and perfusion
range of motion exer
prevention, body positioning, breath-
conservation. An
activity
clearand energy
assessment of the pa
tient's work and home environments may be indi

from aspiration
cated to minimize oxygen demand and energy expen
540
PART V
diture in these settings. Such an assessment includes
impaired, leading to secretion accumulation, postural
review of aids and devices (e.g., wheelchair type,
drainage may need to be instituted, coupled with deep
weight, and size and noninvasive mechanical ventila
breathing and coughing maneuvers.
tion). Aids and devices are selected to minimize en
Although the primary factor contributing to respi
ergy demand such that energy is conserved for other
ratory compromise is respiratory muscle weakness,
activities and undue fatigue is reduced.
the capacity of the respiratory muscles to respond to
The use of supplemental oxygen depends on the
resistive loading is limited. However, ventilatory
severity of the disease. Some patients have no need
muscle training may have some role in selected pa
for supplemental oxygen, some need it only during
tients, particularly children (Adams and Chandler,
exercise, and some patients require continuous oxy
1974; Pardy and Leith, 1984). Improved respiratory
gen with proportionately more delivered during activ
muscle endurance and strength may have a general
ity and exercise compared with rest.
ized effect on functional capacity (Reid and Warren,
1984). Patients with signs of ventilatory muscle fa
management of the patient with muscular dystrophy.
tigue, as opposed to weakness, benefit from ventila
Education includes the reinforcement of preventative
tory support at night. Rest of the respiratory muscles
health practices (e.g., infection control, cold and flu
at night optimizes their function during the daytime.
prevention, flu shots, aerobic exercise, strengthening
Methods of facilitating effecti ve coughing in pa
exercises, nutrition, weight contrOl, hydration, pacing
tients with neuromuscular diseases are extremely im
of activities, and energy conservation). Weight control
portant because they constitute life-preserving mea
is an important goal in patients with chronic neuro
sures. Supported and unsupported coughing methods
muscular diseases because they have the least capacity
are described in detail in Chapters 20 and 21. Patients
to compensate for the cardiopulmonary sequelae of
on noninvasive ventilatory support who are unable to
obesity (Alexander, 1985). Obstructive sleep apnea is
generate adequate peak cough expiratory flow rates
related to hypotonia of the upper airway musculature
can benefit from manual assisted coughing and me
and obesity. Thus activity and sleep patterns need to
chanical insufflation-exsufflation, thereby minimiz
be assessed to ensure sleep is maximally restorative
ing the need for endotracheal suctioning (Bach, 1993;
and not contributing to the patient's symptoms.

Mobilization is an essential component of the long
Barrach, Beck, Bickerman, and Seanor, 1952). Tra

cheostomy is delayed as long as possible. Signifi
term management of the patient with muscular dystro
cantly reduced maximal insufflation capacity, how
phy to optimize the efficiency of oxygen transport
ever, is an indication for tracheostomy.
overall and minimize the sequelae of restricted mobil
Whenever possible, deep breathing and coughing
ity, including circulatory stasis. Maximizing ventila
are coupled with chest wall movement to facilitate
tion with mobilization is limited if the patient has se
maximal inflation of the lungs before coughing by in
vere generalized muscular weakness and increased
creasing pulmonary compliance (Ferris and Pollard,
fatigue. Functional activities provide the basis for the
1960) and maximal exhalation of the lungs during
mobilization prescription. Although heavy resistive
coughing. Body positions are varied and changed fre
strengthening exercise has been advocated for these
quently to simulate shifts in alveolar volume and ven
patients (Vignos and Watkins, 1966), a conservative
tilation and perfusion that occur with normal move
approach, including an exercise program based on
ment and body position changes. Glossopharyngeal
functional goals and energy conservation, is more jus
breathing is a nonmechanical method of assisting
tifiable physiologically. Chest wall mObility exercises
ventilation. The patient is taught to use the tongue
include all planes of movement combined with a rota
and pharyngeal muscles to swallow boluses of air
tional component. Body positioning to optimize lung
past the vocal cords and into the trachea (Bach, Alba,
volumes and airflow rates is a priority. Breathing con
Bodofsky, Curran, and Schultheiss, ) 987). The effi
trol and coughing maneuvers are coupled with body
ciency of training is monitored with spirometry to en
movement and positioning. If mucociliary transport is
sure the patient is able to achieve acceptable vital ca
30
541
pacities. Some patients are able to support their venti
can affect cardiopulmonary function. Such infarc
lation, ventilator-free, for several hours in a day.
tions, however, are I ikely to be lethal. More com
One intervention that is prolonging the life of pa
monly, after a stroke, chest wall movement and elec
tients with muscular dystrophy, as well as of patients
trical activity on the ipsilateral side are reduced
with other progressive neuromuscular diseases, is the
(DeTroyer, DeBeyl, and Thirion,
use of mechanical ventilatory support (Bach,
1992;
1981; Fluck,
1966). Facial and pharyngeal weakness contributes
1981). Home mechariical ventilation provides
to an inability to control oral secretions, swallow ef
a noninvasive method of providing positive airway
fectively, and protect the upper airway. Altered res
pressure through an oral or nasal mask. This provides
piratory mechanics and efficiency reflect impaired
Curran,
considerable advantage over invasive, full body or
chest wall movement, asymmetry, and the degree of
tracheostomy. ventilatory support. Used in conjunc
muscle paresis and spasm.
tion with an insufftation-exsufflation device, pul
Patients with hemiplegia have associated problems
monary complications can be minimized and life ex
that contribute to cardiopulmonary dysfunction.
pectancy increased. Other forms of noninvasive
These patients tend to be older, hypertensive, and
mechanical ventilation include intermittent abdomi
have a high incidence of cardiac dysfunction. Muscle
nal pressure ventilation, rocking bed, negative pres
disuse and restricted mobility secondary to hemiple
sure tank ventilator, and chest shell ventilator. The
gia lead to reduced cardiopulmonary conditioning
type of ventilation is determined individually based
and inefficient oxygen transport. Spasticity increases
on the indications for ventilation and the patient's
metabolical and oxygen demand. Hemiparesis results
status. The use of ventilatory aids as a component of
in gait deviations, which reduce movement efficiency
a comprehensive rehabilitation program maintains
and movement economy. Reduced movement econ
pulmonary compliance and cough efficacy. Introduc
omy results in an increased energy cost associated
tion of these devices early will facilitate increased use
with ambulation, which may reduce exercise toler
as the respiratory muscles progressively weaken.
ance because of fatigue (Dean and Ross,
1993). In
Patients with generalized neuromuscular weakness
addition, ambulating with a walking aid is associated
require prophylactic management given their high
with a significantly increased energy cost compared
risk of developing life-threatening respiratory infec
with normal walking. This increased energy cost re
tions and complications. Prophylaxis should include
duces the patient's exercise tolerance further and in
flu shots, avoiding polluted, smoky environments,
creases fatigue.
smoking reduction and cessation, controlling the

types of food eaten and chewing well to avoid chok
ing, and regular deep breathing, frequent movement,
and change in body positions (even just shifting and
with hemiplegia include the following:
taking some deeper breaths while seated in a wheel
chair) to promote mucociliary transport. An optimal
time to take deep breaths and to cough is during
reserve capacity
transfers, which usually are physically exerting and
Educate about cardiopulmonary manifestations of

hemiplegia, self-management, medications, smok
stimulate hyperpnea.
ing reduction and cessation, nutrition, weight con

trol, and the role of a rehabilitation program
Hemiplegia
Grimby,
1984; Griggs and Donohoe, 1982). A cere
bral infarct involving the vital centers of the brain

rates
Hemiplegia or stroke affects cardiopulmonary func

tion either directly or indirectly (Fugl-Meyer and

and gas exchange
542
PART V
sleep apnea). Thus activity and sleep patterns need to
Protect the airways from aspiration
be assessed to ensure sleep is maximally restorative
and not contributing to the patient's symptoms.
Aerobic excrcise is an essential component of the

long-term management of the patient with hemiplegia
oxygen transport
to optimize the efficiency of oxygen transport overall.
Optimize physical endurance and exercise
Maximizing ventilation with mobilization is limited if
capacity
the patient has severe generalized muscular weakness
and increased fatigue. Although aggressive mobiliza
tion can be supported in these patients (Malouin,
Potvin, Prevost, Richards, and Wood-Dauphinee,
distress, breathing pattern (depth, symmetry, and fre
1992), appropriate selection of patients for such a reg
quency), arterial saturation, cyanosis (delayed sign of
imen, judicious exercise prescription, and monitoring
desaturation), heart rate, blood pressure, and rate pres
must be instituted to ensure the treatment is optimally
sure product. Patients with cardiac dysfunction require
therapeutic and poses no risk to a patient in this high
clearance from a cardiologist before participating in a
risk group. Chest wall exercises include movement in
rehabilitation program and may require ECG monitor
all planes combined with rotation. Body positioning to
ing, particularly during exercise. Subjectively, per
optimize lung volumes and aitflow rates is a priority.
ceived exertion is rated using the Borg scale.
Breathing control and coughing maneuvers are essen
tial and should be coupled with body movement and
response is administered before treatment (e.g., anti
positioning. Exercise is conducted in the upright posi
hypertensive and cardiac medications). Knowledge of
tions to minimize the work of the heart and of breath
the type of medication, its administration route, and
ing during physical exertion. Recumbent positions re
time to and duration of peak efficacy is essential if
duce lung volumes and expiratory flow rates, impair
treatment is to be maximally efficacious.
respiratory mechanics, increase closing volumes, in
crease thoracic blood volume, and increase compres
sive forces on both the lungs and the heart (Dean and
tients with hemiplegia include some combination of
Ross, 1992; Ross and Dean, 1992). Thus significant
education, aerobic exercise, strengthening exercises,
periods and intensities of aerobic exercise should be
spasticity control, postural correction exercises, gait
petformed standing or sitting. Lower-extremity work
reeducation, chest wall mobility exercises, range of
is preferable to upper-extremity work in that the latter
motion exercises, body positioning, breathing control
is associated with increased hemodynamic stress.
and coughing maneuvers, airway clearance interven
Rhythmic exercise of large muscle groups is prefer
tions, activity pacing, and energy conservation. An er
able to static exercise and exercise of small muscle
groups, such as the arms, in that it produces smaller
hemodynamic effects.
Ambulation or wheelchair locomotion should be
as efficient as possible so that the metabolical de
management of the patient with hemiplegia. Educa
mand of these functional activities is reduced. Per
tion includes the reinforcement of preventative health
forming these activities inefficiently on a frequent
practices (e.g., infection control, smoking reduction
basis contributes to an excessive oxygen demand.
and cessation, cold and flu prevention, flu shots, aero
The patient expends considerable energy in perform
bic exercise, strengthening exercises, gait reeducation,
ing these activities uneconomically, which impairs
nutrition, weight control, hydration, pacing of activi
the patient's tolerance and contributes to excessive
ties, and energy conservation). Hemiplegia is often as
fatigue. Conserving energy by performing these ac
sociated with sleep disturbances (e.g., obstructive
tivities more economically from an energetic per
30
spective will
more energy to "PIc-fArm more of
these or other activities.
which has been associated with the disease. The de

gree to which these cardiopulmonary manifestations
neuromuscular weakness
of the disease are offset with

used to treat rest tremor and reverse
their
infec
Prophylaxis should include
been reported.
The upper extremities are rigid and held
abducted from the chest wall during locomotion. The
polluted, smoky
smoking reduction and cessation,
the
rigidity and dyskinesia associated with Parkinson's
disease leads to restricted movement and body
ing, and
tioning. The
deep breathing,
and
movement,
positions (even just
and
breaths while seated in a wheel

nrr,rYI.c>'p
543
use. The
becomes deconditioned from dis

immobile chest, coupled with reduced
body position
contributes to
monary
mucociliary transport. An
breaths and to
Principles
are
nmrSIt:,al therapy management
The goals of
management for the
with Parkinson's disease include the following:

Parkinson's Disease
normal
resulting in the loss of
inhibitory and
199
et

self-
of Parkinson's d
neuronal
smoking reduction a n d
input in the execution of smooth coordinated move

ment
quality of life,
reserve
Parkinson's disease i s associated w i t h reduced

dopamine in the basal
Maximize the
health, and
weight
The clinical manifesta
infection
program
tions of the disease include stooped posture, stiffness

and
tremor of the limbs. Patients with Parkinson's disease
Optimize
and inflexible. Movement initi
Optimize ventilation and perfusion
and slowed
fixed masklike
and gas
once initiated, movement is not

walks with a quick,
volumes and capacities
These factors contribute to an increased energy cost
of movement.
Protect the
tion is
activity is restricted and func

contributing to
aerobic
reduced movement efficiency, and hence re
Facilitate
Although chest wall rigidity and respiratory mus
cle weakness are associated with a restrictive
tory
and efficiency of
Optimize
endurance and exercise
capacity
of lung disease in the Parkinsonian patient (Mehta,

Wright, and
Maximize aerobic
oxygen
duced movement economy.
1978), obstructive type of

has been reported (e.g., reduced
respiratory
mid-tidal flow rates, increase airway resistance, im
distress, breathing
paired distribution of ventilation, and an increase in
arterial saturation, heart rate, blood pressure, and
functional residual
(depth and frequency),
Patients with cardiac dys
and
particularly dur
tive defect may reflect parasympathetic
breathlessness is as
544
PART V
sessed using a modified version of the Borg scale
Multiple Sclerosis
Multiple sclerosis is a demyelinating disease of the
response is administered before treatment (e.g., L
central nervous system. The focal or patchy destruc
dopa). Knowledge of the type of medication, its ad
tion of myelin sheaths is accompanied by an inflam
ministration route, and time to and duration of peak
matory response (McFarlin and McFarland, 1982).
efficacy is essential if treatment is to be maximally
The course of the disease consists of a variable num
efficacious. In addition, patients with Parkinson's
ber of exacerbations and remissions over the years
may be on a beta-blocker to suppress action tremor.
from early adulthood. Exacerbations are also vari
Because such medication reduces the heart rate and
able with respect to severity. The neurological
blood pressure, these patients are prone to orthosta
deficits include visual disturbance, paresis of one or
tic intolerance. In addition, heart rate and blood
more limbs, spasticity, discoordination, ataxia,
pressure responses to treatment and exercises will
dysarthria, weak, ineffective cough, reduced percep
be less valid.
tion of vibration and position sense, bowel and blad
der dysfunction, and sexual dysfunction (Wilson,
Braunwald, Isselbacher, Martin, Fauci, and Root,
tients with Parkinson's disease include some combi
1991). Breathing disturbances, including diaphrag
nation of education, aerobic exercise, strengthening
matic paresis, may occur (Cooper, Trend, and Wiles,
exercises, postural correction exercises, gait reeduca
1985). Autonomic disturbance in the form of im
tion, chest wall mobility exercises, range of motion
paired cardiovascular reflex function at rest and at
tenuated heart rate and blood pressure responses dur
coughing maneuvers, activity pacing, and energy
ing exercise are relatively common in patients with
conservation. An ergonomic assessment of the pa
mUltiple sclerosis (Neubauer and Gundersen, 1978;
Pentland and Ewing, 1987; Senaratne, Carroll, War
ren,and Kappagoda, 1984).
diture in these settings.

management of the patient with Parkinson's disease.
with mUltiple sclerosis include the following:
health practices (e.g., infection control, airway pro
reserve capacity

exercise, nutrition, weight control, hydration, pacing

tection, smoking reduction or cessation, cold and flu

of mUltiple sclerosis, self-management, medica
of activities, and energy conservation).

tions, smoking reduction and cessation, nutri
long-term management of the patient with Parkinson's
tion, weight control, infection control, and the

disease to optimize the efficiency of oxygen transport

overall, including maximizing alveolar ventilation and
mobilizing secretions, as weJl as its musculoskeletal

rates
benefits. Maximizing ventilation with mobilization is

limited by the degree of hypertonicity and rigidity.

and gas exchange
Chest wall exercises include all planes of movement

with a rotational component. Breathing control and
coughing maneuvers are essential and should be cou
pled with body movement and positioning.
30
545
management, modified aerobic exercise, modified
strengthening exercises, pacing of activities, and en
ergy conservation). Multiple sclel'Osis is associated
oxygen transport
with significant fatigue. Thus activity and sleep pat
terns need to be assessed to ensure sleep is maximally
pacity
restorative and not contributing to the patient's symp
toms. By maintaining a log of activity and rest, the
patient can observe relationships between these fac
tors and identify when is the optimal time to rest.
long-term management of the patient with multiple
sclerosis to optimize the efficiency of oxygen trans
product. Patients with cardiac dysfunction require
port overall. In mild-to-moderate cases the goals of
ECG monitoring, particularly during exercise. Sub
aerobic exercise are to optimize cardiopulmonary
jectively, fatigue can be assessed using a modified
conditioning and enhance movement economy. Opti
version of the Borg scale. Perceived exertion is as
mizing cadence of walking or cycling is important to

minimize discoordination, energy expenditure, and
sessed using the Borg scale.

fatigue and maximize safety. In more severe cases the
goal is to maximize ventilation and gas exchange in
spasticity medications). Knowledge of the type of
the patient who has severe generalized muscular
weakness, spasm, and excessive fatigue. Subjective
parameters (i.e., fatigue and exertion) provide the
be maximally efficacious. In addition, knowledge of
basis for the intensity of the exercise program in con
the cardiopulmonary side effects of other medications
junction with objective measures. Parameters, such as
is needed.
intensity and duration, may vary from session to ses
sion depending on the patient's general status, which
diopul monary function and oxygen transport in pa
tends to be variable. Aquatic exercise may be an al
tients with multiple sclerosis include some combina
ternative for patients whose discoordination pre
tion of education, aerobic exercise, strengthening
cludes ambulation and cycling or who are troubled by
exercises (to maintain or reduce rate of decline), re
heat. The use of a fan may also enhance the palient's
duce abnormal muscle tone, postural correction exer
work output.
cises, gait reeducation, chest wall mobility exercises,
Chest wall exercises include all planes of move
range of motion exercises, body positioning, breath
ment with a l'Otational component. Body positioning to
ing control and coughing maneuvers, airway clear
optimize lung volumes and airflow rates is a priority.
ance interventions, fatigue management, activity pac
Breathing control and coughing maneuvers are cou
i n g a nd e nergy conservation. An ergonomic
pled with body movement and positioning. If mucocil
assessment of the patient's work and home environ
iary clearance is impaired leading to secretion reten
ments may be indicated to minimize oxygen demand
tion, postural drainage may need to be instituted
and energy expenditure in these settings.
coupled with deep breathing and coughing maneuvers.
Methods of facilitating effective coughing in pa
management of the patient with multiple sclerosis.
tients with neuromuscular diseases are extremely im
portant because they constitute life-preserving mea
sures. Supported and unsuppolted coughing methods
prevention, flu shots, smoking reduction and cessa
are described in detail in Chapters 20 and 21. When
tion, nutrition, weight control, hydration, fatigue
ever possible, deep breathing and coughing are coor
546
PART V
dinated with chest wall movement to facilitate maxi
ipate actively in a long-term rehabilitation pro
mal inflation of the lungs before coughing and maxi
gram. Patients with cerebral palsy who are able to
mal exhalation of the lungs during coughing. Body
ambulate do so at exceptional energy expenditure
positions are varied and changed frequently to simu
both with and without walking aids (Campbell and
late as much as possible shifts in alveolar volume and
Ball, 1978; Mossberg, Linton, and Friske, 1990).
ventilation and perfusion that occur with normal
Central neurological deficits, generalized hyper
movement and body position changes (Ray et aI.,
tonicity, and musculoskeletal deformity contribute
1974). In addition, body positioning is used to maxi
to increased metabolical demand for oxygen and
mize the patient's coughing efforts.
oxygen transport.
Principles of phYSical therapy management
require prophylactic management given their high

with cerebral palsy include the following:
smoking reduction and cessation, controlling the

reserve capacity
ing, and regular deep breathing, frequent movement,
Educate patient and/or family about cardiopul
and change in body positions (even just shifting and
monary manifestations of cerebral palsy, self
taking some deeper breaths while seated in a wheel
management, medications, nutrition, weight
chair) to promote mucociliary transport. An optimal
control, airway protection, infection control, and
time to take deep breaths and to cough is during
the role of a rehabilitation program
transfers, which usually are physically exerting and
stimulate hyperpnea.

rates
Cerebral Palsy

and gas exchange
Cerebral palsy results from insult to the central ner
vous system usually before birth (e.g., substance
abuse and underoxygenation perinatally) (Wilson et
aI., 1991). The clinical presentation includes spas
ticity and residual deformity from severe muscle
imbalance, hyperreflexia, and mental retardation.
oxygen transport
Although there are varying degrees of cerebral
palsy severity, patients most frequently seen by

pacity
physical therapy have significant functional deficits

and require long-term care. The loss of motor con

trol and hypertonicity of peripheral muscles often
Maximizing aerobic capacity and efficiency of
restrict the mobility of patients such that they are
oxygen transport and optimizing general muscle
wheelchair dependent. Loss of motor function lim
strength pertain to the patient with cerebral palsy that
its p hysical activity and the exercise stimulus
is mild in severity. Unfortunately, many patients seen
needed to maintain an aerobic stimulus and optimal
by physical therapists have poorly controlled spastic
aerobic capacity. Often coupled with motor deficits
ity and extreme cognitive deficits, which preclude
are cognitive deficits and mental retardation. These
full participation in aerobic and strengthening exer
afflictions limit the degree to which the patient can
cise programs. These patients are at risk for the se
follow instructions, perform treatments, and partic
quelae of restricted mobility and recumbency.
30
547
patients often have poor swallowing and saliva con
trol and thus are prone to aspiration and microat
electasis, particularly when recumbent at night. In
ability to reposition themselves at night further
product. Unless mildly affected and not mentally in
increases the risk of aspiration and its sequelae.
capacitated, patients with cerebral palsy are less able
Mobilization is an essential component of the
to provide subjective ratings of treatment response;
long-term management of the patient with cerebral
thus the physical therapist relies particularly on clini
palsy to stimulate aerobic metabolism and optimize
cal judgment in conjunction with the patient's objec
the efficiency of oxygen transport overall, including
tive responses to treatment.
maximizing alveolar ventilation and mobilizing and
removing secretions (Wolff, Dolovich, and Obmin
ski, 1977). Maximizing ventilation with mobilization
spasticity medications). Knowledge of the type of
is limited if the patient has generalized spasticity.
Furthermore, mobilization stimuli are selected specif
ically to minimize eliciting further muscle spasm.

Prescriptive hydrotherapy and equinotherapy (horse
back riding) can provide effective stimulation to the
cardiopulmonary system in the multiply handicapped
tients with cerebral palsy include some combination
individual and minimize the effects of spasticity.
of education, mobilization and coordinated activity
With training, coordination of ambulatory patients
(aerobic stimulation), strengthening e xercises
can be improved and aerobic energy expenditure re
(strength is often difficult to assess and treat because
duced (Dresen, de Groot, and Bouman, 1985). In ad
of overwhelming spasticity), chest wall mobility ex
dition, energy is conserved for performing more ac
ercises, range of motion exercises, body positioning,
tivity. Chest wall exercises includes all planes of
breathing control and coughing maneuvers, and air
movement with rotation. Body positioning to opti
way clearance interventions.
mize lung volumes and airflow rates is a priority.
Breathing control and coughing maneuvers are essen
management of the patient with cerebral palsy.
tial and should be coupled with body movement and
Whenever possible, education is directed at the pa
positioning. If mucociliary transport is impaired lead
tient, but it more likely is directed at the parents and
ing to secretion retention, postural drainage and man
care providers. Education includes the reinforce
ual techniques may need to be instituted with appro
ment of preventative health practices (e.g., infection
priate monitoring to ensure they do not have a
control, cold and flu prevention, flu shots, mobiliza
detrimental effect (Kirilloff, Owens, Rogers, and
tion, coordinated activity, strengthening exercise,
Mazzacco, 1985).
nutrition, weight control, and hydration). Patients
In this patient population, clearing oral secretions
with cerebral palsy can be expected to have abnor
and coughing maneuvers, require special attention.
mal sleep patterns. First, central cerebral involve
Methods of facilitating effective coughing in patients
ment may affect the periodicity of breathing. During
with neuromuscular diseases are extremely important
sleep, the effects of such dysfunction are accentu
because they constitute life-preserving measures. Sup
ated. Loss of normal periodic breathing and inter
ported and unsupported coughing methods are de
spersed sighs impairs mucociliary transport. Secre
scribed in detail in Chapters 20 and 21. Whenever
tions may accumulate and contribute to airway
possible, deep breathing and coughing is coupled with
obstruction and areas of atelectasis. Second, patients
chest wall movement to facilitate maximal inflation of
with cerebral palsy are unable to reposition them
the lungs before coughing and maximal exhalation of
selves during the night in response to both car
the lungs during coughing. Body positions are varied
diopulmonary and musculoskeletal stimuli. Third,
and changed frequently to simulate as much as possi
PART V
548
ble shifts in alveolar volume and ventilation and per

fusion that occur with nomlal movement and
smon
Chronic Cardiopulmonary Conditions
Guidelines for the Delivery of Cardiopulmonary Physical
po
Microaspiratiolls are likely a common
occurrence in this
population,
The
of long-term management for the patient
with spinal cord injury include the following:
at
Maximize the patient's quality of
and well-being and hence
night. Nighttime oositioning must be prescribed for
reserve
require
of spinal cord injury,
ri sk of rlpvpIon.
tions,
medica
reduction and cessation, nutri
tion, weight
infection
and the

alveolar ventilation
Optimize lung volumes and caoacities and flow
rates
ventilation and
and gas exchange
transport.
Spinal Cord Injury

The
Protect the
Facilitate
secretion clearance
manifestations and complica
tions of spinal cord
related to the
are
oxygen transport
Car
level of the lesion (Murray and
and efficiency of
Maximize aerobic
Optimize
diopulmonary impairment results from the loss of

muscles and the
control of the
heart below the
cord lesion. Loss of
Patient
matic innervation results in

Loss of abdominal and intercostal innervation re
duces the
muscle strength and thereby
to
transport, and
the ability to clear the airways. Denervation of the
includes
pattern (depth and frequency), ar
terial
sign of desatura
in that the
product. Patients with high spinal cord injuries are
heart's autonomous function and increased respon
somewhat more hemodynamically unstable and have
siveness of the heart and blood vessels to circulati
more ECO
cathecholamines
dividuals; thus their cardiopulmonary status should
heart and orthostatism are less
The cough
mechanism of quadriplegic patients is ineffective in

the airways
and Oorino, 1992).
than
control in
be monitored during treatment.

ceived exertion is monitored
are
prone to the
effects of restricted mobility
the extent of their
functional motor loss and sensory
spasticity
on cardiopulmonary function (Bach, 1991). Mo

bilization and
cord injured
are essential for the

to maintain
car
of the type of medica
tion, its administration route, and time to and dura

tion of peak
is essential if treatment is to be
maximally efficaciolls.
diopulmonary function and oxygen transport effi
ciency and the optimal strength and endurance of the
respiratory muscles.
tients with soinet! cord iniurY include some combina
30
tion of education, aerobic exercise, strengthening ex
549
the strength and endurance of the respiratory muscles
ercises (to maintain or reduce rate of decline), pos
(Gross, 1980) and may improve the functional capac
tural correction exercises, chest wall mobility exer
ity of some patients. A stronger endurance-trained di
cises, range of motion exercises, body positioning,
aphragm wit! not fatigue as readily as an untrained di
aphragm. Standardizing the resistance of the training
clearance interventions, activity pacing, and energy
stimulus alone, however, is not sufficient to produce
training effect. It is essential that flow rate is con
trolled using a gauge.


because they constitute life-preserving measures. Sup
management of the patient with spinal cord injury.
ported and unsupported coughing methods are de
scribed in detail in Chapters 20 and 21. Whenever pos
sible, deep breathing and coughing is coupled with
chest wall movement to facilitate maximal inflation of
exercise, nutrition, weight control, hydration, pacing
the lungs before coughing and maximal exhalation of
of activities, and energy conservation).
the lungs during coughing. Body positions are v3lied
and changed frequently to simulate as much as possible
long-term management of the patient with spinal cord
shifts in alveolar volume and ventilation and perfusion
injury to optimize the efficiency of oxygen transport
that occur with normal movement and body position
overall, including maximizing alveolar ventilation
changes (Braun, Giovannoni, and O'Connor, 1984).
and mobilizing and removing secretions. With higher
A comprehensive program includes stretching of
lesions, exercise is usually confined to upper-extrem
the chest wall and passive range of motion exercises
ity work in the form of wheelchair ambulation.
of the shoulder girdle. Maximal insufflations are en
Preservation of upper-extremity muscle function and
couraged in optimal body positions. Glossopharyn
minimization of overuse are primary goals from the
geal breathing can enable high quadriplegic patients
outset. Patients can maintain adequate cardiopul
to be freed from mechanical ventilation for hours at a
monary conditioning with wheelchair exercise, how
time. Assisted or unassisted coughing is coordinated
ever, exercise prescription should be conservative to
with deep breathing and rhythmic rocking motion.
maximize the benefit-to-risk ratio of cardiopul
Manual assisted coughing and mechanical coughing
monary conditioning relying of upper-extremity
aids, including functional electrical stimulation and
work. Patients who are able to walk with leg braces
insufflation-exsufflation devices, can be useful
and crutches expend considerable energy doing so. A
(Bach, 1991; Linder, 1993). The pneumobelt is a de
decision needs to be made regarding the benefits of
vice that can facilitate ventilation without a tra
walking at high energy demand vs conserving energy
cheostomy (Miller, Thomas, and Wilmot, 1988). This
for other activities. Chest wall exercises can be used
device counters loss of abdominal tone and helps pre
and should include all planes of movement with a ro
serve normal thoracoabdominal interaction during
tational component. Body positioning to optimize
respiration, which is lost because of reduced rib cage
lung volumes and airflow rates is a priority. Breath
compliance and increased abdominal compliance.
ing control and coughing maneuvers are essential and
Patients with spinal cord injuries, particularly
should be coupled with body movement and position
those with high lesions, require prophylactic man
ing. Coordination of respiration with aerobic activity
agement, given their risk of developing life-threat
and wheeling is taught to maximize work output.
ening respiratory infections and complications. Pro
Ventilatory muscle training has a role in the long
p h y l a x i s s ho uld i n c l u d e flu s h o t s, a v o i d i n g
term rehabilitation of some patients with high spinal
polluted, smoky environments, smoking reduction
cord lesions. Ventilatory muscle training can increase
and cessation, controlling the types of food eaten
550
PART V
and chewing well to avoid choking, regular deep
breathing, airway clearance, and frequent move
of the late sequelae of poliomyelitis, self-man
ment and change in body positions (even just shift
agement, medications, smoking reduction or
ing and taking some deeper breaths while seated in
cessation, nutrition, weight control, infection
a wheelchair is beneficial). An optimal time to take
control, orthoses, mobility and ADL aids and
deep breaths a n d to c o u g h is during transfers,
devices, and the role of a rehabilitation program
which usually are physically exerting and stimulate
hyperpnea.

rates
late Sequelae of Poliomyelitis

and gas exchange
The late sequelae of poliomyelitis are reaching epi
demic proportions as poliomyelitis survivors from the
late epidemic in the 1940s and 1950s reach 35 to 40
years after onset. Three types of poliomyelitis were

oxygen transport
prevalent during the epidemic in the middle of this
century, namely, spinal (the majority of cases), bul
Opti mize physical endurance and exercise ca

pacity
bar, and encephalitic. Many survivors are now pre
senting with disproportionate fatigue, increased

weakness, deformity, pain, reduced endurance, and
breathing and swallowing problems (Dean, 1991;
Howard, Wiles, and Spencer, 1988), and respiratory
insufficiency (Lane, Hazleman, and Nichols, 1974).
Although cardiopulmonary complications were not
product. Subjectively, pain, a feature of the late se
associated with the spinal form of poliomyelitis at
quelae of poliomyelitis, can be assessed using an ana
onset, late-onset breathing and swallowing complica
log scale, perceived exertion is assessed using the
tions can appear as a late effect of the disease (Dean,
Borg scale, and fatigue and breathlessness can also be
Ross, Road, Courtenay, and Madill, 1991). In addi
assessed using a modified versions of this scale.
tion, these patients may be deconditioned and have
poor movement economy (i.e., expend excessive en
response is administered before treatment (e.g.,
ergy because of postural deformities) (Dean and
analgesia). Knowledge of the type of medication, its
Ross, 1993). Thus delayed-onset cardiopulmonary
administration route, and time to and duration of
complications, coupled with the effects of overuse
and general deconditioning, increases the risk of car
mally efficacious.
diopulmonary compromise, reduces the ability to re
cover from these, and increases surgical and anes
diopUlmonary function and oxygen transport in patients
thetic risk.
with the late sequelae of poliomyelitis include some

combination of education, aerobic exercise, strengthen

ing exercises, postural correction exercises, chest wall
mobility exercises, range of motion exercises, body po
with the late sequelae of poliomyelitis include the
sitioning, breathing control and coughing maneuvers,
following:
environments may be indicated to minimize oxygen de
reserve capacity
mand and energy expenditure in these settings. Aids
30
551
and devices are reviewed to optimize energy expendi
ported and unsupported coughing methods are described
ture (e.g., electric wheelchair or scooter vs manual
in detail in Chapters 20 and 21. Whenever possible,
wheelchair) and to reduce cardiopulmonary distress
deep breathing and coughing is coupled with chest wall
(e.g., home mechanical ventilation).
movement to facilitate maximal inflation of the lungs
before coughing and maximal exhalation of the lungs
management of the patient with the late sequelae of
dUling coughing. Body positions are varied and changed
poliomyelitis. Education includes the reinforcement of
frequently to simulate as much as possible shifts in alve
preventative health practices (e.g., infection control,
olar volume and ventilation and perfusion that occur
cold and flu prevention, flu shots, aerobic exercise,
with nonnal movement and body position changes.
strengthening exercises, nutIition, weight control, hy
Progressive loss of pulmonary function in patients
dration, pacing of activities, and energy conservation).
with ventilatory compromise at onset can lead to res
Activity and sleep patterns need to be assessed to en
piratory insufficiency. Comparable with other neuro
sure sleep is maximally restorative and not contribut
muscular conditions, invasive mechanical ventilation
ing to the patient's symptoms. Functional work capac
is avoided. Promising alternatives are nasal and oral
ity and activity tolerance may be increased b y
methods of noninvasive assisted mechanical ventila
balancing activity t o rest, and maintaining fatigue
tion (Bach, Alba, and Shin, 1989). [n addition, airway
below the patient's critical fatigue threshold, i.e.,
clearance can be fUlther assisted with manual assisted
threshold requiring prolonged recovery time.
coughing, glossopharyngeal breathing, mechanical

10ng-tenTI management of the patient with the late se
exsufflation, and mechanical insufflation-exsufflation

(Bach et aI., 1993).
quelae of poliomyelitis to optimize the efficiency of
Poliomyelitis survivors with ventilatory compro
oxygen transport overall. The two principal goals of ex
mise are comparable with other patients with general
ercise are to optimize cardiopulmonary conditioning
ized muscle weakness. Of particular concern in this
and movement economy. Maximizing ventilation with
population, however, is the need to establish the role
exercise is limited if the patient has severe generalized
of mobilization and exercise as a first line of defense
muscular weakness and increased fatigue. Dispropor
in the management and prevention of cardiopul
tionate fatigue and other symptoms experienced by pa
monary dysfunction. However, for those patients
tients with the late sequelae of poliomyelitis have been
whose late effects are due to overuse, additional exer
attributed to overwork of affected and unaffected mus
cise may be detrimental. Modified mobilization and
cles, terminal axon degeneration, and impaired impulse
exercise, however, may be prescribed in an interval
transmission (Dean, 1991). Exercise is therefore pre
schedule (McArdle, Katch, and Katch, 1991) (Chap
scribed judiciously to provide an optimal aerobic train
ter 17). The patient exercises for a period of time and
ing effect without contributing to further otheruse abuse
then rests or reduces to a lower intensity of exercise
(i.e., prescriptive parameters based on subjective re
to aJlow the muscles to rest. In addition to the multi
sponses using semi-quantitative scales in conjunction
tude of benefits of mobilization and exercise on oxy
with objective responses). Walking is the most func
gen transport overall, these interventions also opti
tional type of aerobic exercise, however, aquatic exer
mize respiratory muscle strength and endurance. If
cise provides a useful medium for patients with lower
the patient does not recover within a few hours, the
extremity paresis who require crutches to walk or are
mobilization or exercise stimuli was excessive and
confined to a wheelchair. Reducing physical activity
should be modified. Chest waH mobility exercises to
and exercise is indicated in some patients to optimize
facilitate breathing and coughing may have a role.
aerobic and muscle power. The effect of resting affected

and unaffected muscles enhances functional capacity.

require prophylactic management, given their high
because they constitute a life-preserving measme. Sup
PART V
552
Guidelines for the Delivery of Larruopuunonal
controlling the
Physical Therapy: Chronic Cardiopulmonary Conditions
of food eaten and chewing well
and hypercapnia. With severe chest deof
to avoid choking, regular deep breathing, airway

in
movement and
and
situation.
(even just shifting and taking some

breaths while seated in a wheelchair is benefi
cial). An optimal time to take deep breaths and to
The goals of
cough is during transfers, which usually are

and stimulate hyperpnea.
cally
pulmonary
and right heart failure can result in a
management for the
with thoracic rjptt>rrni
include the
quality of
MUSCULOSKElETAL CONDITIONS
Thoracic Deformities
of thoracic
ications, nutrition, weight control, infection con
can result from abnonnalities

to congenital deformity,
trol, smoking reduction and cessation, and the
. and
acquired disease, and trauma
1988b ).
of the chest wall
reduces the mobility of the bony thorax, thereby in-
VUUlIlILC
Shallow, rapid breath
the work of
ing often results. Minute ventilation is increased at the

and gas
expense of alveolar ventilation. Severe deformity leads

to
lung volumes and caDacities and flow
rates
of the mediastinal stmctures. The heart
Reduce the work of
and rotated, impeding its mechanical
can be
function. Examples of chronic deformities that im

on pulmonary function are kyphoscoliosis sec
ondary to poliomyelitis, tuberculous
and
Other exam-
other causes and
Faci litate
Maximize aerobic
and
of
oxygen transport
of deformity include traumatic injury of the verte
bral column, ribs, and sternum. Routine cardiopul

monary assessment should include a musculoskeletal
examination of the spinal column and thoracic cavity.
Normal pulmonary function and gas

function. Asymmetry of the chest
wall interferes with normal lung
re
of ventilation and
in the
gional
and the distribution of inspired gas (Bake,

and Grimby, 1976; Sinha and
tance of the lung are characteristic of kyphoscolio
distress,
(depth and frequency), ar

(delayed
may con
tribute to altered lung water balance and impaired

lymphatic
The effects of
of desatura
lion), heart rate, blood pressure, and rate pressure

product. Patients with cardiac
tively,
exertion is assessed
the
and breathlessness is assessed usin!l: a modified

version of this scale.
sis. Altered pressure gradients and uneven lung

the
includes dyspnea,
ECG monitoring particularly during exercise. Subjec
compliance and
movement
and thereby
terial saturation,
the elastic resis
increase in work
muscle
Patient
depend on symmetry of cardiopulmonary anatomy

and
Optimize

in pa
tients with thoracic deformity include some combina

tion of
dead space and shunt may be
aerobic
postural correction
30
553
tion, chest wall mobility exercises, range of motion
Patients with chest wall deformities secondary to
neuromuscular conditions require prophylactic man
coughing maneuvers, airway clearance interventions,
agement given their high risk of developing life
threatening respiratory infections and complications.
Prophylaxis should include flu shots, avoiding pol
luted, smoky environments, smoking reduction and

cessation, controlling the types of food eaten and

chewing well to avoid choking, regular deep breath
management of the patient with thoracic deformity.
ing, airway clearance, and frequent movement and
change in body positions (even just shifting and tak
ing some deeper breaths while seated in a wheelchair
prevention, flu shots, smoking reduction or cessation,
is beneficial). An optimal time to take deep breaths
aerobic exercise, strengthening exercises, nutrition,
and to cough is during transfers, which usually are
weight control, and hydration).
physically exerting and stimulate hyperpnea.
Aerobic exercise is an csscntial component of the

long-term management of the patient with thoracic de
formity to optimize the efficiency of oxygen transport
overall. Maximizing ventilation with exercise in pa
Osteoporosis
tients with severe deformity may be limited. OptimiZ
Osteoporosis is a condition associated with reduced
ing alignment to minimize the cardiopulmonary limita
bone mass per unit volume (Smith, Smith, and Gilli
tions of the deformity during physical acti vity,
gan,
exercise, and rest is a priority. Chest wall exercises in
accelerates f a s t e r in w o m e n , p ar t i c u larly after
1991). Age-related bone loss begins earlier and
clude all planes of movement with a rotational compo
menopause, than men. Life-style factors, such as diet,
nent. Body positioning to optimize lung volumes and
exercise, and smoking, have a significant role in re
ailtlow rates is a priority. Breathing control and cough
ducing bone mass. Caffeine has also been implicated
ing maneuvers are essential and should be coupled
as a contributing factor to bone loss secondary to in
with body movement and positioning. If mucociliary
creasing urinary calcium loss.
transport is impaired leading to secretion retention,
Osteoporosis is classified as idiopathic osteoporosis
postural drainage may need to be instituted, coupled
unassociated with other conditions, osteoporosis asso
with deep breathing and coughing maneuvers.
ciated with other conditions (e.g., malabsorption, cal
Ventilatory muscle training may have a role in the
cium deficiency, immobilization, or metabolic bone
management of patients with reduced inspiratory
disease), osteoporosis as a feature of an inherited con
pressures and associated decreases in total lung ca
dition (e.g., osteogenica imperfecta or Marfan's syn
pacity and hypoxemia.
drome), and osteoporosis associated with other condi
tions but the pathogenesis is not understood (e.g.,
tients with musculoskeletal deformity are extremely
rheumatoid arthritis, alcoholism, diabetes mellitus, or
important because they constitute life-preserving mea
chronic airflow limitation) (Wilson et aI., 1991).
sures. Supported and unsupported coughing methods
The most common clinical features are vertebral
are described in detail in Chapters 20 and 2l. When
pain and spinal deformity resulting from vertebral
ever possible, deep breathing and coughing is coupled
compression and collapse. Vertebral bodies tend to
with chest wall movement to facilitate maximal infla
collapse anteriorly, contributing to cervical lordosis,
tion of the lungs before and maximal exhalation during
thoracic kyphosis, postural slumping, and loss of
coughing. Body positions are varied and changed fre
height. Acute episodes may be relieved by restricted
quently to simulate as much as possible shifts in alveo
mobility. Straining and sudden changes in position
lar volume and ventilation and perfusion that occur
can exacerbate an acute episode. C ardiopulmonary
with normal movement and body position changes.
complications of osteoporosis are secondary to spinal
554
PART V
deformity, chest wall rigidity, and cardiopulmonary

deconditioning resulting from restricted mobility.
Patient monitoring includes heart rate, blood pres

sure, and rate pressure product. Patients with cardiac
Osteoporosis is a condition associated with aging
dysfunction require ECG monitoring particularly dur
and older age groups. The pain of acute episodes
ing exercise. Subjectively, pain and discomfort are as
leads to periods of restricted mobility and significant
sessed with an analog scale or modified Borg scale, and
cardiopulmonary dysfunction in older persons (Dean,
perceived exertion is assessed using the Borg scale.
1993). Exercise that is weight bearing and loads the
muscles around bone maintains bone density and de
response is administered before treatment (e.g.,
celerates bone loss thus has a central role in preserv
analgesics). Knowledge of the type of medication,
ing bone health. Generally, the growth and remodel
its administration route, and time to and duration of
lin g of b o n e d e p e n d s h i ghly on t h e e x e r c i s e
prescription parameters (e.g., type o f exercise, inten
mally efficacious.
sity, duration, and frequency). Bone mineral content
is more closely related to cardiopulmonary condition
diopulmonary function and oxygen transport in patients
ing than physical activity level. Furthermore, any
with osteoporosis include some combination of educa
detrimental effect of exercise on osteoporosis appears
tion, aerobic weight-bearing exercise, strengthening ex
to relate more to malalignment and injury rather than
ercises, chest wall mobility exercises, range of motion
activity itself.
exercises, activity pacing, and energy conservation. An

The etiology of osteoporosis is diverse; thus manage
ment needs to consider the underlying pathophysiol
ergonomic assessment of the patient's work and home

environments may be indicated to minimize oxygen de
mand and energy expenditure in these settings.
Education is a principal focus of the long-term man
ogy and that several factors may be contributing to
agement of the patient with osteoporosis. Education in
the presentation of osteoporosis in the same patient.
cludes the reinforcement of preventative health prac
The goals of long-term management for the pa

tient with osteoporosis include the following:
/"
aerobic exercise, strengthening exercises, range of mo
tion exercises, nutrition, weight control, hydration, pac
reserve capacity
ing of activities, and energy conservation).
of osteoporosis, self-management, medications,
long-term management of the patient with osteoporo
nutrition, weight control, smoking reduction and
sis to optimize the efficiency of oxygen transport
cessation, infection control, and the role of a re
overall. Upright, weight-bearing aerobic exercise is
habilitation program
essential to maintain bone density or reduce the rate
of bone loss. Maximizing ventilation with exercise is
limited if the patient has severe generalized muscular
rates
weakness and increased fatigue. Chest wall exercises
can be used and should include all planes of move
and gas exchange
ment with a rotational component. Breathing control
and coughing maneuvers are essential and should be
coupled with body movement and positioning. Strain
oxygen transport
ing, Valsalva maneuvers, and jarring activity and ex
Opt imize physical endurance and exercise
ercise are contraindicated.

capacity
tices (e.g., infection control, cold and flu prevention, flu

shots, smoking reduction and cessation, weight-bearing
tients with osteoporosis are extremely important be
cause they constitute life-preserving measures. Some
30
555
patients fracture ribs and vertebrae during coughing.
of SLE, self-management, nutrition, weight con
Patients at risk should rely on huffing maneuvers that
trol, smoking reduction and cessation, medica
do not require closing the glottis and do not generate
tions, infection control, and the role of a rehabil
high intrathoracic pressures (Hietpas, Roth, and
itation program
Jensen, 1979).

rates
COLLAGEN VASCULAR/CONNECTIVE
TISSUE DISEASES

and gas exchange
Systemic Lupus Erythematosus

Reduce the work of the hem1
Systemic lupus erythemat osus (SLE) is a disease
characterized by the presence of multiple antibodies
that contribute to immunologically mediated tissue
inflammation and damage (Segal, Calabrese, Ahmad,
Tubbs, and White, 1985). The disease affects the

major organ systems, including the central nervous,
oxygen transport

tems. Symptoms include arthralgic and myalgic stiff

ness, pain, and fatigue.

capacity
musculoskeletal, pulmonary, vascular, and renal sys

The cardiopulmonary manifestations of SLE in
clude atelectasis, resulting from inflammation of the
alveolar walls, and perivascular and peribronchial
connective tissue, effusions secondary to lung infarc
tion, reduced surface tension, and splinting secondary
product. Patients with cardiac dysfunction should be
to pleuritic pain. Other manifestations include pleuri
cleared by a cardiologist before being prescribed an
tis with or without effusion, pneumonitis, interstitial
exercise program. Subjectively, discomfort, pain, fa
fibrosis, pulmonary hypertension, diaphragmatic dys
tigue, and breathlessness are assessed using analog
function, pulmonary hemorrhage, systemic hyperten
scales or modified versions of the Borg scale, and
sion, myocarditis, constrictive pericarditis, dysrhyth
perceived exertion is assessed using the Borg scale.
mias, tamponade, pericardial pain, arteritis, and
Medication. that is needed to maximize treatment re
defects of the mitral and aortic valves (Dickey and
sponse is administered before treatment (e.g., analgesic
Myers, 1988). Other manifestations that affect car
and antiinflammatory agents). Knowledge of the type
diopulmonary function include anemia, leukopenia,
of medication, its administration route, and time to and
thrombocytopenia, thrombosis, splenomegaly, ascitis,
gastrointestinal bleeding, nephritis, and renal insuffi
ciency (Wilson et aI., 1991).

tients with SLE include some combination of educa
tion, aerob ic exerc i se, strengthen i ng exerc i scs,
with systemic lupus erythematosus (SLE) include the
postural correction exercises, chest wall mobility ex
following:
ercises, range of motion exercises, body positioning,
clearance interventions, activity pacing, and energy
reserve capacity
556
PART V
deficit. Pulmonary hypertension may be a complicat
ing factor. Broncoal veolar lavage is consistent with
an acute inflammatory process. Cardiomyopathy is
management of the patient with SLE. Education in
associated with ischemia, areas of infarction, and my
cludes the reinforcement of preventative health prac
ocardial fibrosis (Gray, 1989). Fibrosis of the con
tices (e.g., infection control, cold and flu prevention,
duction system predisposes the patient to conduction
flu shots, smoking reduction or cessation, aerobic ex
defects and dysrhythmias. Other cardiopulmonary
ercise, strengthening exercises, nutrition, weight con
manifestations include pericarditis with
trol, hydration, pacing of activities, and energy con
fusion and pulmonary and systemic hypertension
or
without ef
servation). An ergonomic assessment of the patient's
from renal involvement. Half of patients with sclero
work and home environments may be indicated to
derma have renal involvement including intimal hy
minimize oxygen demand and energy expenditure in
perphasia, fibrinous necrosis of the afferent arterioles,

and thickening of the glomerular basement mem
these settings.
brane. Fibrotic changes and stenoses occur in the
long-term management of the patient with SLE to op
small arteries and arterioles systemically. Similar
timize the efficiency of oxygen transport overall, in
changes in the lymphatic vessels may obliterate
cluding maximizing alveolar ventilation and mobiliz
lymph flow.
ing and removing secretions. Parameters of the
Esophageal involvement contributes to regurgita
exercise prescription are based on subjective re
tion of gastric contents. which is exacerbated when
sponses, (e.g., discomfort, pain, breathlessness, and
the patient is recumbent or bends over. Bloating and
perceived exertion in conjunction with objective re
abdominal discomfort may reflect paralytic ileus and
sponses). Optimal types of aerobic exercise include
intestinal obstruction. Ascites and fluid accumulation
walking and cycling. Aquatic exercise may be prefer
in the gut increases abdominal pressure and en
able for patients with musculoskeletal involvement
croaches on diaphragmatic motion.
that precludes walking and cycling. Chest wall exer

cises can be used and should include all planes of
movement with a rotational component. Body posi
tioning to optimize lung volumes and airflow rates is
with scleroderma include the following:
a priority. Breathing control and coughing maneuvers
are essential and should be coupled with body move

ment and positioning. If mucociliary transport is im
paired, leading to secretion r e te ntion, p o s tural

reserve capacity

of scleroderma, self-management, nutrition,
drainage may need to be instituted, coupled with deep

breathing and coughing maneuvers.
weight control, smoking reduction or cessation,

medications, infection control, and the role of a
rehabilitation program
Scleroderma
Scleroderma is characterized by the overproduction

of collagen and progressive fibrosis of cutaneous and
rates
subcutaneous tissues (Gray, 1989). The cardiopul

monary manifestations of this condition result in in
terstitial pulmonary fibrosis with significantly re
and gas exchange
duced vital capacity, diffusing capacity, and arterial
oxygen tension (Bates, 1989; Wilson et aI., 1991).
Reduced static compliance is the primary mechanical

30
and
Maximize aerobic
Chronic Secondary Cardiopulmonary
557
cold and influenza
of
oxygen transport
Optimize
nutrition,
muscle strength and thereby
oxygen extraction
tion). An ergonomic assessment of the patient's

work and home environments may be indicated to
includes dyspnea,
distress,
pattern
and frequency), ar
terial saturation, cyanosis (delayed
of desatura
during exercise. If sup-
oxygen is used, the FIo2 administered is

recorded. Subjectively, breathlessness is assessed
using a modified version of the
ceived exertion and
require
Patients with cardiac
scale of per
of the patient with scleroderma

to
of oxygen
overall.
Chest wall exercises can be used and should include all

planes of movement with a rotational
Body
to
flow rates is a
volumes and air

Breathing control and
maneuvers are essential and should be coupled with
the Borg scale.

Medication that i s needed to maximize treat
ment response i s administered before treatment
movement and positioning. If mucociliary trans

port is impaired leading to secretion
postural
may need to be instituted coupled with
(e.g., immunosuppressive agents and

therapy).
in
minimize oxygen demand and energy

these
heart rate, blood pressure, and rate pressure

ECG monitoring,
of activities, and energy conserva
hydration,
of the type of medication, its
breathing and coughing maneuvers,

efficacy is essential if treatment is to be max
efficacious.
The primary interventions for
car
Ankylosing Spondylitis
Ankylosing spondylitis results in reduced total lung
tients with scleroderma include some combination of
capacity, vital capacity, and inspiratory muscle func

and
tion (Lisboa, Moreno, Fava,
Muhm, and
Ventilatory capacity is preserved
maneuvers,
clearance
that the respi
ratory muscles are not involved. The disease results
and energy
in spinal and chest wall
, thus there
conservation, An ergonomic assessment of the pa

The pa
spondylitis has an increased de
diture in these
function and therefore is

at risk if administered respiratory depressant medica
patients have
antacids between
meals, and do not lie down for a few hours after eat
When recumbent, these patients have the head of
bed elevated to minimize the risk of
of gas
tions or if he or she
strand, I
During
patients with ankylosing spondyli
tis show minimal chest wall
tric contents.
Education is a principal focus of the
thoracic or upper ab
dominal surgery (Grim by, FugJ-Meyer, and Blom
compared with
persons (Elliott et aI., 1985). Although
management of the patient with scleroderma. Educa
workload
tion includes the reinforcement of preventive health
reduced,
capacity, ventilation-perfusion
rather than
558
PART V
or abnormal blood gases is more
to be the limit
(e.g.,
infection
ing factor.
reduction and

with

Aerobic exercise is an e sential component of the

long-term management of the patient with
of life,
spondylitis to
transport overall. Maximizing ventilation with mobi
Educate about
lization is limited if the
weight control, infection

reduction and
smok
and the role of
re
habilitation program
include all planes of movement with

component. Body
to
vol
control
and coughing maneuvers are essential and should be
Optimize lung volumes and
and flow
rates
Venti
with body movement and
latory muscle training in conjunction with exercise

ventilation and perfusion
may have some additional benefit in maximizing aer

obic
and gas
has extreme
Chest wall exercises can be used and should
umes and airflow rates is a priority.
of oxygen
ize the
reserve
of ankylosing spondylitIS, selt-management, nu-
nutrition, weight con-
and hydration),
spondylitis include the

Maximize the patient'
aerobic exer
strengthening
management for the
The goals of
reduction or ces
cold and flu prevention, flu
Facilitate
oxygen transport
Optimize
Rheumatoid Arthritis
Rheumatoid arthritis (RA) is
muscle strength and
disease
that is associated with weI I-documented cardiopul

monary and cardiovascular
with or without
Patient
breathing pattern
including
interstitial fibrosis, pul
monary vasculitis, an increased incidence of bronchi

endo
arterial saturation,
tis and pneumonia
mation), heart rate, blood pressure, and rate pres
c a r d i t is, dysrhythmias, n e ur i t i s a n d v a s c ul itis
1987; S co t t, Wise,
b l o m a n d Nor de mar,
_
interventions for maxlmlzll1g car

tients with ankylosing
include some com
b i n at i o n of e d u cation, e x e r c is e. s t r e nl!th e n i n g
I
Functional
is limited
pain and stiffness
in the affected muscles and joints,

ber of
affected,
the num
and whether the patient
is having an acute episode. Self-limited
ac
tivity and exercise contributes to cardiopulmonary deexercises, range o f motion
Movement such as
control and cougnmg maneuvers,
tioning,
and energy conservation. An ergonomic as

sessment of the
ments may
work and home environ
indicated to minimize oxygen demand
and energy
Education is a
in these
is often in
efficient because of
limited by musculoskeletal
thus submaxi
mal tests are more functional in this popUlation, Tests

of cardiovascular status must be
to enable the
focus of the
without
management of the patient with ankylosing

tis. Education includes the reinforcement of preventa
pain.
Graded low -intensity aerobic exercise for pa

tients with RA from IS to 35 lllinutes three times a
30
Banwell, and
distress,
aerobic capacity, such an
fatigue. Should a
Subjectively,
and general
tlare-up occur while the pa
ar
(delayed sign of desatura
heart rate, blood pressure, and rate pressure
reduced affected joint count, improved activi

reduced joint
pattern (depth and
terial saturation,
exercise prescription results in increased exercise

ties of
559
week can be sufficient to enhance aerobic

(Harkcom,
Chronic Secondary CardioPIJllJlonary Dysfunction
the Borg scale.

tient is on an exercise program, a few days or
response i s administered before treatment
weeks of restricted mobility and abstinence from
steroids, nonsteroidal antiinflammatory
exercise frequently ameliorate the symptoms. Gen
analgesics).
cou
tl.e mobilization (preferably
is essential if treatment is to be maximally
this pe
pled with range of motion exercises
its
of the type of
riod, will minimize the negative effects of reduced
efficacious. Gentle rhythmic,
activity.
prescribed, particularly for patients at risk of loss of
Prolonged use of steroids contributes to bone

Thus physical
and exercise
bone mass
exercise is
to long-term steroid use.

car
The primary interventions for
lions are modified accordingly.
diopUlmonary function and oxygen transport in pa

tients with RA include some combination of educa
Principles of physicallherapy management
tion, aerobic exercise,
exercises,
postural correction exercises, chest wall mobility exbody
range of motion

Maximize the
activity pacing, and energy
clearance
quality of life,
conservation. An
reserve
'J
H.7

diture in these
tion, weight
devices is carried out to maximize the
focus of the
management of the patient with RA. Education in
volumes and
and flow
health prac
cludes the reinforcement of
rates
infection control, cold and flu prevention,

reduction or

and gas exchange
aerobic ex-
strengthening
nutrition,
Reduce the work of

Protect the
Facilitate
Maximize aerobic
and energy
from aspiration
transport
long-term management of the patient with RA to op

timize the
and
of
oxygen transport
both with
of oxygen
overall
to cardiopulmonary conditioning
and improving movement economy. Mild-to-moder
physical endurance and exercise

capacity
Optimize
func
tion and exercise tolerance.

Education is a
A review of mobility aids and
of rheumatoid
medications, infection control, and the
assessment of the pa
muscle
and
ate exercise during subacute periods can be benefi

cial.
efficiency of RA
with
persons. The
l..Iall"'"l
however, is less in RA patients because of limping
560
PART V
Guidelines ror the Delivery of Cardiopulmonary Physical Therapy: Chronic Cardiopulmonary Conditions
and associated deformity and pain. Non-weight

bearing exercise is beneficial in patients with severe
deformity and pain (e.g., aquatic exercise or water
with chronic renal insufficiency include the following:
walking). Given the fluctuations in the patient's con

dition from day to day, exercise prescription is modi

fied frequently to consider the patient's changing
reserve capacity
condition. Chest wall exercises include all planes of
movement with a rotational component. Body posi
of renal insufficiency, self-management, med
tioning to optimize lung volumes and airflow rates is
ications, nutrition, weight control, infection con
a priority. Breathing control and coughing maneu
trol, and the role of a rehabilitation program
vers are essential and should be coupled with body
movement and positioning.

Optimize lung volumes, capacities, and flow
rates
Chronic Renal Insufficiency

and gas exchange
Patients with chronic renal disease have significant
systemic complications. Cardiopulmonary manifes
tations include left ventricular hypertrophy and
congestive heart failure secondary to chronic vol
ume and pressure overload (American College of
Sports Medicine, 1991). Patients have a high inci

oxygen transport
dence of atherosclerosis, coronary artery disease,

pacity
glucose intolerance, and diabetes. Also, generalized

muscle weakness and fatigue compromises func
tional work capacity.

Chronically increased fluid volume, although reg
ulated with dialysis, contributes to increased stroke
work of the heart and cardiomegaly and hyperten
sion. With respect to pulmonary function, increased
fluid volume increases peribronchial fluid and airway
product. Subjectively, perceived exertion is assessed
closure. After dialysis, the reduction in body weight
using the Borg scale.

is related to a reduction in closing volume, increased

vital capacity, and forced expiratory flow rates.
The pulmonary-renal syndromes reflect the close
relationship between the lungs and kidneys. These
syndromes are characterized by altered immunologi
cal status, alveolar hemorrhage, interstitial and alveo
lar inflammation, and pulmonary vascular involve
ment (Matthay, Bromberg, and Putman, 1980).

The kidneys have a primary role in the production
tients with chronic renal insufficiency include some

combination of education, aerobic exercise, strength
and regulation of certain humoral regulators of me
ening exercise, chest wall mobility exercises, range of
tabolism, hemodynamics, fluid balance, and oxygen
motion exercise, body positioning, breathing control
transport (Rankin and Matthay, 1982) Thus pathol
and coughing maneuvers, airway clearance interven
ogy of the kidneys significantly affects those life-sus
tions, activity pacing, and energy conservation. An er
taining processes.
30
561
ditions presented include muscular dystrophy, hemi
plegia, Parkinson's disease, multiple sclerosis, cere
Education is a principal foclls of the long-term
bral palsy, spinal cord injury, and the late sequelae
management of the patient with chronic renal insuffi
of poliomyelitis. The musculoskeletal conditions
ciency. Education includes the reinforcement of pre
presented included kyphoscoliosis and osteoporosis.
ventative health practices (e.g., infection control, cold
The collagen vascular/connective tissue conditions
and flu prevention, flu shots, aerobic exercise,
presented include systemic lupus erythematosus,
strengthening exercises, range of motion exercises,
scleroderma, ankylosing spondylitis, and rheuma
nutrition, weight control, hydration, pacing of activi
toid arthritis. Finally, management of the patient
ties, and energy conservation.
with chronic renal insufficiency is presented. The
principles of management are presented rather than
long-term management of the patient with chronic
treatment prescriptions, which cannot be given with
renal insufficiency to optimize the efficiency of oxy
out consideration of a specific patient. In this con
gen transport overall. Maximizing ventilation with
text the goals of long-term management of each
exercise is limited if the patient has severe general
condition were presented, followed by the essential
ized muscular weakness and increased fatigue. Maxi
monitoring required, and the primary interventions
mal oxygen uptake increases in hemodialysis patients
for maximizing cardiopulmonary function and oxy
along with improvement in other indices of car
gen transport. The selection of interventions for any
diopulmonary conditioning (Painter et aI., 1986). Pa
given patient is based on the physiological hierar
tients may decrease or eliminate the need for antihy
chy. The most physiological interventions are ex
pertension medications. Exercise carried out during
ploited followed by less physiological interventions
hemodialysis treatment sessions is feasible and safe
and those whose efficacy is less well documented.
for appropriate patients. Because hemodialysis treat

ments require sessions of several hours multiple
times weekly, aerobic training (e.g., cycle ergometry)
REVIEW QUESTIONS
can be effectively incorporated into treatment time
I. Describe the chronic cardiopulmonary patho
(Shallom, Blumenthal, Williams, Murray, and Den
physiology secondary to muscular dystrophy,
nis, 1984; Zabetakis et aI., 1982). The exercise pre
hemiplegia, parkinson's disease, multiple sclero
scription of patients with blood glucose abnormalities
sis, cerebral palsy, spinal cord injury, late seque
and coronary artery disease is modified accordingly.
lae of poliomyelitis, kyphoscoliosis, osteoporo
Chest wall exercises can be used and should in
sis, systemic lupus erythematosus, scleroderma,
clude all planes of movement with a rotational com
ankylosing spondylitis, rheumatoid arthritis, and
ponent. Body positioning to optimize lung volumes
chronic renal insufficiency.
and ailflow rates is a priority. Breathing control and
2. Relate cardiopulmonary physical therapy treat
coughing maneuvers are essential and should be cou

ology of each of the above chronic conditions
pled with body movement and positioning.
and provide the rationale for your choice.
SUMMARY
This chapter reviews the pathophysiology, medical
management, and physical therapy management of
chronic, secondary cardiopulmonary pathology.
Specifically, this chapter presents chronic cardiopul
monary dysfunction secondary to neuromuscular,
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PART
VI

of Cardiopulmonary
Physical Therapy:
Intensive Care
Comprehensive Patient Management

in the Intensive Care Unit
Elizabeth Dean
KEY TERMS
Evidence-based practice
Quality care
Function optimization
Scientific evidence
Physiological evidence
Treatment goals
Prevention
Treatment selection and prioritization
INTRODUCTION
(Bar low, Hayes, and Nelson, 1984; Dean, 1985;
Because cardiopulmonary physical therapy in the in
Dean, 1994a; Hislop, 1975; Ross and Dean, 1989;
tensive care unit (lCU) is a specialty in itself, this
Schon, 1983; Worthingham, 1960; Zadai, 1986). A
chapter presents some general aspects of clinical and
superior knowledge of cardiopulmonary physiology,
nonclinical management in this setting. An overview
pathophysiology, pharmacology, and mu ltisystem
of the general goals of treatment and the rationale for
disease and its medical management is essential.
prioritizing treatments according to a physiological
Clinical decision making in the lCU and ration
hierarchy is described. Both clinical and nonclinical
al management of patients is based on a t r i pod
aspects of patient management are presented. Finally,
approach: (1) a knowledge of the underlying patho
issues related to the management of the dying patient
physiology and basis for general care, (2) the physio
are addressed.
logical and scientific evidence for treatment interven
The thrust toward evidence-based p ractice in
tions, and (3) clinical e xp e rie n ce (Figur e 31-1).
health care and the development of conceptual bases
Quality care is a function of these three areas of
for practice have had major implications for car
knowledge and expertise. Evidence-based practice
diopulmonary physical therapy practice in the ICU
and excellent problem solving ability will maximize

567
568
PART VI
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Care
therapist must work within narrow windows of opportu
Knowledge of underlying
pathophysiology
nity to effect an optimal treatment response. Trc<ltments

are v31iable with respect to their intensity, duration, and
frequency. Usually treatments are short and frequent;
thus the maximally beneficial outcome with the least
risk to the patient is the objective of every treatment.
GOALS AND GENERAL BASIS OF MANAGEMENT

Clinical experience
Physiologic and scientific

evidence for treatment
interventions
The ultimate goals of cardiopulmonary physical ther

apy treatment in the lCU include the following:
1. To have the patient alert and oriented to person,
time, and place
FIGURE 31-1
2. To have the patient return to premorbid func
Tripod approach to patient management.
tional level to the greatest extent possible

3. To reduce morbidity. mortality, and length of
the benefit-to-risk ratio of cardiopulmonary physical

therapy interventions (Riegelman, 1991).
hospital stay.
As a precursor to achieving these three overriding
goals, the immediate goals initially relate to the attain
ment of optimal oxygen transport and hence car
SPECIALIZED EXPERTISE OF THE
diopulmonary function and secondly relate to the at
leu PHYSICAL THERAPIST
tainment of optimal musculoskeletal and neurological
Effective clinical decision making and practice in the
function. In the lCU the physical therapist must recog
ICU demands specialized expertise and skill including
nize the implications of cardiopulmonary insuffi
advanced, current knowledge in cardiopulmonary and
ciency on neuromuscular status and that apparent im
multisystem physiology and pathophysiology, and in
pairment of neuromuscular status in not necessarily
medical, surgical, nursing, and pharmacological man
indicative of neurological dysfunction. Rather, re
agement (see the box on p. 569). Physical therapists in
duced cardiac output and blood pressure, hypoxemia,
the lCU need to be first-rate diagnosticians. Given the
hypercapnia, and increased intracranial pressure (lCP)
multitude of factors that contribute to impaired oxygen
may be indirectly responsible for these changes.
transport (Dean, 1983; Dean, I 994b; Dean, 1994c), the

physical therapist must be able to analyze these to de
fine the patient's specific oxygen transport deficits and
Restricted Mobility and Recumbency
problems. Therefore the lCU physical therapist must be
Hospitalization particularly in the ICU is associated
capable of integrating large amounts of objective infor
with a considerable reduction in mobility (i.e., loss of
mation quickly, interpreting this information, and inte
exercise stimulus), and recumbency (i.e., loss of grav
grating it to provide the basis for a treatment prescrip
itational stimulus) (see Chapters 17 and 18). These
tion (i.e., the specific selection, prioritization, and
two factors are essential for normal oxygen transport;
implementation of treatment interventions) (Cutler,
thus their removal has dire consequences for the pa
1985). The integration and interpretation of the vast
tient with or without cardiopulmonary dysfunction.
amount of multiorgan system data is perhaps the single
In terms of a physiological hierarchy of treatment
most important skill in ICU practice and treatment pre
interventions (see Chapter 16), exploiting the physio-.
scription. With this database, the physical therapist
logical effects of acute mobilization, upright position
must identify the indications for treatment, contraindi
ing, and their combination, are the most physiologi
cations, and optimal timing of interventions. The condi
cally justifiable primary interventions to maximize
tion of the ICU patient can change rapidly. The physical
oxygen transport and prevent its impairment.
31
Comprehensive Patient Management in the Intensive Care Unit
569
Specialized Expertise and Skill of the lCU Physical Therapist

Detailed, c omprehensive knowledge of cardiopulmonary physiology and pathophysiology, and phar macology .
Thorough working knowledge of the monitoring systems routinely used in the ICU and an understanding of the inter
pretation of the output of these mon itoring systems ( e. g. ,
ECG,
arterial blood gases, fluid and e lectrolyte balance,
hemodynamic monitoring, chest-tube drainage systems, intracranial pressure m onitoring ). This information is an
integra l component of the physical therapy assessment of the und erlying problems, and for selecting, prioritizing.
and progressing or modifying treatment.
E xte nsive expertise in c ardiopulmonary assessment and treatment presc ription : preferably a minimum of 2 to 3 years
experience in ge ne ral medicine and surgery.
Detailed understanding of multisystem physiology and pathophysiology and the cardiopulm onary manifestations of
systemic disease.
An ability to practice effectively under pressure and in often apparently congested, suboptimal working conditions.
Knowledgeabh:: regarding all emergency procedures including those for respiratory and cardiac aITest, equipment. or
power failure.
K nowledge abl e rega rding the paging system used in the unit for contacting the physical therapist when she or he is
out of the unit and out of the hospital . On-call service, 24 hours a day. 7 days a week is a co mmon practice and
should be considered in units without this service.
Sensiti vity toward each patient's psychosocial situation, culture , and values, and active involvement of the patient
and family in clinical decision making whenever feasible.
Superior communication skills (e.g., ability to work coop era tively with other members of the
lCU team ( see Figure
31-2) and give ve rba l prescntations and discuss patients at rounds).
Recumbency is nonphysiological; it is a position
Specificity of Cardiopulmonary Physical Therapy
that all too often is to what most patients are injudi
Physical therapy interventions must be specifically
ciously confined. Changing the position of the body
geared toward the management of each organ sys
from erect to supine positions results in significant
tem, taking into consideration the pathophysiologi
physiol ogica l changes, which may jeopardize the pa
cal basic for the patient's signs and symptoms and
tient's already compromised or threatened oxygen
rational for each intervention and the physiological
transport system (sec the box on p. 570, at top left)
and scientific evidence supporting t h e efficacy of
the intervention (Dean and Ross, 1992). Physical
(see Chapter 18).

The culmination of these deleterious effects off
therapy provides both therapeutic and prophylactic
sets the increased homogeneity of ventilation and
interventions for the ICU patient. The use of con
perfusion and their matching in the supine position.
servative, noninvasive measures is the initial treat
These effects compound the sU[lerimposed factors of
ment of choice to avert or delay the need for addi
immobility, recumbency-induced central fluid shifts,
ti onal
prolonged lying without the normal stimulation or
supplemental oxygen, pharmacological agents, and
invasive
mo n i t o r i n g
and
t r e a t m e nt,
will to turn the body, and underlying pathophysiol
the need for intubation and mechanical ventilation.
ogy or trauma that may contribute to impaired car
The physical therapist aims toward avoiding, post
diopulmonary function and oxygen transport. Theo
poning, or reducing the need for respiratory support
retically, the more compromised the patient, the
for as long as possible. In addition, the physical
greater the priority is to maximize time spent in the
therapist h e lp s to prevent the multitude of side ef
upright position in conjunction with exploiting the
fects of immobility and prolonged confinement to
benefits of acute mobilization.
bed. A su mm a ry of general information required
570
PART VI
Generallnformatioll Required Before Treating

Normal Physiological Changes When Changing
the ICU Patient
from the Upright to the Supine Position
Medical and surgical histories
Cephalad displacement of the visceral contents and
Gender and age
diaphragm
Premorbid status (e.g., life style. ethnicity. culture,

work situation. stress, cardiopulmonary condi
Compression on the posterior dependent lung
tioning, and oxygen transport reserve capacity)
fields
Smoking history
Cephalad tluid shift to the central circulation
Hydration and nutritional status: deficiencies. obe
Stroke volume and cardiac output
sity, or asthenia
Total lung capacity
Recency of onset and course of present condition
Vital capacity
Existing or potential medical instability
Indications or necessity for intubation and mechani
Residual volume
cal ventilation
Forced expiratory volumes
Invasive monitoring, lincs. leads. anel catheters
Airway resistance
Existencc of or potential for complications and mul

tiorgan system failure
Closing volumes of small airways

Restriction of chest wall and diaphragmatic excursions
Coma
Elevated intracranial pressure (lCP) and the need for
Arterial oxygen levels
ICP monitoring
Cough effectiveness
Preload and afterload and myocardial work
Risk or presence and site(s) of infection

Quality of sleep and rest periods
Myocardial efficiency
Sympathetic stimulation and decreased peripheral
Nutritional support during ICU stay

Pain control regimen
vascular resistance
General Physical Therapy Goals Toward Function Optimization in the ICU Patient
Maintain or restore adequate alveolar ventilation and perfusion and their matching in nonaffected and affected lung
fields and thereby optimize oxygen transport overall
Prolong spontaneous breathing (to the extent that is therapeutically indicated) and thereby avoid, postpone, or mini
mize need for mechanical ventilation
Minimize the work of breathing
Minimize the work of the heart
Design a positioning schedule to maintain comfort and postural alignment (distinct from therapeutic body positioning
to optimize oxygen transport)
Maintain or restore general mobility, strength. endurance, and coordination, within the limitations of the patient's
condition and consistent with the patient's anticipated rehabilitation prognosis (distinct from therapeutic mobiliza
tion to optimize oxygen transport)
Maximally involve the patient in a daily routine including self-care, changing body position, standing, transferring,
sitting in a chair, and ambulating in patients for whom these activities are indicated
Optimize treatment outcome by interfacing physical therapy with the goals and patient-related activities of other
team members, coordinating treatments with medication schedules. and treating the patient specifically. based on
results of objective monitoring available in the ICU and subjective findings
31
571
before treating the ICU patient is presented in the
scribed in Chapter 17 and relate primarily to the sta
box on p. 570, at top right.
tus of the cardiopulmonary, neuromuscular, and mus

culoskeletal systems. In the ICU the negative physio
logical effects of immobility are amplified in severely
Function Optimization
ill and older patients. A primary objective of the
Function optimization refers to promoting optimal
physical therapist, therefore, is to avoid or reduce
physiological functioning at an organ system level, as
these untoward effects on the patient's recovery and
well as promoting optimal functioning of the patient
length of stay in the ICU. Specifically, these goals in
as a whole. In critical care, primary goals related to
clude reducing the deleterious effects of immobility
function optimization are initially focused on car
and pathology on cardiopulmonary and neuromuscu
diorespiratory function. With improvement in oxygen
lar function and reducing the risk of deformity and
transport, increased attention is given to optimal
decubiti. The negative sequelae of relative confine
functioning of the patient with respect to self-care,
ment are largely preventable. Particular care must be
self-positioning, sitting up, and walking. General
taken to avoid pressure sores because these signifi
physical therapy goals related to function optimiza
cantly increase the risk of infection and deterioration.
tion are shown in the box on p. 570, at bottom.
Physical therapists and nurses need to examine rou

tinely for sites of redness, pressure, and potential skin
lesions in every patient, regardless of expected length
Prophylaxis
of stay in the ICU (Stillwell, 1992). The texture of
General aspects of patient care related to physical
bed coverings, their smoothness, bunching of the bed
therapy practice include the role of prophylaxis or
gown, or irritation from lines and catheters to the pa
prevention. The complications of immobility are de
tient need to be routinely monitored.
Specific Patient Information Required Before Treating the ICU Patient

Detailed knowledge of the patient's history, including the differential diagnosis on admission to the rcu, and rele
vant past medical. surgical, and social histories
Detailed understanding and knowledge of the medications administered to the patient, their indications. and side ef
fects, especially those affecting response to physical therapy
Knowledgeable about the stability of vital signs since admission, including heart rate and rhythm, respiration rate and
rhythm. blood pressure, skin color, core temperature, and hemodynamic stability
Detailed knowledge of relevant findings of laboratory tests, procedures, and biopsies, including arterial blood gases,
blood analysis, fluid and electrolyte balance, ECG, x-ray, thoracentesis, central venous pressure (CVP), left arttial
pressure (LAP), pulmonary artery wedge pressure (PAWP), microbiology and biochemistry reports, and urinalysis
If the patient is ventilated, detailed understanding of the rationale for the ventilatory mode and parameters used
With respect to establishing a patient database, do the following: (I) Conduct a thorough, detailed clinical assessment
specific to the patient's condition(s), including inspection, palpation, percussion, and auscultation of the chest, as
well as a neuromusculoskeletal assessment to rule out any secondary effects of cardiopulmonary dysfunction and
to establish rehabilitation prognosis. (2) Establish a physical diagnosis and problem list and prioritize the treatment
goals and overall treatment plan. (3) Determine the optimal assessment and treatment outcome measures and be
knowledgeable about their interpretation. (4) Conduct serial trend measurements to predict the patient's oxygen
transport reserve capacity before treatment and stressing the oxygen transport system
As treatment progresses, record objective and relevant subjective treatmenl outcome measures and revise treatment
goals as indicated by the patient's progress
572
PART VI
Preparation for Treating the ICU Patient
Physical Therapy Uses of Monitoring Systems

in the leU
Patients in the rcu are generally characterized by

some degree of life-threatening medical instability. Be
Establish the indications for and contraindications of
fore treating a give:1 patient in the rcu, the physical
cardiopulmonary physical therapy
therapist should be thoroughly familiar with the spe
Define treatment intensity, duration, and frequency
cific information shown in the box on p. 571.
for optimal treatment outcome

Determine the appropriateness of response to a spe
cific intervention
GENERAL CLINICAL ASPECTS OF THE
Assess the need for supplemental oxygen before,
MANAGEMENT OF THE ICU PATIENT
during, and after treatmcnt
Assessment
Determine appropriate patient positioning between.
The fundamental assessment procedures for the car
during. and after treatments
diorespiratory system are described in detail in Part
Establish whether the patient is responding nega
Two. Laboratory reports, procedures, sputum culture,
tively to treatment and whether treatment should
and x-rays supplement the findings of inspection, pal
be discontinued or modified
pation, percussion, and auscultation of the chest. Of

particular importance are the blood work, arterial blood
gases, ECG, fluid and electrolyte balance, hemody
pulmonary artery pressure and wedge pressure, which
namic Ilionitoring, and intracranial pressure monitoring.
provide an index of myocardial sufficiency and
These are the most commonly monitored parameters in
specifically left heart function. Central venous pres
the ICU in addition to vital signs-respiration rate,
sure gives an indication of fluid loading and the abil
heart rate, temperature, and blood pressure.
ity of the right side of the heart to cope with changes

in circulating body fluids. Pressures related to heart
function give the physical therapist an indication of
Monitoring
pulmonary status and help to determine whether heart
Optimal physical therapy treatment depends on opti
dysfunction is affecting lung function, lung dysfunc
mal use of the monitoring systems available in the
tion is affecting heart function, or both. Existing car
rcu. Monitoring systems can be used to establish
diopulmonary stress alerts the physical therapist to
the indications and contraindications for treatment,
appropriately modify workloads or the physical de
parameters of the treatment prescription and pro
mands of treatment to keep the patient medically sta
gression. in addition to assessing the patient. These
ble, avoid undue fatigue, and deterioration.
are summarized in the box above. Physical thera
Changes in ECG may reflect heart disease, lung
pists need to exploit the considerable amount of ob
disease, altered acid base, and electrolyte and fluid bal
jective data available to them in patient manage
ance. The physical therapist is responsible for identify
ment. A thorough knowledge and routine use of
ing the patient's heart rhythm and ECG changes that
monitoring systems for each patient in the lCU can
might be expected with improvement or deterioration
not be overemphasized in terms of contributing to
in oxygen transport, and secondary to medical man
improved quality of care with less potential risk to
agement, drug intervention and changes in the course
the patient.
of the disease and response to treatment generally.
The monitoring systems described in Chapter 15

provide essential information with respect to the
management of the ICU patient. Information regard
Pharmacological Agents
ing acid-base imbalance and fluid and electrolyte bal
The physical therapist needs a thorough knowledge
ance helps to establish specific treatment goals. The
of the common pharmacological agents used in inten
Swan-Ganz catheter in situ gives the pressures for
sive care (Chapter 43). With this knowledge, the
31
physical therapist can augment the effects of these
573
In addition, narcotics tend to have significant multi
agents and optimize physical therapy treatment re
system effects rather than localized effects. Because
sponse when treatments are coordinated with medica
physical therapy is the most physiological and nonin
tion schedules. Most medications have optimal
vasive intervention available to the ICU patient, it be
dosages for any given patient, optimal sensitivity, and
hooves the physical therapist to ensure that all other
peak-response time. Most medications have side ef
pharmacological agents that are effective and more
fects. Side effects may cause deterioration in the pa
selective than narcotics in achieving the desired ef
tient's condition, create apparent signs and symptoms
fect have been considered.
suggestive of other disorders, or alter response to

treatment. The physical therapist therefore needs to
identify the medications each patient is taking and
TREATMENT PRESCRIPTION IN THE ICU

Physical therapy treatments in the ICU are judiciously
their side effects.

Certain medications, such as bronchodilators,
selected in a goal-specific manner. As a general
sedatives, mucolytic agents, antianginal medications,
guideline, treatments descend in a physiological hier
and analgesics, help the patient to be able to cooper
archy. Mobilization, exercise, and body positioning
ate during treatments. Special consideration must al
should be exploited first with respect to their direct
ways be given to the different peak-response times of
and potent effects on oxygen transport overall. At the
medications used in the ICU. The patient is willing to
other end of the hierarchy (i.e., least physiological in
cooperate more actively in the treatment if pain is re
terventions that have a more limited effect on the
duced, breathing is easier, and mucus is easier to
steps in the oxygen transport pathway) are conven
clear. A better treatment effect is therefore more
tional interventions, such as manual techniques.
likely. These advantages result in more effective use
Mobilization and exercise can be prescribed to ef
of the physical therapist's time, and often a shorter,
fect three physiologically distinct outcomes based on
more cost-effective, efficacious treatment.
their acute effects, their long-term effects, and their
Certain other medications may prevent close moni
preventative effects (see Chapter 17). The treatment
toring of patients during exercise and activity. Patients
prescription needs to focus on which specific effects
on beta-blocking agents, for example, will not show
of mobilization and exercise are required to reverse
the normal changes in heart rate and blood pressure in
or mitigate deficits in the oxygen transport pathway
response to exercise. In addition, beta-blockers con
or prevent impaired oxygen transport. The treatment
tribute to fatigue. Caution must therefore be observed
prescription is different in each case.
when prescribing exercise for these patients. Another
Unlike other patient care areas, the frequency of
classification of drugs called vasopressor agents help
treatments may range from one to several treatments
regulate blood pressure and heart rate. Patients on
daily. The frequency depends on the patient's spe
these agents may also exhibit abnormal exercise re
cific treatment goals, the aggressiveness of treatment
sponses. Hence monitoring vital signs to assess treat
indicated, interfering related problems and their man
ment response may be of limited value for patients on
agement, patient cooperation, and tolerance for the
drugs acting on the cardiovascular system.
physical therapy treatments prescribed. The patient's
Narcotics is a commonly used classification of
oxygen reserve capacity needs to be assessed to en
drug used in the ICU and are often administered
sure that the patient can meet the demands of exercise
jointly with sedatives and tranquilizers. Despite their
stress. The physical therapist needs to assess the pa
beneficial effects on pain relief, narcotics of any clas
tient's tolerance with respect to duration, intensity,
sification of pharmacological agents and particularly
and frequency of treatments, as well as prescribed ex
in combination with other sedative type drugs antago
ercise. Objective and subjective measures of the pa
nize and often prohibit physical therapy treatments
tient's tolerance to the initial assessment and the ob
because of the patient's reduced arousal, monotonous
servations of other members of the team help to
ventilation, and inability to cooperate with treatment.
establish this baseline.
574
PART VI
Guidelines for the Delivery of Cardiopulmonary Physical Thel'3py: Intensive Care
Treatment goals and interventions are described in
progress notes during the ICU stay in order that the team
Part III. Interventions frequently used in the ICU in
responsible for the patient after discharge is able to con
clude those related to mobilization and exercise, body
tinue management with reduced risk of disruption of
positioning, breathing control and coughing, mucocil
care or regression of the patient's condition. The patient
iary transport and mucous clearance interventions,
should be consulted, if possible, and informed at all
such as deep breathing and coughing maneuvers,
times of his or her progress and plans made by the team
chest wall mobilization, postural drainage, percussion,
and family. The patient should be given as many
vibration, shaking, rib springing, relaxation, body
choices as possible about his or her care and be actively
alignment, and general strengthening exercises. These
involved in long-term planning.
interventions are the mainstay of cardiopulmonary

physical therapy. Intensive care physical therapy de
mands particular skill in selecting, prioritizing, and
applying the particular interventions that can effect
the optimal treatment outcome in the shortest time in a
NONCLINICAL ASPECTS OF THE MANAGEMENT

OF THE ICU PATIENT
Team Work
given critically ill patient. For example, a common
Comprehensive patient care in the ICU includes some
scenario in the ICU is the physical therapist's attempt
nonclinical activities. Team work is the cssence of
ing to reduce or reverse the adverse changes observed
optimal patient care, particularly in the ICU. The
in blood gases; that is, falling Pao2 levels and increas
physical therapist interacts frequently with other team
ing Paco2 levels in the patient for whom intubation is
members regarding observations and changes in the
being seriously considered if improvement is not ob
patient's condition, treatment goals, and treatment re
served soon. The focus of treatment for such a patient
sponse (Figure 31-2). In addition to providing therapy
is delineated into two parts. The physical therapist
for patients, the physical therapist is often consulted
first focuses on optimizing oxygen transpOit and car
regarding ambulation, body positioning, lifting, trans
diopulmonary function of the involved lung fields and
ferring, chair sitting, and self-care.
second on maintaining optimal cardiopulmonary func

tion of the uninvolved lung fields.
Contraindications and the awareness of potential ad
Infection Control
verse effects of cardiopulmonary physical therapy are
Personal hygiene and good hygienic practice on the
particular concems in the ICU. The physical therapist
part of the physical therapist cannot be overempha
needs to be well-versed about these. Treatments need to
sized. Patients in the ICU are usually prone to infec
be modified to achieve an optimal treatment effect with
tion. Meticulous hand washing with an antiseptic de
out posing a hazard to the patient. Herein lies one of the
tergent between patients is essential. Soaping for 30
many challenges of intensive care physical therapy.
seconds or more with a thorough scrubbing motion and

followed by thorough rinsing should be carried out.
After contact with infected wounds, saliva, wounds,
Discharge from the ICU
blood, pus, vomitus, urine, or stool, the physical thera
To be recommended for discharge from the ICU, the
pist must be particularly conscientious about washing
patient should not require cardiopulmonary physical
immediately. Given the concerns regarding HIV infec
therapy more than every 4 to 6 hours. The patient
tion and AIDS, physical protection, including gown
should be breathing spontaneously and independently
ing, gloving, capping, and masking, should be routine.
and elicit a cough with or without assistance, prefer

ably one that is effective in clearing secretions. If
alert, the patient should be moving purposefully in
bed before transfer.
Recognition of the Patient as a Person

Although constraints do exist in the high technology
The physical therapist is responsible for documenting
atmosphere of the ICU, the patient's dignity is ob
the physical therapy treatment priorities and frequent
served as much as possible regardless of the reason
31
FIGURE 31-2
Team work in the intensive care unit is essential to facilitate communication and patient
treatment. A, Physical ther<lpist and nurse "bagging" and suctioning the patient. B, Two persons
positioning for dependent, heavy patients prior to portable chest x-ray. C, Respiratory care
practitioners. D, Radiologist. E, Nursing staff.
575
576
PART VI
for admission, the level of consciousness, or belliger

ent and objectionable behavior directed toward the
THE DYING PATIENT

Anticipation of dying and death are traumatic for the
ICU staff. Gestures, such as using the patient's pre
patient, family and friends, and the health-care team.
ferred name, explaining aspects of the patient's care,
The phases of dying (Andreoli, Fowkes, Zipes, and
continually orienting the patient to person, place,
Wallace, 1991; Warner, 1978) that can be anticipated
time, and day, and having an interpreter available if
when caring for the dying patient are presented in the
necessary are widely practiced. A supportive caring
box on p. 577.
atmosphere is created in which the patient is free to
Principles 01 physical therapy management
make choices and ask questions as much as possible.
The dying patient and his or her family and friends

have special needs that must be included in and in
leu as a Healing Environment
fact constitute an integral parl of the patient's over
The physical environment of the IC U has a profound
all care. In general the physical comfort and per
effect on the patient's recovery independent of the
sonal hygiene of the patient, as well as the quality of
level of care received. Windows with pleasant views,
the immediate psychosocial environment, are para
for example, help to orient the patient, and provide a
mount concerns. Compassion, understanding, and
sense of day and night and the passage of time (Fig
respect for the patient and the family must be forth
ure 31-3). Other benefits incl\lde reduced number and
coming from the ICU team. The ability to be atten
types of complications and reduced length of stay in
tive, comforting, and compassionate are invaluable
the ICU and in hospital overall. Physical therapists
personal qualities that need to be developed to a
who are involved in the designing of rcus should
high degree in the critical care area. The tcam needs
consider psychosocial, environmental, technological,
to attend to how the patient, if sufficiently alert, is
and clinical factors.
dealing with the possibility of dying and take their
FIGURE 31-3
An overview of an rcu room. Note large window area and openness of room. Windows help
patients orient to day and night.
31
to the fatigue induced by treatment and by coughing.
Characteristics of the Dying Patient
Facilitated and supported coughing may help reduce
Loss of strength. motion, and reflexes in the legs

and then in the
577
the effort required to cough productively.
anm,
The use of human touch may be the single most
Failure of the peripheral circulation and profuse
important means of communicating with and provid
sweating, causing body cooling
ing support to the dying patient who may be unable
The dying patient tends to turn toward the light
or disinterested in communicating. Supportive touch
Decreased sensitivity to touch and deep pressure
ing and handholding may be even more important to
and pain tends to remain
the patient on life support systems where these may
Often conscious until death
be experienced as a physical barrier between the pa
May experience pain. acute loneliness. and fear
tient and those around him or her.
May increase spiritual neeus, particularly at night
SUMMARY
an interval of 4uiescence just before death
From Andreoli KG, Fo\V cs VK. Zipl!s DP, Wallace AG: COl11pre
hel1.live cardiac care, ed 7, St. Louis. 1991. Mosby.
Cardiopulmonary physical therapy in the ICU is a

specialty in itself. The overriding goals pertain to
returning the patient to a premorbid level of func
tion and in the process minimize morbidity, mortal
ity, and length of hospital stay. The general goals of
critical care are function optimization and prophy
cues from the patient with respect to the role they
laxis. Specific primary goals are defined by the un
need to play. If requested by the patient or family,
derlying cardiopulmonary pathophysiology and
pastoral care services are summoned, preferably be
multisystem dysfunction and its sequelae. Specific
fore death is imminent.
secondary goals are defined by the presence of or
If life support systems are being continued, the
the potential for musculoskeletal and neuromuscll
physical therapist may provide treatment to keep
lar dysfunction. This chapter elaborates on some
the patient as comfortable as possible. Conservative
general a s p e c t s of treating ICU p a tients. The
prophylactic cardiopulmonary physical therapy
knowledge base and experience of physical thera
may be provided to reduce the work of breathing.
pists working in the area are presented. A broad
Treatments are kept to a minimum in terms of num
overview of the objectives of treatment and the ra
ber and duration if death is inevitable. Range of
tionale for prioritizing treatments according to a
motion exercises may help to reduce the discomfort
physiological hierarchy is described. General clini
of immobility and facilitate nursing management
cal and nonclinical aspects of patient management
and the basic care of the patient. Analgesics may be
are discussed. Finally, issues related to the manage
continued along with other medications to reduce
ment of the dying patient are addressed.
pain and sufl'ering and maximize comfort. If so,

these are prudently timed with treatments if appro
priate. In the presence of life supports the patient's
needs may have to be anticipated somewhat more
than without life supports because they severely
limit communication. The dignity and modesty of
REVIEW QUESTIONS
I. Describe the elements of evidence-based practice
in cardiopulmonary physical therapy.

2. Describe the general goals and principles of car
the patient continue to be observed even after death
diopulmonary physical therapy in the intensive
has occurred.
care unit.
The patient who has had life supports removed re
3. Describe the role of monitoring in cardiopul
ceives the same level of palliative care as the patient
monary physical therapy care of the critically-ill
with supports. Weakness and wasting may contribute
patient.
578
PART VI
Guidelines for the Delivery of Cardiopulmonary Physical The.-apy: Intensive Care
References
Dean. E" & Ross, J. (1992). Discordance between cardiopulmonary
Andreoli, K.G .. Iowke,. V.K., Zipes , D.P.. & Wallace. A.G. (1991).
COlllprehensi!'e cardiac care, (7th ed.). St Louis: Mosby.
phy iology and physical therapy. Chest. 101. 1694-1698.
Hi slop. J.H. (1975). Tenth Mary Mc M illain lecture. The not-50-im
Barluw, D.H .. H ayes. S.c., & Nelson . R.O. (1 984). the scientist
practitioner. research and accountability in clinical (lI1d educa
possible dream. Physical Thi'rapy. 55. 1069-1080.

Riegelm an . R.K. (1991). Millillli illg lII e dico l lIliswkes. The art
tion "ettillgs. New York: Pennagon Press .
of lIledical decision II/akillg. Boston: Little_ Brown and
Cutler. P. (1985). Problem soil'ing in clinical medicine. from data

to diagnoSis. (2nd
cd.). B altimore : Williams & Wilkins.
Company.
Ross. J
Dean, E. (1983). Research. The right way. Clinical Mal1af'emcnr,
& D ean . E. (1989). Integrating physiological princi ples
into the comprehensive management or cardiopulmonary dys
3. 29-33.
function. Physica l Tlltrop),. 69. 255-259.
Dean. E. (1985). Psychobiolugical adaptation model fur physical
Schon. D.A. (1983). Til" rejleClil'e practitiollel'. HOlV IJruje.uilllwls
therapy practice. Physical Therapy. 65. 1061-1 06R.

Dean. E. (1994a). Oxygen tran sport : A physiologically-based con
thillk ill act io ll. New York: Basic Books.
Stillwell. S. ( 1 992 ) . Mosby's critical care lIursill!; referellce, St
ceptual I'ramework for the practice of ca rdiopulmonary physio

ther apy. Physiotherapy. 80, 347-355.
Louis: Mosby.
Wo rth i ng ham. C. (1960). The de velopment of physical therapy as
Dean. E. (1994b). Physiotherapy skills: Positioning and mobili/.a
a profession through research and publica tion . Physical Ther
tion of the patient. In B.A. Webber & J.A. Pryor. (Eds.). Phys
iother(l!I.1' lor Respimtorr and Cardiac Prnhlellls. Edinburgh:
apy.40.
573-577.
Zadai. C.C. (19 86) . Pathokinesiology: The clinical implications

from a cardiopulmonary perspective. Physica l Therapy. 66
Dean. E. (1994c). Invited cOlllmental), to "Are incentive spirometry.
intermittent positive pressure breathing. and deep breathing exer
cises effectivc in the prevention of pos toperative pull11on ry
complications after upper abdominal surgery? A systematic
ovcrvi w and meta-analysis." Physica l Therapy. 74. 10-15.
368-371.
CHAPTER
32
Intensive Care Unit Management of

Primary Cardiopulmonary Dysfunction
Elizabeth Dean
KEY TERMS
Cardiopulmonary failure
Primary cardiopulmonary dysfunction
Coronary artery disease
Restrictive lung disease
Obstructive lung disease
Status asthmaticLls
INTRODUCTION
not treatment prescriptions. Rather, each patient must
This chapter presents the principles of cardiopul
be assessed and treated individually taking into con
monary physical therapy in the management of criti
sideration all factors that contribute to impaired oxy
cally ill patients with primary cardiopulmonary dys
gen transport (i.e., immobility, recumbency, extrinsic
function that can lead to cardiopulmonary failure. The
factors related to the patient's care, intrinsic factors
categories of conditions presented are obstmctive lung
related to the patient, and the underlying pathophysi
disease, status asthmaticus, restrictive lung disease,
ology) (Chapter 1). For examples of treatment pre
and coronary art ry disease (medical and surgical con
scriptions for specific patients refer to the companion
ditions). Each category of condition is presented in
volume to this book entitled Clinical case studies in
two parts. First, the related pathophysiology and perti
cardiopulmon(/ry phY.licaltherapy.
nent aspects of the medical management of each con

dition are pres nted. Second, the principles of physi
cal therapy management are discussed. These are not
mutually exclusive for each category because consid
erable overlap may exist when conditions coexist.
CARDIOPULMONARY FAILURE
Pathophysiology
The heart and lungs work interdependently; thus fail
It should be emphasized that these principles are
ure of one organ has significant imp] ications for the

579
580
PART VI
TABLE 32-1
Classification of'Respiratory Failure by Cause and Mechanisms
Origin
Drugs
Metabolic
Neoplasms
Injections
Trauma
Other
BRAIN
Narcotics
Barbiturates
Hyponatremia
Hypocalcemia
Plimary
Metastatic
Meningitis
Encephalitis
Direct injury
Increased
Central alveolar
hypovcntilation
Sedatives
Hypercapnia
Abscess
Poisons
Alkalosis
Bulbar polio
Anesthetics
Hyperglycemia
pressure
Obstructive sleep
apnea
Myxedema
NERVES AND
MUSCLES
Curariform drugs
Arsenic
Aminoglycosides
Hypophosphatemia Primary
Hypomagnesemia
Metastatic
Polio
Tetanus
Direct injury
Motor neuron
disease
Myasthenia gravis
Multiple sclerosis
Muscular dystrophy
GuilJain-Barre
syndrome
UPPER
AIRWAY
Tonsillar
adenoid
Epiglottitis
Vocal cord
LaryngotraCheitis
paralysis
hyperplasia
Tracheoma
Goiter
lacia
Polyps
Cricoarytenoid
Malignant
arthritis
tumors
Laryngeal
edema
CHEST
BELLOWS
Flail chest
Burn with
keloids
Sclerodenl1a
Pleural inter
position (fibrosis,
fluid, tumor, air)
Spondylitis
Scoliosis
Kyphosis
CONTRIBUTING
FACTORS
Massive obesity
A cites
lleus
Pain
Recumbency
LOWER
AIRWAY AND
PARENCHYMA
Malignant
Benign
Viral
(bronchiolitis,
broncho
pneumonia)
Bacterial
(bronchitis,
pneumonia,
abscess,
bronchiectasis)
Fungal
Mycoplasma
From Civelliu JM, Taylor RW, Kirby RR: Crilical care, Philadelphia, 1988, JB Lippincolt.
Contused
lung
Bronchospasm
Hea11 failure
congestive restric
tive OilSlIlJctive
COPD
Rcspiratory distress
syndrome
Interstitial lung
disease
Atelectasis
Cystic fibrosis
Pulmonary emboli
32
Intensive Care Unit Management of Primary Cardiopulmonary Dysfunction
function of the other organ (Vincent and Suter, 1987;

Weber, Janicki, Shroff, and Likoff, 1983). Insuffi
ciency or failure of the cardiopulmonary system
refers to the inability of this system to maintain ade
quate oxygen and carbon dioxide homeostasis.
Pulmonary failure reflects a gas exchange defect or
defect of the ventilatory pump. Table 32-1 shows the
classification of pulmonary failure by specific causes
and the mechanisms involved. Some common predis
posing conditions include primary cardiopulmonary
conditions, (e.g., chronic lung disease, overwhelming
pneumonia, and myocardial infarction) and secondary
cardiopulmonary conditions (e.g., motor neuron dis
eases, spinal cord injury, stroke, and muscular dystro
phy) (Chapter 30). The oxygen and carbon dioxide
tensions that have been used to define failure are vari
able because they depend on factors such as premor
bid status, general health, age, prior blood gas profile,
581
PATIENT WITH OBSTRUCTIVE LUNG DISEASE

Obstructive lung disease can result in ventilatory fail
ure and admission of the patient to the intensive care
unit (ICU), or this disease can complicate manage
ment if the patient is admitted for other reasons
(Boggs and Wooldridge-King, 1993; Un derhill,
Woods, Froelicher, and Halpenny, 1989). If conserv
ative management fails or is unlikely to improve crit
ically impaired oxygen transport and gas exchange
and to adequately remove copious and tenacious se
cretions, intubation and mechanical ventilation are in
dicated (Chapter 41). Complicating factors include
impaired oxygen delivery, polycythemia, impaired
respiratory mechanics secondary to lung damage and
increased time constants impairing optimal inhalation
and exhalation, flattened hemidiaphragms, rigid
and the time frame for the development of failure. Ar

terial blood gases and pH are essential in the assess
ment of cardiopulmonary failure, which is usually di
agnosed when the Pa02 falls below 50 to 60 mm Hg
and the PaC02 rises above 50 mm Hg (Shoemaker,
Thompson, and Holbrook, 1984).
Primary cardiac failure reflects failure of the my
ocardium to pump blood to the pulmonary and sys
temic circulations and maintain adequate tissue per
fusion (Austin and Greenfield, 1980). Significant
dysfunction of the left ventricle can lead to pul
monary vascular congestion and cardiogenic pul
monary edema ( i . e . , c o n g e s t i v e h e a r t f a i l u r e )
(Matthay, 1985). Diseases o f the heart that can lead
to failure include significant myocardial damage as a
result of infarction or myopathy, valvular heart dis
ease, and congenital defects.
Both primary pulmonary and cardiac failure can be
classified into acute and chronic stages. The compen
sation mechanisms that occur in the two stages are
distinct. With adequate physiological comp:nsation,
patients can tolerate some degree of chronic failure.
Patients with a mild degree of failure can live I'eason
ably independent lives. Moderate failure is signifi
cantly more limiting, thus these patients may require
home ventilatory support (e.g., supplemental oxygen
and nighttime ventilation), and severe failure requires
FIGURE 32-1
hospitalization and mechanical ventilatory support.
Patient receiving mechanical ventilation.
582
PART VI
banel-shaped chest wall, increased accessory muscle
tion from the oropharyngeal cavity can be reduced by
use and work of breathing, reduced diffusing capac
suctioning through the airway with the cuff of the air
ity, impaired mucociJiary transport, secretion accu
way inflated, in addition to suctioning the oropharynx'
mulation, ineffective cough mechanism, increased
after suctioning via the airway.

Suctioning can be performed frequently in a pa
oxygen consumption, increased work of the heart,

and general debility and weakness.
tient with an artificial airway and is less traumatic.
The goal of intubation and mechanical ventilation
Patients should be suctioned only as indicated be
is to provide an airway and adequate alveolar ventila
cause this procedure can produce significant desatu
tion, which is based on arterial blood gas analysis. A
ration (up to 60%), particularly in the ventilated pa
tidal volume and a respiratory rate that provide satis
tient (Walsh, Vanderwarf, Hoscheit, and Fahey,
factory blood gas and pH values are established and
1989). Administration of 100% oxygen for 3 minutes
maintained unless the clinical condition changes. The
before and after suctioning (i.e., hyperoxygenation)
precise regulation of mechanical ventilation helps to
minimizes this desaturation effect. This can be ac
restore adequate blood gases and cardiopulmonary
complished by manually bagging the patient before
function, reduce the work of breathing, rest fatigued
treatment (i.e., manual hyperventilation) or by preset
ventilatory muscles, and provide an optimal fraction
ting the mechanical ventilator (Fell and Cheney,
of inspired oxygen (FIo2) and humidification (Figure
1971). Risk of aspiration of gastric contents is re
32-1) (Wilson, 1992).
duced by the use of a nasogastric tube.
Minute ventilation can be seriously impaired with a
A common cause of acute rcspiratory failure is ad
leak in the mechanical ventilator circuitry. The tube
vanced chronic airflow limitation (Civetti, Taylor, and
connecting sites are often the sites of air leakage. Com
Kirby, 1988). The pathophysiological deficits include
plete disconnection at the endotracheal or tracheostomy
significant loss of alveolar tissue, increased compli
connection may occur in those patients with high pul
ance of alveolar tissue, hyperintlated chest wall, im
monary resistance. Close monitoring of the exhaled
paired respiratory mechanics, flattened hemidi
tidal volume and end tidal carbon dioxide will ensure
aphragms, impaired breathing efficiency, and reduced
the patient is receiving sufficient ventilation.
diffusing capacity. Proportional changes in lung vol
Positive end expiratory pressure (PEEP) is useful
umes and capacities in patients with chronic airway
in promoting greater opportunity for gas exchange at
limitation compared with healthy persons are pre
end-cxpiration in mechanically ventilated patients.
sented in Figure 8-5, p. I SO. The primary abnormality
However, venous return, myocardial perfusion, and
is a significantly increased residual volume and inspi
cardiac output may be impaired during positive pres
ratory reserve volume and hence total lung capacity.
sure ventilation with PEEP administration (Jardin, et
Failure of oxygen transport ensues secondary to venti
aI., 1981; Kumar, Pontoppian, Falke, Wilson, and
lation and perfusion mismatch, ventilatory muscle fa
Laver, 1973). Excessive stimulation to cough in these
tigue, reactive pulmonary hypertension, and right ven
ventilated patients shOUld be avoided because this ac
tricular failure. Correcting the complications of
centuates the cardiovascular side effects of PEEP.
respiratory failure, however, is often more problem
Continuous positive airway pressure (CPAP) can
atic than treating the specific cause. Hypoxemia and
maintain airway patency during spontaneous ventila
hypercapnia are often present. Hypoxemia is usually
tion. This mode of ventilation, however, seems to be
improved with supplemental oxygen in the absence of
prcferred in children, whereas PEEP is used more
significant diffusion defect or shunt.

Cardiovascular complications are among the most
commonly in adults.
Interfcrence with the gag reflex in the patient with
prevalent observed in ventilatory failure. Marked hy
an endotracheal tube increases the risk of aspiration
percapnia (increased arterial P(02) with acidemia (re
of the oropharyngeal and gastric contents and can re
duced pH) can produce extreme vasodilatation and
sult in pneumonitis and pneumonia. Risk of aspira
hypotension resulting from the local action on blood
32
vessels (Boggs and Wooldridge-King, 1993). Mild
583
Nutrition
hypercapnia can produce reflex vasoconstriction and
Critically ill patients are hypermetabolical. Metaboli
hypertension. Occasionally systemic hypertension is
cal demand and oxygen consumption are increased
observed during weaning from the ventilator with the
secondary to healing and repair, increased tempera
presence of a moderate degree of hypercapnia.
ture, altered thermoregulation and after surgery. Pa
Right heart failure, cor pulmonale, is a well
tients with chronic cardiopulmonary limitation are
known complication of chronic lung disease and con
often undernourished because of the effort required to
gestive heart failure. Both hypoxia and reduced pH
purchase food, prepare, and consume it. Furthermore,
cause pulmonary vasoconstriction and an increase in
these patients have an increased oxygen consumption
pulmonary artery prcssure. Consequently, reversing
and energy expenditure secondary to the increased
bronchospa sm, hypoxemia, hypercapnia, a n d
work of breathing (Petty, 1985; Rochester and Esau,
acidemia can often reduce pulmonary vasoconstric
1984). Without adequate nutrition, patients incur the
tion, lower pulmonary artery pressure, and thereby
effects of deconditioning faster, are debilitated, are
improve hemodynamics.
less capable of responding optimally to therapy, and
The end stage of respiratory failure results in a pro
are more susceptible to infection. Intravenous hyper
gressive increase in airway resistance, work of breath
alimentation, or external hyperalimentation, is typi
ing, oxygen consumption, and carbon dioxide produc
cally instituted early to maintain optimal nutritional
tion. In areas of bronchial obstruction, marked
status and to avoid excessive physical wasting and
alveolar hypoventilation results and ventilation and
deterioration. If a tracheostomy has been pelformed,
pelfusion are severely mismatched. Hypoxemia and
the patient is able to eat normally.
respiratory acidosis produce reactive pulmonary hy

pertension and further ventilatory failure. Profound
carbon dioxide retention, refractory hypoxemia, and
The principles of management of acute respiratory
respiratory acidemia may terminate in a fatal dys
failure are based on interventions that will enhance
rhythmia (Gibson, Pride, Davis, and Loh, 1977;
oxygen transport (i.e., oxygen delivery, oxygen
Macklem and Roussos, 1977; Rochester and Arora,
consumption, and oxygen extraction), and facilitate
1983; Vincent and Suter, 1987; Weinstein and Skill

man, 1980; Wcissman, Kemper, Elwyn, Askanazi,
Hyman, and Kinney, 1989).
carbon dioxide removal (Gallagher and Civetta,
1980). Thus the steps of the oxygen transport path

way that have been identified as impaired or threat
Acidemia from respiratory causes with a pH of
ened by the patient's condition (i.e., immobility, re
less than 7.25 is often harmful with respect to dys
cumbency, and extrinsic and intrinsic factors in
rhythmia production. Conversely, hypoventilation is
addition to the underlying pathophysiology) (Chap
equally harmful, and pH elevations greater than 7.5
ter I) are the focus of treatment. Based on a de
may cause neurological and cardiovascular complica
tailed analysis of these factors, treatments are se
tions. In acute respiratory failure with profound
lected, prioritized, and applied to optimize the steps
acidemia, intravenous use of bicarbonate is used to
in the pathway that are affected. These may include
buffer the hydrogen ion concentration until the under
treatments to maximize the patency of the airways,
lying disorder is corrected. Bicarbonate infusion is
increase alveolar ventilation, facilitate mucuciliary
guided by frequent pH measurements.
transport, facilitate airway clearance, optimize the
Transport of oxygen and carbon dioxide to and
mechanical position of the diaphragm, optimize
. from the tissues depends on adequate pulmonary and
ventilation and perfusion matching, optimize pH,
systemic circulation. Frequently, blood volume has to
eliminate carbon dioxide, optimize peripheral circu
be restored by fluids or blood replacement or both.
lation and tissue perfusion, and reduce the work of
Inotropic agents are used to maintain adequate circu
breathing and of the heart. To optimize oxygen
lation by augmenting myocardial contractility.
transport, the primary goals of physical therapy
584
PART VI
include the following:
treatments with medications so the
l. To improve or maintain arterial oxygen tension

(Pao2) or prevent its deterioration
its deterioration
or
and pH or prevent its detedoration
levels
around rest
Mobilization and exercise are at the top of the hi
3, To improve or maintain arterial carbon dioxide

The means by which these
erarchy of physiological treatments; thus the potent

and direct effects of these interventions are ex
are fulfilled de-
first (see Chapter I
on each patient's clinical presentation and

the
control, and coor
maximal effect is
dinating treatments with peak energy periods and
2, To improve or maintain arterial oxygen satura

tion
Intensive Care
factors that contribute t o cardiopul
monary dysfunction.
the upright
into
cardiopulmonary function and
promotes
gas exchange. Chairs should be available at the side

of every ICU bed to provide greater opportunity for
Mobilization
the Datien! to be upright. The benefits of the upright
Mobilization and ambulation are
for normal
IUIU glCtll functioning of the human body (i.e., to

stress and
stimulate exercise stress and
(Dean and
thereby optimize oxygen
propped up in
during
the physical labor of lifting
transfers. These devices are designed to be
1992b). Although oatients in the ICU are

to move,
are different to
bed. Stretcher chairs are particularly useful in reduc
tioned under the patient while recumbent in bed and
sit up, stand, sit in chairs, take a
then mechanically configured into a chair. One po
and in some circumstances, ambulate
tential danger, however, is overreliance on these de
across the unit even if they are ventilated (Macken
vices, Even minimal ability of the patient to assist
few
and Ciesla,
mobilization
is prescribed to exploit its

long-term cumulative
(I) acute effects, (2) the

and (3) the
These effects are
effects
cally distinct and need to be
with his or her bed

minutes and
in the ICU, critically ill patients can move

limits.
is
among those activities that are the most metaboli

cally
for ICU patients
Parrent and
per, 1
Askanazi,
and Kinney,
outcome that can be
the patient'S
with passive interventions. The
expected
fundamental goal is enhanced recovery, reduced
Murphy,
Weissman and Kem
tolerance to be
which also reduces the

mobilized. What
cost is the greater
Given that cardiopulmonary physical
so, the pa
tient's oxygen transport system deconditions fur-
address each patient's problems. With the monitoring

and be moved within safe
assistants. These minimal ef
forts must be exploited. Without
specifically to
must
and
be exploited, even i f the maneuver takes several
reduced morbidity and mortalitv. and re

duced ICU and hospital stay.
Significant benefit can be gained from
the ventilated
provided there are no absolute
to meet a given increase in oxygen demand must be
contraindications to being upright i n terms of car
determined before treatment. Even
diopulmonary
car
therapy stresses the oxygen

as a means of
the func
ventilated patient is the

and Jones,
tion and efficiency of this system, unnecessary or

excessive energy
neuromuscular and muscu
loskeletal status, and skin
Ambulating the
whenever
1972). The potential
i s undesirable and
Mobilization and
thus should be minimized. Interventions that can
exercise must be
minimize oxygen demand include relaxation,
the exercise stimulus is therapeutic
cious body
provides an
stressor to the oxygen transport pathway,
to facilitate oxygen trans
is not hazardous),
port, coordination of treatments with other interscheduling treatments at appropriate
specifically to ensure that
Standing and
even a few steps can be ex
32
tremely strenuous for the ICU patient with respect to

oxygen demand, considering that this patient is hy
permetabolical. Such activities need to be introduced
gradually and with continuous monitoring to ensure
the patient does not exceed the prescribed therapeutic
intensity needcd to maximize oxygen transport.
Standing and walking are coordinated with other as
pects of the patient's care and should be carried out
in several stages. Monitoring of the ECG and arterial
saturation of the critically ill patient performing ac
tivities such as standing or walking cannot be
overemphasized. By disconnecting these monitors,
the physical therapist is working blindly and poten
tially dangerously because the leads do not reach or
585
Body positioning
Body positioning is a potent therapeutic intervention
that promotes optimal oxygen transport and gas ex
change in two ways; one, from the physiological
benefits accrued from the specific positions them
selves, and two, from the physiological hcndits ac
crued from physically changing from one position to
another (see Chapter 18). Body position can be used
preferentially to augment alveolar volume, alveolar
ventilation, ventilation and perfusion matching, res
piratory mechanics, cough effectiveness, eentral and
peripheral hemodynamics and fluid shifts, mucocil
iary transport, and secretion clearance (see Chapter
18). Both ventilation and perfusion are enhanced in
becausc of movement artifact. In anticipation of an
the inferior lung fields. Thus in postural drainage po
increased workload, ventilatory parameters for the
sitions the superior lung being treated is neither pref
ventilated patients may require adjusting. A greater

concentration of oxygen should be delivered for at
least 3 to 5 minutes before the activity and continued
afterward for 10 minutes or so until the patient has
recovered from the increased exertion and the heart
erentially ventilated nor perfused. The less affected

lung fields therefore may be contributing more sub
stantially to improving arterial gases. Hence the
physical therapist must consider the goals of treat
ment with respect to pulrnona:-y function in both the
rate and blood pre. sure have returned to within 5% to
involved and less-involved lung fields. During pos
10% of baseline values.
tural drainage, the length of time in a given position
Active movement has greater therapeutic effect

on oxygen transport than assisted or passive move
ments; thus the benefits of active movements are ex
ploited first. Movement recruiting large muscle
groups minimizes the disproportionate hemodynamic
stress associated with movement of small muscle
groups or movements requiring excessive dynamic
stabilization (Hanson and Nagel, 1987). If active
needs to be monitored to avoid drainage of secre

tions into the less involved, functional, inferior lung
fields and to avoid the possibility of compression at
electasis in the inferior lung (Dcan, 1985; Leblanc,
Ruff, and Milic-Emili, 1970).
Although positions can be predicted that will opti
mize ventilation and pert'usion matching, each patient
will respond differently, depending on such factors as
movements cannot be performed or excessively
pathology, age, weight, depth of breathing, and me
stress the oxygen transport system, then active as
chanical ventilation (Clauss, Scalabrini, Ray, and
sisted movements arc indicated. Passive movements
Reed, 1968; Ray et aI., 1974), Thcrefore the patient's
have a role primarily when the patient is paralyzed
response to specific positioning must be observed,
or' so hemodynamically unstable that the patient de
documented, and objectively monitored with respect
teriorates with active movement. With respect to car
to the effect on oxygen transport variables.
diopulmonary benefits, passive movement stimulates

changes in ventilatory and circulatory patterns
(West, 1995). These can be particularly beneficial in
patients who have significant mobility restriction,
however, they should not substitute for active and
active-assisted movements, which are associated
with even greater benefit because they are higher
order activities on the physiologically based treat
ment hierarchy (see Chapter 16).
Another important goal of body positioning is to

potentiate position-dependent fluid shifts to optimize
cardiovascular function. For this reason the patient
should be positioned upright as often as possible. In
addition, there are other beneficial effects of the up
right position on pulmonary function (e.g., maximizc
lung volumcs and capacities, minimize alveolar col
lapse, decrcase airway resistance, increase lung eom
pliancc and, therchy, reduce ventilator system pres
586
PART VI
sure). To maximize the effect of gravity on promot
increased before postural drainage and treatment to
ing fluid shifts, the legs should be positioned depen
help compensate for any physical stress imposed
dently at frequent intervals. In a patient who is not
by treatment. Oxygen, however, should always be
100% and inspired for at least 3 min
self-supporting with or without assistance, fluid
increased to
shifts can be stimulated with a high Fowler's posi
utes before and after suctioning. Should arterial de
tion coupled with the use of the bed knee-break. Be
saturation be apparent during treatment, oxygen
tween sessions of therapeutic body positioning, a
may need to be increased. If the patient is sponta
schedule of four-point turning (supine, left side,
neously breathing without oxygen, supplemental
prone, right side) is ideal and should be attempted
oxygen may also be indicated during treatment to
even in the ventilated patient if not strictly con

traindicated (Dean,
1994).
avoid desaturation in some patients. Oxygen ad

ministration must be knowledgeably regulated by
Extreme body positions have been reported to
the ICU team based on arterial blood gas results.
have beneficial effects on oxygen transport in pa
Severe hypoxemia is known to result in irreversible
tients with acute respiratory failure. The head-down
tissue damage within minutes, but hyperoxia can
position has been shown to reduce respiratory distress
also produce harmful effects within hours. By max
in some patients with obstructive lung disease
imizing alveolar ventilation, gas exchange, and
1954). The abdominal viscera are
ventilation and perfusion matching, supplemental
(Barach and Beck,
displaced cephalad, thereby elevating the typically
oxygen can be opti mally used and the effects of
flattened hemidiaphragms and placing them in a me
acidemia minimized.
chanically advantageous position. This effect may be
Treatment for respiratory acidosis is aimed at in
mimicked in other body positions by manual abdomi
creasing alveolar ventilation to improve the ex
nal compression and abdominal binders. In some pa
change of carbon dioxide and oxygen. Because the
tients, however, the additional load imposed by the
r e s p i r a t o r y c e n t e r is d e p ressed by i n creased
increased intraabdominal pressure on the underside
amounts of carbon dioxide (carbon dioxide narco
of the diaphragm may inadvertently increase the
sis), the lowered oxygen tension of the blood be
work of breathing and increase respiratory distress.
comes the stimulus for respiration. If the patient in
The prone position has been reported to be beneficial
hales
in patients with acute respiratory fai I ure (Douglas,
stimulation for respiration may be removed. For
Rehder, Beynen, Sessler, and Marsh,
1977; Piehl and

1976). A variant of the prone position, semi
this reason, oxygen is never given to patients with
Brown,
carbon dioxide narcosis.
prone, may be more beneficial in some patients by re
high
c o n c e n t r a t i on s
Low flow oxygen
of
oxygen,
the
(I to 3 Llmin) is given to a pa
ducing intraabdominal pressure. In addition, the
tient with chronic pulmonary disease who maintains a
semi-prone position may be safer and more comfort
chronically elevated arterial Pe02 in the presence of
able for the mechanically ventilated patient. The pre
arterial hypoxemia. If intermittent positive pressure
scription of any body positioning must be based on
breathing is indicated, compressed or room air is used
its anticipated benefits on oxygen transport. The
instead of oxygen in this situation.
more extreme positions should be introduced in pro
Severe hypoxemia usually suppresses cardiac out
gressive stages and the patient's response monitored
put to some degree. Cardiac output may be further
to ensure the response is favorable.
compromised immediately after a patient is placed on

a mechanical ventilator because of impaired venous
return by the elevated transpulmonary pressure
Supplemental oxygen
(Jardin et aI.,
1981). An attempt is made to carefully
Supplemental oxygen is usually administered con
balance ventilation with an optimal or adequate car
tinuously, whether the patient is ventilated or not,
diac output by shortening inspiratory time and by
to maintain Pa02 level within an optimal range

(Dantzker,
1991). Oxygen concentrations can be
minimizing transpulmonary pressures by using lower

tidal volumes.
32
Intensh'e Care Unit Management of Primary Cardiopulmonary Dysfunction
Bagging
Dean and
Drlctl:ce in some ICUs is bagging, A self
manual
is temporarily connected to
the
is to pro
I 992a), Thus these less
less physiological conventional proce
are manually inflated for a few

breaths, The purpose of
587
and
should be considered
after other more supported and
physiological treatments have been
Fur-
breaths during treatment, to
because of their documented adverse ef
maintain some degree of
end-expiratory
fects, it is essential that the patient be continuously
pressure, to assess lung
and to facilitate
monitored for safety reasons and to establish a favor
the effect of instillation of a small volume of saline
able treatment outcome, For the unconscious or para-
vide some
solution into the tracheobronchial tree to loosen se

cretions, Bagging must be performed
Ag
can
The use
is contro
in conjunction with
versial. Some clinicians
needed to examine the role of

of this
and the effect
on mucous removal.
to bag the patient after
suctioning to a void the
of the
pressure pushing the mucus distally, Others maintain

that because of the adherent quality of the mucus to
the walls of the
patient, the ventilator or self-inflating bag can

be used to increase inflation volumes, Research is
Instillation
Instillation is another procedure that should be used
and the dilatation of the air

does
ways in response to positive pressure,
not propel the mucus distally, Rather, it is believed
in
A mucolytic effect of saline
has not been well established, Beneficial

however, may be more apparent in neonates,
before suctioning promotes air entry dis
that
tal to the mucous
and movement of
cen
on expiration,
Certain body
ventilator is
lem when a
prob
The patient in
used,
tion to fluid balance to carefully
of the ventilator is greatly reduced
The
head is
when the
below the hips
because of an increase in total pulmonary resistance

caused
the pressure of the abdominal contents,
tural
fluid, Normally the
of the tracheobronchial tree is therefore

larly important in the
tidal volume can
an assistant while the pllysical ther
aids the patient with bronchial
With
the physical therapist
needs to ensure the
is adequately ventilated
than tidal breath every minute or
so, As soon
cant additional source of
alveolar gas is saturated with water vapor. The
tioning, The effect of humidification can be assessed
the use of the

and takes a
and fluid volume, Inhaled humidified air is a
10 another and during some pos
positions,
be maintained
hydration
from erosion and potential infection, This is partiCLI
to maintain pressure when
from one
atten
failure needs
bag
Therefore the use of a

may be
Mucociliary transport and secretion clearance
secretions, Thick
secretions suggest humidification may be

and the patient may be systemically
If the effects of mobilization on
port and secretion accumulation have been
and further secretion clearance is
breathing is en
possible,
of the
by the
suc
requmng
may be indicated, Postural
may be
couraged in conjunction with postural drainage, The
contraindicated in patients with unstable vital
small airways dilate
and is usually contraindicated immediately after feed-
on
and cause
mucus to peel away from the walls; thus, during expi

mucous
are moved toward the trachea,
to which chest wall percussion, shaking,

and vibration facilitate this movement is
the literature (KiriJloff,
l!l
and meals, In some

tients on continuous 24-hour tube
after
are
has been discontinued for 15 minutes.
The cuff in the artificial
and Maz-
however, pa
A sequence
588
PART VI
and vibration may be indicated in conjunction with
clearance. Patients should not breathe below the end
postural drainage. Manual techniques have been asso
of normal tidal ventilation to avoid airway closure.
ciated with desaturation, atelectasis, musculoskeletal

trauma, discomfort, cardiac dysrhythmias, and arrest
(Kirilloff, et aL, 1985); therefore these techniques
Weaning from the mechanical ventilator
must be applied rationally and with attention to all
The physical therapist and the respiratory therapist
monitoring systems and changes in signs and symp
are primarily responsible for weaning the patient off
toms. The precise sequence, the duration, intensity,
mechanical ventilation. Thus coordinating their goals
and frequency of treatment is based on treatment out
and working together to ensure the weaning process
come rather than ti me. The application of manual
is carried out expediently and with the least risk of
techniques in the head-down position is contraindi
weaning complications (e.g., postextubation atelecta
cated in patients with acute myocardial infarction and
sis, aspiration and hypoxemia) is a priority (Marini,
increased intracranial pressure. Relative contraindica
1984; Shoemaker et aI., 1984). Blood gas analysis
tions include hemorrhage, bronchopulmonary fistula,
and pulmonary function provide the indications for
acute chest trauma, lung abscess, and gastric reflux
weaning. Ideally, the patient's spontaneous tidal vol
(Boggs and Wooldridge-King, 1993).
ume should approximate that delivered by the venti
The specific postural drainage positions to be used
lator. Forced vital capacity should be two to three
are determined based on the pathology, x-ray, and
times the patient's required tidal volume (Figure
clinical examination. The recommended positions for
32-2). Weaning is not usually indicated if the patient
the bronchopulmonary segments involved should be
requires PEEP greater than 5 cm H20 or FIo2 greater
approximated as closely as possible (Chapter 19) and
than 0.4. In addition, patients who are unable to gen
only modified if there are clear indications to do so.
erate a negative inspiratory pressure of -20 mm Hg
Frequently, specific positioning in the ICU is com
or greater are unlikely to be able to generate suffi
promised as a result of the patient's status, intoler
cient intrathoracic pressures for deep breathing and

.
airway clearance and thus are poor candidates for
ance to lying flat or being tipped, or limitations im

posed by the monitoring apparatus or ventilator.
weaning. Minute ventilation and maximum voluntary

ventilation can be measured at bedside and contribute
to the decision whether to wean. Although weaning
Breathing and cOl)ghing maneuvers
protocols differ depending on the patient and the ven-
If the patient is nonventilated or recently extubated,

body positioning and breathing and coughing maneu
vers are emphasized to promote mucociliary transport
and secretion clearance (Bennett, Foster, and Chap
man, 1990), decrease minute ventilation and respira
tory. rate, increase tidal volume, and improve arterial
blood gases (Barach, 1974; Casciari, Fairshter, Harri
son, M o r r is o n, Blackhurn, a n d Wi l s o n, 1981).
Breathing exercises are believed to be most effective
if pursed-lips breathing is performed in conjunction
with mechanical pressure applied over the abdomen
(Irwin and Tecklin, 1985; Mueller, Petty, and Filley,
1970). To derive the maximal benefits, breathing and

coughing maneuvers should be performed in body
positions that are most mechanically and physiologi
FIGURE 322
cally optimal. In addition, they are performed in the
Spirometer for bedside measurement of TV, ve, and
postural drainage positions to augment mucociliary
minute volume.
32
589
tilatory mode used, general guidelines for this com
include tachypnea, dyspnea, labored breathing, audi
mon ICU procedure are outlined in the box below.
ble wheezing, tachycardia, cyanosis, anxiety, and

panic. If the patient is able to cooperate wilh spiro
metric testing, the degree of reduced vital capacity,
PATIENT WITH STATUS ASTHMATICUS
peak flow, and forced expiratory volume provide in
dices of the severity of airway obstruction (Brunner
Status asthmaticus is a potentially life-threatening sit
and Wolff, 1988).
uation (Petty, 1982; Gaskell and Webber, 1988). The
Medical management is aimed at administering
pathophysiological features include marked airway re
drugs and fluids to reduce hypoxemia with oxygen,
sistance secondary to bronchospasm, edema, and mu
decrease airway inflammation and resistance, and
cous secretion and retention. The work of breathing is
hence reduce the work of breathing and anxiety. In
markedly increased, resulting in respiratory distress.
travenous sodium bicarbonate helps to reverse respi
A cycle results in which the patient becomes more hy
ratory acidosis and possibly m e tabolic acidosis
poxemic and hypercapnic secondary to alveolar hy
(Civetta, et aI., 1988).
poventilation, 'bronchospasm increases, and reactive
pulmonary hypertension may ensue along with a fur

ther incrcase in the work of breathing and anxiety.
The prime objective of physical therapy is to optimize
The classical signs and symptoms of a severe asth
oxygen transpolt and possibly avoid or delay the need
matic attack that may progress to status asthmaticus
for mechanical ventilation. If ventilation becomes
General Steps in Weaning a Patient From the Mechanical Ventilator

1. An individualized weaning schedule is designed for each patient in which periods of time are spent off the venti
lator and on a T tube thaI delivers appropriate oxygen and humidity
2. The initial time period off the venti lator is carefully selected; mornings are often good times
3. (a) Physical activity should be at a minimum d uring this period (e. g. , not during or after physical therapy. not
after meals. rests,
4.
or
procedures, and not during family visits) (b) Supplemental oxygen and humidity are given
The physical therapist offers support and reassurance
5. Vital signs. and signs and symptoms of respiratory distress are monitored continuously during weaning
6. The patient is not left unattended in the initial weaning sessions until periods off the ventilator are reliably toler
ated well for several successive minutes
7. (a) Deterioration of vital signs, blood gases. and evidence of distress indicate that the patient will have to return
\0
ventilatory assistance imminently (b) Rest periods of at least an hour are strategi cally interspersed in the
weaning schedule
8. B lood gases are performed at regular intervals (e.g .. 15, 30. 60, 90, and 120 minutes or more or less frequently as
indicated)
9. If blood gases stabilize within acceptable limits during the weaning period and the patient is generally tolerating
the procedure well. the time off the ventilator is increased
10. Patients with underlying cardiopulmonary disease who are older, malnourished, obese, or smoke can be expected
to take longer to be completely weaned from the ventilator
II. Weaning is generally faster in patients who have required a shorter period of mechanical ventilation
12. To hasten the weaning process, intermillent mandatory ventilation (lMV) has been reported to be useful in some
patients. Others, however. have observed that the use of IMV tends to fatigue the patient and delay the patient's
progress in wcaning. Thus IMV must be used cautiously. and individual variability must be considered in terms
of its effectiveness.
PART VI
590
necessary, prognosis for recovery is poorer (Petty,

Physical
can augment the medical
management of the
with status asthmaticus. In
expiration and to maintain the patency of the

and relaxed
small airways.
emphasized
with periodic
an attempt to avert intubation and mechanical ventila
huffing and avoidance of forced
tion the physical therapist coordinates treatment with
vers
medications
the
bronchodilators, mus
control, en
matching, promotes
mucociiiary
and secretion
reduces
and teaches the patient CO coordinate rewith general
movement. Cau
Despite
Nunn, Cole
and Laws,
man, Sachithanandan,
cle relaxants. steroids. and supolemental oxygen).
maneu
Roth, and
1965).
ve noninvasive management,
blood gases may deteriorate and mechanical ventila

tion may be inevitable, Relaxation,
alveo
lar ventilation, and reducing airway
and ob
struction continue to be the primary

means of achieving these
however.
differ when the patient
ventilated. Optimal prescriptive body
tion needs to be observed to avoid stimuli that poten
is
tiate bronchospasm and deterioration of the
positioning is the intervention of choice. Secretion
condition
clearance is achieved by judicious suctioning. Suc
that increase
tory distress rather than relieve it, chest wall percus

forced
maneuvers,
bag
and possibly instillation). Attention to relaxation
tioning is
as required because it can con
tribute to reduced oxygenation,
collapse, and
atelect asis, increased arousal, increased work o f

and generallv increased respiratory distress,
and reduction of excessive oxygen demands is a

as was described for the patient with chronic air
flow limitation. Certain
be avoided, for
positions may have to

in
because of the
colerance and exacerbation of symptoms in those po-

sitions. Because of the relationship of altered pul
positioning
'
PATIENT WITH RESTRICTIVE LUNG DISEASE
Acute
failure can be associated with
mary restnctlve
monary fibrosis). This is distinct from restrictive de
cautiously within the patient's tolerance.
fects secondary to neuromuscular and musculoskeletal
Those body positions that reduce respiratory distress

and the work of
Guillain-Barn
diseases
and neuromuscular
and maximize alveolar ven
tilation, oxygen saturation and blood gases, are the
neuromuscular disorders that can
respira
tory failure in the absence of underlying primary
of choice.
problems in status asthmaticus are alveolar
airway obstruction secondary t o
(Chapter
likely be
33). If
on
bronchospasm, mucosal edema, and secretions. Thus

maximizing alveolar ventilation and
transport are priorities
mu-
1989). Other
dysfunction may,
the chest
or both may be involved.
and an ineffective cough. The physical therapist coor
fore reflect ventilatory
dinates treatment with the
failure, or both. The
and clear
the
sons other than cardiopulmonary disease. The lung

The underlying cause of
medications to fa
will
admitted to the ICU for rea
because of an inefficient breathing pattern
mucociliary
the
assistance.
management of
include significantly increased work of
cilitate
interstitial
disease
distress) must be
in patients in
failure may there

failure, gas
restrictions ro
monary function need to be identified and treated in

treatment. Obstructive and re
a n c e of s e c r e t i o n s w i t h b r e a t hi n g c o n t r o l and
dividually t o
modified chest wall percussion.
stricti ve patterns of cardiopulmonary frequently
and huff
Obtaining a productive cough

is a
thus the contribution of both types of defects

to a patient's oxygen
should be determined.
Typically, in restrictive lung disease, all lung volumes
and
591
Intensive Cafe Unit Management of Primary Cardiopulmonary Dysfunction
32
are
tidal volume can
be relatively normal
considerations.
condition and
the
150). Patients
Movements may be totally assisted but more oftcn
with severe interstitial pulmonary fibrosis have in
are likely to be active-assisted and active. No mat
creased pulmonary artery pressures with an associated
ter how weak the patient may be, active-assisted
increase in
p.
ventricular work
and active movements a r e the mainstay of the
and
1989). These patients desaturate very
movement interventions performed by the physical
Restrictive ventilatory
near-upright positions. Assisted or passive move
is commonly as
sociated with both medical and
conditions.
The principles of management of acute respiratory

with these differ in that medical
failure
unless
ments should not be

indicated
the
is unable to execute these

alone). Even modest at
movements
tempts at active-assisted movements, with perhaps

only a minimal number of repetitions, benefit the
conditions are associated with underly

versible
in
particularly if these can be
whereas in the
pa
considerably more both in terms of treat
tient the pulmonary restriction is reversible. The
ment
natural course of disease in the medical patient will
loskeletal function than assisted movements that do
sta
be determined in part by the patient's
related to cardiopulmonary and muscu

endurance, and
not contribute to muscle
tus. The majority of surgical patients, however, will
coordination.
have had normal
sisted movements will contribute to the
function before surgery and
application of totaUy as
s
the development of cardiopulmonary complications
deconditioning and physical deterioration. Regard
of whether mechanical
less of the type of mobilization, the patient is ob
Chapter
34).
tissue
carbon
for arterial
served
discomfort,
regulation of blood pH, and an ef
and extent of
output are priofltles.
fective
oxygen is often effective in
if ass isted-acti ve and acti v e move

tissue oxy
ments are
in conditions associated with restrictive

disease in the absence of a right to left shunt.
In the presence of
supplemental oxygen does
performed.
Assisted movements are indicated to promote oxy

gen
via their effects on ventilatory and cir

Additionally, the
culatory patterns
is to maintain joint range of motion and

tive
can also be
if the
function,
is
ventilated), reduce risks of
cardiopulmonary compl
of
soft tissue in particu
lar. Care must therefore be taken to

movements
these
the complete range of movement
reduce muscu
for each joint, with special attention to rotatory com
loskeletal deformities and skin breakdown, and pro
ponents of joint movement. Lax joints can maintain
for
mote comfort. It is essential with body
any purpose that the patient is not confined unneces
range of motion daily. Lax
range with one

joints are
and vulnerable to excessive
sarily and does not assume any position for too
strain. Protection may best be effected in these joints
Although lines, leads, monitoring dev
by
these are anchored as se
catheters may be
as
with sufficient length to allow the
patient to move spontaneously, be mobilized as much

IJV'''HL!lv,
..
as many positioning
as
range. In the presence of
the ICU, as much and as often as
that may be particularly beneficial in
One
given
or limb splinting
from two or more excursions through full range

the distribution of ventilation and blood flow
body movement, par
ticularly in upright positions, is always a priority in
the ex
because of discomfort the involved joints will benefit
and facilitate routine patient care.

Mobilization and
the joint more slowly
tremes of joint range and just short of complete
is
body and range of motion
particu
larly of the upper limbs. If the patient is able to
592
PART VI
however, greater cardiopulmonary stress occurs with
Optimizing oxygen transport using body positioning
upper limb exercise; thus heart rate, ECG, and blood
and then nonphysiological interventions may then
pressure need monitoring. Lower-extremity move
need to be considered. Furthermore, extreme caution
ments, such as hip and knee flexion, may help to posi
needs to be observed in positioning these patients and
tion the diaphragm for improved excursion. Lower-ex
moving their limbs because they are at risk of sublux
tremity movements will also increase venous return,
ations, pressure sores, bruising, and strains.
which may or may not be desirable, depending on the
Interventions to promote mucociliary transport and
patient. The goals of upper- or lower-extremity work
secretion clearance are applicable to all situations in
must therefore be clearly defined. Possible benefits
which secretions, mucosal edema, bronchospasm, or a
and untoward effects must be identified to ensure the
combination of these factors occur. If postural drainage
patient benefits optimally from the prescribed exercise.
is indicated to further facilitate mucociliary transport
The treatment of choice in all patients is to stimu
and secretion clearance, caution needs to be exercised
late those conditions that maintain optimal oxygen
to avoid inducing bronchospasm and hypoxemia; thus
transport in health or approximate those conditions as
the use of percussion should be considered carefully.
closely as possible. That is, the most physiological

interventions are exploited first and the least physio
logical interventions are exploited last or when more
PATIENT WITH RESTRICTIVE LUNG DISEASE

physiological interventions are not possible. Physio

logical interventions such as mobilization may be
The initial priority of management in the acute phase
contraindicated in patients whose oxygen delivery is
of myocardial infarction (MI) is the correction of the
too low. Without some reserve capacity in oxygen
immediate problems including dysrhythmias, my
transport, the patient cannot sustain the additional
ocardial insufficiency, reduced cardiac output, hy
metabolical load that mobilization imposes. Patients
poxemia, chest pain, and anxiety followed by imple
who are this critical are often put on neuromuscular
mentation of a progressive rehabilitation program
blocking agents to reduce muscle tone and thereby
ranging from the acute medically stable phase to post
reduce oxygen demand. Because these patients are in
discharge rehabilitation phase (Andreoli, Fowkes,
induced paralytic states, mobilization is not possible.
Zipes, and Wallace, 1991; Froelicher, 1987; Irwin
Means of Reducing Myocardial Work Load in Patients With Cardiopulmollary Disease

1. A quiet environment without excessive noise and stimulation.
2. Low-intensity activity until medical stability has been maintained and patient shows signs of physical improvement.
3. Progressive mobilization begun in conj unction with patient's medical status, ECG stability, and unchanging or re
solving enzyme levels.
4. Reduce patient's anxiety about his or her condition, self-care activities, and family and work responsibilities.
5. Gentle mobilization exercises, deep breathing, and coughing are usually begun immediately as a prophylactic
measure, although crepitations are frequently audible in the bases of the lungs of coronary patients; treatments
need to minimize pulmonary congestion and cardiac stress.
6. Relaxation is often promoted with low-intensity activity. All levels of activity, including breathing exercises, are
ped'ormed in a coordinated, rhythmic manner. Breath holding. Valsalva maneuvers, and isometric muscle contrac
tions, (i.e., isometric exercise and exercise involving significant muscle or postural stabilization) are absolutely
contraindicated during all activities in patients with coronary artery disease and should not be performed in any
stage of a rehabilitation program.
32
593
and Tecklin, 1985). Before admission to the coronary
cluding generalized or localized pain anywhere over
care unit, continuous monitoring of the heart rate and
the thorax, upper limbs, and neck, palpitations, dysp
rhythm is established. An intravenous line is rou
nea, lightheadedness, syncope, sensation of indiges
tinely started for the administration of medications
tion, hiccups, and nausea.
and fluids. An arterial line may be started for serial
Depending on the degree of myocardial infarction
blood sampling for blood gases and enzyme mea
and damage, varying lengths of modified mobility
sures. Initially, pain medications, coronary vasodila
may be recommended (Andreoli, Fowkes, Zipes, and
tors, and diuretics are frequently used to minimize the
Wallace, 1991). During this period, the physical ther
work of the heart, anginal pain, and discomfort.
apist concentrates on rhythmic breathing exercises,
Drugs such as morphine serve to depress the respira
gentle coughing exercises or huffing, modified posi
tory drive; thus the physical therapist must be aware
tioning with the bedhead elevated at least 15 degrees
of corresponding changes in vital signs. Less potent
to facilitate the gravity-dependent mechanical action
sedatives and tranquilizers are more routinely pre
of the heart and thereby reduce myocardial oxygen
scribed. Increascd pain and anxiety potentially
demand. The patient is encouraged to perform deep
worsen the patient's cardiac status by increasing my
breathing and coughing every hour during the day.
ocardial oxygen demand and altering normal breath
Bed exercises including rhythmic, unresisted, hip and
ing pattern and gas exchange.
knee and foot and ankle exercises are usually per
The primary purpose of oxygen administration to
formed every 4 hours or so, or when the patient turns
the cardiac patient is to reduce hypoxemia, myocar
in bed. The patient is cautioned to exercise one leg at
dial work, and angina. Dyspnea, however, is com
a time, sliding one heel up and down the bed, guard
monly observed in the initial phases of myocardial
ing against lifting the leg off the bed. These exer
infarction and can be effectively controlled by sup
cises; when performed correctly and coordinated with
plemental oxygen administered by nasal cannulae or
inspiration and expiration require relatively little ef
mask. Oxygen may also correct potential ventilation
fort or additional physical stress to the MI patient.
perfusion mismatching and hypoxemia. Oxygen is
Comparable with the management of the postopera
always administered with humidity to avoid drying
tive patient, these exercises are performed prophylac
the airways.
tically to reduce the risk of venous stasis and forma
Blood gas analysis is performed within an hour of
tion of thromboemboli. In addition, they may help to
initiating oxygen therapy to establish a baseline of ar
regulate more coordinated breathing, encouragc deep
terial saturation. In this way, oxygen dose can be al
breaths and mucociliary transport, and rcduce atelec
tered to regulate blood gases and acid base balance.
tasis. The patient is cautioned against performing the

VaJsalva maneuver and straining because these activ
ities increase intrathoracic pressure and reduce car
MEDICAL CARDIAC PATIENT
diac output.
Electrocardiographic (ECG) monitoring of the car
A primary principle of the management of the patient
diac patient is the responsibility of all members of the
after myocardial infarction is to reduce myocardial
health-care team involved in the patient's care. The
oxygen demand and workload. The myocardium
physical therapist has a special responsibility to be
needs rest to promote optimal healing. Judicious rest
proficient in ECG interpretation in the coronary care
of the myocardium is a priority that can often be bal
unit because physical therapy is one of the most
anced with gentle rhythmic, non static movements.
metabolically demanding interventions for patients
The box on p. 592 illustrates several ways of reduc
(Dean et aI., 1995; Weissman et aI., 1984). The phys
ing myocardial workload in patients with cardiopul
ical therapist often has the responsibility of initiating

new activities with the cardiac patient, which might
monary disease.
The physical therapist should be watchful at all
include sitting over the edge of the bed, engaging in
times for signs of impending or silent infarction, in
self-care (particularly involving the arms being main
594
PART VI
tained in a raised position), getting in and out of bed,
duration, and frequency of these activities (Bjore,
sitting in a chair, going to the bathroom, walking
1972; Froelicher, 1987). The patient's tolerance and
around the room or in the hallways, and eventually
changes in ECG and vital signs are used as indicators
exercising on the treadmill or ergometer. Changes in
for establishing and modifying the treatment program.
the ECG must be watched for, particularly when in
These physiological parameters must be observed
troducing new activities and increasing the intensity
carefully as the patient progresses to optimize the po
of workload in activities. Careful attention to ECG
tential benefits of the therapeutic regimens as early as
changes and serum enzyme levels will contribute to
possible without endangering the patient.
enhanced physical therapy care of the acute MI pa
Patient education and prevention of infarction are
tient by optimizing the treatments prescribed and the
particularly important for the cardiac patient. As
margin of safety with which activities are performed.

Congestive heart failure may be unavoidable in
soon as the patient is alert and able to cooperate, in

formation about his or her condition with guidelines
cases of severe infarction or even milder infarction
about activity, diet, and stress management is rein
coupled with lung disease. Fluid intake and output
forced. The more involved and informed the patient
and daily weight measurements promote early detec

tion of congestive heart fai lure. Routine fluid intake
by an intravenous line should not exceed 20 to 30 ml
per hour. Signs of imminent and established conges
tive heart failure appear in the box below. The work
of the heart can be significantly reduced in the up
right position (Levine and Lown, 1952).
All cardiac patients are prone to anxiety about their
conditions and prognoses. The patient is given realis
tic guidelines at each stage of recovery with respect to
the level of activity that can be safely performed,
which can potentially avert deterioration and promote
recovery. Involving the patient in rehabilitation plan
ning from the onset facilitates the patient's planning
realistically for the future and may help to reduce the
depression often experienced by the acute MI patient.
The initial rehabilitation program is planned with
the long-range rehabilitation goals in mind. The pro
gram designed for the cardiac patient is progressive in
terms of types of activities, usually beginning with ac
tivities of daily living and with respect to the intensity,
Signs of Imminent Congestive Heart Failure

Development of tachydysrhythmias
Development of a ventricular gallop
Pulmonary crackles and other persistent advenlitiae
Development of dyspnea
Development of increased jugular venous pressure
and distention
FIGURE 32-3
Patient following open heart surgery (4 hours
postoperative).
NOTE:
patient on mechanical ventilator,
mediastinal drains, receiving blood, IV's, on EKG, CVP,
Swan Ganz, Arterial Blood Gas lines.
32
595
Guidelines to Stages of Physical Therapy in the Open Heart Surgical Patient

Stage I
Patient may be seen in the postanesthesia and recovery room for a physical therapy assessment; the patient is usually
extubated within 24 hours after surgery. Although the patient must be permilled to rest as much as possible in the
initial 24-hour period, judicious body positioning is instituted to stimulate physiologic "stir-up." Usually once ex
tubated, the patient is positioned side to side for deep breathing and coughing at least four times in the first 24
hours and low-intensity mobilization is initiated. Medications are administered before lreatment to ensure optimal
effect during treatment. Depending on the findings of x-ray, physical examination, and arterial blood gases, the pa
tient may require vibrations and possibly percussion. Postural drainage positions are modi lied to avoid tipping the
patient head-down and causing increased myocardial strain. A sputum sample for culture and sensitivity testing
may be taken at this time. The patient can usually tolerate being dangled over the edge of the bed for a few min
utes. Special care is taken for all hem1 patients to avoid the Valsalva maneuver, forced coughing, and huffing and
,
to maintain a semirccumbent or upright position for treatment. Blood pressure is checked before, during, and after
treatment. Mobilization is progressed.
Stage 2
Deep breathing and coughing maneuvers coupled with mobilization are continued. Positioning for enhanced alveolar
ventilation and ventilation and pelfusion matching may be indicated. If secretion accumulation is a problem and
the patient too unstable to be optimally mobilized or positioned, postural drainage and possibly percussion and/or
vibration may be indicated. Upper limb and neck exercises are introduced. Neck exercises are withheld if central
venous pressure lines are still in place in the neck veins. The patient can sit in a chair at bedside as tolerated. The
patient is encouraged to stand erect for a minute or so on transferring back and forth to the chair.
Stage 3
The patient can take ShOl1 walks as tolerated. Ambulation is not begun until arterial lines and the Swan-Ganz catheter
have been capped or removed. Vital signs are monitored before and after standing and walking. Deep breathing
and coughing maneuvers are continued even if the chest is clear, until the patient is up and about within reasonable
limits as tolerated. The patient is encouraged in grooming and self-care.
Stage 4
Deep breathing and coughing should be done by the patient without supervision. The presence of atelectasis on x-ray
or from assessment findings. however, would indicate the need for continuation of mobilization and body position
ing with breathing exercises. Ambulation is increased as tolerated.
Stage 5
Palient can participate in individual or class activities, concentrating on trunk mobility, upper-extremity range of mo
tion, coordinated breathing activities, posture. biomechanics, and increasing the patient's endurance gradually.
Stage 6
The palient can attempt six to eight stairs if progress has been satisfactory and as indicated. Aortic repairs in the first
week or so are prone to rupture. Elevation of the blood pressure is therefore avoided to reduce the risk of break
down of the aortic suture line.
Stage 7
The patient depends primarily on ambulation for maintaining optimal alveolar ventilation and mucociliary transport
rather than brealhing and coughing exercises. The patient is cautioned to balance a period of exertion with a period
of rest. The pat ient may be discharged. The physical therapi st ensures the patient fully understands the specific de
tails of the home exe rci se progrdm. The emphasis of exercise for cardiac patients conlinues to be
-
011
rhythmic, co
ordinated dynamic movements on discharge, avoiding isomelric, static exercise. If possible, the patient is invited to
participate in a reconditioning and health promotion program as an oUlpatient in a physical therapy department.
NOTE: The physical therapist must guard againsl excessively intense treatmenl of open heart surgical palienLs or other patients who are on a
prophylactic course of anticoagulants.
596
PART VI
is in self-management, the greater the likelihood of
cate different practices, depending on their facilities,
receptivity and adherence to a rehabilitation regimen
experience of the surgical and ICU team, and the in
after discharge.
cidence of postoperative complications and survival

for that institution.
The physical therapist must guard against exces
PATIENT AFTER OPEN HEART SURGERY

sively intense treatment of open heart surgical pa

tients or other patients for whom periods of relatively
Patients scheduled for open heart surgery are treated
restricted mobility (4 to 5 days) are anticipated. Tn ad
as high-risk surgical candidates because of the nature
dition to the fact these patients may be hemodynami
and invasiveness of this type of surgery (Figure
cally unstable initially, these patients may be suscep
32-3), regardless of their general level of health be
t i b l e to s o f t t i s s u e bruising f r o m being on a
fore surgery (Trekova, Dementyeva, Dzemeshke
prophylactic course of anticoagulants.
vich, and Asmangulyan, 1994). Whenever possible,
Physical therapy follow-up should continue sev
patients prepare for surgery in advance by decreasing
eral months beyond discharge at which point the pa
or stopping smoking, by avoiding exposure to respi
tient should be well integrated into a cardiac rehabili
ratory tract infections, by avoiding stress, by eating a
tation program. Continuity and continuation of
balanced diet, and by getting adequate sleep. In addi
physical therapy throughout the entire rehabilitation
tion, patients can benefit from a modified, prescrip
period, from acute- to long-term, cannot be overem
tive exercise program before surgery to maximize
phasized given that achieving a maximal recovery
their aerobic capacity and thereby improve their peri
from surgery is the priority.
operative course.
In the preoperative period the physical therapist
may spend additional time with patients scheduled
SUMMARY
for open heart surgery to provide teaching of the
This chapter describes the principles of cardiopul
basic anatomy and physiology related to surgery to be
monary physical therapy in the management of criti
performed, the effect of anesthesia, the role of intuba
cally ill patients with primary cardiopulmonary dys
tion and mechanical ventilation, the incision lines to
function. Cardiopulmonary failure secondary to
be expected over the chest and the legs if veins are to
chronic lung disease and heart disease are described.
be removed for bypass surgery, the lines, leads, chest
Cardiopulmonary physical therapy management is
tubes, and catheters that will be in place after surgery,
based on the specific underlying pathophysiological
and the course of recovery the patient might expect
mechanisms of these various disorders. Tbese princi
barring complications (Chapter 26). The emphasis on
ples, however, cannot be interpreted to be guidelines
patient education in most open heart surgery units
for specific treatment in that each patient is an indi
may contribute to the generally low incidence of
vidual whose condition reflects mUltiple factors con
complications and mortality.
tributing to impaired cardiopulmonary function or
Some guidelines for physical therapy management
threatening it (i.e., the effects of restricted mobility,
of the open heart surgical patient appear in the box on
recumbency, extrinsic factors related to the patient's
p. 595. These guidelines are to be applied thought
care, and intrinsic factors related to the patient in ad
fully and cautiously with regard to each specific pa
dition to the underlying pathophysiology).
tient's condition and observed recovery. These guide

lines suggest the upper limit of intensity of physical
therapy if all is progressing well initially and sh0uld
REVIEW QUESTIONS
be reduced if warranted by the patient's condition.
1. With respect to critically ill patients with the fol
Progression from one stage to the next is based on an
lowing conditions, describe the pathophysiology
optimal and reliable treatment response at each level
of primary cardiopulmonary dysfunction, car
before proceeding. Different institutions may advo
diopulmonary failure, obstructive lung disease,
32
status asthmaticus, restrictive lung disease, and
Dean, E. (1994). Physiotherapy skills: Positioning and mobiliza

tion of the patient. In B.A. Webber
coronary artery disease.

2. Relate cardiopulmonary physical therapy treatment
597
& lA. Pryor. (Eds.). Pfly.l'
iotherapv for respiratory and cardiac problems. E dinburg h:

interventions to the underlying pathophysiology of
Dean, E., Murphy, S., Parrent, L., & Rousseau, M. (1995). Meta
each of the above conditions in the critically ill pa
bolic consequences of physical therapy in critically-ill p atients.
tient and provide the rationale for your choice.
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Intensive Care Unit Management

of Secondary Cardiopulmonary
Dysfunction
Elizabeth Dean
KEY TERMS
Burns
Musculoskeletal trauma
Head injury
Neuromuscular dysfunction
Morbid obesity
Spinal cord injury
INTRODUCTION
management are not mutually exclusive for each cat
This chapter describes the principles and practice of
egory. Rather, considerable overlap may exist when
cardiopulmonary physical therapy in the manage
conditions coexist. The principles presented are not
ment of secondary cardiopulmonary dysfunction that
treatment prescriptions. Each patient must be as
can lead to cardiopulmonary failure. Some common
sessed and treated individually taking into considera
categories of conditions described include neuro
tion the contribution of immobility, recumbency, ex
muscular disease, morbid obesity, musculoskeletal
trinsic factors related to the patient's care, and
trauma, head injury, spinal cord injury, and burns.
intrinsic factors related to the individual patient (see
Each category of condition is presented in two parts.
Chapter 16), in addition to the underlying pathophys
First, the related pathophysiology and pertinent as
iology. For examples of specific treatment prescrip
pects of the medical management of the condition
tions refer to the companion volume to this book en
are presented. Second, the principles of physical
titled Clinical case studies in cardiopulmonary
therapy management are discussed. Guidelines to
physical therapy.
599
600
PART VI
PATIENT WITH NEUROMUSCULAR DISEASE

mobility and recumbency, in addition to the patho

physiological consequences of respiratory failure.
GuiUain-Barre syndrome, myasthenia gravis, muscu
Provided the patient has some residual muscle
lar d y s t r o p h y , mUl tiple scl e r o s i s, s t r o k e , p o
power, the balance between oxygen demand and
liomyelitis, and neuromuscular poisonings are com
supply will determine the degree to which mobiliza
mon neuromuscular disorders that can precipitate
tion can be exploited to maximize oxygen transport.
respiratory failure in the absence of underlying pri
The treatment goals for these patients are to maxi
mary lung disease (Cooper, Trend, and Wiles, 1985;
mize oxygen delivery, enhance the efficiency of
Cu rran and Col b e rt , 1 9 8 9; Dean, Ross, Ro ad,
oxygen uptake and utilization, and thereby reduce
Courtenay, and Madill, 1991; Fug l-Me yer and
the work of breathing. In these patients, minimizing
Grimby, 1984; Griggs and Donohoe, 1982; Lane,
oxygen demand overall (i.e., during mobilization as
Hazleman, and Nichols, 1974). If paralyzed, the pa
well as at rest) is a priority. Mobilization needs to
tient will likely be dependent on ventilatory assis
be prescribed in body positions that enhance oxygen
tance. Cardiopulmonary physical therapy has a cen
transport and its efficiency so that the benefits of
tral role in minimizing the need for mechanical
mobilization can be exploited more fully without
ventilation in these patients because their prognosis
worsening arterial oxygenation (Dean, 1985). The
for weaning is poor. Progressive respiratory insuffi
patient requires continuous monitoring of oxygen
ciency is best addressed early with the institution of
transport and hemodynamic monitoring to ensure
nighttime ventilation at home (Curran, 1981) before
the exercise stimulus is optimally therapeutic and
the development of failure and necessity for hospi
not excessive.
talization. Patients with progressive neuromuscular
Although the mechanisms are different, patients
diseases (e.g., muscular dystrophy) are living longer;
with neuromuscular dysfunction can benefit from
thus cardiopulmonary insufficiency wil I be com
body positioning to reduce respiratory distress much
pounded by age-related changes of the cardiopul
like a patient with chronic airflow limitation (Barach,
monary system (Dean, 1994a; Leblanc, Ruff, and
1974). Upright and lean-forward positions will re
Milic-Emili, 1970).
duce distress to the greatest extent.
Neuromuscular conditions contribute to cardiopul
The patient's body position and length of time in
monary dysfunction in numerous ways (Chapters 21
any one position must be carefully monitored and
and 22). With progressive deterioration of inspiratory
recorded to minimize the risks of positions that are
and expiratory muscle strength and endurance, respi
deleterious to oxygenation and to ensure that a bene
ratory insufficiency and failure can ensue (Black and
ficial position is not assumed for too long because of
Hyatt, 1971). Depending on the specific pathology,
the diminishing benefits over time. This is particu
such deficits include reduced lung volumes and flow
larly important for the patient who is incapable of po
rates, reduced alveolar ventilation, increased airway
sitioning him or herself, who is incapable of commu
resistance, ventilation and perfusion mismatch, im
nicating a need to turn, and in whom muscle wasting,
paired mucociliary transport, mucous accumulation,
bony prominences, and thinning of the skin may pre
reduced cough and gag reflexes, relatively unpro
dispose the patient to skin breakdown.
tected airway secondary to impaired glottic closure
Patients who are hypotonic and generally weak
and weakness of the pharyngeal and laryngeal struc
and debilitated fail to adapt normally to position-de
tures, and increased work of breathing.
pendent fluid shifts and thus are Illore prone to ortho

static intolerance (Marini and Wheeler, 1989). Gravi

A patient with restrictive pulmonary disease sec
tational stimulation is essential to maintain the

volume regulating mechanisms. Tilt tables should be
used judiciously given the potential risks in these pa
ondary to neuromuscular conditions is at consider
tients, which is compounded by the loss of the lower
able risk of succumbing to the negative cardiopul
extremity muscle pump mechanislll. Because of po
monary and cardiovascular sequelae of reduced
tential adverse reactions to fluid shifts and the
33
Intensive Care Unit Management of Secondary Cardiopulmonary Dysfunction
601
potential for desaturation. falling Pao2 levels and dys
sential that these attempts are maximized (i.e., the
rhythmias. the patient's hemodynamic status must be
patient optimally rested and medicated le.g., bron
monitored closely during gravitational challenges.
chodilators, analgesia, reduced sedation and nar
The importance of chest waH mobility to optimize
cotics] is physically positioned to optimize length
three-dimensional chest wall excursion in chronic
tension relationship of the diaphragm and abdominal
neurological patients is emphasized in Chapters 2 I
muscles, positioned vertically to optimize inspiratory
and 22. This goal is particularly challenging in the
lung volumes. and expiratory flows and avoid of as
neurological patient with acute respiratory insuffi
piration, and is provided thoracic and abdominal
ciency. The goal is to promote alveolar ventilation,
support during expiration to maximize intrathoracic
reduce areas of atelectasis. and optimize ventilation
and intraabdominal pressures) (see Chapter 21).
and perfusion matching and breathing efficiency to
These supportive measures will ensure that the bene
augment and minimize reliance on respiratory sup
fits of the normal physiological cough mechanism,
port (i.e., supplemental oxygen and mechanical venti
which is the single best secretion clearance tech
lation) while minimizing respiratory distress. This is
nique, is maximized (i.e., the most productive cough
especially important because patients with neuromus
with the least energy expenditure) (Bennett, Foster,
cular conditions are poor candidates for being
and Chapman, 1990; Hasani et aI., 1991; Kirilloff,
weaned off mechanical ventilation (Petty, 1982). In
Owens, Rogers, and Mazzocco. 1985; Zinman,
addition these patient are prone to microaspirations.
1984). Forced chest wall compression or forced ex
Promotion of mucociliary transport is therefore es
piratory maneuvers are contraindicated (Nunn, Cole
sential to facilitate clearing of aspirate and minimize
man, Sachithanandan, Bergman, and Laws, 1965).

Impaired mobility, inability to cough effectively,
bacterial colonization and risk of infection.

Another major problem for patients with restric
decreased airway diameter, and bronchospasm con
tive lung disease secondary to generalized weakness
tribute to impaired mucociliary transport and secre
and neuromuscular disease is an ineffective cough.
tion accumulation. In addition, impaired glottic clo
Cough facilitation techniques (e.g., body positioning,
sure and increased risk of reflux in this patient
abdominal counter pressure, and tracheal tickle can
population exposes the airway to risk of aspiration.
be used to increase intraabdominal and intrathoracic
Prophylactically, multiple body positions and fre
pressures and cough effectiveness. A natural cough,
quent position changes will minimize the risk of se
even when facilitated, is preferable and more effec
cretion accumulation and stasis. If mechanically
tive in dislodging mucus from the sixth or seventh
ventilated. these patients are suctioned as indicated.
generation of bronchi than repeated suctioning. Even
If pulmonary secretions become a significant prob
a weak, facilitated cough may be effective in dis
lem despite these preventative measures, postural
lodging secretions to the central airways for removal
drainage positions are selected to achieve the opti
by suctioning or for redistributing peripheral secre
mal effect (i.e., secretion mobilization and optimal
tions (Hasani, Pavia, Agnew. and Clarke, 1991).
gas exchange). Given the treatment response. man
Huffing, a modified cough peJformed with the glottis
ual techniques of which manual vibration would
open and with abdominal support. may help to mobi
have the greatest physiological justification, may
Jize secretions in patients with generalized weakness
yield some benefit.
(Hietpas, Roth, and Jensen. 1979). In some cases,
Patients with chronic neuromuscular dysfunction
suctioning may be the only means of eliciting a
and residual musculoskeletal deformity pose an ad
cough and clearing secretions simultaneously.
ditional challenge to the cardiopulmonary physical
Coughing attempts are usually exhausting for these
therapist in that cardiopulmonary function is less
patients. Thus ample rest periods must be inter
predictable because of altered lung mechanics
spersed during treatment, particularly for the venti
(Bake, Dempsey, and Grimby, 1976) and possibly
lated patient. Coughing maneuvers need to be strate
cardiac dynamics. Thus clinical decision making is
gically planned. Even though the patient may be
more experiential in these patients who require
only to effect a series of a few weak coughs, it is es
close monitoring.
602
PART Vl
OBESITY
The obese patient can be treated aggressively pro
Restriction of cardiopulmonary function secondary to
vided there are no contraindications and he or she is
morbid obesity is called the alveolar hypovenlilalion
being fully monitored. Treatments need to be intense,
syndrome or Pickwickian syndrome. In this syndrome
to the limits of the patient's tolerance, provided this
the weight of excess adipose tissue over the thoracic
is not contraindicated. An aggressive approach is es
cage and abdominal cavity restricts chest wall move
sential given that the obese patient is at greater risk of
ment and movement of the diaphragm and abdominal
deteriorati ng between treatments than a nonobese
contents, respectively, during respiration. In very
counterpart. Recumbency is tolerated poorly by an
heavy individuals, cardiopulmonary function can be
obese patient. Positional decrements in Pa02 and
significantly impaired, resulting in hypoxemia and
Sa02 can induce dysrhythmias. The weight of the ab
cardiopulmonary failure. The major pathophysiologi
dominal viscera limit diaphragmatic descent and ele
cal mechanisms include significant alveolar hypoven
vate the resting position of the diaphragm, impeding
tilation, reactive hypoxic pulmonary vasoconstriction,
its mechanical efficiency.
increased pulmonary vascular resistance, myocardial
These patients need to be aggressively mobilized;
hypertrophy, increased right ventricular work, altered
both whole body exercise stress and range of motion
position of the thoracic structures, abnormal compres
exercises between mobilization sessions. Active and ac
sion of the heart, lungs, and mediastinal structures, ab
tive assisted upper-extremity range-of-motion exercises
normal position of the heart, cardiomegaly, increased
are associated with increased hemodynamic stress; thus
intraabdominal pressure, elevated hemidiaphragms
the patient must be monitored closely. Lower-extremity
with resulting pressure on the underside of the di
exercise, such as pedaling and hip and knee flexion and
aphragm, impaired cough effectiveness, impaired mu
extension exercises, may help position and improve the
cociliary transport, mucous obstruction of airways,
excursion of the diaphragm. Lower-extremity move
airway narrowing, bronchospasm, impaired mechani
ment will augment venous return. Depending on the pa
cal efficiency of diaphragmatic excursion, and im
tient and the work of the heal1, the effect of lower-ex
paired respiratory mechanics and breathing efficiency
tremity movement will need monitoring to ensure that
(Bates, 1989). In addition, such patients are likely to
myocardial work is not increased excessively.
have poor cardiopulmonary reserve capacity sec
The erect upright position is optimal to augment
ondary to increased metabolical rate and minute venti
ventilation and reduce the work of the mechanical
lation at submaximal work rates, increased metabolic
ventilator and the risk of barotrauma. The upright po
cost of breathi ng, and increased work of breathing.
sition, coupled with leaning forward, displaces the
Moderately heavy patients whose pulmonary function
abdominal contents forward, thereby reducing in
is normally not compromised may exhibit cardiopul
traabdominal pressure and facilitating diaphragmatic
monary dysfunction when their oxygen transport sys
descent. The posterior lung fields, particularly of the
tems are stressed because of illness.
bases, are at risk for dynamic airway closure and at
Mechanical ventilation can be a challenge in that
electasis. Numerous positions and position changes
the system pressure required to inflate the lungs may
ensure that the dependent alveoli remain open. The
predispose the patient to barotrauma. Furthermore,
time spent in the supif!e position should be mini
high system pressures contribute to reduced stroke
mized. In fact, greater emphasis should be placed on
volume and cardiac output. Adequate circulation is
nursing these patients in the upright position (i.e., the
essential to fulfill the goals of medical management
position of least risk and its variants). In addition to
(i.e., to optimize tissue oxygenation and carbon diox
its pulmonary benefits, the upright position can re
ide removal). Thus a delicate balance between ade
duce compression of the heart and mediastinal struc
quate alveolar ventilation, cardiac output, and periph
tures and there is a potential decrease in stroke vol
eral circulation is maintained.
ume and cardiac output. The weight of the chest wall,
33
Intensiye Care Unit Management of Secondary Cardiopulmonary Dysfunction
in addition to the weight of internal fat deposits in
603
are taught comparable with those described for the
and around the cardiopulmonary unit, can compro
patient with neuromuscular disease. Body positioning
mise cardiac output and contribute to dysrhythmias.
to facilitate coughing and supported coughing need to
Thus during all body position changes the patient
be instituted to maximize cough effectiveness. These
should be monitored hemodynamically to ensure the
maneuvers should be carried out in conjunction with
position is being tolerated well. Obese patients often
hourly extreme position shifts.
slump after being positioned in the upright position.
Morbidly obese patients have a high incidence of
It is crucial that the position of these patients is
upper airway obstruction and sleep apnea secondary
checked frequently and corrected. The slumped posi
to floppy compliant pharyngeal tissue. Thus the qual
tion can be counterproductive in that the benefits of
ity of their sleep and rest is suboptimal, and they are
the upright position are significantly reduced and can
apt to desaturate significantly while sleeping. These
lead to deterioration.
patients are also at high risk for esophageal reflux
Although obese patients do not tolerate the prone

position well, the semi-prone position can be benefi
and aspiration. The optimal resting position is with

the head of bed up.
cial by simulating the benefits of the upright lean-for

ward position on the displacement of the abdominal
viscera (Ross and Dean,
1992). This position also
PATIENT WITH MUSCULOSKELETAL TRAUMA

simulates the prone abdomen-free position, which is

associated with even greater benefit than the prone
abdomen-restricted position (Dean,
1985). The bene
fits of the prone position for the obese individual in
Crush and penetrating injuries of the chest are com

monly seen in the ICU (Moylan,
1988). Damage to
the chest wall, lung parenchyma, and heart contribute
clude increased lung compliance and enhanced gas
to the risk of cardiopulmonary failure (see box on
exchange and oxygenation. The full prone abdomen
p.
restricted position is contraindicated in the obese in
and abdomen may also contribute. Fractures of long
dividual with cardiopulmonary failure, however, be
bones and pelvis are associated with fat emboli,
cause this position can compromise diaphragmatic
which pose the threat of pulmonary embolism. In ad
604). Associated injuries of the head, spinal cord,
descent and contribute to further cardiopulmonary
dition, fluid loss in multiple trauma contributes to
distress and failure and possibly cardiac arrest.
loss of blood volume, hypovolemia, and hcmody
Mucociliary transport is slowed and ineffective in
namic instability. The more extensive the injuries, the
obese patients with cardiopulmonary failure. Fre
greater the pain and need for analgesia. Pain con
quent body positioning will facilitate mucociliary
tributes significantly to reduced alveolar ventilation,
transport and lymphatic drainage. The postural
airway closure, and inefficient breathing patterns.
drainage positions can be effective in mobilizing se
Paradoxical motion of the chest wall associated
cretions should accumulation become a problem.
with flail chest and rib fractures results from instabil
Manual techniques are not likely to add much benefit
ity of portions of the rib cage after trauma to the
particularly in the morbidly obese patient. Suctioning
chest. If severe, patients may require surgical stabi
is essential to clear pulmonary secretions from the
lization of the ribs or stabilization by continuous ven

tilatory management. Chest wall injuries and rib frac
central airways.
The obese individual is at risk for postextubation
tures are particularly painful.
atelectasis. Thus aggressive mobilization and numer
The presence of blood or air in the chest cavity
ous positions and frequent position changes need to
and in the potential spaces of the pericardiai sac and
be continued.
intrapleural cavity impairs cardiac distension and
The spontaneously breathing obese patient has a
contraction, impairs venti lation, promotes retention
weak ineffective cough, which will be even less ef
of secretions, interferes with effective clearance, and
fective after a period of intubation and mechanical
impairs lymphatic drainage (Marini and Wheeler,
ventilation. Deep breathing and coughing maneuvers
1989). Resolution of effusions can be facilitated with
604
PART VI
sion. A tension pneumothorax results when air col
Factors COlltributillg to Cardiopulmonary

Failure After Trauma and Their Diagnostic Signs
lects under tension in the pleural cavity. The tension

pneumothorax promotes lung collapse on both the ip
silateral and contralateral sides, which furlher threat
Airway Obstruction
ens respiratory failure. Phrenic nerve injuries inhibit
Respiratory insufficiency
diaphragmatic function (Dureuil, Viires, and Canti
Respiratory distress
neau, 1986). The position of the affected hemidi
Impaired blood gases
aphragm rests higher in the thoracic cavity, which

may restrict ventilation to the lung base and con
Inadequate Ventilation
tribute to airway closure and basal atelectasis. Di
Reduced thoracic movement
aphragmatic injuries directly affect ventilation in two
Paradoxical thoracoabdominal movement
ways. First, the bellows action of the lungs is com
Tension Pneumothorax
promised. Second, the lung is displaced by herniation
Cyanosis
of the abdominal contents into the thoracic cavity.

Analysis of blood gases in the patient with post
Unilaterally absent breath sounds
traumatic injuries of the chest often shows severe hy
Distended neck veins
poxemia and moderate elevations of arterial PC02.
Subcutaneous emphysema
The presence of acidemia is common, which may
Cardiac Tamponade
have both respiratory and metabolical components.
Distended neck veins

Muffled heart sounds
Narrowed pulse pressure
Severe restlessness and dysp nea in a patient with
Paradoxical pulse
chest injury are classic indications of respiratory fail
Open Pneumothorax
ure. Auscultation and percussion can usually reveal
Decreased breath sounds
an underlying pneumothorax or hemothorax. Tension
Penetration of thoracic wall
pneumothorax is confirmed by chest x-ray or aspira

tion of the chest with a needle and syringe.
Myocardial Contusion
Flail chest refers to fractures involving the chest
Dysrhythmia
cage where there are two or more fractured ribs at
Flail Chest
two or more sites. This results in instability of the
Loose segment
chest wall. The so-called flail segment is usually ap

parent on physical examination. Paradoxical move
Multiple palpable fractured ribs
ment of the flail segment can often be observed. The
Decreased or moist breath sounds
chest is depressed rather than elevated over the site
Modified from Moylan, J. A. (Ed.). (1988). Trauma surgery.

Philadelphia: .IB LippincOl1.
during inspiration. Rib fractures are indicated by ten

derness and crepitations on physical examination and
from x-ray findings. Nonventilatory management of
chest injuries in the absence of severe hypoxemia is
preferred in these patients.
mobilization and body positioning. These interven

tions reexpand underlying atelectasis and help restore
fluid balance by their effects on lymphatic drainage.
Rib Fractures
Furthermore, by shifting the effusion fluid, atelectatic
Simple uncomplicated rib fractures often receive no
areas can reexpand. The presence of a pneumothorax
specific treatment. Pain from complicated fractures
or hemothorax can severely compromise lung expan
may be treated with intercostal nerve blocks and tran
33
scutaneous electrical nerve stimulation and analgesia.
605
ventilator. Small leaks can be tolerated and are usu
Optimizing alveolar ventilation and mucociliary trans
ally compensated for by a n increase in tidal or
port and avoiding pulmonary complications are pri
minute ventilation.
mary goals. Strapping the chest is avoided because this

further restricts and compromises chest wall expansion.
The CUITent method of therapy for flail chest is in
ternal stabilization of the chest and use of a mechani
Multiple Trauma
The management of multiple trauma is a major chal
cal ventilator. Slight hyperventilation will usually re
lenge for the rcu team. Multisystem involvement
duce the respiratory drive of most patients to allow
and complications often present a precarious situation
the ventilator to take over the full work of breathing.
in which priorities have to be defined for each indi
The flail segment is then stabilized by internal expan
vidual situation. Multiple trauma can include head in
sion of the lungs. The treatment ensures adequate
jury, chest wall injuries, fractures, lung contusions,
ventilation with the least pain possible. After 2
diaphragm injury, pleural space disorders, internal in
weeks, the flail segment is usually stable.
juries, thromboemboli, fat emboli, and cardiac contu
When the patient can maintain a reasonable tidal
sions. Shock and adult respiratory distress syndrome
volume and normal blood gases, weaning is begun.
may ensue (see Chapter 34). The clinical picture of
As soon as tidal volume and forced vital capacity are
the patient with mulliple trauma is compounded by
within acceptable limits, oxygen can be administered
the mobilization and positioning restrictions imposed
through an endotracheal tube with a T tube assembly.
(Ray et aI., 1974). Positive end-expiratory pressure
Arterial blood gases are monitored closely after the
(PEEP) is frequently used to reduce the effects of
ventilator has been discontinued. Once the blood
lung congestion secondary to shock or adult respira
gases are in acceptable ranges over a reasonable pe
tory distress syndrome (ARDS) (McAslan and Cow
riod of time (i.e., 12 to 24 hours) the endotracheal
ley, 1979). Arterial blood gases are assessed to evalu
tube is removed.
ate the effectiveness of PEEP in effecting improved

oxygen transfer.
Pneumothorax and Hemothorax

Air or blood in the pleural cavity after chest trauma
Multiple Fractures
must be removed through a chest tube. For a pneu
Multiple trauma patients are assumed to have spinal
mothorax the chest tube is positioned in the second or
involvement, particularly of the cervical spine, until
third intercostal space in the midclavicular line. For a
ruled out with appropriate scans and x-rays. Mean
hemothorax the chcsl tube is positioned in the sixth
while the physical therapist performs repeated assess
intercostal space in the posterior axillary line. Usually
ments to establish a baseline and recommend posi
the chest tubes are sutured and taped into position and
tions for the patient that will ma ximize oxygen
therefore are not easily dislodged. If the tubes are
transport. Treatment to enhance oxygen transport and
pulled out, subcutaneous emphyscma or a pneumotho
mucociliary lransport is primarily restricted to body
rax results. A pneumothorax will also result if the tube
positioning using log rolling maneuvers and a se
is disconnected from the underwater seal. This is the
lected range of motion exercises (i.e., not of the head
reason for securing the collecting reservoirs of a chest
and neck, and possibly shoulders).
tube drainage system with tape to the floor. Mobiliz
Fixation, traction. and casting of fractures and dis
ing and frequency repositioning the patient facilitates
locations of the limbs complicate the management of
chest tube drainage and reexpansion of collapsed alve
the trauma patient. Restrictions to mobilization and
oli. Care is taken to avoid kinking or straining chest
body positioning arc primary concerns of the physical
tubes during patient treatment.
therapist (Mackenzic, 1989). Mobilization in the up
A bronchopulmonary fistula can be responsible
right position provides both a gravitational stimulus
for a major loss of the tidal volume delivered by the
and an exercisc stimulus, both of which are essential
606
PART VI
to optimize oxygen transport. This is preferable to
the trauma patient to reduce excessive oxygen con
mobilization exercises in the recumbent position. In
sumption and promote comfort (Malamed, 1989).
some cases, traction can be transferred from over the
Active relaxation refers to relaxing the patient
end of the bed to over a chair. A strict routine of body
through participation of the patient in relaxation pro
positioning is maintained, although severe limitations
cedures. Passive relaxation refers to relaxing the pa
often exist with respect to the specific positions and
tient using passive procedures (e.g., body positioning,
the degree of turning permitted. Lower limb traction
physical supports, talking slowly and calmly, and tak
can be maintained when the patient is positioned in a
ing adequate time for conducting treatments). Taking
modified sidelying position. Coordinating treatments
time to implement mobilization is essential. First,
with analgesia schedules reduces the patient's pain
mechanically moving and having patients who have
and fatigue, thereby improving tolerance to and pro
mUltiple injuries move requires a prolonged period of
longing the treatment. These patients usually tolerate
time. In addition, however, the cardiovascular and
the head-down position well provided head injury
cardiopulmonary systems of critically ill need time to
does not complicate the clinical picture.
adapt to new positions physiologically and to control
The acute effects of mobilization that will benefit
concommitant discomfort. Prolonged periods of time
the patient with musculoskeletal trauma include aug
may be required to turn a patient, dangle him or her
mentation of ventilation, perfusion, ventilation and
over the bed, or transfer him or her to chair with con
perfusion matching, and promotion of mucociliary
tinuous monitoring. Every effort is made to maintain
transport and cough effectiveness. General mobiliza
the patient's spirits, reduce stress, and encourage a
tion exercises and propriocepti ve neuromuscular fa
positive attitude toward active participation early in
cilitation (PNF) can be used to promote a mobiliza
the rehabilitation program that begins in the ICU.
tion stimulus. Cycle pedals can be attached to a chair
Care must be taken to avoid undertreating or
or the end of the bed to provide a low-intensity exer
overtreating trauma patients. A clear chest can
cise challenge for some patients. Maximal work out
rapidly regress because of general immobility and
put can be achieved within the patient's capacity
limitations to body positioning imposed by traction
using an interval training type schedule (i.e., schedule
and pain. Treatments should always be coordinated
of work to rest periods). A mobilization program that
with the patient's analgesics to optimize treatment re
promotes the long-term effects of exercise can be pre
sponse and for the patient's comfort. Whenever pos
scribed that involves as many large muscle groups as
sible, the patient should be equipped with slings and
possible in rhythmic, dynamic exercise.
pulleys and weights at bedside and a monkey bar
Frequent deep breathing and coughing is continued
overhead for bed mobility and upper-extremity exer
during and between treatments, depending on whether
cise. In addition to their cardiopulmonary benefits,
the patient requires mechanical ventilation. Body posi
PNF patterns are useful in preparation for slings and
tioning is carried out within the limits of the patient's
pulleys. The use of PNF patterns for trauma and post
traction and casts. Impaired mucocil iary transport is
operative patients can be well tolerated by these pa
treated with body positioning and frequent position
tients. All activities are taught in conjunction with
changes. Secretion accumulation may require postural
breathing control exercises and coordination with the
drainage. Modified positions may be indicated because
respiratory cycle.
of the positioning restrictions imposed by the fractures,

traction, and fixation devices. If indicated manual tech
n i q u e s may be c o u p l e d with postu ral drainage
(Mackenzie, Shin, Hadi, and Ilnle, 1980). Care must
PATIENT WITH HEAD INJURY

be taken to ensure the addition of manual techniques is
Hypoxemia is observed in many patients with injury
beneficial and is tolerated by the patient.
to the central nervous system (Demling, 1980). This
Relaxation interventions, both active and passive,
may reflect primary damage to the cardiopulmonary
should be integrated into the treatment regimen for
centers of the brain or secondary effects of associated
33
trauma. Arterial blood gases are therefore closely

monitored in these patients.
Acute cerebral edema with sudden increase in in
tracranial pressure (ICP) and reduction in cerebral
pelfusion pressure, rapidly affects central control of
respiration (Borozny, 1987). Advancing cerebral
edema is evidenced by deterioration in level of con
sciousness, pupillary reflexes, ocular reflexes, pattern
of respiration, and exaggerated muscle tone and pos
ture. The sequence of these clinical signs corresponds
to progressively increasing ICP from the cortex to
ward the medullopontine region. With involvement of
the brain stem, respiration becomes variable and inco
ordinate. With loss of central control and imminent
cessation of breathing, respiration is shallow and
ataxic. The appearance of the jaw and laryngeal jerk
with each inspiratory effort suggests a poor prognosis.
Physical therapy and the patient's normal routine
may have a dramatic effect on the ICP. ICP can be el
evated indirectly by an increase in intrathoracic pres
sure as a result of physical therapy or suctioning.
Turning and positioning may produce obstruction to
cerebral venous outflow. Noxious stimuli, such as ar
terial and venous punctures or cleansing wounds, can
elevate ICP and relatively innocuous stimuli, such as
noise or pupil checks. Wbether these factors elevate
607
ICP depend on cerebral blood volume and intracranial

compliance. On cerebral stimulation, a chain reaction
is initiated. Cerebral activity is increased, which in
turn elevates metabolical rate, blood flow, and hence
volume and ICP. Alternatively, increased cerebral
blood volume secondary to gravitational effects, in
creased ICP, and reduced cerebral perfusion pressure.
The head of the bed is usually maintained between
30 and 40 degrees to promote venous drainage and
thereby reduce ICP. The patient's head and neck can be
fixed in a neutral position by halo traction or by sand
bags positioned on either side (Figure 33-1). Mechani
cal hyperventilation is used to maintain PC02 below
normal limits but above 20 mm Hg. Arterial blood
gases are checked during or immediately after hyper
ventilation. Prolonged hyperventilation is avoided.
Barbiturate coma may be induced to decrease the
cerebral metabolical rate for oxygen and hence cere
bral blood flow. The reduction in cerebral metaboli
cal rate exceeds the reduction in blood flow and thus
oxygen supply exceeds demand, which is a desirable
treatment outcome. Invasive hemodynamic monitor
ing is instituted in conjunction with barbiturate
coma because barbiturates contribute to hemody
namic instability.
A complication of head injuries is acute lung in
' ......... IIIft,-
--
.
' .
. . .
FIGURE 33-1
Patient following neurosurgical procedure; head of bed elevated 20 degrees to help reduce ICP.
608
PART VI
jury, specifically, neurogenic pulmonary edema (see
may be acceptable provided the pressure returns to
Chapter 34). Antonomical nervous system dysfunc
normal immediately after the removal of the pres
tion contributes to hypertension and neurogenic pul
sure-potentiating stimulus. Prolonged elevation of
monary edema. The endothelial tight junctions in the
ICP suggests low cerebral compliance and the possi
pulmonary capillaries leak protein into the intersti
bility of potential brain damage unless pressure is re
tium along with fluid. Constriction of the lymphatic
duced. Thus all interventions must be performed
vessels may also contribute to fluid accumulation by
guardedly with due consideration being given to cor
impeding the removal of lung water. Increased fluid
responding changes in ICP. Typically, management
accumulation in the interstitium may progress to the
of patients with central nervous system trauma in
alveoli contributing further to impaired gas exchange
cludes judicious tracheal suctioning, a stringent turn
and reduced lung compliance.
ing regimen, lung hyperinflation with the manual

breathing bag in the nonventilated patient, or deep
breathing with occasionally increased tidal volumes

or sighs in the ventilated patients.
Physical therapy priorities in the management of the
If the ICP is unstable and a risk of brain damage
patient with cardiopulmonary dysfunction secondary
exists, physical therapy should follow sedation. Ide
to head injury appear in the box below.
ally, treatments should be peIformed when the ICP is
In cases of abnormally elevated ICP, mechanical
low and intracranial compliance is satisfactory. The
hyperventilation and maintenance of Pe02 around 25
head-down position is contraindicated. Noise and
mm Hg are effective measures to reduce cerebral
noxious stimulation that increases rcp should be kept
edema by reducing blood flow. Intracranial pressure
to a minimum.
may increase with treatment and in particular with
If the ICP is elevated, all noxious stimuli should
turning or suctioning. An ICP of up to 30 mm Hg
be removed. In severe conditions a decision may
Physical Therapy Priorities in the Management of the Patient with

Cardiopulmonary Dysfunction Secondary to Head Injury
I. Prevention of cerebral hypoxia by maintaining a patent airway

2. Reduction of intracranial pressure and optimal cerebml perfusion pressure
3. Position the patient within the limits of fracture stabilization and elevated intracranial pressure to promote alveo
lar ventilation and ventilation and pert'usion matching
4. Position the patient to reduce pathological patterns of muscle synergy and thereby promote ventilation and re
duce oxygen consumption
5. Position the patient to reduce myocard ial stress

6. Avoid a ctivities and stimuli that increase ICP
7. Reduce atelectasis
8. Shift lung fluid accumulations and areas of atelectasis
9. Promote lymphatic dr ainage
10. Promote m ucocil i ary transport and reduce pooling of secretions. and risk of chest infection
II. Reduce the work of breathing and improve the efficiency of the muscles of respiration, particularl y if long-term
disability is a risk
12. Perform active, active-assisted, or passive movements as soon as possible to enhance cardiopulmonary function
and secondarily to preserve musculoskeletal and neuromuscular function and reduce the risk of thromboemboli
33
609
have to be made by the team to limit or withdraw in
sions, is cardiopulmonary complications. Lung vol
terventions that lead to an excessive ICP increase that
umes are reduced with the exception of residual vol
does not remit instantly (e.g., physical therapy, posi
ume that increases. Interestingly, vital capacity in
tioning, suctioning, or neurologic assessment).
creases in the supine compared with the sitting
Movement of the limbs is performed gently and in a
position in quadriplegic patients. However, this does
relaxed manner. Patients in a comatose state may expe
not counter the negative effects of reduced functional
rience passive limb movement noxiously. Intracranial
residual capacity (FRC) and increased airway closure
pressure may be elevated as a result. Passive move
in this position and reduced flow rates.
ments, however, may have the added benefit of pro
Spinal cord injuries above C3 result in loss of
moting improved tidal ventilation in the nonventilated
phrenic nerve i n n e r vati on, necessitating a t ra
patient by providing afferent stimulation to the respira
cheostomy and mechanical ventilation. The lower the
tory center via peripheral muscle and joint receptors.
level of the spinal cord lesion, the lower the car
Severe head injury may produce flexor or extensor
diopulmonary risk. All patients with spinal cord in
posturing. These synergies may be inhibited by ap
juries are at risk for developing atelectasis and pneu
propriately positioning the patient. Judicious body
monia. The coughing mechanics of quadriplegic
positioning, in turn, reduces oxygen consumption and
patients are abnormal and contribute to ineffective air
the patient's overall energy requirements.
way clearance (Estenne and Gorino, 1992). In addi
Neurophysiological facilitation of respiration has
tion the quadriplegic patient is at risk for developing
been proposed as a treatment intervention to improve
pulmonary emboli. Prophylactic low-dose heparin is
ventilation, coughing, and breathing pattern in the un
used routinely unless the presence of pulmonary em
conscious patient (Bethune, 1975). Neurophysiologi
boli is suspected and higher dosages are indicated.
cal facilitation techniques include cocontraction of
Patients with suspected spinal cord injuries usually
the abdominal muscles, vertebral pressure, intercostal
undergo immediate spinal fixation on admission. De
stretch, lifting the posterior basal areas of the lungs,
pending on the level of injury detennined by clinical
and perioral stimulation. Although these techniques
signs and x-rays, traction, and fixation may be local
are believed to stimulate reflex involuntary respira
ized to the head and neck or spinal support and cast
tory movements, there is no evidence to support their
ing may be required in the thoracic or lumbar regions.
efficacy in the management of the unconscious pa

tient. Comparable with conventional chest physical
therapy procedures, reported benefits associated with
neurofacilitation cannot be discriminated from the
Because of the need to maintain relative immobility
potent and direct physiological effects of increased
in the acute stabilization period of suspected spinal
arousal, body positioning, and mobilization on oxy
cord injury, therapeutic body positioning rather than
gen transport (Dean, 1994b). These latter effects have
mobilization is a primary intervention for optimizing
been well documented.
oxygen transport. Although modified body position
Although arousing the patient and increasing oxy
ing can be achieved, the provision of optimal care
gen consumption occurs with cardiopulmonary physi
under these restricted conditions is a singularly im
cal therapy, arousal and oxygen consumption are
pOl'tant challenge to the physical therapist, particu
generally minimized to reduce hemodynamic and
larly with respect to the management of adequate
metabolical demands in head-injured patients.
oxygen transport while the patient is in the ICU. Pa

tients with high spinal cord lesions can be positioned
in all positions within the limits of the cervical trac
PATIENT WITH SPINAL CORD INJURY
tion device being used, barring head injury. Both
head and foot-tipped positions, however, are intro
The principal cause of death in the early stages of
duced cautiously and with hemodynamic monitoring
acute spinal cord injury, particularly for the high le
because both positions can have significant car
610
PART VI
diopulmonary and hemodynamic consequences sec
respiratory muscles. In some centers, patients are
ondary to spinal nerve loss and hence sympathetic
started in the weaning period on respiratory muscle
nerve loss to the peripheral blood vessels. Turning
training. The physical therapist must be well versed
frames such as the Stryker frame facilitate turning
and practiced in this procedure before using it in con
and tipping these hemodynamically labile patients in
junction with weaning the quadriplegic patient off the
the supine and prone positions (Douglas, Rehder,
ventilator. Because of the potential risk of inappropri
Beynen, Sessler, and Marsh, 1977).
ate application and of danger to the patient, respira
Effective body positioning, despite the need in

some cases for extensive modification, may be suffi
tory muscle training must be effected knowledgeably

to optimize its benefits for each individual patient.
cient to optimize oxygen transport secondary to im

proved regional ventilation and perfusion to all lung
fields. In the spontaneously breathing patient, deep
Respiratory Muscle Training
breathing and coughing maneuvers need to be cou
Respiratory muscle weakness and fatigue, two physio
pled with position changes to optimize mucociliary
logically distinct entities, are probably much more
transport (Alverez, Peterson, and Lunsford, 1981;
common in the ICU than appreciated. These states
Braun, Giovannoni, and O'Connor, 1984). Some pa
need to be recognized and detected early because both
tients may not tolerate numerous positions and posi
can cause respiratory muscle failure (Macklem and
tion changes and thus have impaired mucociliary
Roussos, 1977). The distinction between the two con
transport. If secretion accumulation and stasis de
ditions is that weakened muscles respond to resistive
velop, postural drainage can be instituted; however,
muscle training, whereas fatigued muscles do not. Ex
tipping must be attempted very cautiously. Patients
posing fatigued respiratory muscles to resistive loads
should be monitored closely during and after treat
can accentuate respiratory failure. The indication for
ment. Because of their well-documented side effects
respiratory muscle training, therefore, is weak rather
(Kirilloff et aI., 1985) and the hemodynamic lability
than fatigued respiratory muscles. Rest is indicated for
of acute quadriplegic patients, percussion and vibra
fatigued respiratory muscles. Whether the respiratory
tion are applied cautiously, should they be indicated,
muscles are weak or fatigued must be established be
depending on the severity of any complicating frac
fore prescribing respiratory muscle training.
ture-dislocation(s), the stability of fixation, the condi
The combination of immobilization and cardiopul
tion of the lungs, the presence of chest wall injuries,
monary involvement secondary to multiple trauma
and hemodynamic lability.
may result in similar disuse atrophy and weakness of
The high-frequency oscillating ventilator may
the diaphragm as observed in other skeletal muscles.
have some benefit in the management of mUltiple
Respiratory muscle weakness and fatigue can be a
trauma patients with spinal injuries who require ven
component of both obstructive and restrictive pat
tilation. The advantages of the high-frequency oscil
terns of lung disease. Patients with spinal cord in
lating ventilator include improved spontaneous mu
juries do not have the same advantage of performing
c o c i l i a r y clearance and r e d u c e d i n c i d e n c e of
coordinated general body activity and relaxation ma
atelectasis (Gross and King, 1984). Weaning quadri
neuvers to help reduce the work of breathing. This
plegic patients off the ventilator requires special skill
contributes to a marked decrease in respiratory mus
because of the lost function of the respiratory mus
cle strength and endurance resulting in reduced vital
cles. For these patients, weaning can be particularly
capacity, rib cage mobility, and the ability to cough.
fatiguing, frightening, and frustrating. Patients are
For these reasons, patients with paralysis and demon
weaned lying supine when they are alert and able to
strated respiratory muscle weakness are particularly
cooperate. Short periods off the ventilator on the T
well suited for respiratory muscle training. The quad
piece are used initially. Use of the accessory muscles
riplegic patient has lost the function of the intercostal
of respiration and any other muscular reserves are en
muscles which are important muscles of inspiration
couraged to compensate for the loss of function of the
and are responsible for thoracic cage expansion. In
33
611
addition, the absence of the abdominal muscles,
fatiguing factors as eating a meal, talking, exposure to
which are the primary expiratory muscles, drastically
heat and humidity, sitting upright, overcoming a respi
reduces the ability to cough effectively and to per
ratory tract infection, and so on.
form a forced expiration. The diaphragm and the ac
A candidate for respiratory muscle training is
cessory muscles of inspiration, namely the scaleni
equipped with an individual resistive breathing pack
and sternocleidomastoid muscles, then become the
age containing the valve, mouthpiece, noseclip, flow
quadriplegic patient's respiratory muscles.
regulator, and a series of resistors that attach to the
These factors as well as the effects of heat, humid

ity, and the vertical position, all predispose the quad
inspiratory side of the valve (Figure
33-2). It is es
sential that flow rate is controlled in that patients can
riplegic individual to the development of respiratory
negate the training effect of a set resistor by chang
muscle weakness and failure. The physical therapist
ing flow rate.
can help avert the effects of respiratory muscle weak

ness with respiratory muscle training.
An initial pretraining assessment is performed to

determine the appropriate resistor with which to com
Respiratory muscle training with a regimen of pro
mence training. The progression to the next level of
gressive resistive breathing has been demonstrated to
resistance is based on specific criteria of endurance
improve the strength and endurance of respiratory
on the current resistor. Once the resistor has been
1980; Loveridge and Dubo,

1990; Pardy and Leith, 1984) and improve functional
capacity in some patients (Reid and Warren, 1984).
shown in the box on p.
Resistive breathing exercise is aimed at the prevention
pacity can be measured routinely to monitor change
of respiratory failure by increasing the strength and
in diaphragmatic function. The level of inspiratory
muscles (Gross and King,
chosen, a typical training session includes the steps
612.
Maximum inspiratory mouth pressure and vital ca
particularly endurance of the key muscle of inspira
resistance and the duration for which the patient can
tion, the diaphragm. Because the diaphragm is skeletal
use each resistor are indications of the endurance of
muscle, it can be reconditioned using a series of inspi
the inspiratory muscles. Measurement of vital capac
ratory resistance maneuvers. A stronger, endurance
ity and maximum inspiratory and expiratory mouth
trained diaphragm will not fatigue as quickly as an un
pressures provide an index of the strength of the in
trained diaphragm when exposed to such potentially
spiratory muscles.
FIGURE 33-2
Handheld resistive breathing training devices. Left, P-Flex; resistance level is altered by changing
settings on dial. Right, DHD device; resistance level is altered by inserting stopper with different
size orifice into inspiratory port.
612
PART VI
General Steps Involved in Respiratory Muscle Training and Its Prescription

I. The patient is usua lly in the sitting or upright position for training initial l y unless sitting is not yet indicated
2. The noseclip is attached snugly
3. The mouth pi e ce is p l aced securel y in the individual's mouth and a l l ows him or her to select an indi v i dual rate and
pattem of breathing
4. The patient adjusts flow rate to that designated and maintains it with feedback from the flow regulator
5. Breathing is performed comfortably without force
6. The patient is instructed to stop the exercise by letting go of the valve if the resistance becomes too difticu lt
or
if
lightheadedness or dizziness occur
7. When the individual has adjusted to the resistance in the initial training position. an attempt can then be made to
train at the same load in other positions
8. The parameters of the respiratory muscle training is determined by thc patient" s baseline: specific paramcters of
the prescription include initial resistance, the flow rate, the number of repetitions, the number of sets. the fre
quency of sessions. and progression
Modified from Hornstein S: Ventilatol), muscle training.

jury Unit, Shaughnessy Hospital,
J 984,
Vancouver.
clinical guide for physiotherapis/s, Unpublished
manual
of the Spinal Cord
In
Be.
Celtain precautions must be observed with respira
plicate the clinical picture further and seriously
tory muscle training. Each time a new resistance is
threaten tissue oxygenation (Cahalane and Deming,
tried, the physical therapist should be with the patient.
1984; Cane, Shapiro, and Davison, 1990). Hemoglo
The patient selects his or her own rate and pattern of
bin has a higher affinity for binding with carbon
breathing. The inspiratory rate is usually constant.
monoxide than oxygen. A carboxyhemoglobin level
Too shallow breathing is inefficient, and too slow,
greater than 20% denotes carbon monoxide poison
deep breathing may result in accumulation of carbon
ing. Levels in excess of 50% may produce irre
dioxide. The patient is cautioned about avoiding hy
versible neurological damage. The principal danger
perventilation. The physical therapist, or the patient
of carbon monoxide poisoning is that arterial Paoz
when he or she is capable, should check the valving
can be adequate and tissue oxygen tension inade
system on the respiratory muscle trainer before each
quate. Administration of high levels of oxygen is an
training session to ensure it is functioning properly.
initial priority to reduce the half-life of carbon

monoxide to 1 hour from several hours.
Depending on the severity and extent of the burns,
PATIENT WITH BURNS

treatment ranges from conservative medical interven

tions to multiple surgeries related to progressive de
Cardiopulmonary complications are common in pa
bridement and skin grafting. Both second and third
tients with smoke inhalation with or without severe
degree burns can result in severe disfigurement and
burns and are a major cause of death (Marini and
disability. Second-dcgree burns are partial thickness
Wheeler, 1989). Smoke and chemical inhalation pro
burns and tend to be painful. Third-degree burns are
duce edema, bronchospasm, cough, mucosal slough
full thickness burns; these tend to be anesthetic in that
ing, hemorrhage, hoarseness, stridor, and profuse
the nerves themselves have been destroyed. Body po
carbonaceous secretions. Irritation of the alveoli and
sitioning to optimize oxygen transport is life-preserv
acute pulmonary edema can result in a condition re
ing; however, positioning and limb splinting must also
sembling adult respiratory distress syndrome (see
be considered from the outset to minimize defonnity
Chapter 34). Carbon monoxide poisoning may com
and restore optimal neuromuscular and musculoskele
taJ statllS.
and preventing infec
is effectively treated with the ad
tion.
ministration of oxy g e n a n d m a in t a i n i n g c l e a r
airways. I f the
oxygen is
is breathing spontaneously,
via nasal cannulae or mask at tlows
on the arterial oxygen sat
of I to 5 L/min,
di
pulmonary edema consists typically of
Treatment is directed at improving arterial satura

fluid
Treatment of
monary circulation in these
in the burn
must address both these aspects of management.

tion,
613
33
uretics, and mechanical ventilation. Positive end ex

piratory pressure is usually indicated in the ventilated
Mist or aerosol inhalation is also used to
burn
reduce the thickness of pUlmonary secretions.
halation
In
are common in burn

heat trauma, and chemical
uration. Moisture can be administered through a face
ing from smoke
tent with a heated nebulizer. Fluid balance is
and gas inhalation.
larly
usually administered
in the burn patient because of the
to hospital, the
On admission of the burn

patency of the airway is assessed
Heat may cause
and bronchial edema. If
which is essential to the retention and
occlusion
compartmentalization of body fluids and in the regu
from
lation of fluid and electrolyte loss from the body. In
formed. If indicated early, intubation may avoid res
edema threatens, intubation is per
these patients may lose blood because of in
distress within the critical 24-hour period

after admission. Particular care
at the time of the accident. There is also a
given to children
to
and older adults with inhalation injury because these
the time medical attention is available and IV tluid
have a higher risk of developing secondary
without tluid replacement from before the
complications.
resuscitation commenced. Because of the nature of

even when tluid resuscitation has
fluid
balance remains a challenge until con
and
siderable healing and
has occurred. Fluid and
imbalances have considerable implica

tions for hemodynamics and cardiopulmonary func
15) and contribute to
tion
management.
An
the
in anticipation of progres
which would make the insertion of air
sive
impaired thermoregulation, hypermetabolism and in

creased energy expenditure, ileus and
disten
sion, pain, and infection. Eschar formation associated

cally restricts chest wall movement and can lead to
respiratory failure. Tissue edema that can continue for
may be inserted initially with burns to

airway, and
nrp'\iPI1fP
with circumferential burns of the chest wall mechani
instability, which necessitates modification of the

physical
must be
tient and
a few
after the bum contributes to increased tis
sue pressure and
tissue
potentiat
tissue ischemia and necrosis. Late complications
way considerably more difficult hours or days later.
include gastrointestinal bleeding
Ventilatory assistance is indicated with evidence of
ulceration and the continued high risk of infection.
to stress
to smoke inhala
throat, airway,
and burns of the nose,
lungs, and chest wall. A nasotracheal tube i s pre

ferred to
tracheostomy tube because complications
with a tracheostomy tube are greater in burn patients.

Cardiopulmonary
lated to
are
re
or tluid overload in the initial stage.
Acute pulmonary edema and

preventable with careful fluid
nous pressure can be
pressure more
Central ve
verely i
to
prevent atelecta
and improve or main
Pulmonary function may be se

r e d as t h e n e t result of i n halation
burns and trauma to the chest wall,
and
tluid imbalance.
artery
reflects the status of the
with inhalation
of the
sis and retention of

tain gas
in the burn patient
pulmonary edema.
maintain the
are largely
because of severe fluid loss and may remain at low

values
physical therapy is often required

immediately for the
physical
modified in the burn
often has to be
1984). Mobi
614
PART VI
lization to enhance oxygen transport is exploited as
traindicated over freshly grafted skin; however, man
much as possible, however, because of blood volume
ual vibration may be transmitted from a more distal
and hemodynamic problems, orthostatic intolerance
site to a lung field that cannot be vibrated directly.
may limit mobilization and positioning alternatives.
Risk of aspiration is increased if tube feedings are
With more severe burns and more extensive burn dis
not discontinued for at least I hour before treatment.
tribution, body positioning is the primary interven
A nasogastric tube is often used and should be cor
tion. Positioning to effect an optimal therapeutic ef
rectly positioned particularly during treatment.
fect on oxygen transport is challenging because of the
Stimulating exercise and gravitational stress may
significant physical limitations that may exist. Given
initially consist of being in the upright position prefer
that body positioning profoundly influences ventila
ably with the legs dependent, performing selected
tion and perfusion matching (Clauss, Scalabrini, Ray,
limb movements and dangling over the edge of the
and Reed, 1968), the reduced number of positioning
bed for a few minutes if this can be tolerated. how
alternatives will contribute to shunt, ventilation and
ever, in patients with severe burns and significant
perfusion mismatch, and hypoxemia. This effect will
fluid imbalance, active and active-assisted movements
be accentuated if the patient is mechanically venti
in an upright position that can be tolerated, may sub
lated (see Chapter 32).
stitute. As the patient's tolerance increases, free un
Patients who have skin grafts require particular
supported sitting can progress to standing and walk
care when moving or positioning because of the dan
ing. Ambulation during ventilator-assisted breathing
ger of sheering forces of the graft, which can disrupt
should always be considered for any patient for whom
the circulation, nutrition, and healing of the new skin.
this activity is not contraindicated. The upright posi
Sterile procedures must be observed at all times. The
tion and physical activity in the upright position are
physical therapist is usually required to cap, gown,
likely to enhance markedly the patient's cardiopul
mask, and glove before treating the patient with ex
monary and neuromuscular function, and improve the
tensive exposed areas and to cover the chest with a
patient's strength and endurance in preparation for
sterile drape. Facilitating mucociliary transport is a
long-term rehabilitation. If sitting up and ambulation
priority if the patient has significant mobility and po
are not imminent, appropriate limb movements,
sitioning restrictions because of the burn severity.
preferably active, can help provide an exercise stimu
Wherever possible, mobilization in conjunction with
lus that can enhance oxygen transport. Passive full
multiple body positions and position changes is at
range of motion exercises, in addition, are required to
tempted to maximize mucociliary clearance (Wolff,
maximize joint range (a distinct goal from that to en
Dolovich, Obminski, and Newhouse, 1977). If secre
hance oxygen transport), wherever possible.
tions have accumulated, positioning for postural
Positioning to minimize deformity is a priority
drainage requires the same consideration as position
given the potential consequences for cardiopul
ing for improved alveolar ventilation and ventilation
monary function and oxygen transport, as well as
and perfusion matching. In the spontaneously breath
musculoskeletal and biomechanical reasons. Position
ing patient, postural drainage positions can be used
ing a burn patient regardless of the goal should con
selectively to increase alveolar volume in the superior
sider alignment, pressure points, muscle balance, and
lung fields and alveolar ventilation to inferior lung
effect on healing and grafted skin.
fields, in addition to purposes of drainage of the su
Certain precautions have to be observed in the
perior bronchopulmonary segments. However, if the
management of the burn' patient. First, skin loss con
patient is mechanically ventilated, the superior lung
tributes to substantial fluid loss, often resulting in la
fields are preferentially ventilated (see Chapter 32).
bile fluid and electrolyte imbalance. This situation
Should the addition of manual techniques be indi
enhances myocardial irritability and the risk of dys
cated, percussion may not be comfortably tolerated in
rhythmia. Hemodynamic and ECG monitoring is per
the presence of first and second degree burns. Manual
formed routinely during physical therapy treatment.
vibration may substitute. Manual techniques are con
Second, large areas of skin loss increase the risk of
33
infection; therefore the

therapist must be fa
miliar with sterile technique.
Barach, A.L. (1974). Chronic obstructive lung disease: Postural re

of dyspnea. Archives oj Physical Medicine & Rehabilila
lion,
495-504,
SUMMARY
Bates, D.V. (1989). Respiralory JU i leli on
This chapter describes the principles and practice of
Bennett, W.D., Foster, WM,
secondary to neuromuscular and
monary
musculoskeletal conditions that can lead to cardiopul

monary failure.
of conditions included are
neuromuscular conditions_ musculoskeletal condi

tions, morbid obesity, head
spinal cord injury,
and burns. A detailed
of the underly
pathophysiology of these conditions and their

medical management provides a basis for defining
and
the physical
treatment.
The principles described in this chapter cannot be in

terpreted as treatment
in that each pa
tient is an individual whose condition reflects multifactors contributing to
oxygen transport
care, and intrinsic factors related to the

dition to the
in ad
pathophysiology).
plied Physiology,
69, 1670-1675.
Bethune. D.o, (1975). NeurophysiOlogical facilitation of respira

tion in
unconscious adull patient. Physiotherapy Canada,
27(5),
Black, L.F.,
& Hyatt, R.E. (1971). Maximal static respiratory pres
sures in generalized neuromuscular disease. American Review

oJRespiralOJ), Diseases, 103,641-650.
M.L. (1987). Intracranial hypertension: Implications for
the physiotherapist. Physiotherapy Canada, 39, 360-366.
Braun, S.R., Giovannoni, R.,
& O'Connor, M. (1984). Improving
the cough in patients with spinal cord injury. American Journal

oj P ilfl ical Medicine, 63, 1-10.
& Deming, R.H. (1984). Early respiratory abnor
Cahalane, M.,
malities from smoke inhalation. .Iournal oj the A m eri can Med

ical Associalion, 25,
Cane, R.D., Shapiro, B.A.,
care
Davison, R. (1990). Case silidies in
me d ic ine (2nd cd.). St. Louis: Mosby.
Clauss, R.H., Scalabnni, BY, Ray, J.F., Ill,
Reed, G.E. (1968).
Effects of changing body position upon improved vemilatio!l
Circulalion, 37(SuppL 4), 214-217.

& Wiles, C.M. (1985). Severe di
aphragm weakness in multiple sclerosis. Thorax, 40, 631-632.
perfusion relationships.
Cooper, C.B., Trend, P.S.,
Curran, FJ. (1981). Night vent.ilation
REVIEW QUESTIONS
body respirators for pa
tients in chronic respiratory failure due to late stage muscular
Curran, F.J.,
& Colbcr!, A.P. (1989). Ventilator management in
Duchenne muscular dystrophy and postpoliomyelilis syn
\P{''''IfU/f
drome: twelve years' experience. Archives of Physi cal
morbid
musculoskeletal trauma, head
spinal cord
injury, and burns.
Dean, E, (1985). Effect of body position on pulmonary function.
65, 613-618.
Dean, E.
ment interventions to the underlying
Cardiopulmonary development. In B.R. Bonder
&M.B.
ology of each of the above conditions in the criti

the rationale for
your choice.
Medi
cine and Rehabilila/ion, 70, 180-185.

Physical
2. Relate cardiopulmonary
cally ill patient and
Gnd Rehabilitation,
62.
describe the
of cardiopulmonary dysfunction
neuromuscular
Archives oj Physical Medicine
dystrophy.
1. With respect to critically ill

lowing
& Chapman, WF (1990). Cough
enhnnced mucus clearance in the normal lung. Journal
the effects of restricted mobility,
recumbency, extrinsic factors related to the patient's
(Eds.). Philadelphia: FA Davis.
Dean, E. (l994b). Invited commentary on "Are incentive spirom

etry, intermittent positive pressure breathing, and deep
breathing exercises effective in the prevention of postopera
p ul m o n a r y c o m p l i c a t i o n s a f t e r u p p e r a b d o mi n a l
P
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Mackenzie, C.F., Shin, B., Hadi, F., & Imle, P.e. (1980). Changes
in total lung/thorax compliance following chest physiothernpy.
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Dureuil, B., Viires, N., & Cantineau, J.P. (1986). Diaphragmatic

contractility after upper abdominal surgl'l'y . Joumal ofl\pplied
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Macklem, P.T, & Roussos, e.S. (1977). Respiratory muscle fa
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Complications, Adult Respiratory

Distress Syndrome, Shock, Sepsis,
and Multiorgan System Failure
Elizabeth Dean
KEY TERMS
Acute lung injury
Respiratory failure
Adult respiratory distress syndrome
Sepsis
Multiorgan system failure
Shock
Perioperative complications
INTRODUCTION
physiological deficits in these complex conditions is
The purpose of this chapter is to describe some com
the basis for efficacious management in addition to re
mon complications seen in critically ill patients. Com
ducing the risk of an untoward treatment response and
plications arising from the following conditions are
preventing worsening the patient's condition.
included: respiratory failure, surgery, acute lung in

jury and adult respiratory distress syndrome, shock,
sepsis, and multiorgan system failure. Second, the im
plications for cardiopulmonary physical therapy are
presented. Complications add further complexity to
RESPIRATORY FAilURE
Metabolical Dysfunction
the diagnosis of the multiple factors contributing to
The range of complications associated with respira
impaired oxygen transport and to the challenge of pre
tory failure that can further impair tissue oxygenation
scribing effective treatment. Understanding the patho
are described in the box on p. 619. The metabolical

617
618
PART VI
consequences of these complications and impairment
(Fenwick, Dodek, Ronco, Phang, Wiggs, and Russell,
of oxygen transport are lifc threatening for the pa
1990). This so-called pathological dependence of
tient. Thus prevention of their development is a prior
oxygen consumption on oxygen delivery occurs
ity. Should complications develop, however, early
when the cells are inadequately extracting and using
detection and definitive management becomes the
oxygen even in the presence of supranormal oxygen
priority if the patient is to survive.
delivery levels. This phenomenon is observed in pa
A hallmark of these complications is the impair

ment of multiple steps in the oxygen transport path
tient with adult respiratory distress syndrome and

shock (discussed later this chapter).
way, which adds to the complexity of management
Given physical therapy is one of the most meta
(Dantzker, 1991). The three major components of
bolically demanding rcu interventions (Dean, Mur
oxygen transport can be affected individually or in
phy, Parrent, and Rousseau, 1995; Weissman and
combination (i.e., oxygen delivery, consumption, and
Kemper, 1993), the physical therapist needs to be
extraction) (Pallares and Evans, 1992; Wysocki, Bes
able to calculate this safety margin to prescribe the
bes, Roupie, and Brun-Buisson, 1992).
type of treatment and its parameters (i.e., intensity,
In health the ratio of oxygen consumption to deliv
duration and frequency) such that treatment is maxi
ery is low (i.e., 23%, which ensures an over supply of
mally beneficial and associated with the least risk to
oxygen as a safety margin) (see Chapter I). This
the patient.
safety margin also ensures that most patients are able
The ultimate treatment outcome measures are
to recover from insults to the oxygen transport sys
markers of oxygen tissue metabolism (Dantzker,
tem. However, if the insult is extreme, such as that
1993; Nightingale, 1993; Pallares and Evans, 1992).
resulting from complications of respiratory failure,
In addition, hourly assessment of oxygen delivery,
surgery, acute lung injury and adult respiratory dis
consumption, and extraction provide the basis for di
tress syndrome, shock, sepsis, and multiorgan system
recting management of oxygen transport deficits.
failure, significant metabolical dysfunction secondary

to tissue hypoxia can result (Guiterrez, 1991).
The relationship between oxygen consumption
Pulmonary Dysfunction
and delivery has elucidated our understanding of he
Complications of the cardiopulmonary system can
modynamic and metabolical changes observed in
lead to respiratory failure (see box on p. 619) (Boggs
critical illness (Vincent, 1991). The phenomenon of
and Wooldridge-King, 1993; Civetta, Taylor, and
oxygen-delivery dependence of oxygen consumption
Kirby, 1988). Some of these relate to being mechani
occllrs when a patient's oxygen transport system is
cally ventilated. Certain technical problems related to
unable to supply sufficient oxygen to meet basal oxy
the cuffs used in conjunction with artificial airways
gen demand (Phang and Russell, 1993). Oxygen de
may occur (e.g., overinflation, distortion, and hernia
livery below 300 ml 02/min/M2 limits the oxygen
tion of the orifice of the tube). Mucous plugs can oc
diffusion gradient and reduces oxygen extraction and
clude the endotracheal tube or tracheostomy and im
utilization at the ceLlular level. This is termed the
pede ventilation. The common complications can be
critical/evel of oxygen delivery. When oxygen deliv
reduced if the tube is changed frequently and if mini
ery exceeds 300 ml/min/M2, oxygen consumption
mal amounts of air are used for cuff inflation.
does not depend on delivery. Thus the greater the de
Prolonged endotrach al intubation can result in la
livery in relation to consumption the greater the
ryngeal edema, ulceration, and fibrosis. Mechanical
safety margin. When oxygen transport is so severely
ventilation may also rupture a bleb on the surface of
compromised that oxygen delivery falls below the
the lung and produce a pneumothorax with rapid ten
critical level, anaerobic metabolism is triggered.
sion development. Chest tubes are inserted immedi
However, anaerobic metabolism may also be trig
ately to relieve the tension. Blebs occur when alveoli
gered at levels of oxygen delivery that exceed the
rupture, causing air to track to subpleural sites.
normal critical threshold for anaerobic metabolism
Mechanical ventilators can be a source of infection.
34
Complications, Adult Respiratory Distress Syndrome, Shock, Sepsis, and Multiorgan System Failure
ated with some complications (see Chapter
Complications of Respiratory Failure
619
15). In
fection may lead to bacteremia and septicemia. Judi

cious selection and application of any invasive proce
Life-threatening impairment of oxygen transport

and tissue oxygenation
dure is warranted to minimize undue hazard. The

presence of these catheters limits head and neck posi
Fluid ,md electrolyte imbalances
tions and requires mobilization be carried out cau
Cardiac dysrhythmias and hemodyn,lmic instability
tiously within the patient's hemodynamic tolerance.
Myocardial dysfunction
Metabolical dysfunction
Acid-Base Abnormalities
Thromboembolism
Neurological dysfunction
Any combination of acid-base imbalance may occur
Gastrointestinal dysfunction
either acutely or chronically during respiratory fail
Renal dysfunction
ure. Severe alkalemia associated with potassium and

chloride losses may occur after mechanical ventila
Metabolical and blood sligar irregularities
tion and can precipitate serious cardiovascular and
Infection
15) (Petty,
1982). Significantly impaired oxygen delivery to pe
neurological complications (see Chapter
Nutritional deficits
Complications of intubation and mechanical ventila
ripheral tissue may contribute to increased anaerobic
tion, including increased risk of infection
metabolism and metabolic acidosis (Fenwick, Dodek,
Complications of oxygcn therapy
Ronco, Phang, Wiggs, and Russell,
1990).
Fluid and Electrolyte Abnormalities

T':L: physical therapist can help minimize this risk by
Fluid retention can occur with prolonged mechanical
not directly handling the ventilator attachments that
ventilation in a patient with no evidence of cardiac
communicate with the air flow channels. Condensation
failure. Pulmonary edema, weight gain, decreased pul
from the hose should not be drained toward the venti
monary compliance, and reduced oxygen transport are
lator or toward the patient. The physical therapist
common signs. Fluid overload is a common cause of
should be maskcd and gloved when connecting and
this fluid retention. Mechanically ventilated patients
disconnecting the patient to and from the ventilator.
are therefore usually maintained underhydrated. Be
Oxygen toxicity is a significant clinical complica
cause of a tendency for sodium retention and hence
tion of mechanical ventilation. Mechanical ventila
fluid retention, intravenous saline solution is kept to a
tors have precise oxygen controls to deliver the low
minimum. Humidifiers attached to mechanical venti
est possible inspired oxygen concentration needed to
lators are responsible for adding a considerable
maintain arterial oxygen tensions. Because of the ia
amount of water by absorption through the lungs.
trogenic complications of high FIo2 levels (i.e., deni

trogen atelectasis and oxygen toxicity) excess oxygen
above the patient's needs is never indicated other
than short periods of hyperoxygenation before suc
Cardiac Dysrhythmias
Cardiac dysrhythmias are a common complication of
tioning or in preparation for, during, and immediately
respiratory failure. In addition, patients in respiratory
1971; Shoe
failure tend to be older adults who as a group have a
after mobilization (Fell and Cheney,

maker,
1984).
greater incidnce of dysrhythmias secondary to cardiac
Flow-directed pulmonary artery catheters (i.e.,
disease. Electrocardiographic monitoring is therefore
Swan-Ganz catheters), commonly used in the inten
essential for all patients requiring ventilatory assis
sive care unit (lCU) for monitoring patients who de
tance in addition to patients with overt or suspected
velop hemodynamic complications, are also associ
heart disease. Both atrial and ventricular tachydys
620
PART VI
rhythmias are seen in acute respiratory failure. Sinus
over the lower legs to minimize venous pooling and
tachycardia and premature ventricular contractions,
assist venous return (see Chapter 32). JOBST and
however, are particularly common. With rapid lower
TED stockings also may be applied over the feet
ing of arterial Pe02, ventricular fibrillation, or even
and legs to increase circulatory transit time in the de
death may occur.
pendent areas and reduce circulatory stasis.
In the presence of respiratory failure and in the ab

sence of cardiac disease the management of cardiac
dysrhythmias lies predominantly in the correction of
Myocardial Dysfunction
blood-gas abnormalities. Effective supportive man
As in any clinical situation, acute myocardial infarc
agement can usually be achieved with pharmaceutical
tion can occur during the management of acute respi
agents. Intravenous injection of lidocaine followed by
ratory failure. The risks are increased because pa
continuous infusion is useful in managing premature
tients in respiratory failure tend to be older and more
ventricular contractions, which may be the precursor
susceptible to positional hypoxemia. The probability
of potentially fatal tachydysrhythmias and cardiac ar
of heart failure and associated dysrhythmias is in
rest. Electrolyte replacement may also be required.
creased and significantly compounds the problems of
A thorough understanding of the clinical presenta
the patient in respiratory failure.
tion, electrocardiographic diagnosis, and correct man

agement of cardiac dysrhythmias is fundamental to
the optimization of physical therapy treatments in the
Gastrointestinal Dysfunction
ICU and minimizing any risk to the patient. Cardiac
Peptic ulcer is commonly associated with chronic
dysrhythmias resulting from any cause necessarily re
airway obstruction. The stress of respiratory failure
quire ongoing evaluation and therapy.
predisposes the patient to peptic ulceration. Pro
The physical therapist must be able to treat the

patient optimally and safely within the restrictions of
found hemorrhage may occur and blood replace

ment is necessitated.
any dysrhythmia in addition to other medical or sur
Gastric dilation may occur in patients who are re
gical conditions. The implications of the dysrhyth
ceiving mechanical ventilation. Gastric dilation is
mia on the patient's clinical presentation and for
best managed by means of a nasogastric tube and in
treatment selection and response must be recognized
termittent suction. Care must be exercised to avoid
by the physical therapist and considered in designing
hypokalemia and hypochloremia caused by excessive
the treatment plan.
gastric suctioning. Special care is also taken to avoid

fecal impaction, particularly in the paralyzed patient.
This risk can be reduced with suitable fluid balance,
Thromboembolism
mobilization, frequent turning in conjunction with ap
A high incidence of pulmonary thrombosis or em
propriate trunk and lower limb movements.
bolism exists in patients in acute respiratory failure.

Early diagnosis and management of pulmonary
thromboembolism have been greatly facilitated by the
Neurological Dysfunction
use of serial ultrasound procedures and scans. Physi
A close correlation exists between the state of con
cal therapy has a key role in preventing the develop
sciousness and the arteri 1 P02 and Pe02. In addition,
ment of t hromboemboli by p r o moting f r equent
changes occur in alertness, personality, memory, and
changes in position, specific bed exercises, particu
orientation with altered blood gases. Motor changes
larly of the lower limbs, and passive range of motion
also occur, including generalized or localized weak
exercises if indicated. It is essential that movement
ness, tremors, twitching, myoclonic jerks, gross
and repositioning are performed regularly to maxi
clonic movements, convulsions, and flaccidity. Neu
mize their cardiopulmonary protective benefits. Pneu
rological complications of respiratory failure must be
matic extremity cuffs apply pressure intermittently
differentiated from those of nonpulmonary origin.
34
The physical therapist must be aware of the spectrum
621
teredo The presence or absence of cyanosis may be an
of neurological complications that can result from
unreliable sign because peripheral cyanosis can occur
respiratory failure and recognize that apparent im
despite adequate arterial P02. Morbidity and mortality
provement of neurological signs may reflect im
has been reported to be reduced in patients with se

vere respiratory failure and system involvement when
proved cardiopulmonary status.
Sllpranormal levels of oxygen delivery was achieved

(Hayes, Yau, Timmins, Hinds, and Watson, 1993;
Renal Dysfunction
Waxman and Shoemaker, 1980; Yu, Levy, Smith,
The development of renal failure greatly compro
Takiguchi, Miyasaki, and Myers, 1993).
mises the chances of the patient's survival. Renal

failure can result from gastrointestinal bleeding, sep
sis associated with shock, drug-induced nephrotoxic
ity, and hypotension, Urinary outputs are maintained
with adequate fluid and diuretics, with care not to in
duce pulmonary edema. Dialysis may need to be in
Common Postoperative Complications

Hypoxemia
stituted if more conservative management fails
Hypercapnia
(Phipps, Long, and Woods, 1991). If dialysis is antic
Increased work of breathing
ipated, the physical therapist should review existing
Increased work of thc heart
treatment goals to mOdify treatment accordingly,
Fluid shifts and third spacing

Fluid and electrolyte imbalances
POSTOPERATIVE COMPLICATIONS
Metabolic and blood sugar abnormalities

Reduced blood volume
Respiratory failure in the postoperative patient is usu

ally associated with a low Pao2 and a high Paco2. This
situation is likely to be more common than generally
appreciated. If the patient is in good general health
and is free from underlying cardiopulmonary disease,
Reduced cardiac OUlput

Reduced tissue perfusion and oxygenation
Anemia
Pain
recovery is usually rapid. Otherwise, more severe
Alveolar hypoventilation
complications and cardiopulmonary failure may result
Airway collapse
and progress to a life-threatening situation. The effects
Atelectasis
of surgery on oxygen transport and on the varioLls

organ systems are described in Chapter 28. Common
postoperative complications and their causes appear in
the box at right and the box on p. 622.
Physiological shunting
Ventilation and ped'usion mismatching
Impaired mucociliary t ransport
Mucus accumulation and stasis
Pneumonia
Hypoxemia
Thromboemboli
The most common postoperative complication is hy

poxemia secondary to alveolar hypoventilation, re
duced functional residual capacity (FRC), airway clo
sure, and postsurgical atelectasis (Leblanc, Ruff, and
Pulmonary embolus
Coaglliopathies
Sepsis
Milic-Emili, 1970; Marini, 1984; Ray et aI., 1974).
Shock
Adequate oxygenation, however, can be present de
MlIltiorgan system failure
spite hypoventilation when oxygen is being adminis
622
PART VI
Factors Contributing to Postoperative Complications That Affect Oxygen Transport

Pre morbid cardiopulmonary status
Premorbid oxygen transp0l1 (aerobic) capacity
Premorbid systemic disease
Premorbid general health and immune status
Smoking history
Age and gender
Lifestyle factors-nutlitional status. stress, work situation. family situation, psychosocial support system. and substance abuse
Obesity
Pregnancy
Perioperative pain and anxiety
Perioperative reduced arousal
Perioperative reduced mobility
Perioperative recumbency
Perioperative medications (e.g .. narcotics)
Perioperative nutritional deprivation
Perioperative reduction in normal sleep quality and quantity
Type of surgery
Extent of physical manipulation and compression of lung parenchyma, phrenic nerves, diaphragm. and the heart
Perioperative fever and increased oxygen consumptions
Duration of surgery
Position assumed during surgery
Duration of static positioning during surgery
Type. depth, and duration of anesthesia and sedation
Use of an airway
Use of mechanical ventilation
Oxygen therapy
Neuromuscular blockade
Fluid loss and chest tube drainage
Fluid accumulation and third spacing
Infusion of blood products
Site. number. and extent of incisions
Dressings and binders
Traction and splinting devices
Placement of lines, leads, catheters. and monitoring devices
Invasive monitoring equipment (e.g., Swan-Ganz catheter, Foley catheter, intracranial pressure monitor. central
venous line, arterial lines, intravenous lines, and intraaortic balloon counter pulsation pump)
Need for cardiopulmonary bypass machine
Duration on cardiopulmonary bypass machine
Infection
34
Comp,lic:ti(ms, Adult Respiratory Distress Syndrome, Shock, Sepsis, and
Pain
these
in addition to the effects of anesthesia, fre
contributes to alveolar hypoventilation and
atelectasis after abdominal or thoracic surgery.
.....'''r<mn
increase with the magnitude of the op
erative procedure and

and the
of anesthesia required
premorbid risk factors. These abnor
malities observed in the
period are
and
Rapid, shallow, and monotonous breathing may be

spontaneously adopted by the patient to avoid pain
and
623
System Failure
alveolar
FRC, and residual vol

decreased in
minute ventilation is fa-
Because of the
alveolar ventilation is compromised by the in

creased ratio of dead space to tidal volume. Further
crease in FRC (30% o r m o r e), c o m p liance is
more, in the absence of
vv"",-,a,,,"u,
breaths, coughs, and
atelectasis may develop in the underventilated

portions of the
The ventilation-perfusion ratio
and therefore the work of
is in
creased, Hypoxemia secondary to transpulmonary

shunting usually becomes maximal within 72 hours
is disturbed because blood flow to underventilated
after surgery, and often is completely resolved with
physiological shunting
conservative management within seven days. The
tends to
may be
although Peo2
on the mode of 100% oxygen ad-
will
An abnormally
Low oxygen flows and low amounts of
monary pressure is then needed to reinflate these at
tend to be delivered via nasal cannulae.

flows can deliver higher amounts of
electatic alveoli.
masks and masks with reservoir bags.
Pulmonary Embolism and Deep Vein Thrombosis
ial blood gases. The
embolism is a potentially life-threatening

complication. Pulmonary embolism usually results
from a thrombus forming in the veins of the lower
limbs,
in the
atrium, or in the
tricle. Patients may be at risk if

chronic heart failure or if
nant, or
oral
ven
have varicose
are
arter
always be taken into account when
preg
is selected to provide ade
quate oxygenation with
lowest oxygen concentra
tion possible.
Based on the
assessment, arterial blood
gases, fluid and
balance, hemodynamic
status, and x-ray, a decision is made as to which

hierarchy will opti
treatments on the
mize oxygen transport and what
rr""tr"""nh
The patient with a pulmonary thromboembolism
will be
used for each treatment.
usually has a sudden onset of
and mobilizing them wherever possible will
chest pain, and apparent
Occasionally,
maximize FRC and reduce closing volumes and
heart failure follows.
are often elevated.
hence enhance gas
P waves, and inverted T
bundle branch
waves may be seen. No abnormality may be noted on
to treatment because of
this can b e discussed at
for
and cir
Treatment consists of primary

with
oxygenation of pe
ripheral tissues. Anticoagulants, such as
are
rounds and other medications should be considered

so that the
is able to
.. nl",n'r
f'"
more. Thus
even extreme body positioning will achieve more fa
infused intravenously to minimize further formation
vorable results
of thromboembolic substrates.
(1973;
and Geraghty
Ray, and Reed, 1968; Oou-
Beynen,
and
1977;
Piehl and Brown, 1976).
Endoctracheal intubation and mechanical ventila
of lung volume,
and gas
What
even minimally
their lack of alertness which must be explained. If the

patient is unable to
chest x-ray.
culatory
and
these
heart strain may be evidenced on ECG. Right
tion may be indicated if blood gases fail to
uniformly occur after anesthesia
and tissue dissection. The extent and duration of
with conservative management. The treatment

ties for the ventilated patient before and during
624
PART VI
weaning are presented in Chapter 32. Special atten

tion in the postoperative patient is given to the pul
monary complications associated with diminished
ability to move spontaneously, surgical pain, restric
tions imposed by dressings and binders, diminished
ability to cooperate, and to periodically hyperventi
late the lungs.
Facilitating mucociliary transport is a primary goal
in these patients. Impaired mucociliary transport can
be precipitated by alveolar hypoventilation, perhaps
the most common cause of postoperative complica
tions. Sufficient impairment can lead to mucous sta
sis, airway obstruction, atelectasis, and infection.
Multiple positions, including upright positions and
360-degree axial turns, and multiple position changes
facilitates mucociliary transport. In the event of mu
cous accumulation and difficulty in removing pul
monary secretions, specific body positions are se
lected to optimize postural drainage of the affected
bronchopulmonary segments and to maximize alveo
lar volume and ventilation. The addition of manual
techniques can be detrimental in severely ill patients
(Mackenzie, 1989; Poelaert, Lannoy, Vogelaers,
Everaert, D ecruyenaere, Capiau, and Colar dyn,
1991), thus their use needs to be considered carefully.
Suctioning may be most effective immediately be
fore and after position changes. The appropliate oxy
gen transport variables are monitored to assess treat
ment outcome and minimally to ensure the patient
who may be unstable is not deteriorating. If the pa
tient begins to deteriorate, treatment is discontinued
until the patient stabilizes. Why the patient deterio
rated is determined so that a decision can be made as
to whether treatment can be reintroduced, and if so,
what modifications are indicated.
Pain management is integral to the management of
the surgical patient. Noninvasive and nonphannacologi
cal pain control strategies need to be exploited for all
surgical patients to augment or reduce the need for po
tent analgesics especially narcotics. Chapter 28 de
scribed some physical therapy pain control strategies for
surgical patients that can be applied with modification to
the patient with surgical complications. Of these, use of
electrotherapy modalities, such as transcutaneous elec
trical nerve stimulation, may be limited in the ICU be
cause of electrical interference with monitoring devices.
Rest is prescribed as judiciously as treatment inter

ventions to enable the patient to physiologically restore
between and within treatments. This is particularly im
portant for ICU patients who are hypermetabolical and
have increased oxygen demands. Particular care must
be observed in prescribing treatment threshold parame
ters for these patients. Suprathreshold states can be as
sociated with an inappropriate balance between oxy
gen delivery and oxygen consumption such that the
patient becomes compromised (e.g., hemodynamically
unstable, cardiopulmonary distress is precipitated, or
both). A greater volume of a mobilization stimulus,
however, may be delivered to these patients with an in
termittent mobilization regimen than with a single pro
longed course of mobilization. Thus the benefits that
would be accrued would be correspondingly increased.
Prevention of thromboemboli is a major treatment
objective and is best achieved with mobilization, body
positioning, passive movements, and physical devices,
such as pneumatic cuff devices and stockings, to aug
ment low-dose anticoagulants in patients at risk. Pa
tients who develop pulmonary emboli are treated
medically and physical therapy needs to be corre
spondingly modified to minimize oxygen consump
tion until the embolus resolves and the patient is in no
imminent danger.
ACUTE LUNG INJURY ANI) ADULT RESPIRATORY
DISTRESS SYNDROME
Acute lung injury results from damage to the alveolar

epithelium (Gattinoni et aI., 1994). The extent of the
damage reflects damage to the type I and type II alve
olar cells. Damage to the type I cells results in alveo
lar edema, atelectasis, and loss of lung compliance
secondary to loss of structuraJ integrity of the alveoli
provided by the type I alveolar cells. Damage to the
type II cells also contributes to atelectasis and loss of
lung compliance, but the mechanism relates to im
pairment of the production of surfactant and pul
monary fluid that covers the alveolar epithelium.
Pulmonary edema refers to the accumulation of
vascular fluid in the interstitial spaces and alveoli. In
acute lung injury the mechanism of pulmonary edema
involves increased water movement across the pul
monary endothelial cells and increased permeability
34
Complications, Adult Re5ioirato:rv
and Multiorgan System Failure
625
of the endothelium to protein. This type of pulmonary
Acute lung injury is characterized as a clinical spec
edema is referred to as noncardiogenic pulmonary
trum of parenchymal cell dysfunction. Mild injury re
in ori
edema. Pulmonary edema that is
results from left ventricular failure. An increase
flects predominantly endothelial cell
and
noncardiogenic edema. Severe injury reflects a progres
in hydrostatic pressure damages the interstitial
sion to both endothelial and
spaces, which normally provide an effective barrier
and adult respiratory distress syndrome
between the pulmonary circulation and alveoli. The
clinical spectrum of acute lung injury and the clinical
critical distinction between the two
manifestations of mild and severe
of pul
pulmonary edema
monary edema is that
primarily involves the movement of water across the
alveolar or
of the edema
and
MILD
AU
HYPOXEMIA
MILD
MILD
O2 responsive
causes of ARDS include shock, severe trauma or in

fection, overwhelming
and inhaled tox
ins. Increased vascular
that
response is a common feature.
MODERATE
All
SEVERE
All
Late ARDS
SIGNIFICANT
SEVERE
PEEP
resp onsive
HH
nonPEEP
responsive
SIGNIFICANT
SEVERE
PEEP responsive
02 or
to
ENDOTHELIAL
CELLS
INTERSTITIUM
EPTHELIAl CELLS
TYPE 1
PERMEABILITY tt
EDEMA
TYPE 2
METABOLIC
DYSFUNCTION 1 +
METABOLIC
DYSFUNCTION 4+
EDEMA ttt
EDEMA ttt
SLOUGHING
ttt
HYPERMITOSIS
SLOUGHING
tttt
METABOLIC
CONSOLIDATION
tttt
FIGURE 34-1
manifestations
and in
to the alveolar-capillary membrane. Some of the
ARDS
LUNG
COMPLIANCE
insult to the
ARDS results from
of the
the amount of fluid accumulation.
of moderate in
jury falls between these two extremes.
pulmonary edema involves the movement of

and water into the interstitial and alveolar
The
are shown in
34-1. The clinical
alveolar capillary membrane, whereas noncardio
spaces. The clinical consequences reflect the location
cell dysfunction
the spectrum of acute
severe disease. (From Shapiro BA, Peruzzi WT: Changing

review of the literature and suggest clinical correlates,
injury from mild to
inventilatator management: a
117:121-133,1991.)
626
PART VI
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Intensive Cm'e
Fluid seeps into the interstitial spaces and over
alveoli open and thereby optimizes gas transfer at
whelms the alveoli, leading to p u lmonary edema.
end e xpiration. Arterial oxygenation is usually im
Lung compliance and gas exchange are severely
proved with PEEP because the effect of shunting is
compromised. Thus the patient presents with severe
reduced and a given Fl02 tends to be more effective.
trates appear on x-ray. Arterial hypoxemia results pri
Although the Fl0 2 may be reduced, which reduces the

possibility of oxygen toxicity, supranonnal oxygen
marily from underventilated but pelfused lung units
delivery can be beneficial in these patients (Bishop et
dyspnea and hypoxemia. Diffuse pulmonary infil
1993).
and right to left shunt. In this situation, hypoxemia is
aI.,
relatively refractory to increases in Fl0 .

2
Fibrinogen in the fluids leaking into the alveoli
of multiorgan system failure reduced.
contributes to fibrosis and reduction of lung compli
junction with arterial blood gases is essential for fol
Survival may be improved and frequency
Further monitoring of respiratory status in con
ance associated with ARDS. Increased lung surface
lowing the progress of the syndrome. In addition to
tension and alveolar collapse tend to result from an
the oxygen transport variables the principal parame
inactivation of surfactant with the accumulation of
ters monitored in ARDS are reduced lung compli
fluid in the alveolar spaces. Thus reduced lung com
ance, tachypnea, and the concentration of inspired
pliance produces
oxygen needed to maintain acceptable levels of the
significant decrease in FRC in the
arterial blood gases.
patient with ARDS.
48
The signs and symptoms of ARDS may take up to
ARDS is characterized by a major pathophysio
hours to be fully manifested. The prognosis for
logical restrictive component. Hence the principles of
survival of patients is
40%
to
60%.
Hypoxemia is a
principal feature of the syndrome, and results from a

right to left shunt, whereby fluid-filled alveoli are in
management of restrictive lung disease can be effec

tively applied. Changes in lung compliance and Fl0
2
requirements provide guidelines to treatment re
effectively ventilated. Hyperventilation and labored
quired, treatment response, and course of the syn
respiration can be expected in conjunction with hy
drome. Patients with ARDS require close monitoring
poxemia. Oxygen therapy has little effect in the pres
and often frequent treatments aimed at promoting op
ence of shunting. Hypercapnia is not usually a major
timal gas exchange because of the severity of the syn
problem in the ARDS patient.
drome and high incidence of mortality associated
The metabolical perturbations that can result in

clude problems with oxygen delivery, consumption
with it. Special attention is given to body positioning

to promote ventilation and perfusion matching and
and extraction as discussed previously. When oxy
mucociliary transport and to minimize the effect of
gen delivery falls below the critical level, anaerobic
restriction of diaphragmatic and chest wall excursion.
metabolism is triggered resulting in increased lactate
Some patients, for example, benefit from side lying
production. Elevated serum lactates are associated
in which excursion of the inferior hemidiaphragm is
with a poor prognosis.
favored. Other patients, however, seem to detel;orate

from apparent restriction of the inferior lung in side

Intubation and ventilatory support are implemented if
lying. Each patient's condition and specific areas of

lung involvement must be taken into consideration
when prescribing a turning regimen. The effect of the
arterial blood gases are severely affected and rerspi
patient's body position on blood gases helps to estab
ratory distress worsened. An endotracheal tube can
lish a suitable regimen on a rational basis.
be placed t h r o u g h t h e n o s e o r mouth or a tra
The sitting position optimizes lung capacity. The
cheostomy can be performed. The tidal volume is set
use of a reclining chair at the bedside perhaps should
10
mUkg of the patient's body weight. The
be considered more often in the management of pa
patient usually establishes the respiratory rate, al
tients with acute lung inj u ry. Theoretically, the poten
though it may be rapid. A positive end expiratory
tial function of all lung fields will be benefited with
pressure (PEEP) of around 12 cm H20 maintains the
the lungs in a more upright position. Patients who are
at about
34
too unstable to tolerate upright positions may respond
627
tribute to intracellular digestion and calcium deposi
favorably to extreme body positions and the prone
tion. Once the lysosomes have ruptured and intracel
position (Albert, Leasa, Sanderson, Robertson, and
lular digestion is triggered, irreversible cell damage
Hlastala, 1987; Langer, Mascheroni, Marcolin, and
ensues, impairing oxygen extraction and uptake
Gattinoni, ] 988).
(Wysocki, Besbes, Roupie, and Brun-Buisson, 1992).
Severely affected patients may require neuromus
The pathology of shock and the effect on the res
cular blockade to reduce their oxygen demand and
piratory membranes of the mitochondria follow a
enable them to respond to ventilatory assistance more
similar course regardless of cause. Swelling of the in
effectively. Handling and positioning patients on neu
terstitial tissue disrupts the perfusion of the pul
romuscular blockade requires particular care because
monary capillaries. Congestive atelectasis and pul
these patients lack muscle tone to protect their mus
monary edema ensue. In the advanced stages, hyaline
cles and joints. Rotating beds can be extremely bene
membrane changes and pneumonitis may occur.
ficial for these patients who are either too hemody

namically unstable or difficult to turn manually.
These mechanical beds slow ly rotate side to side
through an arc, thus changing the patient's body posi
Foremost, the physical therapist must be knowledge
tion continuously (Gentilello et aI., 1988; Pape,
able about the relationship of oxygen delivery and
Regel, Borgman, Sturm, and Tacherne, 1994).
consumption in these patients, as well as the implica

tions of the pathophysiological processes on oxygen
extraction. The type of treatments and their pat'ame
SHOCK
ters are based on a careful analysis of oxygen trans
Common causes of shock include hypovolemia, sep
port variables. Treatments are prescribed within the
ticemia, heart failure, and direct insult to the central
patient's safety margin. Physical therapists in the
nervous system. Some of the classical features of
ICU must also be knowledgeable about the signs and
shock are hypotension, reduced cardiac output, tachy
symptoms associated with impending and frank
cardia, hyperventilation, diaphoresis, pallor, confu
shock. By recognizing and understanding the compo
sion, nausea, and incontinence. Inadequate tissue per
nents of the different types of shock and the effect on
fusion results in extracellular acidemia and loss of
the cardiopulmonary system, the physical therapist
potassium ions from the cells. The pulmonary blood
can better prescribe a rational treatment plan for the
vessels constrict in response to hypoxemia, which
short- and long-term management of the patient.
tends to increase pulmonary artery pressures.
Although physical therapy may be limited in re
Failure of cellular function secondary to shock can
versing the signs and symptoms of shock, physical
result from a deficiency of substrate for energy pro
therapy can help to restore and maintain optimal car
duction, a reduced ability to use the nutrients for en
diopulmonary function, reduce the risk of complica
ergy production, or both. The pathophysiological
tions associated with immobility and with recum
mechanisms responsible include hypoperfusion of the
bency, and maintain physical status at the best
tissues, hormonal and metabolical cellular changes,
possible optimal level during the episode and in an
and the toxic effects of the metabolical changes. Col
ticipation of the patient's recovery. The primary ob
lectively, these produce cellular damage. With hy
jective, however, is to minimize oxygen demand. A
poperfusion and decreased oxygen delivery and other
minimal objective is not to worsen the patient's con
nutrients, the production of adenosine triphosphate is
dition by imposing excessive metabolical demand.
reduced. The maintenance and repair of cell mem
This is the case in patients whose oxygen delivery is
branes is disrupted, resulting in swelling of the endo
approaching the critical level with respect to oxygen
plasmic reticular and eventually the mitochondria.
consumption dependence. Excessive demands in
Persisting cellular hypoxia contributes to rupture of
these patients can be life threatening.
the lysosomes, which releases enzymes that con
Patients in shock are usually unresponsive. The
PART VI
628
course of the shock episode is often complicated with
The fluid is drained after about 30 minutes. Car
the sequelae of immobility and recumbency. The spe
diopulmonary physical therapy is most effective if
cific goals related to optimization of cardiopul
performed after the fluid has been completely drained
monary and musculoskeletal function and prevention
from the peritoneum. After drainage of the fluid the
of further complications associated with cardiopul
diaphragm is at a more optimal functional length for
monary function in particular are priorities.
respiration, which potentially can improve treatment
Specific concerns for the patient in shock include
response. If hemodialysis is indicated, the patient is
the need for short, efficacious treatments and avoid
connected to a unit that dialyzes the blood externally.
ance of unnecessary fatiguing of the patient. Treat
This process takes several hours and is usually re
ment goals are therefore critically appraised and pri
peated every few days.
oritized throughout each day to target physical
In the end stages of shock, as for other severely ill
therapy treatment only to the very immediate and es
medically unstable patients, physical therapy may
sential needs of the patients. Prudent patient position
constitute primarily supportive care and comprehen
ing is a priority because of the relative immobility
sive monitoring.
and reduced spontaneous movement observed in

these patients and recumbency. Approximations to
the upright position (i.e., head of bed up and foot of
SEPSIS AND MULTIORGAN SYSTEM FAILURE
bed down) can augment sympathetic stimulation and
Sepsis is the response to bacteremia or other by prod
improve hemodynamic status and reduce sympath
ucts of bacteria in the blood. The clinical features of
omimetic medications. In addition, this position sim
sepsis include fever, tachycardia, tachypnea, and res
ulates the upright sitting position (although not per
piratory alkalemia. Metabolical abnormalities are
fectly) with re spect to i t s beneficial effects on
also a common feature of sepsis. Sepsis is the most
pulmonary and cardiac function.
common predisposing factor contributing to multior
Late stages of refractory shock leading to renal
gan system failure (MOSF), which typically involves
failure may necessitate dialysis. In peritoneal dialysis
failure of more than two organ systems (Carrico,
a liter of fluid with a high osmotic fluid content is in
Meakins, and Marshall,
jected into the patient's abdomen to draw fluid out.
34-1 shows the major organs affected and their clini-
1993; Vincent, \993). Table
TABLE 34-1
Presentation of Multiorgan System Failure
CLIN[CAL PRESENTAnON
SYNDROME
Lungs
Hypoxemia, lung compliance, diffuse infiltrates
Acute lung injury/AROS
Kidneys
Creatine> 2 mg/dl
ORGAN
Urine output
Liver
<
Oliguric ARF
500 m1l24 hr
Urine output> 500 m1l24 hI'
Nonoliguric ARF
Bilirubin 2 mg/dl, SGOT and LOH
Jaundice
Intractible hyperglycemia or hypoglycemia
Hepatocyte failure
Cholecystitis
Acalculous cholecystitis
Gut
Upper gastrointestinal bleed
Stress ulceration
Coagu lation
Thrombocytopenia, prolonged PT and PTT
Hypofibrinogenemia DIC
Heart
Hypotension, Cl
Heat1 failure
CNS
Response only to painful stimuli
Obtundation
Modified from Civetta.
J.M., Taylor, R.W., &
ARF.
SCOT.
acute renal failure;
coagulalion;
PT.
Kirby,
R.R. (1988).
Critical care. Philadelphia:
serum glutamic oxaloacetic transaminase;
prothrombin time;
PIT.
partial prothrombin time;
LDH.
C/, c ardiac
index
JB Li ppi ncott
lactate, dehydrogenase;
DIC,
disseminaling intravascular
34
cal manifestations (i.e., pulmonary, gastrointestinal,
629
fective Floz. Even though the patient wi II likely bene
hepatic, renal, cardiovascular, hematological, and
fit more from some positions than others, frequent
central nervous systems). The cascade of pathophysi
body position changes, preferably 360-degree turning
ological features of this MOSF is believed to be pre
regimen, are still necessary to avoid the sequelae of
cipitated by mUltiple mediator systems. The release
static body positioning. Semi-prone positions can
of these mediators impairs oxygen delivery and uti
substitute well for full prone positions if the patient is
lization of oxygen by the cells. Thus the supply of the
too hemodynamically unstable. Semi-prone positions
major energy source to the cell, adenosine triphos
may be tolerated better by the patient and may be
phate, is reduced which leads to structural and func
safer. Even though hourly position changes may not
tional damage of the various organ systems. The mor
be feasible in these severely ill patients, prolonged

periods in a static position (more than 2 hours) is
tality rate ranges from 60% to 80%.

Conditions that predispose a patient to MOSF in
clude sepsis, overwhelming infection, multiple
deleterious to the patient. Thus a balance between

these two concerns must be achieved.
trauma and tissue injury, inflammation, and tissue
Promoting optimal mucociJiary transport remains a
perfusion deficits. Patients who are older, have
priority even in the absence of secretion accumula
chronic diseases, are immunosuppressed or have a se
tion. Frequent position changes and numerous posi
vere initial presentation have an increased risk of fail
tions ensure pulmonary secretions are continually

being redistributed to prevent accumulation and en
ure and mortality.
hance removal. Should postural drainage be indicated,

these positions may need to be modified. Head-down
positions in particular may not be tolerated well.
The patient with sepsis and MOSF, like the patient in
Based on a careful assessment, the relative benefits of
shock, is gravely ill and unlikely to be able to cooper
superimposing manual techniques must be established
ate with treatment. The principles for management
in that these procedures are associated with increased
are comparable with those for managing the patient
metabolical demand to which the patient is not readily
in shock, however, oxygen delivery is likely to be
able to adapt. Increasing the oxygen demand of these
consistently compromised in these patients. If oxygen
patients may worsen their condition.
delivery is critically low, oxygen consumption de

pends on oxygen delivery and the patient is in
of metabolical acidosis (see Chapter
state
I). In this situa
SUMMARY
tion, where oxygen delivery is compromised to the
This chapter presents several major complications
point of not meeting tissue oxygen demands, the goal
that occur secondary to various conditions in the in
of treatment is to maximize oxygen delivery (Bishop
tensive care unit. Complications add significantly to
et aI., 1993; Yu, Levy, Smith, Takiguchi, Miyasaki,
the complexity of the physical therapy diagnoses of
and Myers, 1993) and minimize oxygen demand so
the patient'S underlying problems with respect to
that oxygenation of vital organs is threatened to the
oxygen transport and cardiopulmonary management.
least extent. Thus the physical therapist must estimate
The complications highlighted in the chapter include
the oxygen reserve capacity (i.e., the balance between
those that impair multiple steps in the oxygen trans
oxygen demand and oxygen) in every assessment to
port pathway and hence jeopardize metabolism at the
select optimal treatment, which is associated with the
cellular level. This sequence of events is most fre
least risk. Treatments are selected to improve the effi
quently associated with the complications of respira
ciency of oxygen transport and utilization a n d
tory failure, surgery, adult respiratory distress syn
thereby reduce the work of the heart and o f breathing.
drome, shock, sepsis, and multiorgan system failure.
Above all, treatment should not worsen the patient's
Physical therapy treatments in critical care areas
oxygen transport status. Selective body positioning
are typically short, frequent, and should always be ef
can augment oxygen transport and maximize the ef
ficacious. Patients with the complications, however,
630
PART VI
are usually severely compromised and often unable to

cooperate with treatment necessitating particularly
short and frequent sessions. Because of the severity
of illness, patients with the complications described
often require treatments that are more passive (i.e.,
stress the oxygen transport system minimally, thus
are lower on the physiological treatment hierarchy).
These patients require frequent and comprehensive
monitoring (often several times daily) of their oxygen
transport capacity (i.e., the relationship between oxy
gen delivery and consumption, and oxygen extrac
tion, to establish if and when treatment is indicated,
and the specific parameters of treatment. If a patient
is thought to be too unstable for treatment at a given
time, continued monitoring of her or his status is es
sential so that small windows of opportunity can be
exploited during stable periods. During periods of
monitoring rather than active treatment intervention,
the physical therapist continues to have an impoltant
role in recommending body positions and frequency
of body position changes so that these can yield the
manual for
Cane, R.D.,
critical care medicine ( 2nd ed.), St. Louis: Mosby.

Carrico, C.J. , Meakins, 1 ,L.,
&
J.e. (1993),
Marshall,
Multiple
organ failure syndrome, The gastrointestinal tract: the motor of

MOF. Archives of Surge/y, 121, 197-208.
Civetta, 1.M., Taylor, R,W.,
&
Kirby, R.R. (1988), CrilicaL care.
Philadelphia: 18 Lippincott.
Clauss, R.H., Scalabrini, BY. Ray,
1.F, III, & Reed,
G.E. (1968).
Effects of changing body position upon improved ventilation

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Dean, E" Murphy, S., Parrent, L.,
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Rousseau, M. (1995), Meta
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Proceedings of the World Confederation of Physical Therapy
Cogress, Washington, De.
Dantzker, D.R. (1991). Cardiopulmonary critical care (2nd ed.).
Dantzker, D.R. (1993). Adequacy of tissue oxygenation, Critical
Care Medicinc, 21, S40-S43.
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acute respiratory failure: the prone position, American Review
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Fenwick,
l,e.,
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Russell, 1 , A. (1990), Increased concentrations of plasma lactate
REVIEW QUESTIONS
predict pathologic dependence of oxygen consumption on oxy
1. Describe the complications associated with respi
gen delivery in patients with adult respiratory distress syn

drome, loumal of Crilical Care, 5, 81-86,
ratory failure.
2. Describe the implications for cardio ulmonary
physical therapy of respiratory failure, surgical
complications, acute lung injury, adult respira
tory distress syndrome, shock, sepsis, and multi
Gattinoni, L., Bombino, M., Pelosi, P., Lissoni, A., Pensenti. A.,
R., &
Fumagalli,
Tagliabue,
M,
Lung structure and function in
different stages of severe adult respiratory distress syndrome,

loumal of the American MedicaL Association, 2 71 , 1772-1779,
Gentilello,
L,
Thompson, D.A., Tonnesen, A,S" Hernandez, D" Ka
padia, A,S., Allen, S.1., Houtchens, B.A.,
organ system failure.
Effect of a rotating
bed
& Miner, M.E. (1988),
on t he incidence of pu I monary complica
tions in critically ill patients. Crilica! Care Medicine, 16,783-786.

Gutierrez, G. (1991). Cellular e nergy metabolism during hypoxia.
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P., Paredes, R.M., & Clauss, R.H. (1974). Immobility, hypox
prospective, randomized, controlled study. Crilica/ Care Medi
emia, and pulmonary arteriovenous shunting. Archives oj
cine, 21,830-838.
Surgery, 109, 537-541.
Care oJth
PART
VII
Guidelines for the Delivery of

Therapy: Special Cases
The Neonatal and Pediatric Patient
Victoria A. Moerchen
Linda D. Crane
KEY TERMS
Bronchopulmonary dysplasia
Hyaline membrane disease
Chest physical therapy with
Patent ductus arteriosus

Pediatric cardiac rehabilitation
infants/children
Childhood asthma
Pediatric pulmonary rehabilitation
Cystic fibrosis
Pulmonary development
Endocardial cushion defect
Transitional circulation
Handling for ventilation
Trunk-ventilation interaction
INTRODUCTION
(3) present principles and precautions of direct respi
Pediatrics entails a "special" application of cardiopul
ratory care; and (4) incorporate these principles into
monary physical therapy. This chapter stresses that
suggestions for practice.
cardiopulmonary development and its related vulner
This chapter begins with a brief description of crit
abilities form the basis for cardiopulmonary practice
ical events and important characteristics of cardiac
with neonatal and pediatric patients.
and pulmonary development. Relevant diagnoses are
The objectives of this chapter include to: (l) re
then presented to build onto this developmental per
view cardiopulmonary development and related vul
spective and to stress that cardiopulmonary pathology
nerabilities; (2) relate developmental pathologies to
and ventilatory compromise are often related to de
issues of adequate ventilation and oxygen transport;
velopmental vulnerabilities. Finally, treatment ap

635
636
PART VII
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cases
proaches are described, including pediatric cardiac
men ovale allows right-to-left blood flow through the
rehabilitation, pulmonary care for neonatal and pedi
atria, bypassing the lungs (Yao, 19H3). Left ventricular
atric patients, pediatric pulmonary rehabilitation, and
output (LVO) is well-oxygenated blood that then enters
developmental motor approaches for trunk and venti
the ascending aorta and flows to the brain and upper

body. The ductus arteJiosus similarly allows the lungs
latory muscle function.

A knowledge of cardiopulmonary development,
to be bypassed, as most of the right ventricular output
congenital and d evelopmental cardiopulmonary
(less well-oxygenated than the LVO) flows to the de
pathology, and pediatric cardiopulmonary treatment is
scending aorta and from there to the lower body.
essential for any therapist serving children. Most pedi
Fetal blood flow to the lungs is minimal, secondary
atric patients require ongoing attention to respiratory
to high pulmonary vascular resistance during fetal cir
function, whether as a primary focus of physical ther
culation. Only 10% to 12% of evo goes to the lungs
apy or as an inherent aspect of motor development.
(Koff, 1993; Phelan, Olinsky, and Robertson, 1994),
This chapter is relevant to therapists who perform di
with the function of nourishing the developing lung
rect cardiopulmonary care and to therapists who incor
tissue rather than providing gas exchange.
porate a cardiopulmonary awareness into developmen

tal motor therapy.
Neonatal circulation
Adult-like circulation occurs at or shortly after birth,
with separation from the placenta and ventilation of
CARDIOPULMONARY DEVELOPMENT
the lungs resulting in closure of the ductus venosus,
The application of cardiopulmonary physical therapy
foramen ovale, and ductus arteriosus. This process,
to infants and children requires a special understand
referred to as transitional circulation, occurs early in
ing of developmental cardiopulmonary anatomy and
neonatal life and increases the efficiency of oxygen
physiology. Knowledge of normal development and
uptake and transport (Heyman and Hanley, 1994;
its inherent points of vulnerability will help the
Rudolph, 1970).
reader understand some of what is known about car

diopulmonary pathology in pediatric patients.
The initiation of breathing and the removal of lung

fluid increases pulmonary blood flow. Whereas fetal
circulation was characterized by high pulmonary vas
cular resistance and low systemic resistance, separa
Cardiac Development
tion from the placenta causes a rise in systemic resis
Differences in fetal and neonatal gas exchange ac
tance and a decrease in pulmonary vascular resistance.
count for differences in the anatomy and physiology
As this shift in relative pulmonary and systemic resis
of fetal and neonatal circulation. A basic review of
tances occurs, sites of intercommunication (shunts)
developmental circulation is essential for discussion
close, and the ventricles shift from working in parallel
of congenital heart defects and the role of pediatric
to working in series (Heyman and Hanley, 1994).
Closure of Foramen Ovale. The increased left atrial
cardiopulmonary physical therapy.
pressure that occurs during transitional circulation re
Fetal circulation
sults in apposition of the valve of foramen ovale
Placental oxygenation is a major characteristic of
against the interatrial septum, functionally closing this
fetal circulation. Additionally, in fetal circulation
site of fetal circulatory shunting (Rudolph, 1970). In
blood flow through the right and left sides of the
most infants, anatomical closure occurs 2 to 3 months
heart occurs in parallel, such that cardiac output is ac
later (Emmanouilides and Baylen, 1988; Yao, 1983).
tually combined ventricular output (eVO) (Heyman
Closure of Ductus Arterioslls. Functional closure or
and Hanley, 1994). This is possible as a result of
constriction of the ductus arteriosus occurs postnatally
shunts in fetal circulation (Parks, 1988).
within the first IS to 72 hours in response to increased
Two points of shunting during fetal circulation are at
arterial oxygen saturation (Daniels, Hopman, Stoelinger,
the foramen ovale and the ductus arteriosus. The fora
Busch, and Peer, 1982). Anatomical closure of ductus
35
637
arteriosus occurs by 2 to 3 weeks in most term neonates
diaphragm of a newborn has fewer type I (high oxida
(Rudolph, 1970). It is important to note that the respon
tive) muscle fibers (25% compared with 50% in adult)
siveness of the ductal smooth muscle to arterial oxygen
(Muller and Bryan, 1979). This difference predisposes
tension and to endogenous prostaglandins is impacted
an infant to earlier diaphragmatic fatigue when stressed.
by gestational age (Pack, 1988; Yao, 1983).
A biomechanical difference between the infant

and child is the circular and horizontal alignment of
the ribs and the concomitant horizontal angle at
Pulmonary Development
which the diaphragm inserts on the ribs during new
Structural and functional characteristics of pulmonary
born and early infant chest development (Massery,
development in infants and children are significant
1991; Muller and Bryan, 1979). This, along with the
because they may contribute to aspects of respiratory
more cartilaginous nature of the rib cage, results in
vulnerability (Muller and Bryan, 1979).
less efficient chest wall mechanics. The result, again,

is increased work to breathe. (See Chapter 37 for a
Newborn respiration
more complete discllssion of chest development).
The pulmonary anatomy of t h e term i n f a n t i s

markedly different from the adult but also different
Respiration in the child
from the child. An infant's airways are narrower from
Two residual strllctural differences exist beyond the
the nares to the terminal bronchioles. This presents a
newborn period and have potential implications for
point of pulmonary vulnerability because a smaller
pulmonary vulne rabili ty in the child. First, the some
diameter airway is more easily obstrllcted by mucus,
what horizontal angulation of the ribs persists unti I
edema, foreign objects, and enlarged lymphatic tis
approximately 7 years of age and results in less effi
sue. The infant also has a high larynx (Laitman and
cient chest wall mechanics (Muller and Bryan, 1979).
Crelin, 1980). Although this position of the larynx
Secondly, lymphatic tissue (especially adenoids)
enables the newborn to breathe and swallow simulta
grows rapidly until about 6 years of age (Sinclair,
neously, it may also contribute to predominant pat
1978) and can continue to be a potential source of
terns of infant nasal breathing, which can result in in
upper airway obstruction.
creased work to breathe during any compromise of
As infants and children grow and develop, how

ever, most structural and functional disadvantages
the nasal airway.

Even without airway compromise, the work of
disappear. An aspect of growth and development that
breathing is increased during the neonatal period.
can be protective for infants and younger ch i ld re n is
The initial low compliance of the newborn's lungs
alveolar multiplication. This begins in the rirst year
requires increased effort for ventilation, which re
of lire and continues until approximately 8 years of
sults in a high rate of respiration and increased oxy
age (Blackburn, 1992; Thurlbeck, 1975).
gen consumption.
Although the process of transitional circulation al
lows more efficient O2 transport in the neonate than
in the fetus, gas exchange in the newborn is still
Cardiopulmonary Considerations
in the Preterm Infant
somewhat inefficient because of immature alveolar
All of the cardiopulmonary structural and functional
structure and function. The surface area for gas ex
characteristics of neonates that have been previously
change is 1120 that of an adult (Johnson, Moore, and
discussed apply to the premature infant. Additionally,
Jefferies, 1980), and the diffusion distance across the
there arc signi["jeant gestationa l characteristics and as
alveoli-capillary membrane is increa sed as a result of
pects or cardiopulmonary vulnerability that are more
thick alveolar walls (Blackburn, 1992).
pronounced and create more problems in premature
Functional characteristics of infant pulmonary de
infants Cfable 35- I).
velopment are also significant to understanding possi
Recall that the transitional circulation of a term
ble contributions to pulmonary distress in infants. The
newborn includes a decrease in pulmonary vascular
638
PART VII
TABLE 35-1
Factors Contributing to Cardiopulmonary Dysfunction in the Premature Infant*
ANATOMICAL
PHYSIOLOGICAL
Capillary beds not well developed before 26 weeks' gestation
Increased pulmonary vascular resistance leading

10
Type II alveolar cells and surfactant production not mature
right-to-Ieft shunting
Decreased lung compliance
until 35 weeks' gestation; elastic properties of lung not

well developed; lung space decreased by relative size of
the heart and abdominal distention
Decreased responsiveness of the ductus arteriosus to oxygen
Left-to-right shunting
tensions; delayed ductal closure

Type I, high-oxidative fibers compose only 10% to 20% of
Diaphragmatic fatigue: respiratory failure
diaphragm muscle
Highly vascular subependymal germinal matrix not resorbed
Decreased or absent cough and gag reflexes; apnea
until 35 weeks' gestation, increasing the vulnerability of the

infant to hemorrhage
Lack of fatty insulation and high surface area to body-weight ratio
Hypothermia and increased oxygen consumption
*Modified from Crane, L.D. (J 995). Physical Therapy for the Neonate with Respiratory Disease. In S. Irwin & lS. TeckJin (Eds.).
Cardiopulmonary physica/therapy. St. Louis, Mosby.
resistance over the first day. In preterm infants, how
Most significantly, the immature status of car
ever, lung immaturity and abnormal surfactant func
diopulmonary anatomy in preterm infants predisposes
tion (Jobe, 1988) may result in retained high pul
them to h ypoxia under any conditions that require in
complia nce),
creased oxygen (Blackburn, 1992). Cardiopulmonary
hypoperfusion, and respiratory distress syndrome
pathophysiology and/or the stressors inherent to med
(Walther, Benders, and Leighton, 1992). Persistent
ical care often present challenges beyond the adaptive
pulmonary hypertension will reinforce persistent
capacities of these fragile little systems.
m o na r y
resistance
(p o o r
lung
right-to-Ieft shunting through the ductus arteriosus

(Nude! and Gootman, 1983; Rudolph, 1980). In fact,
respiratory distress syndrome (RDS) has been identi
fied as the best predictor of prolonged patency of duc
tus arteriosus (Milne, Sung, Fok, and Crozier, 1989).
As the respiratory distress of the premature infant
COMMON PEDIATRIC DIAGNOSES

The sections that follow present and discuss specific
cardiac and pulmonary diagnoses. Common neuro
muscular or developmental diagnoses that have in
improves with neonatal intensive care, cardiopulmonary
herent to them the risk of compromised respiration or
vulnerabilities can then occur in the opposite circulatory
associated cardiopulmonary disease are also dis
direction. Given the gestationally related responsiveness
cussed. The diagnoses presented are not all inclusive
of ductus arteriosus to oxygen, some preterm infants re
but merely represent an attempt to give the reader a
tain patency of the ductus even when pulmonary vascu
preliminary knowledge of underlying pathologies and
lar resistance falls (Archer, 1993). The result is Ieft-to
medical management of diagnoses commonly en
right shunting that may lead to congestive heart failure
countered in the practice of pediatric cardiopul
(Nudel and Grootman, 1983; Parks, 1988).
monary physical therapy.
3S
639
TABLE 35-2
Common Pediatric Diagnoses and Associated Heart Defects
DlAGNOSIS
HEART DEFECTS
Duchenne's muscular dystrophy
Cardiomyopathy (adolescence)
Fetal alcohol syndrome
Ventricular septal defect

Tetralogy of Fallot
Pulmonary value stenosis
Friedreich's ataxia
Ventricular hypertrophy
Congestive heart failure
HIV-l infection
Myocarditis
Ventricular dysfunction
Juvenile rheumatoid arthritis
Pericarditis
Marfan syndrome
Aortic aneurysm
AorticlMitral insufficiency
Noonan's syndrome
Dystrophic pulmonary valve (Pulmonary stenosis)
Prematurity
Trisomy 13 (Patau's syndrome)

Atrial septal defect
Trisomy 18 (Edwards' syndrome)

Patent ductus arteriosus (large)
Trisomy 21 (Down syndrome)
Endocardial cushion defect

Atrial septal defect
Tetralogy of Fallot
Turner's syndrome
Williams syndrome
Coarctation of the aorta

Supravalvular aortic stenosis
Supravalvular pulmonary stenosis
Cardiac Diagnoses
the most common heart defect during the neonatal
Patent ductus arteriosus, endocardial cushion defects,
period (Musewe and Olley, 1992). In term newborns,
and tetralogy of Fallot are the cardiac defects dis
however, PDA accounts for 10% of congenital heart
cussed within the limits of this chapter. Additionally,
disease (Mitchell, Korones, and Berendes, 197 I).
Table 35-2 provides a summary of common develop
Gestational age, the presence of lung disease, the
mental diagnoses and their associated cardiac defects.
size of the ductus, and the direction of the shunt me

d i a t e the clini c a l f e a t u r e s of P D A (Gr e e n e ,
Mavroudis, and Backer, 1994; Musewe and O lley,
Patent ductus arteriosus (PDA), already introduced as
1992). The preterm infant with very low birth-weight
a cardiopulmonary complication in preterm infants, is
will have the most extreme clinical picture. An infant
640
PART VII
Guidelines for the Delivery of Cardiopulmonary Physical Thempy: Special Cases
obvious
of mitral valve regurgitation (Merrill et ai., 1994).
clinical presentation. Tachycardia, an ejection sys
For infants with complete ECD, early surgical repairs
or child with a large ductus will also have
an
tolic murmur, bounding peripheral pulses, increased
are indicated (Bender, Hammon, Hubbard, Muirhead,
respiratory distress, and poor feeding or poor weight
and Graham, 1982; Graham and Bender, 1980).
gain are the classical signs of PDA (Archer, 1993;
Tetralogy of Fallot
Greene et ai., 1994; Musewe and Olley, 1992). In the
(TOF) is named for its "tetrad" of
term infant, PDA may be more clinically silent, espe
Tetralogy of Fallot
cially when the ductus is small (Parks, 1988).
defects: ventricular septal defects, right ventricular
Medical management of PDA includes nonsurgi
outflow obstruction, right ventricular hypertrophy,
cal use of indomethacin or direct surgical closure of
and aortic override (Bove and Lupinetti, 1994; Pin
the PDA (Musewe and Olley, 1992).
sky and Arciniegas, 1990). A neonate with TOF will

have symptoms dependent on the extent of right ven
Endocardial cushion defects and
tricular tract obstruction, which results in decreased
artrioventricular defects
pulmonary blood flow and the presence of right-to
Endocardial cushion defects (ECD) represent a spec
left shunting (Bove and Luppinetti, 1994). The clas
trum of defects characterized by malformation of the
sic picture is one of cyanosis, especially with crying
atrial septum, the mitral and tricuspid valves, and/or
(EmmanouiIides and Baylen, 1988; Pinsky and
the ventricular septum (Emmanouilides and Baylen,
Arciniegas, 1990).
1988). Combinations of these defects are categorized
In neonates, initial medical management may in
as complete, transitionaVintermediate, and partial, de
clude treatment of hypoxemia by pharmacologically
pending on degree of ventricular septal deficiency
maintaining patency or reopening the ductus arterio
(Merrill, Hoff, and Bender, 1994; Spicer, 1984). In
sus for additional pulmonary blood flow (Driscoll,
the complete fOlm of ECD, all of the structures are
1990; Freedom and Benson, 1992). The elimination of
deficient. In the partial form, only an atrial septal de
conditions that produce hypoxemia may also include
f e c t w i t h a cleft mit ral valve is present ( E m
pharmacological agents to increase systemic vascular
manouilides and Baylen, 1988; Merrill e t ai., 1994;
resistance and decrease myocardial contractility (Bove
Parks, 1988).
and Lupinetti, 1994). Surgical repairs are generally
T h e r e is marked variation in the underlying

anatomy of this class of cardiac defects, such that
performed within the first year (Bove and Lupinetti,
1994; Starnes, Luciani, Latter, and Griffin, 1994).
clinical features are equally varied and difficult to in

clusively summarize. In neonates with a complete de
fect, heart failure may manifest in infancy. However,
neonates with milder forms of this defect may not be
Pulmonary Diagnoses
The section that follows provides a brief discussion
symptomatic until much later in development (Parks,
of common pulmonary disorders for which chest
1988). Additionally, endocardial cushion defects are
physical therapy is indicated. Additional physical
frequently associated with other cardiac defects (Em
therapy treatment is described later in this chapter.
manouilides and Baylen, 1988).
Hyaline membrane disease
Although the total incidence of endocardial cush

ion defects in infancy is 1 % to 4%, the incidence in
The most common respiratory disorder in premature
infants and children with Down syndrome is 40%
infants is hyaline membrane disease (HMD) or infant
(Freedom and Smallhorn, 1992). In fact, in these chil
respiratory distress syndrome (IRDS or RDS). Occur
dren a complete ECD is the most common cardiac
ring almost exclusively in preterm infants younger
malformation (Spicer, 1984).
than 37 weeks' gestation, HMD results from lung im
Operative management of infants and children
maturity and an inadequate amount and regeneration
with ECD depends on the morphology of the defect,
of surfactant (Phelan et ai., 1994). Surfactant func
the degree of pulmonary hypertension, and the extent
tions to decrease alveolar surface tension and thus en
35
641
abies the neonate to stabilize terminal air spaces (Wal
with severe BPD (Berman, Katz, Yabek, Dillon,
lis and Harvey, 1979). Surfactant deficiency results in
Fripp, and Papile, 1986; Gerhardt, Hehre, Feller, Re
alveolar collapse and increased effort to breathe.
infenberg, and Bancalari, 1987). Right-sided heart
Clinical signs of respiratory distress resulting from
failure (cor pulmonale) is a common sequelae of this
HMO occur early (usually within I to 2 hours) and
disease, especially in the first few years. Addition
persist for at least 48 to 72 hours (Farrell and Avery,
ally, BPD survivors demonstrate an increased inci
1975). Respiratory failure is 'common in these infants,
dence of neurodevelopmental sequelae, including
necessitating oxygen therapy and assisted ventilation.

Chest physical therapy (CPT) is commonly indi
cerebral palsy and general development delay (North

way, 1979; Vohr, Bell, and Oh, 1982).
cated in the management of infants with HMO. There
Chest physical therapy is an important component
is usually a marked increase in airway secretions in
of the management of an infant with BPD. Airway
the "recovery" state of the syndrome (after approxi
clearance problems are common due to submucosal
mately 2 to 3 days), which is exacerbated by oxygen
and peribronchial smooth muscle hyperplasia, in
therapy and endotracheal intubation (Crane, 1981;
creased mucous secretions, oxygen therapy, and fre

quent lower respiratory tract infections. Infants with
Finer and Boyd, 1978).
BPD also frequently have poor growth, which may be
Bronchopulmonary dysplaSia
a consequence of a higher resting V02, such that
As more preterm newborns survive neonatal respira

tory distress, the prevalence of chronic lung disease
or bronchopulmonary dysplasia (BPD) has increased
caloric needs are greater (Weinstein and Oh, 1981).
Transient tachypnea of the newborn
(Parker, Lindstrom, and Cotton, 1992). Although
Transient tachypnea (TTNB) is another neonatal
controversial, the etiology of BPD is usually linked
problem considered in the differential diagnosis of
with positive pressure ventilation and oxygen therapy
HMD/RDS. It is associated with delayed clearance of
in the treatment of respiratory distress during the
amniotic fluid from the lungs, results in early presen
neonatal period. The risk of BPD is highest in
tation of respiratory distress, and is most common in
younger, low-birth-weight premature infants (Abman
full-term and postterm neonates (especially if deliv

ered by cesarean) (Avery, Garewood, and Brumley,
and Groothius, 1994).

Northway, Rosan, and Porter's (1967) classic de
1966; Emmanouilides and Baylen, 1988). Chest
scription of BPD includes four pathological stages.
physical therapy is occasionally indicated for infants
The f irst stage invo lves s ymptoms si milar t o
with this problem, but TINB is uSllally self-limited.
HMD/RDS, but b y the fourth stage, BPD has pro

gressed to include characteristics of chronic lung dis
ease (Voyles, 1981).
Meconium aspiration syndrome

Meconium is the content of fetal and newborn bow
Clinically, infants with BPD often present with
els. Although the cause of meconium passage is
rales, wheezing, cyanosis, hypoxemia, increased inci
highly debated (Bacsik, 1977), once meconium is
dence of lower respiratory tract infections, and abnor
present in the uterine environment the risk for aspira
mal chest radiographs by I month postnatally
tion is significant. It is generally accepted that meco
(Abman and Groothius, 1994). Medical management
nium aspiration most frequently occurs with the first
of BPD is primarily supportive. Long-term oxygen
postnatal breaths of term or postterm infants (Gre
therapy is often necessary for infants who exhibit
gory, 1977), but it may also occur with gasping in
persistent severe hypoxemia.
utero just before delivery (Katz and Bowes, 1992;
The cardiopulmonary outcome of BPD is variable,
Wiswell and Bent, 1993). Research has supported tile
ranging from near normal pulmonary function by age
contention that meconium aspiration syndrome
3 to 5 in children who had milder forms of BPD, to
(MAS) is often preventable if the upper and lower
continued poor cardiopulmonary function, chronic
a i r w a ys a r e s u c t i o n e d immedi atel y after b i r t h
distress, and ongoing oxygen dependence in children
(Wiswell, Tuggle, and Turner, 1990). The lower air
642
PART VII
ways especially should be suctioned in infants deliv
i n g c a u s e of s y m p t o ms in ch ildren with HIV
ered through thick, particulate ("pea soup") meco
(Marold a, Pace, Bonforte, Kotin, Rabinowitz, and
nium in amniotic material (Gregory, 1977).

Aspiration of meconium can result in serious and
Katlan, 1991). In infants with perinatally acquired

HIV, pneumocyctis carnii pneumonia (PCP) fre
devastating pathophysiology. Most commonly, the
quently occurs within the first 15 months of life
meconium will partially or completely block the
(Connor et aI., 1991). The risk of mortality during
peripheral airways (Wiswell and Bent, 1993). At
the infant's first episode of PCP is high (Bagarazzi,
electasis is the classic finding, but with partial ob
Connor, McSherry, and Oleske, 1990; Bernstein,
struction, hyperexpanded areas will also be ob
Bye, and Rubinstein, 1989; Scott et aI., 1989).
served as a result of air that was inspired but then
The clinical presentation of PCP includes failure
trapped in distal, small airways. Common compli
to thrive, cough, dyspnea, tachypnea, fever, hypox
cations of MAS include tension pneumothorax, per
emia, and chest radiograph evidence of prominent air
sistent pulmonary hypertension, and bronchiolitis
b r onchograms
and pneumonitis secondary to chemical irritation
(Bagarazzi et aI., 1990; Berdon, Mellins, Abramson,
and mUltiple
cysts
or
bullae
from the components of the meconium (Wiswell
and Ruzal-Shapiro, 1993; Bernstein et aI., 1989).
and Bent, J 993). A d d itionally, long-term pul
PCP is most often diagnosed after bronchoalveolar
monary sequelae have been reported (MacFarlane
lavage studies (Phelan et aI., 1994).
and Heaf, 1988; Swaminathan, Quinn, Stabile,

Bader, Platzker, and Keens, 1989).
Treatment is supportive and includes antibiotic

therapy, antiretroviral therapy, nutritional support,
Medical management of MAS is supportive, with

supplemental oxygen and, if necessary, mechanical
and mechanical ventilation as needed (Bagarazzi et

aI., 1990; Phelen et aI., 1994).
ventilation. Chest physical therapy is especially advo
Asthma
cated during the first 8 hours of life, although it may

be necessary for a longer period of time if the infant
Although asthma is discussed in detail in Chapter 4, a

discussion of pediatric pulmonary problems would
requires assisted ventilation.
not be complete without some discussion of this com
Pneumonia
mon cause of childhood lung disease. An estimated
Neonatal Pneumonia. The most common organisms
8% to 10% of children in the United States have
producing neonatal septicemia associated with pneu
asthma, with asthma accounting for the most lost
monia in neonates are group B streptococcus and He
time from school and 33% of pediatrician visits per
mophilis inJluenzae (Emmanouilides and Baylen,
year (Magee, 1991).
1988). Neonatal pneumonia mimics HMD/RDS in

clinical presentation and chest radiographs.
Childhood asthma can begin at any age, and its

clinical etiology and clinical course are variable.
Aspiration Pneumonia. Aspiration is an unfortunate
Children with early medical histories including very
result of small children's "indiscreet curiosity" (War
low birth weight, bronchopulmonary dysplasia, and
ing, 1975) in exploring their environment and relying
respiratory syncytial virus infection may be at in
on their mouths for sensory learning. Aspiration can
creased risk for developing asthma (Pullen and Hey,
also result from gastroesophageal reflux and de
1982; Rickards, Ford, Kitchen, Doyle, Lisseden, and
creased upper airway neuromuscular control (Oren
Keith, 1987; Smyth, Tabachnik, Duncan, Reilly, and
stein and Orenstein, 1988).
Levison, 1981).
Bronchial drainage techniques are often indicated
Medical management usually includes avoidance
as part of the medical management of infants and
of known precipitants, adrenergic drugs, and corti
children after aspiration to aid with airway clearance
costeroids (in chronic, severe cases). Chest physical
and reduce the possibility of bacterial superinfection.
therapy for this disease includes patient and family
Pneumocystis Carnii PneumonialHIV-lnJected
education in breathing control, relaxation, effective
Children. Pulmonary involvement is often the lead
coughing, and exercise. Older children, in paJticular,
35
643
may benefit from CPT especially when they are re
breathing (ACB) technique, use of a positive expira
sponding slowly to pharmacological treatment alone
tory pressure (PEP) mask, autogenic drainage (AD),
(Asher, Douglas, Airy, Andrews, and Trenholme,
and use of the flutter device, have been shown to be
1990). Exercise, also highly effective in the treatment
effective in assisting sputum expectoration, often in
and management of asthma, is discussed in a later
greater amounts and in less time per treatment
section on pulmonary rehabilitation.
(Konstan, Stern, and Doershuk, 1994; Mahlmeister,

Fink, Hoffman, and Fifer, 1991; Pryor, 1991; Pryor
Cystic fibrosis
and Webber, 1979; Schoni, 1989).
Cystic fibrosis (CF) is a complex autosomal-reces
Although postural drainage, percussion, and vibra
sive disorder that affects the exocrine glands. Defini
tion remain the treatment of choice for infants and
tive diagnosis of CF includes positive family history,
children who are unable to be instructed in tech
obstructive pulmonary disease, recurrent pulmonary
niques that use patterns of voluntary breathing, other
infection, intestinal malabsorption and poor growth,
techniques are available for children who can follow
the
specific breathing instructions and who can perform a
presence
of
Slaphylococcus
aur eus
or
Pseudomonas aeruginosa i n the respiratory tract,
reliable pulmonary function test. Children as young
and, most importantly, a positive sweat chloride test
as 2 to 3 years can be taught to "huff' as part of FET
(Cystic Fibrosis Foundation, 1990).
(Pryor, 1991), the PEP mask has been used with chil
The chronic pulmonary disease in CF is related
dren as young as 3Y2 years (Mahlmeister et aI., 1991),
to increased secretion of a b n o rm a lly v i s c o u s
and AD can reportedly be taught to children as carly
mucus, impaired mucociliary transport, airway ob
as 4 to 6 years of age (DeCesare and Graybill, 1990;
struction, bronchiectasis, overinflation, and infec
Sci1oni, 1989). The benefits of each technique should
tion. Radiographic changes are most pronounced in
be carefully considered relative to each child's cogni
the upper lobes, especially the right (Wood, Boat,
tive, respiratory, and motor planning abilities when
and Doershuk, 1976).
choosing or modifying the child's program for airway
The early institution of prophylactic pulmonary
clearance.
physical therapy, including postural drainage and the
Ventilatory muscle training is an important aspect
judicious use of antibiotics, provides effective mea
of pulmonary treatment in older children with CF.
sures for controll ing or slowing the effects of bron
Studies have demonstrated that training to improve the
chiolar and bronchial obstruction. Involvement of the
endurance of ventilatory muscles decreases dyspnea
child and family in pulmonary care is particularly im
and increases general exercise tolerance in patients
portant. Family understanding of the nature of the
with CF (Keens, Krastins, Wannamaker, Levison,
disease and the purpose of each therapeutic measure
Crozier, and Bryan, 1977; Reid and Loveridge, 1983).
promotes successful management of the child. A
The role of general exercise in the cardiopul
home program of CPT should be established for each
monary management of children with CF is specifi
child, taking into consideration the child's ongoing
cally discussed within the context of pulmonary reha
pulmonary needs and the family's unique contribu
bilitation. However, it is important to realize that
tions and constraints.
some debate exists as to whether exercise can replace
Bronchial drainage is an aspect of conventional
more traditional airway clearance techniques. Pryor
treatment for CF that in recent years has gained sev
(1991) has suggested that exercise should be an addi
eral options that allow both efficacy and patient in
tional component rather than a substitute for breath
dependence (Davis, 19(4). Airway clearance tech
ing techniques. Cerney (1989) in contrast, reported
niques are described in detail in Chapter 20, but
that some children with mild disease may be able to
alternatives to traditional percussion and postural
use regular exercise in place of bronchial drainage
drainage warrant mention within the context of CPT
treatments. The severity of the disease process and
for children with CF. Specifically, the forced-expi
the child's condition at any one point in time, will
ration technique (FET) as part of the active cycle of
clearly mediate the appropriateness and effectiveness
644
PART VII
of exercise as either a component or as a primary
These deviations and other aspects of ventilatory
means of airway clearance.
compromise are discussed with regard to motor diag
Special respiratory problems associated

with intubation and tracheostomy
Once an infant or child develops respiratory failure,
noses common to pediatric practice.
Cerebral palsy
Children with cerebral palsy generally have weak trunk
intubation and mechanical ventilation are usually re
and postural muscles, which, when combined with atyp
quired. The goals of medical management are then to
ical neural mechanisms, produce atypical movement
treat the cause of the respiratory failure as aggres
pattems and functional alignment deviations. The trunk
sively as possible and to wean the child from me
and respiration relationshi[ls described in Table
chanical ventilation as quickly as possible.
consistent with the clinical picture of external pul
If a child's condition necessitates long-term me
35-3 are
monary development in children with cerebral palsy.
chanical ventilation, or if an artificial airway is needed
Although the extent of mobility impair ment is
to bypass an upper airway obstruction, a tracheostomy
variable between children, hypoventilation, increased
is usually petformed (Scott and Koff,
1993).
Infants and children who have a tracheostomy and
work to breathe, inefficient cough, increased risk for

aspiration, and poor breath support for vocalization
1993). Limited active mobility
are intubated for long periods of time require vigorous
can occur (Alexander,
prophylactic airway management, such as bronchial
and the use of habitual patterns with little deviation
drainage and airway suctioning. Chest PT, including

postural drainage and vibration emphasizing right
upper lobe segments, has been shown to significantly
decrease the incidence of postextubation atelectasis in
infants intubated for more than 24 hours (Finer, Mori
artey, Boyd, Phillips, Stewart, and Ulan,
1979).
Pulmonary Considerations in Neuromuscular

and Motor Diagnoses
Although cardiopulmonary symptoms may not be
the primary reason for referral to physical therapy in
children with neuromuscular and general motor de
velopmental diagnoses, these children do have motor
involvement that can result in respiratory and pos
tural muscle weakness, immobile chests, and hy
p oventilation. Furthermore, many of these children
have had medical histories remarkable for cardiopul
monary complications or have diagnoses that entail
progressive processes that will result in cardiopul
monary compromise.
Table
35-3 provides an extensive summary of the
interactions between trunk musculature and ventila

tion in children with atypical development. Although
the biomechanical deviations noted are frequently
seen in children with atypical tonal presentations,
FIGURE 35-1
they are also common in children with scoliosis, ster
Flattened anterior chest with marked rib flaring in a child
nal deformity, or general immobility of the thorax.
with cerebral palsy.
35
645
TABLE 35-3
Functional Relationships of Trunk Control and Respiration
BIOMECHANICAL
POSTURAUfRUNK CONTROL
RESPIRATORY
COMPONENT
CONSEQUENCES
CONSEQUENCES
Passive lumbar lordosis
Ineffective cough
Weak abdominal obliques
Protruding tummy
High chest
Lower rib flaring
Retained horizontal rib alignment
Decreased trunk rotation

Unable to weight shift
Tight rectus abdominis may lead to
Dependence on rectus abdominis
pectus excavatum
Child may use diapl1ragm for trunk
control, limiting its function as a
primary muscle of respiration
Decreased support of abdominal
contents under diapmagm
Anterior upper chest cannot adequately
Forward shoulders
Tight pectoralis minor
Scapula pulled laterally and anteriorly,
expand
away from the thoracic wall

Upper thoracic flexion
Weak serratus anterior
Wcak upper fibers-medial edge of

scapula Icaves the thoracic wall
Decreased structural reinforcement

of the posterior chest wall
Interdigitation of the lower fibers of
serratus anterior with the external
abdominal oblique will interact to
affect the dynamic stability of the
rib cage
Decreased active upper
Approximation of upper ribs
Kyphotic upper trunk
thoracic extension
scapular retractors
-7
decreased oxygenation of the upper

lobe
Decreased rib cage stability
-7
decreased upper chest mobility
Passive overlengthening of the
Serratus anterior will elevate the ribs

rather than stabilize the scapula
-7
abdominal breathing
Decreased structural support for the

respiratory muscles to work from
against the thoracic wall
Modified from Moerchen

the
Neurology Report
V A:
Respiration and motor development: a systems perspective,
with the permission of the Neurology Section,
Neural Rep 18 (3): 8-10, 1994.
Reprinted from
APTA.
of the center of gravity beyond the base of support
chest excursion and should be incorporated into a
contribute to thoracic stiffness. A high chest, flat
home program. Mobilization of the ribs and thoracic
tened anteriorly, with excessive rib flaring, is com
spine are important precursors to improving chest ex
mon in these children (Figure 35-l).
cursion during ventilation.
Therapeutic attention to respiration should first
Chest PT may be indicated if the child develops a
identify possible aspiration and suggest modifications
primary pulmonary complication. Prophylactic pos
for positioning during feeding. Additionally, certain
tural drainage can also be integrated into many sen
postures for sleep and play may be less restrictive for
sory stimulation programs for more severely involved
646
PART VII
children. Additional "handling" to address ventilatory

function will be discussed in
subsequent section on
motor approaches to respiratory treatment.
Myelomeningocele
Myelomeningocele or spina bifida are diagnoses that
physical therapists generally equate with issues of am
bulation and mobility. However, central ventilatory
dysfunction is prevalent in infants, children, and ado
lescents who also have an associated Arnold-Chiari
type II malformation (Hays, Jordan, McLaughlin,
Nickel, and Fisher, 1989; Swaminathan et aI., 1989;
Ward, Jacobs, Gates, Hart, and Keens, 1986).
The Arnold-Chiari type II malformation, which oc
curs in 90% of infants with myelomeningocele, is a
hindbrain malformation consisting of a caudal helllia
tion of the cerebellum and brain stem into the cervical
canal (Charney, R orke, Sutton, and Schut, 1987).
Ventilatory problems associated with a symptomatic
Arnold-Chiari type II malformation include inspira
tory stridor (vocal cord paralysis), central apnea, and
respiratory distress (Hays et aI., 1989; Hesz and Wol
raich, 1985; Oren, Kelly, Todres, and Shannon, 1986).
However, abnormal ventilatory patterns have also
been observed in asymptomatic infants (Ward et aI.,
1987) and adolescents (Swaminathan et aI., 1989).

Ventriculoperitoneal shunting (management of hy
FIGURE 35-2
An 8nterior cut-out and elastic support in a body
jackel/spinal orthosis aids diaphragm function.
drocephalus) and, if necessary, cervical decompres

sion are the surgical approaches to treatment of life
Down syndrome
threatening ventilatory complications in this population.

Other
p u lmonary
issues
in
c h ildren
with
Impaired pulmonary function in children with Down
myelomeningocele warrant discussion. TtUnk weakness
syndrome is clearly related to generalized weakness of
and hypotonia are observed early in the motor develop
trunk musculature (Dichter, Dmbee, Effgen, and Pal
ment of infants and toddlers who have shunted hydro
isano, 1993). The postural deviations common in these
cephalus. Additionally, in children with thoracic and
children reflect (Figure 35-3) inefficient muscle func
high lumbar level lesions, abdominal muscle SUpp0l1 for
tion for both ventilation and movement
diaphragm function may be insufficient. The use of ab
1994). Again the ttUnk-ventilation relationships delin

eated in Table 35-3 summarize the subtle but significant
dominal binders, and spinal othoses/body jackets with
(Moerchen,
(anterior) diaphragm cut-outs and an elastic inse11 are
clinical presentation of external pulmonary develop
indicated to aid in diaphragm function (Figure 35-2).
ment in these children. Too often only motor develop
Although progressive scoliosis is not the natural history
ment is addressed by physical therapists who are treat
of children with spina bifida, it is a symptom of unstable
ing children with Down syndrome. Respiration needs to
neurology (tethered cord), and attention to ventilatory
be considered if therapy goals include increased vocal
ability is necessary both for general monitoring and for
izations or improved tolerance for exercise.
possible preoperative evaluation.
Pulmonary hypoplasia may also challenge the res
35
647
FIGURE 353
A, Characteristic posture of a child with Down syndrome/hypotonia. Note the abdominal protrusion
and sternal retraction. B, Rib flaring with upper extremity movement; the abdominal obliques are
not stabilizing the lower ribs.
(1994). Respiration and Motor Development: a Systems Perspective.

18(3), 8-10. Reprinted with the permission of the Neurology Section, APTA.
Photos from Moerchen, V.A.

Neurology Report,
piratory function of these children. Cooney and Thurl
Muscular dystrophy
beck (1982) observed a consistent combination of de
Duchenne's muscular dystrophy involves end-stage
creased numbers of alveoli and larger alveolar ducts
respiratory failure that results from progressive respi
in individuals with Down syndrome, not related to age
ratory muscle weakness, thoracic deformity, reduced
or incidence of heart disease. Although these re
lung compliance, retained secretions, ventilation
searchers had a small sample size, their results do sug
peIi'usion imbalance, and hypoxemia (Bach, O'Brien,
gest that trisomy 21 may result in lung vulnerability.
Krotenberg, an d Alba, 1987; Smith, C alverley,
648
PART VII
Edwards, Evans, and Campbell, 1987). In 70% to
niIe rheumatoid arthritis (JRA) may have inflamma
90(;1(:
tion of thoracic joints or may splint through their
strictive respiratory complications (Bach et aI., 1987;
trunks when they try to move painful extrcmities.
Smith et aI., 1987).
With thcsc children, brcathing exercises will have a
Physical therapists are typically involved in treat
role both in pulmonary carc and in pain management.
ment of these paticnts for preservation of motor func
Put simply, children who make cumpensatiuns in
tion. Early attention to ventilation, however, is war
their movement patterns to accomlllodate pain, weak
r a n t ed. P r o phyla c t i c spi n a l f u s i o n to pre v e n t
ness, or deformity, may limit the mechanics of their
scoliosis-related compromise o f ventilation i n these
thoraces. Con versel y. chi I dren who cannot ade
patients considers both the progrcssion of the spinal
quately oxygenate may make compensations in their
curvature and vital capacity (YC) (Rideau, Glorion,
movement patterns to SUpp0l1 ventilation. Clearly, at
Delauber, Tarle, and Bach, 1984).
tention to ventilation should be an inherent aspect of
Chest physical therapy should be a component of

the overall rhysical therapy management of children
observing motor development and quality of move

ment in all children.
with muscular dystrophy. Deep breathing, coughing,

and activitics to addrcss cndurance arc recommended
but will require ongoing modification as the disease
progresses. Inspiratory muscle training in these chil
dren remains controversial. Although some researchers
PHYSICAL THERAPY TREATMENT APPROACHES

Postoperative Pediatric Cardiac Rehabilitation
havc del11on. trated improved endurance of ventilatory
Postopcrative physical therapy consists largely of
muscles (DiMarco, Kelling, DiMarco, Jacobs, Shields,
techniques to increase respiration, mobilize secretions,
and Altose, 1985; Martin, Stern, Yeates, Lepp, and Lit
and progress physical mobility. Positional rotation for
tle, 1986; Stern, Martin, Jones, Garrett, and Yeates,
pulmonary care is pussible if the child has a stabilized
1991), other researchers have suggested that inspira
sternum. Breathing exercises and coughing will need
tory resistance may over-tax respiratory muscles that
to be modified based on the child"s age and cognitive
are all'eady near fatigue due to working against incom
level. Huckabay and Daderian (1990) reported im
pliant structures (lungs, thorax) (Smith, Coakley, and
proved postoperative cooperation in children 3 to 10

years of age when choice making was incorporated
Edwards, 1988).
Respiratory dependence does occur as the disease
into a breathing program.
progresses. Protocols for point of initiation and type
Immobilization after cardiac surgery is to be
of mechanical ventilation are being studied. There is,
avoided as much as medically possible. Passive range
however, agreement that close monitoring of YC and
of motion may be initiated immediately, with care to
of nocturnal hypoventilation can allow respi ratory
avoid compromising arterial lines. Ambulation is
support to be implemented before the onset of acute
generally initiated once the child is extubated and has
respiratory failure (Bach, Alba, Pilkington, and Lee,
had atrial and groin lines removed (Johnson, 199 I).
1981; Bach et aI., 1987; Curran, 198 I).
Child and family education as part of pediatric

cardiac rehabilitation has been observed to reduce
Miscellaneous conditions
parent and child anxiety related to safe levels of
Multiple other pediatric diagnoses and musculoskele
pllysical activity (Balfour, Drimmer, Nouri, Penning
tal conditions include clinical presentations (strength,
ton, Hemkens, and Harvey, 1991; Calzolar et ai,
alignment, and limited mobility) that should cue the
1990; Mathews et ai, 1983). Although studies of pe
therapist'S attention to pulmonary function. Syn
diatric cardiac rehabilitation have been focused on
dromes that involve sternal deformity such as Marfan
children older than 6 years, monitored exercise has
syndrome or Poland's syndrome will clearly entail
been shown to safely produce an increase in peak
possible ventilatory compromise. Children with juve
oxygen consumption and a decrease in resting heart
35
649
Nouri, P e n n i n g t o n,
of lymph nodes, making it vulnerable to extrinsic
Hemkins, and Harvey, 1991; Calzolari et aI., 1990;
compression. Important considerations and essentials
Mathews et aI., 1983).
of a positional rotation program for infants are out
r a t e (B a l f o u r, Dri m m e r,
Exercise prescription for cardiopulmonary rehabili
lined in the box below.
tation of older children who have undergone cardiac re
It is important to note that premature infants do
pairs at an early age will require careful monitoring.
tolerate and benefit from prone positioning. Studies
Lower exercise V02 values, lower cardiac output, and
have demonstrated improved oxygenation, tidal vol
lower values of diffusion capacity of the lung for car
ume, dynamic lung compliance, and synchrony of
bon monoxide have been observed in response to exer
chest wall movement when preterm infants are put in
cise in children who have undergone cardiac surgery as
prone positions (Hutchinson, Ross, and Russell,
compared with the responses of age-matched controls
1979; Lioy and Manginello, 1988; Martin, Harrell,
(Gildein, Mocellin, and Kaufmehl, 1994; Tomassoni,
Rubin, and Fanaroff, 1979).
Galioto, and Vaccaro, 1991). Exercise recommenda
Positional rotation is generally performed manu
tions include submaximal performance (Tommassoni et
ally every 2 hours, and, although this provides pul
aI., 1991) and technique training to increase the biome

chanical efficiency of movement while decreasing the
associated metabolical costs (Gildein et aI., 1994).
Essentials of a Positional ROUl/ion Program

Chest Physical Therapy for Neonates and Infants
I.
The plimary goal of chest physical therapy for neonates

and infants is to improve airway clearance. If tech
niques of bronchial drainage can increase the diameter
of the airways through secretion mobilization, then
ventilation may also be improved and the work of
breathing reduced. These techniques should be judi
ciously applied for prophylaxis and treatment in infants
who have or are at risk for developing airway clearance
problems. Applying bronchial drainage techniques to
infants requires a thorough understanding of each in
Care should be taken to coordinate any change

in the infant's position with other nursing proce
dures to avoid unnecessary stimulation.
2.
Infants should never be left unattended when in

a head-down position.
3. Vital signs should be monitored closely by res

piration and heart rate monitors. The alarms
should be turned on.
4. The infant's chest should be auscultated for ad

ventitious breath sounds after positioning.
5. While the infant is in a drainage position, secre

tions will be more easily mobilized. The infant's
fant's condition and the precautions and considerations
trachea or endotracheal tube should be suctioned
inherent to any technique or combination of techniques.
as needed.
6. Avoid placing the infant in a head-down posi

tion for approximately I hour after eating to
Positional rotation
Frequent changing of position will prevent prolonged
dependency of any one portion of the lung, so that
pooling of secretions can be limited/avoided and im
proved ventilation can be achieved (Menkes and
Britt, 1980; Ross and Dean, 1989). Whereas posi
tional rotation programs for adults emphasize the
lower lobes, positional programs for infants must em
phasize all lung areas (Figures 35-4 to 35-6). The
upper lobes and right middle lobe are common sites
of airway collapse and atelectasis in infants, and the
avoid aspiration of regurgitated food.
7. Any change in the infant's position should be

done slowly to minimize stress on the cardiovas
cular system.
8. Infants with umbilical arterial lines can be

placed on their abdomens. However, one should
always check that the line has not been kinked.

9. Some infants might require modified drainage
positions. Infants with severe cardiovascular in
stability or suspected intracranial bleeding
should not be placed in a head-down position.
right middle lobe bronchus is surrounded by a collar
650
PART VII
J.
FIGURE 35-4
Sequence for positional rotation.
Position I.-Segments that come off the left lower bronchus posteriorly are drained by positioning
the infant on his right side, three-foUl1hs prone with a head-down angle. Position 2.-The posterior
segment of the right upper lobe is drained by positioning on the left side, three-fourths prone with
the bed flat. Position 3.-The anterior segments of the upper lobes are drained by positioning
supine with the head of the bed elevated or flat. Position 4.-Segments that come off the right
lower lobe bronchus posteriorly are drained by positioning on the left side, three-fourths prone with
a head down angle.
35
4.
5.
FIGURE 35-4-cont'd
Position 5.-The posterior segment of the left upper lobe is drained by positioning on the right
side, three-fourths prone with the head of the bed elevated. Position 6.-Segments that come off
the tracheobronchial tree anteriorly are drained by positioning supine with a head-down angle.
Positu)1Is 7 and 8.-Segments such as the right middle lobe or lingula that come off the
tracheobronchial tree anterolaterally will be drained in a three-fourths spine position, slightly head
dow (see Figure 35-5, p. 652).
NOTE:
Babies on ventilators may also be positioned prone. This is usually done by the therapist
rather than in a routine positional rotation (see Figure 35-6, p. 652).
651
652
PART VII
FIGURE 35-5
FIGURE 35-6
Three-fourths supine position for right middle lobe. Lingula
Premies (even those on ventilalOrs with numerous
is the same three-fourths supine position with the patient
catheters) may be placed prone when care is taken.
lying on his right side.
monary benefit, it may also contribute to the disrup
ing less than 800 grams) usually require and benefit
tion of homeostasis that has been documented to
from modification of the head-down position. Hori
occur in the course of neonatal intensive care (Long,
zontal to slightly elevated positioning of the head may
Philip, and Lucey, 1980; Yeh, Lilien, Leu, and
be best (Thoresan, Cowan, and Whitelaw, 1988). This
Pildes, 1984). Use of nursery beds that provide con
modification primarily is due to the high incidence of
tinuous positional oscillation (from right side to
intraventricular hemorrhage in premature infants
supine to left side, and so forth) might provide an op
(Crane, Zombek, Krauss, and Auld, 1978; Emery and
tion that allows the benefits of position change while
Peabody, 1983). Other precautions for Trendelenburg
also minimizing the homeostatic disruption. Murai
positioning of infants include but are not limited to
and Grant (1994) demonstrated that continuous posi
abdominal distention, congestive heart failure, dys
tional oscillation as part of a total chest physical ther
rhythmias, hydrocephalus, frequent episodes of apnea
apy program decreased the duration of oxygen sup
and bradycardia, and acute respiratory distress.
p l e m e n t a ti o n w i t h o u t a d v e r s e ly e f f e c t i n g t h e
cardiopulmonary status o f the neonates.
Chest percussion and vibration

Percussion and vibration are used in conjunction with
Postural drainage
postural drainage to augment the effect of gravity in
Postural drainage (PD) positions to promote gravity
the removal of secretions. There are several ways to
assisted drainage of specific segmental airways can be
perform percussion on infants. For a larger infant, it
safely applied to infants and children. In the acute care
is possible to use a cupped hand, similarly to per
setting, however, many of the head-down positions
cussing an adult's chest. For a smaller infant, some
are modified according to tolerance and precautions or
modification of this technique is needed. Chest per
contraindications (Table 35-4). The rule for modifica
cussion for a smaller infant is accomplished by the
tion of any position for PD is that the position used
use of tenting three fingers, four fingers, or using any
should be as close to the classical (anatomically cor
of the commercially available percussion devices
rect) position for that segment as safely possible. Ex
made for neonates (Figure 35-8). A small anesthesia
amples of the classical PD positions for each bron
mask or "palm cup" can also be used effectively.
chopulmonary segment are pictured in Figure 35-7.

Tiny infants (especially premature infants weigh-
Precautions for chest percussion in the infant in

clude but are not limited to unstable cardiovascular or
3S
653
TABLE 35-4
Precautions and Contraindications for Postural Drainage in a Neonate*
POSITION
PRECAUTION
CONTRAINDICA TlON
Prone
Umbilical arterial catheter
Untreated tension pneumothorax
Continuous positive airway pressure

in nose
Excessive abdominal distention
Abdominal incision
Anterior chest tube
Tendelenburg position
Distended abdomen
(head down)
Untreated tension pneumothorax
SEHlIVH* (grades I ancllI)
Recent tracheoesophageal fistula repair
Chronic congestive heart failure or
Recent eye or intracranial surgery
cor pulmonale
Intraventricular hemorrhage (grades III
Persistent fetal circulation
and IV)
Acute congestive heart failure or cor

pulmonale
Apnea and bradycardia

Infant exhibiting signs of acute
respiratory distress
Hydrocephalus
Less than 28 weeks' gestational age
'Subependymal hemorrhage/intraventricular hemorrhage.

From Crane LD: Physical therapy for the neonate with respiratory disease. ln [rwin S, Tecklin JS, editors:
therapy,
SI. Loui"
1995,
Cardiopulmonary physical
Mosby.
oxygenation status (although percussion may be pro
bration will depend on the day-to-day medical status of
vided safely if continuous transcutaneous monitoring
the infant and the infant's response to treatment.
is available), coagulopathy, subcutaneous emphy

sema, or intraventricular hemorrhage. Additionally,
Airway suctioning
percussion is generally contraindicated over a healing
Sterile airway suctioning is discussed in detail in
thoracotomy incision or if the child displays ilTitabil
Chapter 42. However, some special considerations
ity and signs of rcspiratory distress with the treatment.
for suctioning the a i rway of an infant need to be
Vibration is accomplishcd either through manual vi
highlighted (Durand, Sangha, Cabal, Hoppenbrowers,
bratory motion of the therapist's fingers on the infant's
and Hodgman,
chest wall (Figure 35 -9) or through the use of a me
Volpe,
1989; McFadden, 1981; Perlman and
1983).
chanical vibrator. An electric toothbmsh can be adapted
1. If possible, suction with a transcutaneous oxy
by padding the bristle portion with foam (Cun'an and
gen monitor in place. These monitors give con
Kachoyeanos, ) 979). Vibration has been observed to
tinuous feedback regarding the infant's oxy
occasionally increase irritability and may be less well
genation status.
tolerated than percussion. The most common precau
2. Bagging should be done only with a bag at
tion for vibration is increased irritability with the devel
tached to a pressure manometer to ensure that
opment of bradycardia alld respiratory distress.
sufficient prcssures are being used without ex
The decision to use chest percussion and vibration

will depend on the reviewed principles and precautions,
the medical condition of the infant, and the infant's tol
erance to handling. Continuation of percussion and vi
ceeding the maximum safe le v els (these l imits

should be similar to the ventilator settings).
3. Suction for no more than 5 seconds with each

catheter withdrawal.
654
PART VII
Guidelines for the Delivery of Cardiopulmonary Physical Therapy: Special Cllses
- --:---
'-
:.-
FIGURE 35-7
Postural drainage with an infant. A, Both upper lobes-apical segments. B, Left upper lobe-
anterior segment. C, Right upper lobe-anterior segment. D, Lingula.
35
FIGURE 35-7-cont'd
E, Right middle lobe. F, Right upper lobe-posterior segment. G, Left Lipper lobe-posterior
segment. H, Both lower lobes-apical (superior) segments.
655
656
PART VII
FIGURE 35-7-cont'd
I, Both lower lobes-anterior basal segments. J, Left lower lobe-lateral basal segment; Right
lower lobe
arduac (medial) segment. K, Both lower lobes-posterior basal segments. L, Right
lower lobe-lateral basal segment.
35
657
FIGURE 36-8
'Tenting" of the finger for percussion of premies or small children.
FIGURE 36-9
Manual chest wall vibration of a premie.
4. Infants should be carefully hyperoxygenated
tions and imitating a therapist's demonstration of deep
when hyperventilated so as to minimize hyper
breathing, coughing, and active exercise. Chest physi
oxia and hypoxia. Bagging usually does not
cal therapy in children is focused on improving venti
10 seconds
lation, improving the efficiency of breathing, increas
5. Monitor the blood pressure of preterm infants be
on muscles of respiration, improving posture, and ad
need to continue for more than 5 to

to maintain adequate oxygen levels.
ing general strength and endurance with an emphasis
fore, during, and after suctioning. Change in
dressing relaxation, breathing control, and pacing.
blood pressure may indicate increased intracra
The application of chest PT with children often re
nial pressure and risk for intracranial hemOtThage.
quires patience and creative adaptation (Figure 35-
10). The challenge is to make it seem less like a treat

ment and more like a game. It is important, however,
Chest Physical Therapy for Children
to be honest in your explanations and to speak to the
The goals for chest physical therapy with children
(2
years and older) include more than improving airway

clearance. Children are capable of following direc
child with respect and at a level appropriate to the

child's age and development.
Involving the family in PT treatment of a child can
658
PART VII
FIGURE 36-10
A, B, C, Few areas of health care delivery require creative adaptation and problem solving to the
extent that pediatrics does.
be invaluable. In some cases the parent may do most
tant to have his position changed, changing the loca
of the "hands-on" and repeat instructions to the child
tion of the television may be helpful. Be creative!
under the direct guidance of the therapist. This
Young Children. In younger children (18 months to 3
arrangement will also help reinforce parent and fam
years) deep breathing is usually encouraged by blow
ily education for carry-over of home therapy.
ing bubbles, tissue paper, mobiles. or simple horns. To

achieve maximal chest expansion, the child should be
Positional rotation
positioned on each side while playing blowing games
The goal of positional rotation and postural drainage
or singing. The theory behind the side lying position is
is to prevent the accumulation of secretions and to aid
that the downside lung ventilates more effectively (see
in their removal. Any child who is immobile, receiv
Chapter 18). Additionally, if the poorly ventilated
ing artificial ventilation, or not expanding his chest
lung is uppermost, stretch techniques can facilitate
adequately should have his position changed at least
deeper breathing (see Chapter 22).
every 2 hours. Recall that positional changes will en
Spontaneous coughing in younger children often
hance oxygen transport and promote pulmonary
occurs with a change in position or with crying. For
drainage (Ross and Dean, 1989). If the child is reluc
the child who does not cough spontaneously or whose
35
659
FIGURE 35-11
Whistles such as these encourage increased inspiration and controlled, sustained expiration to make
the whistle components move
(left:
a fish with a wheel that moves at its back fin;
middle:
a race car
that drives around a track making whirling sounds; right: a ball that moves up and down in a train).
cough is inadequate to clear secretions, nasopharyn
treat ment by therapists helps to decrease the inci
geal suctioning may be necessary.
dence of postoperative complications.
Older Children. School-age children can be more
Preoperative teaching is extremely important for
specifically instmcted in various breathing exercises,
both the child and the family. Parents can often be
such as diaphragmatic breathing, pursed-lip breathing,
more anxious than the child, so patient and family ed
and segmental lateral costal breathing. They may also
ucation is important. The level of preoperative train
be candidates for using relaxed deep breathing for
ing with the child will depend on the child's age.
control and pacing of activity. Cooperation with this
If the child is very young (under 2 years), the thera
age group, however, still remains higher if some as
pist will meet with the parents and explain the purpose
pect of therapy is fun. Elaborate whistles are available
of bronchial drainage treatments, potential airway clear
that encourage deep breathing as a fun means to an
ance problems, and possible complications. The pre
end of making the whistle components move (Figure
ventative nature of these treatments should be stressed,
35-11). Additionally, pediatric incentive spiro meters
and procedures that might be done with the child after
are available with cheerfull"cool" pictures to make
surgery should be demonstrated and discussed. These
respiration exercises more like a game (Figure 35-12).
might include: (I) positioning, (2) chest percussion,
Older children (not infants) can be stimulated to

cough by applying a firm pressure over the trachea in
(3) vibration, and (4) airway suctioning. In addition, al

ways allow time for the parents to ask questions.
the suprasternal notch. Beware t h a t coughi ng,
If the child is able to understand simple concepts,
whether spontaneous or stimulated, may elicit gag
the therapist can, in addition to parent orientation, in
ging and vomiting, especially if airway clearance is
stmct the child in various breathing games, use of an

incentive spirometer, coughing, and general upper
scheduled too soon after a child has eaten.
and lower extremity exercises.
Preoperative and postoperative care
In older children (8 years or older), postoperative
The efficacy of postoperative chest PT is highly re
procedures can be explained and demonstrated. The
lated to preoperative care. The appropriate applica
importance of bronchial hygiene should be stressed
tion of preoperative assessment, instruction, and
during demonstration of deep breathing and cough
660
PART VII
are atelectasis, infection secondary to pooling of se

cretions, and airway obstruction. Infants and children
with the following characteristics will be at risk for
developing postoperative pulmonary complications:
(I) preexisting lung disease, (2) thoracic or upper ab

(3) prolonged post
operative bedrest or restricted mobility, and (4) neu
dominal location of the incision,
romuscular involvement that affects the ability to be

mobile and to cough and deep breathe.
Postoperative treatments generally focus on in
creasing ventilation, coughing, and active mobility.
Specific bronchial drainage is used only if the child is
unable to clear his or her airways or is at risk due to
chronic lung disease.
After high abdominal or thoracic surgery, there
may be a tendency for the child to splint on the side
of his or her incision. Arm, shoulder, and trunk
movement should be encouraged to prevent any post
operative complications. For the younger child, chest
mobility can be encouraged by clapping the hands
overhead or by dramatizing songs such as The Itsy
Bitsy Spider. More conventional exercises may be
taught to the older child.
Children tend to mobilize very quickly (unless
their movement is limited secondary to motor in
volvement or to a specific surgical procedure). Once
the child is out of bed and moving about, with clear
lungs and an effective cough, postoperative CPT
treatments can generally be discontinued.
FIGURE 35-12
A pediatric incentive spirometer. (Photo provided courtesy
of DHD Medical Products. Used by permission.)
Pediatric Pulmonary Rehabilitation

Rehabilitation programs for pediatric patients with
chronic lung disease include the same components
and have essentially the same goals as adult pul
ing. The child can be shown how to splint the inci
monary rehabilitation. The major difference is related
sion using a pillow or stuffed animal to assist with
to different diagnoses being most prevalent in the
comfort while coughing. Do not tell the child that
children versus adult age groups. Asthma and CF are
coughing will not hurt; be honest but reinforce that
the most common diagnoses of children who are can
splinting will help. Teach the child diaphragmatic
didates for pulmonary rehabilitation.
and pursed-lip breathing with an inspiratory-hold ma
Exercise and asthma
neuver, and, if appropriate, teach the child how to use

an incentive spirometer.
Exercise and conditioning are very important compo
Postoperative pulmonary complications may not
nents of the treatment of the child with asthma. Im
be as prevalent in the pediatric age group as in adults,
proved chest and trunk mobility, control of breathing,
but they still occur. The most common complications
strength, posture, and an increased tolerance to exer
35
cise are all goals that can be addressed in the design
661
oxygen desaturation during exercise in children with
of exercise programs for these children (Magee,
CF (Coates, 1992). Loutzenhiser and Clark (1993),
1991; Seligman, Randel, and Stevens, 1970).
however, suggested that severity of CF is not the pri
Part of a pulmonary rehabilitation program may
mary limiting factor in the exercise capacity of these
involve providing recommendations for the child's
children. Clearly, any aerobic exercise program de
participation in physical education (PE). Certain as
signed for older children with CF will require careful
pects of exercise relative to pul monary function in
monitoring of pulmonary support during exercise.
children with asthma need to be communicated to the

PE teacher. Running is the form of exercise most
likely to aggravate exercise-induced asthma, espe
cially if performed in a cool, dry environment. Swim
Motor Approaches to Maximize Trunk

and Ventilatory Function
ming, by contrast, is an excellent activity. Continuous
Attention to pulmonary function is easily accom
or high burst exercise might induce bronchospasm,
plished within any "handling" approach to motor
whereas short periods of exercise (less than 6 contin
therapy for children with trunk weakness, tightness,
uous minutes) may be beneficial for conditioning
alterations in tone, or general immobility. Most "han
wi thout bronchial aggravation (Magee, 1991). PE
dling" consistent with a neurodevelopmental tech
teachers should also be aware that the child may need
nique (NDT) approach lends itself readily to a dual
to use a preexercise aerosol to participate in PE with
focus on movement quality and ventilation. Extrinsic
out pulmonary consequence (Magee, 1991).
pulmonary development is clearly interrelated with

musculoskeletal and motor development of the trunk.
Exercise and cystic fibrosis
Treatment should begin with assessment and ini
Physical activity designed to improve exercise toler
tial handling for functional range of motion through
ance helps children with CF to mobilize secretions
the trunk. This will typically require elongation of the
and to improve body image. The development of an
pectoral, sternocleidomastoid, upper trapezius, and
exercise program for children with CF should be done
rectus abdominis muscles. Manual lowering of the rib
on a individualized basis and a preexercise assessment
cage will also be necessary to work toward maximiz
should include but not be limited to the following:
ing chest mobility (Figure 35-13).
I. Assessment of range of motion, strength, and
Passive elongation of muscles must always be

followed by active elongation. Controlled prone
posture.
2. Complete chest evaluation.
extension off the ball is both fun for the child and
3. Evaluation of ADL tolerance and limitations.
effective for the therapist (Figure 35-14). Manual
4. Inspiratory muscle strength (maximal inspira
guidance for upper extremity abduction and exter
tory ncgativc pressure at the mouth) and en
nal rotation will facilitate active elongation of the
durance testing. This inspiratory endurance
pectoral muscles via active firing of the scapular
testing can be done with an inspiratory muscle
retractors. The ball can be used to impart move
training device by having the child breathe for
ment and support the lower rib cage. This elon
a predetermined length of time at progressively
gates the anterior trunk (rectus abdominis), length
increased resistances until tolerance is reached.
5. Exercise tolerance testing, performed with

ECG, blood pressure, and oxygen monitoring.
A basic exercise program for children with CF
ens intercostal muscles, and facilitates increased

upper chest expansion.
Handling to achieve proprioceptive input of the
scapulae on the posterior thorax, will help reinforce
should include activities to strengthen the back and
active thoracic extension and anterior chest expan
shoulder extensors, to elongate the trunk t1exors, and
sion. The therapist's hands can stabilize the rib cage
to address overall endurance. The role of more vigor
to reinforce abdominal oblique function during
ous exercise and fitness training in these children is a
movement (Figurc 35-15).
issue of debate, based on inconsistent incidence of
Activities requiring alternating extension-rotation
662
PART VII
FIGURE 35-13
Manual lowering of the rib cage.

NOTE:
Arrows indicate direction of therapist's hand movement (caudal and medial).
FIGURE 35-15
FIGURE 35-14
Handling to facilitate active upper thoracic extension, as a
Handling to reinforce upper chest expansion and abdominal
means of actively opening the anterior chest and
oblique stabilization of the lower ribs.
lengthening rectus abdominis while supporting the lower
rib cage on the ball.
35
663
and flexion-rotation will recruit control of the abdom
4. Compare the goals of chest physical therapy for
inal obliques and maintain active upper trunk exten
infants and older children. What are the similari

ties and differences?
sion. Bubble blowing, whistle toys, and singing are

excellent means o f monitoring the ventilatory
5. When treating infants to improve airway clear
changes that occur with active use of increased upper
ance, what are the precautions/considerations of:
chest expansion. As tidal volume increases, vocaliza
positional rotation?
tions should increase in frequency, sound higher, and
postural drainage?
become louder.
percussion?
vibration?
airway suctioning?
The concept of functional carry-over is central to

the treatment approach presented here. Addressing
ventilation and trunk control simultaneously has intu
itive appeal based not only on shared musculoskeletal
relationships but also on the necessity of pulmonary ,
6.
How might neuromotor (neuromuscular) dys

function affect pulmonary development and con
tribute to possible postoperative complications?
7. Describe goals, precautions, and suggested monitor
tolerance for motor activity.
ing for exercise in children who have the following:
SUMMARY
Cardiopulmonary physical therapy with infants and
a history of cardiac surgery
asthma
cystic fibrosis?
children is presented starting with issues related to

development and developmental vulnerabilities. Spe
cific cardiopulmonary diagnoses in pediatrics are de
scribed and treatment recommendations are provided.
Cardiopulmonary development and function are pre
sented as the basis for indications and precautions for
treatment of neonatal and pediatric patients.
The link between pulmonary and motor function
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The Aging Patient
Elizabeth J. Protas
KEY TERMS
Aging
Exercise changes
Autonomic
Pulmonary changes
Cardiovascular changes
INTRODUCTION
linear but curvilinear, with changes accelerating after
Cardiopulmonary and autonomic nervous system
age 65. Thus many of the physiological studies that
functions are dynamic and undergo changes as people
have been done with 60 year olds may not apply to in
age. It is important for physical therapists to be aware
dividuals who are 80, 90, or 100 years old. Most of the
of changes that are to be expected with normal aging
studies that
to better understand the impact of disease and impair
als have been conducted with subjects who are under
ment on these functions. In addition, a clear under
age 65. A vast majority of these studies only used men
are
available on exercise in older individu
standing of how these systems respond to exercise
as subjects or had a small number of women in the
training will assist the clinician in prescribing and
sample. Gender may be an important variable in rela
evaluating exercise interventions in elders.
tion to exercise and aging, but there is limited data
Unfortunately, aging is a bit more complicated to
available on this issue. Another consideration is the
understand than just the issue of chronological age. As
composition of study populations. With increasing age,
people age, greater variability occurs between individu
there is a greater incidence of disease. Latent cardiovas
als, making predications about any one individual more
cular disease and histories of chronic illnesses are com
difficult. The trends of some changes are probably not
mon in older populations. Comorbidities are frequently

669
670
PART VII
encountered in elders. It may be more uncommon to

have a person over age 75 without any problems than to
have a healthy older individual. As a physical therapist,
I may be more interested in the responses of a frail 85
or 90-year-old woman who has a history of hyperten
sion, coronary artery disease, and diabetes than some
one who is healthy at this age because this reflects the
population who is referred to physical therapy. The oc
currence of disease states in study populations may im
pact the cardiopulmonary responses to exercise. Fi
nally, the study of the physiological aspects of exercise
and aging is still evolving. The literature can be confus
ing and contradictory, making conclusions and general
izations difficult. An attempt is made to provide some
direction in this confusing maze of infonnation.
An additional issue is a model of aging that might
sort out some of the determinants of aging. (Figure
36-1) The model identifies biological factors, disuse,
disease, and psychosocial concerns as determinants of
aging. Biological factors address genetics, gender, cel
lular mechanisms, and metabolical, and physiological
responses that influence aging. Disuse is implicated in
more sedentary life styles led by many elders, which
results in loss of exercise capacity (Bortz, 1993). Ca
pacities that decline as a result of disuse should be re
versible or attenuated with exercise training. The em
phasis in this chapter is on the biological and disuse
characteristics of aging. The impact of various dis

eases is discussed in other chapters. Psychosocial is
sues related to exercise and aging are not discussed.
CARDIAC CHANGES WITH AGING
Aerobic Capacity
The aerobic capacity is the maximum ability to per

form exercise with large muscle groups. This ability
is produced by the interaction of the lungs, heart, and
peripheral tissues. The most common indirect mea
sure of the aerobic capacity is the maximum oxygen
consumption (Vo2ma,), or the maximum oxygen used
during exercise. The Vo2max is directly related to the
cardiac output (the amount of blood pumped by the
heart) and the arteriovenous oxygen difference (the
amount of oxygen extracted in the periphery). The
cardiac output is the product of the heart rate times
the stroke volume. The aerobic capacity reflects the
central cardiac function and the efficiency of the pe
ripheral tissues to extract and use oxygen.
The Vo2max declines with age between 0.40 to
0.50 ml/kg/min per year in men and between 0.20 to
0.35 mllkg/min per year in women (Figure 36-2)
(Buskirk and Hodgson, 1987). The reduction is ap
proximately 10% per decade. The decline is larger in
V02max
(ml/kg/min)
Disuse
Biological
factors
--
I
L:J
--
Psychosocial
factors
50
1
45
40
35
30
25
20
15
10
5
o
20-29
30-39
40-49
50- 59
Age (years)
60- 75
FIGURE 36-2
Decline in maximum oxygen consumption
Disease
FIGURE 36-1
from
permission Hossack KF, Bruce RA: Maximal cardiac
A model of aging which identifies the major determinants

underlying the aging process.
(Vo2max)
age 20 to 75 in both men and women. (Redrawn with
function in sedentary normal men and women: comparison
of age-related changes, J App/ Physio/53:799-804, 1982.)
36
The Aging Patient
671
men than women; however, the capacity of the males
ation of the myocardial fibers, sufficient venous re
is larger than the females (Hossack and Bruce,
turn to rapidly fill the heart, and the timing of the
1982). Vo2max is related to body size, which tends to
atrial contraction to contribute to the end diastolic
be smaller in women than men. Increases in body
volume. Relaxation is hampered possibly by an in
weight as people age results in reduced V02max even
crease in ventricular stiffness, although there is lim
if the aerobic capacity remains the same, since rela
ited evidence of this in humans (Lakatta, 1993). The
tive oxygen consumption is related to body weight.
period of the isovolumic myocardial relaxation (be
Reduced physical activity with aging also con
tween aortic valve closing and mitral valve opening)
tributes to a loss of Vo2ma".
is prolonged. Likewise the peak rate of left ventricu
Considerable disagreement exists about the mecha
lar filling during early diastole is reduced in older,
nisms that contribute to the decline in V02max with
healthy men and women compared with younger in
age. Both cardiac and peripheral changes contribute to
dividuals. Despite the changes in early diastole, the
the loss. A reduction in maximum cardiac output ac
resting left ventricular end-diastolic volume remains
counts for 50% to 100% of the total reduction in
the same because of an enhanced left atrial contribu
V02max (Dempsey and Seals; Ogawa et aI., 1992;
tion to ventricular filling. This is accompanied by an
Saltin, 1986). Decreased maximum arteriovenous
enlarged left atrium and an audible fourth heart sound
oxygen consumption accounts for whatever is not due
in most older adults (Lakatta, 1993; Fleg, Gersten
to decreased maximal cardiac output. A major compo
blech and Lakatta, 1988).
nent to the decline in maximal cardiac output is a de
Considerable disagreement exists about what hap
creased maximal heart rate (Ogawa et aI., 1992; Hag
pens to diastolic function during exercise. Some re
berg, 1987). The decline in heart rate is linearly
cent studies suggest that end-diastolic volume during
related to age and occurs in both sedentary and active
exhaustive exercise increases in older men but not it
elders (Sidney and Shephard, 1977). Reduced maxi
women (Lakatta, 1993). Filling pressures during ex
mal stroke volume has also been observed as people
ercise in men increase with age (Ehrsam, Perruchoud,
age (Ogawa et aI., 1992) Recent studies suggest de
Oberholzer, Burkhart, and Herzog, 1983). In addi
creased stroke volume is associated with a decrease in
tion, peak left ventricular diastolic filling rate during
total blood volume in healthy older men and women
submaximal and maximal exercise decreases with
(Dempsey and Seals, 1995; Davy and Seals, 1994;
aging (Levy, Cerqueria, Abrass, Schwartz, and Strat
Stevenson, Davy, Reiling, and Seals, 1995). Most evi
ton, 1993; Schulman, Lakatta, Fleg et al. 1992) De
dence suggests that decreased V02max with aging is re
creased filling rate is associated with increased ven
lated to decreased maximal heart rate, stroke volume,
tricular stiffness and prolonged relaxation times
and arteriovenous oxygen difference, although each
(Ehsani, 1987).
component's contribution varies (Dempsey and Seals,
1995; Lakatta, 1993),
Resting measures of systolic and cardiac pump

function do not change with aging. The resting end
systolic volume and stroke volume do not change
with age. Likewise, the ejection fraction at rest (end
Cardiac Mechanics
diastolic volume - end-systolic volume/end-diastolic
The most consistent cardiac structural change is a
volume) is similar in healthy older and younger indi
modest increase in left ventricular wall thickness in
viduals (Lakatta, 1993).
80 year olds compared with 20 year olds (Lakatta,
Unlike resting systolic function, the pumping func
1993), attributed to an increase in size of cardiac my
tion of the heart changes considerably in response to
ocytes and is exaggerated by hypertension and/or
exercise. Myocardial contractility as measured by the
coronary artery disease (Lakatta, 1993). After age 80,
ratio of end-systolic volume to systolic arterial pres
the left ventricular wall thickness again decreases.
sure declines during exercise as people age (Lakatta,
The cardiac filling or diastolic properties of the
1993). The end-systolic volume increases, whereas
heart are altered with age. Diastole requires a relax
the ejection fraction decreases during exercise. These
672
PART VII
changes reduce stroke volume
exercise. Re
duced contractile performance is related to a decrease
Special Cases
catecholamines is most often cited as the reason for

"'
"<"vu
in maximal heart rate with
(Rodehef
in the response to beta-adrenergic stimulation,
f e r, Gerste nbl
changes in the myocardium, increased
Lakatta, 1984). Relatively intense endurance training
blood
pressure, a n d v e n t r i c u l a r w a l l abnorma l i t i e s
W e i sfeld, and
for a year or more can increase
1995).
(Dempsey and
Beck er,
stroke volume in
Ogawa, Miller,
and Jilka, 1991;
Spina,
Impact of
Training on Aerobic Capacity
older women have been attributed
and Cardiac Mechanics

Older persons who continue to be active reduce the
decline of 10% per decade in
1987). A recent metaanaly
sedentary adults
sis of 29 studies including 1030 men and 466 women

between the ages of 61 and 78 and endurance trainconcluded that endurance
increases functional
(Spina,
Kohrt, Martin, Holloszy, and Ehsani,
1993). This apparently occurs desoite intensive en

durance
over a year-long
The diastolic changes thal occur with
endurance trained 13 rigor-
screened older men

low
and short duration of exercise
sessions. The analysis suggests that a
68-
can be
et al., 1993).
reversed by exercise training

Levy et al.
increasing age, a shorter length of

Vo2rnax before
ence rather than central changes in cardiac function
in young elders
Less improvement was seen with
and
to
in arteriovenous oxygen differ
rate of decline in Vo2max to 5% per decade compare

with an
and
Adaptations to exercise training in
age
60 to 82
68) and II younger men in their twenties for 6

months. The training increased
and
submaximal,
rates for the older group comparable

seen in the younger group (Levy et
with the
year-old individual who exercises for 30 minutes
aI., 1993). End-diastolic peak volume at rest and ex
three times per week for 4 to 6 months can improve
ercise also increase after lengthy endurance training
14%
and
Similar
occur in both men and women (Kohn,
Vo2max i n the
with endurance
in
which pro
in cardiac
relaxation
This implies that
c oxidase levels
and Stratton, I
1992;
in the
in elders. The
on maximal cardiac
(Ehsani, 1
Taffet,
McBride, and Michael, 1990;
skeletal muscles account for some of the

increase in
decreases
reduces the decline of left ventricular
pressure, enhances fatty acid oxidation, and increases
duces a wider arteriovenous oxygen difference in

both older men and women
reduces the age
have shown that exercise training increases calcium
are not
clear. One consistent finding is greater extraction of

oxygen in the exercising skeletal
1991). Thus
response are uncertain in humans. Studies in rats
1991; Warren et
The mechanisms underlying
(Ehsani et
associated diastolic changes. The mechanisms of this
and Edington, 1
All of these
have been associated with reduced diastolic
of exercise
i s uncertain
can either
Exercise
can also
remain the same or increase after exercise training,
mance in older men as reflected by the increase in the
depending on the effect of training on maximal stroke
exercise stroke volume. Increased
volume and maximal heart rate. Maximal heart rate
ume occurs with an increased exercise
remains the same in older men
of activity
that the decline in maximal heart

on factors other than exercise and physiHagberg,
and Hol-
A decrease in response to circulating
stroke vol
frac
tion, a decrease in end-systolic volume, and greater

left ventricular wall mass (Ehsani et
Seals et al.,
1994). These changes apparently do not occur in

older,
women
Table 36-1 contains a summary of these
et
1993).
36
TABLE 36-1
160
Cardiac Changes With Aging*

BECAUSE
OF AGING
Blood pressure
(mm/Hg)
120
100
Oxygen consumption
Heart rate
Stroke volume
J,
J,
J,
i
H
i,H
J,
J,
i
i, H
Arteriovenous oxygen
difference
Cardiac output
80
60
--+-Systolic
-D-Diastolic
40
Cardiac function
20
Diastolic
o --------
35
40
45
50
55
60
65
70
75
Left ventricular wall
i, J, after 80
J,
H
i
i
J,
i
J,
i ,Hi
J" Ht
i,Ht
Left ventricular
filling rate
End-diastolic volume
Age
FIGURE
36-3
Changes in systolic and diastolic bl.ood
Systolic
age. (Redrawn with permission from Timiras PS:
Myocardial contractility
End-systolic volume
Ejection fraction
Cardiovascular alterations with age: atherosclerosis, coronary

heart disease and hypertension. In Timiras, PS:
basis of aging and geriatrics.
i increase; J, decr as : H no change;

=
673
140
AFTER
EXERCISE
TRAINING
Maximum Exercise
thickness
The Aging Patient
over the age of
tin women
Physiological
Boca Raton, Fla., 1988, CRe.)
70 (Lipsitz, 1989). Orthostatic intoler
ance is associated with decreased resting diastolic

function, decreased stroke volume, extreme inactiv
ity, and, in individuals with hypertension, high levels
Vascular and Autonomic Changes with Aging
of systolic blood pressure (Harris, Lipsitz, Kleinman,
Aging results in an increase in arterial stiffness be

cause of a loss of elastin and an increase in collagen
(Lakatta,
1993; Roach and Burton, 1959). Arterial
wall thickness and diameter and resting systolic pres
and Cornoni-Huntley,
1991).
There are decreases in baroreceptor and cardiopul
1993; Cleroux,
1989) Arterial and venous dilation are reduced,
monary reflexes with aging (Lakatta,

et a\.,
36-3) (Lakatta, 1993). It is
but vasoconstriction is relatively spared. The heart
unclear whether peripheral vascular resistance in
demonstrates an overall decrease in responsiveness to
creases in normotensive older adults. Changes in the
autonomic stimulation. Older individuals experience
sure also increase (Figure
structure, size, and reactivity of the arteries increase
higher central venous and mean arterial pressures, but
the work of the left ventricle and have been directly
lower forearm blood flow and forearm vascular resis
implicated in the increase in cardiac myocyte size.
tance in response to passive leg raising (Cleroux et aI.,
Complaints of dizziness when an older patient
1989). During submaximal and maximal exercise, ar
moves from supine to standing are frequently en
terial blood pressure is either unchanged or increased
countered by the physical therapist. Postural hypoten
when comparing younger and older subjects (Seals,
sion, or orthostatic intolerance, generally does not
1993). There also appears to be impaired peripheral
occur in healthy community dwelling elders but is
vasodilation in skeletal muscle in response to exercise
common in debilitated, institutionalized individuals
(Ogawa et a\.,
1992). Redistribution of blood flow
674
PART VII
during exercise normally involves the shunting of
chest wall (Dempsey and Seals, 1995). The lung's
blood from inactive limbs and viscera. There seems to
elastic recoil depends on the composition of the con
be an enhanced vasoconstriction in inactive muscles
nective tissue, the structure of the connective tissue,
during dynamic exercise in healthy older men (Taylor,
and alveolar surface tension produced by surfactant

(Dempsey and Seals, 1995). Very limited evidence
Hand, Johnson, and Seals, 1992).
suggests that the structure of the connective tissue

may be the primary mechanism for age-associated
Effect of Exercise Training on Vascular
change in elastic recoil. Chest wall stiffness is ac
and Autonomic Function in Aging
companied by an increase in chest anterioposterior
Exercise training improves peripheral bloodflow in
diameter, coastal cartilage calcification, nan'owing of
skeletal muscle in 60-year-old men and women (Mar
the intervertebral disks, and changes in the rib to ver
tin, Ogawa, Kohrt, Malley, Korte, and Stoltz, 1991).
tebrae articulations (Crapo, 1993).
Systolic and mean arterial blood pressure responses
Decreases occur with the alveolar-capillary sur
to submaximal exercise are lower in physically active
face area, the alveolar septal surface area, and the
adults compared with sedentary individuals (Martin
total surface area of lung parenchyma (Brody and
et aI., 1991). Endurance training also increases mus
Thurlbeck, 1985). This reduces the surface area avail
cle sympathetic nerve activity and plasma norepi
able for gas exchange.
nephrine concentrations at rest and during a moderate
Loss of elastic recoil with aging is directly associ
isometric handgrip, indicating elevated sympathetic
ated with reduced forced expiratory flow. Limitations
nerve activity in response to exercise (Table 36-2)
in exhalation are caused by airway narrowing and
(Ng, Callister, Johnson, and Seals, 1994).
closure at all lung volumes; thus reducing forced ex

piratory volume in I second (FEV1) (Dempsey and
Seals, 1995) Early airway closure also produces an
PULMONARY FUNCTION
early closing volume and a relati ve increase in the
Structural and Functional Changes With Aging
total residual volume. The combination of reduced

elastic recoil and increased chest wall stiffness leads
Two major changes with aging of the pulmonary sys
to a decrease in the forced vital capacity in older indi
tem are decreased elastic recoil and stiffening of the
viduals. Flow rates are also significantly lower in

women and African-Americans than in Caucasian
men at any age (Dempsey and Seals, 1995).
Respiratory muscle strength, as reflected by the abil
ity to create pressure over a range of lung volumes and
TABLE 36-2
flow rates, is similar when comparing healthy 30 and 70
Vascular and Autonomic Changes With Aging*

BECAUSE
OF AGING
i
i
Arterial wall thickness

Systolic blood pressure
Diastolic blood pressure

Orthostatic tolerance
and
Vasoconstriction
pressures have been reported to decrease 15% between
the sixth and eighth decades (Figure 36-4) (Enright,
t
t
these observed differences are similar to the differences
?
?
Central venous pressure
AFTER
EXERCISE
TRAINING
Arterial and venous dilation
year olds (Johnson and Dempsey, 1991) This suggests

that respiratory muscle strength does not change with
aging; however, maximal inspiratory and expiratory
Kronmal, Manolio, Shanker, and Hyatt, 1994). Perhaps

observed with submaximal and maximal cardiac re
sponses with the dynamic pressure measures over dif
ferent volumes and flows considered submaximal.
Changes in the surface area result in a decrease in
"i
?
increases;
decreases;
H =
unchanged;
insufficient data on older adult subjects
the diffusion capacity of the lung (Murray, 1986).

Both the loss of surface area and a decrease in pul
36
The Aging Patient
675
monary capillary blood volume contribute to reduced
mains unchanged as people age, although the vital ca
and uneven ventilation to perfusion matching in el
pacity for elders is reduced. Likewise, as exercise and
ders. The resting partial arterial pressure of oxygen
the tidal volume increase there is a slight drop in the
declines 5 to 10 mm Hg between ages 25 and 75
ratio of dead space to tidal volume. This drop is not
(Dempsey and Sea Is, 1995). These changes do not af
effected by aging, although the older person will
fect the arterial oxymyoglobin saturation or oxygen
breathe more (have a higher minute ventilation) in re
content. Paralleling changes in the peripheral vascu
sponse to submaximal exercise.
lature, pulmonary vascular resistance and pulmonary

arterial pressure at rest increase (Table 36-3).
The work of breathing is increased during exercise

as people age as a result of a number of factors.
Higher ventilation during exercise requires the devel
opment of higher pleural pressures; thus increasing
Changes in Pulmonary Responses to
the work required. In addition, an increase in the end
Exercise With Aging
expiratory lung volume with increasing exercise re
In addition to the structural and functional changes at
sults in breathing that occurs at a stiffer point in the
rest, a number of significant changes occur in breath
lung-volume relationship. The increased stiffness im-
ing during acute exercise. Expiratory flow limitations

occur at lower exercise intensities as people age. A
normal, healthy 69 year old will begin to experience
TABLE 36-3
flow limitations even in response to moderate exercise
Pulmonary Function Changes With Aging*
(Dempsey and Seals, 1995). Practically, this may be
BECAUSE
OF AGING
experienced by the individual as having greater diffi

culty "catching his or her breath" during exercise.
Normally as people exercise, the tidal volume in
creases directly with increasing exercise intensity up
to about 50% to 60% of the vital capacity. This re
Structure and Function

Elastic recoil
Chest wall stiffness
Alveolar-capillary surface area
200
180
160
140
120
100
80
60
40
20
Forced expiratory flow
MEP(cmHpl
,--
Total residual volume
,-r--
Men
lD.Women
-
Forced vital capacity

Maximum inspiratory and
J,
i
J,
J,
i
J,
J,
expiratory pressure
Ventilation-perfusion matching
Partial arterial pressure oxygen
Oxygen saturation
Pulmonary vascular resistance
J,
J,
H
i
Exercise response
i
i
i
i
Expiratory flow limitation
o f--
65-69
Minute ventilation
70 - 74
75-79
80-84
Work of breathing
Age
Respiratory muscle oxygen

consumption
FIGURE 36-4
Arterial hypoxemia
Decrease in maximum expiratory pressures between ages
Pulmonary artery pressure
65 to 84 for both men and women. This is a measure of
H,i
i
i
Pulmonary wedge pressure
respiratory muscle strength. (Redrawn with permission

from Enright PL, Kronmal RA, Monlio TA, Schenker MB,
Hyatt RE: Respiratory muscle strength in the elderly, Am J
Respir Cril Care Med 149:430-438, 1994.)
'i
increases; J,
Tsubmaximal
t maximal
=
decreases; H
unchanged
AFTER
EXERCISE
TRAINING
PART VII
676
Guidelines for the Delivery of Cardiopulmonary Physical Therapy:
Cases
elastic recoil on the ventilatory mus
diffusion and may contribute to ventilation
greater pressure development by the
maldistribution ( Dempsey and
1995)
inspiratory muscles. The increase in expiratory flow

resistance likewise requires greater pressure
muscles. Both the inspiratory
ment by the
changes increase the work of breath
and
Effects of ExerCise Training on Pulmonary Function

Aerobic training in elders can reduce some of the
ing. The increase in the work of breathing increases
that have been described. There are limited or
the respiratory muscle oxygen consumption so that
no studies that address some of the changes, such as
the
chest wall
muscles alone can
12% of the total
10% to
oxygen
during
maximal exercise in a sedentary 70-year-old man

)""W.N'"
(995).
and
young
What is also apparent is that the reserves used to
artery pressure.
who are 60 to 70 years
which does
insights into what exercise might do for
not
respond to exercise represent a greater percent of the
or
The studies that are available deal with relatively
the those in their
or beyond.
Aerobic training can significantly decrease sub-
available capacity. An older individual can exceed

50% of inspiratory muscle capacity even during mod
Jones,
program with
erate exercise. This is in contrast to the younger indi

vidual who
exceeds 50% of the capacity with
exercise
and
Thus the reserve
maximal minute ventilation
36-5)
et
pleural pressure is reduced in eI
al., 1993). Decreased minute ventilation is accompa
v irtue of the fact that greater caoacitv is
nied by a decrease in carbon dioxide production, the
capacity to
ders
women over a 12
and demonstrated a 7.7% drop in the sub
needed even for moderate exercise.
respiratory exchange ratio (carbon dioxide produc
The variability characteristic of exercise r e
tion/oxygen consumption), and the blood lactate level
sponses in older individuals is particularly evident
for any
when
et aI., 1986; Warren et aI., 1993). Thus the improved
and
gas
cular hemodynamics. I n
demonstrate only slight
most individuals
in arterial blood-gas
ventilatory
than an
d e m on s t r a t e a r t e r i a l h y p o x e m i a w i t h e x e r c i s e
proved
1995). Some studies suggest
after
may have more to

in the
do with improved
but a small number of individuals

and
level of submaximal exercise (Makrides
rather
Im
on the pulmonary system
metabolical efficiency results in the
production of less carbon dioxide; therefore the
that this response may be a factor of fitness level.
do not have to work as hard to eliminate the carbon
More fit older individuals showed progressive arter
dioxide. The important functional results of these
and carbon dioxide retention during
ial
changes are that the older adults will
laud, and Masse-Biron, 1994;
et aI., 1994).
The pulmonary artery pressure is increased with

at any oxygen consumption or cardiac output
during exercise (Reeves,
and
less
experience a lower perceived exertion,
mild-to-moderate exercise (Prefaut, Anselme, Cail
and use a lower
of their maximal ventila
tory capacity during exercise (Jones,

Exercise training also increases maximal ventila-
\989).
maximal exercise
12-week
In addition, the maximal pulmonary artery pressure at
et
pro
maximal exercise is reached at substantially lower oxy
gram referred to above increased maximum minute
gen consumption and cardiac output in older individu
ventilation
als
36-5) (Jo n e s, I
with younger persons. The pulmonary

pressure also increases with age and can exceed
25 mm Hg
Seals, I
peak supine exercise (Dempsey and

Limited data suggest that these
pres
14% in
s/week at an
women
.
Figure
These w o me n walked 5
of 78% of the maximal
treadmill heart rate or 118 beats/minute on average,

so the program was not very strenuous but
IJH;'UWc.C'u
sures may in tum induce pulmonary edema during in
substantial
tense exercise in elders. Pulmonary edema would limit
training can improve submaximal ventilatorv effi
in maximum ventilation. Exercise
70
Ventilation
(L/min)
677
The Aging Patient
36
REVIEW QUESTIONS
which occur
What are the
1.
with
in the cardiovascular
What outcomes will exercise
2.
pro
duce in an older adult's cardiovascular sys

tem?
3.
What are the major
that occur with
in the autonomic nervous

and which of these
sponse to
can be influenced by execise

What are the major
4.
that occur in the
pulmonary system with
and in reo
to exercise?
5.
Describe the possible impact of exercise

on the
system.
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FIGURE 365
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14:60-65. 1993).
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Sports Medicine, 14, 60-65.
The Patient with Neuromuscular or

Musculoskeletal Dysfunction
Mary Massery
KEY TERMS
Adverse musculoskeletal changes
Paradoxical breathing
Chest development
Planes of ventilation
Effects of gravity
Gravity
Respiratory impairments
Impaired phonation support
Respiratory muscles
Musculoskeletal deficits
Sleep disorders
Neuromuscular deficits
Triad of ventilation
Nighttime hypoxemia
INTRODUCTION
muscular and/or musculoskeletal deficits and what
It is often observed in a rehabilitation setting that
clinicians can do to minimize or eliminate these
patients with neurological deficits continue to ac
complications. The focus of this treatment approach
quire respiratory problems long after their acute
is primarily aimed at the physical therapist (PT).
phases have subsided. Research has repeatedly doc
Every effort is made to explain specific physical
umented a decrease in pulmonary function for the
therapy concepts so that all clinicians, occupational
chronic neurologically impaired patient, yet many
therapists (OTs), speech language pathologists
therapists do not appear to fully comprehend why
(SLPs), respiratory therapists (RTs), and nurses
this occurs. This section tries to elaborate the causes
(RNs), family members, and others can benefit from
of respiratory complications secondary to neuro
the ideas presented in this chapter.

679
680
PART VII
DIAGNOSES ADDRESSED
ing may respond better to techniques that act primarily
The following treatment ideas are applicable for all
on the subconscious and require little cognitive partici
neurological and orthopedic diagnoses including the
pation. Finally, the differcnce between rehabilitation
following: spinal cord injuries (SCI), head traumas,
and habilitation must be understood. Rehabilitation in
cerebral vascular accidents (CV A), multiple sclerosis
volves restoring function, and habilitation teaches
(MS), amyotrophic lateral sclerosis (ALS), Parkinson's
functioning for the first time. Children with acquired
disease, cerebral palsy (CP), muscular dystrophy (MD),
deficits in utero or shortly after birth have never expe
polio myelitis (polio), spina bifida, and neuropathies as
rienced normal movement patterns. Therefore they
well as back, neck, and shoulder injuries or dysfunc
cannot depend on the memory of past motor experi
tion. However, it is by no means an exhaustive list. The
ences to help con'ect abnormal motor patterns the way
primary consideration for application of these treatment
adults going through rehabilitation can. This important
techniques is the residual physical deficits left by a neu
difference must be accounted for when developing
rological or musculoskeletal insult. Therefore a patient
their treatment programs.
presenting with hemiplegia will be treated with tech

niques geared toward promoting increased function on
the involved side, regardless of how the original deficit
PLANES OF VENTILATION
was acquired (e.g., from a CVA, head trauma, or CP).
This neuromuscular/musculoskeletal treatment ap
Likewise, tetraplegia or paraplegia not only refers to
proach is based on the premise that ventilation does
patients that have suffered from SCls but any patient
not take place in a one-dimensional plane but rather as
that presents with tetraplegic or paraplegic deficits.

However, three aspects of neurological/muscu
a three-dimensional activity. The chest expands in an

anterior-posterior plane, an inferior-superior plane, and
loskeletal disorders must be clarified here to assist the
a lateral plane (Figure 37-1). Too often, therapists treat
therapist in discerning which techniques, described
patients with neuromuscular and/or musculoskeletal
later, are appropriate for his or her particular patient.
dysfunctions with apparent disregard for this ex
(1) progressive vs. nonpro
tremely important fact. This one-dimensional fallacy
(2) cerebral vs. noncerebral injuries,
has been perpetrated by techniques taught to new ther
and (3) rehabilitation vs. habilitation. Single-insult in
apists that describe the patient's breathing program in
The three aspects follows:

gressive injuries,
juries, such as SCTs, traumatic brain injuries, CVAs,
only one or two postures, most often supine and sit
CPs, or cervical whiplash, are nonprogressive. The
ting. To be effective, we must acknowledge this three
damage was only inflicted once and does not repeat it
dimensional movement of the thorax and use this con
self. Progressive diseases, on the other hand, such as
cept when determining treatment protocol.
MS, ALS, Parkinson's disease, MD, or scoliosis, show

increasing physical deficits over time. Goals for these
groups will be different, with maximal respiratory
functioning stressed for the single-insult diagnoses and
EFFECTS OF GRAVITY
If chest expansion takes place in three planes, the ef
comfort and ease of ventilation stressed for progres
fect of gravity on these planes must be considered.
sive diagnoses. Similar treatment consideration is
Physical therapists would not exercise a weak muscle
given for patients with detrimentally affected cerebral
without taking into account the effect of gravitational
functioning, such as with traumatic brain injuries,
pull on that muscle, tbereby making the positioning
CVAs, and Parkinson's disease, versus those whose
of the limb in space an important consideration in
deficits are at the spinal level, such as with SCIs, neu
treatment planning. This same consideration must be
ropathies, myopathies, and polio. Patients with only
given for the weakened ventilatory muscles. Gravity
spinal involvement may respond favorably to complex
can assist, resist, or have no effect on the movement
techniques and demonstrate better conscious carry
of the chest wall, according to the chest's position in
over, whereas those with impaired cerebral function
space. Consider weakened intercostal muscles. Plac
37
TIle Patient with Neuromuscular or MuscuJoskeletal Dysfunction
681
in abdominal tone (many SCIs, Guillian-Barre syn

drome, or spina bifida), intestinal positioning be
comes an important factor in respiratory functioning.
The abdominal wall acts as the anterior support
for the intestines, causing the intestines to sit high in
the abdominal cavity (see Chapter
2). This forces the
diaphragm to rest high, at approximately the level of

the fifth rib in an erect posture (Figure
37-2). The di
aphragm contracts, drawing its origins toward its in

sertion (concentric contraction). These muscle fibers,
which originate down as low as the tenth rib, must
rise up superiorly and then medially toward the cen
tral tendon (see Chapter
2). This movement pattern
causes primarily superior and lateral expansion of

the lower chest. Without abdominal wall support, the
intestines shift inferiorly and anteriorly, the "beer
belly" effect, allowing gravity to position the di
aphragm lower in the abdominal cavity (Figure
373). This p u t s t h e d i a p h r a g m at an e x t r e m e
mechanical disadvantage. Instead o f having t o rise
up and over the intestines, the lateral fibers of the di

aphragm can now move more horizontally to reach
the central tendon, thereby significantly reducing ex
cursion in all three planes of expansion. This adverse
positioning may be so significant as to cause a nega
FIGURE 37-1
tive lower chest expansion on inspiration for patients
Planes of respiration (anterior-posterior, inferior-superior,
with tetraplegia. Quantitatively, this may be seen as
and lateral).
much as
Y2- to I-inch decrease rather than increase in
overall lower chest expansion, measured at the

ing a patient with this deficit in a supine position for
xiphoid process, when the patient proceeds from
initial treatment in his or her rehabilitation program
maximal expiration to maximal inspiration.
and then asking the patient to "breathe up into your
Since gravity causes the intestines to shift, the ef
hands" is asking the patient to attempt the most diffi
fect on the diaphragm will be most dramatic in a
cult gravitational posture first (breathing into the an
gravity-dependent position, such as sitting or stand
terior plane with gravity resisting the movement). It
ing, rather than in a gravity-eliminated position, such
would seem more appropriate to start retraining tech
as supine. Thus the imponance of providing the pa
. niques in a gravity-eliminated posture for anterior
tient with an external abdominal wall support in these
chest expansion, such as side lying, or a gravity
upright postures should be undeniably clear. Al
assisted posture, such as hands-knees, and then
though not as effective as the abdominal muscles
progress to gravity-resisted postures, such as supine.

Gravity also affects the positioning of the in
testines under the diaphragm. In the normal, neuro
themselves, abdominal supports help restore the nat

ural mechanical advantage of the diaphragm (see
Chapter 22).
logically intact person, this seems to have a minor ef
In addition to changing muscle effectiveness,
fect on respiratory functioning. However, for many
gravity also affects bony structures. Obviously, this
neurologically impaired persons with a marked loss
affects a growing child more so than a fully devel
682
PART VII
FIGURE 37-2
Proper mechanical positioning of the diaphragm relative to the abdominal viscera. Note the high
dome shape of the diaphragm.
oped adult, but both will be affected. Bones grow ac
plays an extremely crucial role in the skeletal devel
cording to stress laid on them, thus abnormal stresses
opment of the chest in the newborn. Normal, neuro
produce abnormal bony developments. For persons
logically intact infants move freely in and out of pos
with severe neurological deficits, gravity becomes the
tures, such as prone, hands-knees, and standing, as
main force acting on the bones and joints, unopposed
they progress developmentally, allowing gravity to
by normal muscle action. This can result in many
alternately assist or resist the movements. Through
skeletal deformities, such as flattening or flaring o f
this, the infant begins to strengthen and develop mus
the lower anterior rib cage, narrowing of the upper
cle groups and learn to interact with the gravitational
chest, loss of normal spinal curves, and chest cavus
force in his or her environment.
deformities. Prevention of these deformities, rather
This combination of normal movement patterns in
than their cure, must be the aim of a good long-term
a gravitational field, along with genetic predisposi
ventilatory program for the neurologically impaired.
tion, accounts for the normal development of the

bones, muscles, and joints that comprise the chest
GRAVITY: EFFECTS ON CHEST DEVELOPMENT
wall. Conversely, infants with severe neurological

impairments do not have that same freedom of move
Thus far the effects of gravity on the planes of venti
ment within their environments. This applies to chil
lation, muscle function, and bony changes in the
dren with congenital deficits, such as CP or spina bi
adult have been discussed. This same force, gravity,
fida, or for children who acquire deficits at an early
37
The Patient with Neuromuscular or Musculoskeletal Dysfunction
683
FIGURE 37-3
Independent upright posturing in a patient with congenital quadriplegia. Note relationship of rib
cage and abdominal viscera.
developmental age, such as some CY As, head trau
neck renders the upper accessory muscles nonfunc
mas, or SCIs. These children become subjugated to
tional as a ventilatory muscle. The infant's arms are
the effects of gravity on their growing and develop
held in flexion and adduction across the chest, signif
ing bodies because they are unable to independently
icantly hampering lateral or anterior movement of the
counteract its constant presence. A variety of reasons
chest wall. This all points to underdevelopment of the
may account for their inability to change their own
upper chest region in the newborn. The infant, forced
(I) muscle weakness, (2) tonal

problems (e.g., spasticity or flaCCidity), (3) reflex
dominance, (4) incoordination, or (5) a combination
to be a diaphragmatic breather, shows greater devel
positions in space:
of the above. Typically, these children spend signifi

cantly more time in supine than in any other posture,
which can lead to undesirable changes in the thorax.
opment of the lower chest and hence leads to the tri

angular shaping of the rib cage.
From
3 to 6 months of age, the infant begins to de
velop more trun k extension tone, they spend more

time in a prone on elbows position, and they begin to
Understanding the basic steps and principles in
reach out into the environmenr with the upper extrem
normal chest development is essential for accurately
ities. This facilitates development of the anterior
assessing abnormal chest deformities often seen in
upper chest. Constant stretching helps to expand the
this physically challenged population. Initially, the
anterior upper chest both anteriorly and laterally. An
newborn's chest is triangular in shape, narrow and
increase in intercostal and pectoralis muscle strength
flat in the upper portion, and wider and more rounded
improves the infant's ability to counteract the force of
37-4). The infant's short
gravity on the anterior upper chest in supine, leading
in the lower portion (Figure
684
PART VII
FIGURE 37-4
Newborn chest configuration. Note triangular shape.
FIGURE 37-5
A and B, I O-month old infant chest configuration. Note shape of chest changes and angle of ribs.
37
The Patient with Neuromuscular or Mu culoskeletal Dysfunction
685
to the development of a slight convex configuration of
Children with severe neurological deficits often
the area and a more rectangular shaping of the thorax
show a very different picture of chest development.
from a frontal plane.
Frequently, they do not develop adequate upper
The next significant development occurs when
extremity and neck muscle control (e.g., weak mus
the child begins to independently assume erect pos
cles, tone problems, reflex dominance, or incoordina
tures (e.g., sitting, kneeling, or standing). Until this
tion), causing their upper chests to retain the more
time, the ribs are aligned 'fairly horizontally, with
primitive triangular, flattened shape. Inadequate mus
narrow intercostal spacing (see Figure 37-4). In fact
cle control or chronically shortened neck muscles
the newborn's chest only comprises approximately
also renders the accessory muscles less able to assist
one tbird of the total trunk cavity. As the child be
if needed in ventilation. In some cases the child's di
gins to move up against the pull of gravity, the ribs
aphragm remains so strong and unbalanced by the ab
rotate downward (more so in the lower ribs), creat
dominal and intercostal muscles that it creates a
ing the sharper angle of the ribs as seen in the adult
cavus deformity (pectus excuvatum) at the sternum
(Figures 37-5 and 37-6). This markedly elongates
(Figure 37-7). This occurs when the intercostal mus
the rib cage until it eventually occupies more than
cles are incapable of maintaining the anterior chest
half of the trunk cavity. A comparison of chest x
wall's position against gravity and the abdominal
rays of newborns and adults, as well as pictures of
muscles are weak or flaccid, thus not stabilizing the
infants, clearly shows these developmental trends
lower borders of the thorax. This may also eventually
(see Figure 37-4 to 37-6). Development trends are
cause an anterior flaring of the lower ribs.
summarized in Table 37-1.
Most of these children with severe neuromuscular
FIGURE 37-6
Normal adult chest x-ray. Chest shape is rectangular, ribs angled downward, upper and lower chest
equally developed.
686
PART VII
impairments require significant assistance to maintain
rectus abdominus, as seen in many children with spastic
an upright posture, therefore they spend more time in a
tetraplegia CP, the chest will become flattened anteri
recumbent position. Thus the rib cage tends to show
orly, yet flared laterally in the lower ribs (Figure
less downward rotation and elongation than that of the
These children are unable to stabilize the lower lateral
37-8).
normally developing child. In some cases of prolonged
borders of their rib cage and are unable to counteract
supine posturing combined with hyperactivity of the
gravity's influence on the anterior chest wall move-
TABLE 37-1
Chest Development Table
Chest
Infant
Ad ul t
Size
Occupies one third of the trunk cav ity
Occupies greater than one half trunk cavity
Shape
Triangular frontal plane
Rectangular frontal plane
Circular anterior-posterior plane
Elliptical anterior-posterior plane
Upper chest
Narrow
Wide
Flat apex
Convex apex
Circular
Elliptical
Flared lower ribs
Integrated with abdominals
Ribs
Evenly horizontal
Rotated downward; especially inferiorly
Intercostal spacing
Narrow
Wide
Limits movement of ribs
Allows for individual movement of ribs
Lower chest
Diaphragm
Accessory muscles
Adequate
Adequate
Minimal dome shape
Large dome shape, greater excursion
Nonfunctional
Functional
FIGURE 37-7
Pectus excavation deform i t y (secondary to spinal cord injury and resultant muscle imbalance).
37
687
ments. Thus we see these adverse musculoskeletal
occurs because of pressure gradients between the air
changes, which limits the breathing patterns options.
outside the lungs and the air inside. These gradients
As long as the neurological deficits are present,
are achieved through movements in the chest wall.
these children will never develop normally. However,
Muscle contractions provide the power to move the
frequent position changes, inhibition of undesired
chest wall. If these muscles do not overcome the ef
tone, facilitation of weakened chest muscles, promo
fect of gravity because of weakness, paralysis, abnor
tion of preferred breathing patterns, and incorporation
mal tone, or inadequate muscle control, the chest will
of ventilatory strategies with movement will stimu
be unable to expand in all three planes of ventilation,
late normal chest development. Optimum respiratory
thus limiting pulmonary function. Because of this im
function cannot be expected from a severely underde
portant fact, all muscles originating or inserting into
veloped chest.
the chest wall become "ventilatory muscler" The box

on p. 688 lists these muscles and how they affect chest
expansion and other specific respiratory function.
MUSCULAR AND TONAL INFLUENCES
They are listed in the following two distinct groups:
ON CHEST DEVELOPMENT
the primary muscles needed for normal ventilation
Adverse effects of gravity are counteracted by func

tioning musculature. Recall that inspiration/expiration
(the triad of normal ventilation) and all other acces

sory muscles of ventilation. Impairment to any of
these muscles may result in respiratory deficits.
Another factor that determines a muscle's effec
tiveness as a chest wall mover is neurological tone in
the muscle. Rigidity of movement, as seen in some
patients with head traumas and Parkinson's disease
will render the chest immobile, severely limiting its
ability to expand in any plane. Spasticity, more often
to a lesser degree than rigidity, can render the chest
immobile. Spasticity (i.e., SCI, CP, some head
trauma), is frequently activated by quick movement of
the affected muscle either actively or passively. A
quick activity like coughing may activate this abnor
mal tone and work against the patient as he or she
tries to produce an effective cough. The other extreme
of abnormal muscle tone is flaccidity or lack of any
muscular tone, as seen with some SCIs, CY As, and
MD. In this case the muscle is entirely unable to move
the chest wall or to counteract the effects of gravity.
Of the three types of abnormal tone, flaccidity is the
most adversely influenced by the effects of gravity.
At the same time, postural reflexes and their effect
on muscle tone must be considered. For instance, the
tonic labrinthyne reflex (TLR) increases extensor
tone when the person is supine and increases flexor
tone when that person is prone. For patients with CP,
for example, this reflex may stay a dominant force in
FIGURE 37-8
their motor control, interfering with their ability to
Musculoskdetal changes secondary to static positioning
move freely in supine and prone positions. Because
and neurological deficit.
of this, a child with CP with increased extensor tone
688
PART VII
Trunk Muscles and Their Function in Ventilation

Muscles of Velltilatioll-Three-Dimensional Movements
Triad of lIormal velltilatioll
Diaphragm
Major muscle of passive ventilation
Innervation-phrenic nerve-C3 to C5
Primary movement-all three planes
Dependency on intercostal and abdominal muscles
Concentric contractions--quiet and forceful inhalation
Eccentric contractions---controlled exhalation and speech
Intercostals
Primary function-stabilizes rib cage
Innervation-Tl to T2
Primary movement-concentric contractions
Lateral and superior expansion in lower chest during both quiet and forceful inhalation. Anterior expan
sion occurs to a lesser degree.
Anterior and superior expansion in upper chest, lateral expansion occurs to a lesser degree.
Forceful exhalation-primarily medial and inferior compression in lower chest, posterior and inferior
compression in upper chest
Eccentric contractions-needed for controlled exhalation and speech
Abdominals
Stabilizes inferior border of rib cage-provides mid trunk control
Innervation T6 to L I
Provides visceral support
Provides positive pressure support for the diaphragm
Provides necessary intrathoracic pressure for an effective cough
Accessory muscles
Erector spinae
Stabilizes thorax posteriorly to allow for normal anterior chest wall movement to occur
Innervated at TI to S3
Pectoralis muscles
Provides upper chest anterior and lateral expansion
Innervated C5 to TI
Can be a substitute rib cage stabilizer after paralysis of the intercostal muscles
Serratus anterior
Provides posterior expansion of rib cage when upper extremities are fixated
Innervated C5 to C7
Only inspiratory muscle that is paired with trunk flexion movements rather than tnlllk extension mo.ements
37
The Patient with Neuromuscular or Musculoskeletal Dysfullction
689
Trunk Muscles and Their Function in Ventilation-cont'd

Scalenes
Provides superior and anterior expansion of the upper chest
Innervated C3 to C8
Sternocleidomastoid
Provides sup e ri or and anterior exp ansi on of upper chest
Innervated C2 to C3 and accessory cranial nerve
Trape zi us
Provides superior expansion of the upper chest

Innervated C2 to C4 and accessory crani al ne rve
will see an even greater increase in that abnormal
DECREASED CHEST EXPANSION
tone if placed supine. That will make it more difficult
Muscle weakness or abnormal tone, combined with
for the child to attempt any flexion phase of a breath
the effects of gravity that were previously discussed,
ing pattern in supine (coughing or exhalation). Chil
serve to decrease the ability of the chest to expand in
dren should not be left supine as the therapist teaches
one or all three planes of ventilation. Quantitatively,
them altered breathing patterns. If the goal of that
chest expansion can be measured via lung volumes
treatment session is to promote controlled exhalation
by taking vital capacity readings and comparing them
maneuvers, the child would have been positioned for
with the norms, and it can be measured by taking
failure rather than success. Therefore positioning of
chest excursion measurements during inhalation with
the patient and tonal inhibitory or facilatory tech
a tape measure in three places: under the axilla, just
niques become of vital importance when developing
beneath the nipple line, and on the lowest most ribs
a treatment plan for maximizing respiratory function.
(8,9, and 10). Although both methods give an objec

tive measurement, neither technique can assess which
SPECIFIC RESPIRATORY IMPAIRMENTS
planes of ventilation are being compromjsed. Subjec
The first half of this chapter discusses the forces that
ing factors. The box on p. 690 gives detailed sum
influence the functioning of the neurologically im
maries of such assessments for persons with aU levels
paired chest. Understanding these forces allows one
of SCls. These characteristics can be extrapolated to
to discern the impairments that will appear as a di
subjective chest assessments of other neurological
tive assessment skills are needed to dctermine limit
rect or indirect result of those neurological deficits.
and/or musculoskeletal disorders, especially where
Decreased chest expansion, abnormal or inefficient
weakness is present.
breathing patterns, abnormal bony changes, de

creased cough effectiveness, decreased coordination
of breathing with functional activities, decreased
COMPENSATORY BREATHING PATTERNS
ability to phonate, and decreased ability to self-main
Limitations in chest expansion inevitably lead to
tain bronchial hygiene can all be direct results of se
changes in breathing patterns. Severely involved
vere neurological deficits. These specific impair
CV As or head trauma patients may show severe ab
ments are addresseu now in detail.
normalities in their breathing patterns in response to
PART VII
690
Neuromuscular Effects
Oil
Respiratory FU1lction in Spi1lal Cord Injuries
Paraplegia: Primarily Tl to T5
I.
Weakened and/or absent
2.
Intercostal
Erector spinae
Planes of ventilation limited
3.
Abdominal
Slight decrease in anterior and lateral expansion
Resulting in
Slight to moderate decrease in chest expansion and vital capacity (YC)
Decreased ability to build up intrathoracic and intraabdominal pressures
Decreased cough effectiveness
Possible paradoxical breathing
Tetraplegia: C5 to C8
I.
2.
3.
Missing aforementioned muscles and weakened
Pectoralis
Sen-atus anterior
Scalenes
Marked decrease in anterior and lateral expansion
Slight decrease in posterior expansion
Resulting in
Significant decrease in chest expansion and VC
Significant decrease in forced expiratory volume (FEY)
Significant decrease in cough effectiveness
Paradoxical breathing in acute phase and perhaps longer
Tetraplegia: C4
I.
2.
3.
Missing aforementioned muscles and weakened
SClllenes
Di aphragl1l
Marked decrease in anterior and lateral expansion
Slight decrease in inferior and superior expansion
Resulting in
More pronounced limitations in all three planes of ventilation
Possible decrease in tidal volume (TY)
Possible need for mechanical ventilation
37
691
Neuromuscular Effects on Respiratory Function in Spinal Cord Injuries-cont'd

Tetraplegia: Cl to C3
I.
2.
Missing aforementioned muscles and weakened and/or absent, the last of the remaining accessory muscles
Sternocleidomastoid (SCM)
Trapezius
3.
All severely limited including superior expansion
Resulting in
Significant decrease in TV
The need for full-time mechanical ventilation (at least in acute phase)
impairments to their respiratory centers in the brain

stem. This chapter focuses on compensatory breathing
patterns that develop as a result of muscular weakness
or paralysis, high tone, or pain. Details of breathing
Possible Compensatory Breathing Patterns after

a NeurologicallnjurylDisease
pattern changes secondary to brain stem lesions can
Paradoxical breathing (see-saw breathing)
be found in Chapter 22. The compensatory patterns

discussed here are itemized in the box at right.
There are two types of paradoxical, or "see-saw,"
breathing. The first is caused by a strong diaphragm
in the absence of the two other triad muscles, inter

costal muscles and abdominal muscles (e.g., polio,
tetraplegia, or paraplegia). Normal diaphragmatic ex
cUl'sion requires the muscular support and function of

the intercostal and abdominal muscles to optimize the
paradoxical breathing.
abdomen rises excessively
Paralyzed diaphragm
lower chest collapses
upper chest rises excessively
Diaphragm and upper accessory muscles only

Upper accessory muscles only (all three "triad"
Asymmetrical breathers (hemiplegia, unilateral

disorders)
of the stabilizing contraction of the intercostal mus

cles (Figure 37-9). This is the more common form of
muscles paralyzed)
excessively because of flaccid abdominal muscle

tone, and the upper chest collapses because of a lack
upper chest collapses
(paralyzed intercostals)
diaphragm's contractions. In this type of paradoxical

breathing the diaphragm contracts, the abdomen rises
Paralyzed intercostals and/or abdomina Is
Lateral or "gravity eliminated" breathers (weak

ness not paralysis)
Shallow breathers (typically associated with high

tone)
The second type of paradoxical breathing occurs

when there is diaphragm paralysis while the upper
accessory muscles are still intact. The abdominal
muscles may or may not be functional. The see-saw
primarily in a superior plane. Anterior and lateral ex
action here is the opposite motion of that described
pansion may also occur if the intercostal and pec
previously (Figure 37-10). With this type of paradox
toralis muscles are functioning. Generally, this com
ical breathing, the abdomen draws inward during in
pensatory breathing pattern requires some kind of
spiration and the upper chest rises. The upper acces
assisted ventilation, at least part time, because the di
sory muscles c o n t r a c t , exp a n d i n g the r i b c a g e
aphragm normally supplies most of the expansion
692
PART VII
FIGURE 37-9
Paradoxical breathing, strong diaphragm, absent accessory muscles and abdominal muscles.
W((I'
FIGURE 37-10
Paradoxical breathing, diaphragm paralysis.
necessary to maintain adequate oxygenation levels.
Another type of compensatory breathing pattern oc
Total accessory muscle breathing is generally inca
curs when the intercostal and abdominal muscles are
pable of providing adequate independent long-term
paralyzed but the diaphragm and upper accessory mus
ventilation because of the likelihood of respiratory
cles still function (i.e., tetraplegia, Cs to Cs; and para
muscle fatigue.
plegia, T I to T5). These patients learn to counterbal
37
693
FIGURE 37-11
Shortened neck musculature secondary to accessory muscle breathing pattern.
ance the strength of the diaphragmatic pull by using
Neurological insults that affect the chest asymmet
their sternocleidomastoid muscles and possibly their
rically, such as with CV As and some head traumas,
scalene, trapezius, and pectoralis muscles. Allowing
show another type of compensatory breathing pattern.
for superior and possibly some anterior and lateral ex
These patients can still acti vely ex pand their unaf
pansion of the chest, this compensatory breathing pat
fected side in all three planes of ventilation. Often,
tern prevents the collapse of the upper chest seen in
they accentuate this asymmetry to achieve more ex
paradoxical breathing. This must be cognitively coor
pansion on their unaffected sides. This may be seen
dinated with the inspiratory phase and is generally a
as increased sidebending toward their involved side
more effective breathing pattern. On subjective breath
(Figure 37-13). This leads to inadequate venti lation
ing assessment, these patients often present with short
on the affected side, which puts these patients at a
ened neck muscles (Figure 37-11). Intercostal retrac
higher risk of developing respiratory complications
tions, or the collapsing of the intercostal spaces on
secondary to inadequate ventilation. In addition, the
inspiration, may be seen here. The paralyzed inter
adverse effects on their posture can lead to undesired
costal muscle tissue will be sucked in toward the lungs
musculoskeletal changes over a prolonged period of
during the creation of negative pressure within the
time especially for the pediatric patient. Prevention of
chest, thus the observance of the retractions (Figure
these secondary changes is of utmost importance.
37-12). This may be the most accurate way of assess
Patients with generalized weakness, such as with

Guillain-Barre syndrome, some myopathies, neu
ing intercostal paralysis without an EMG test.

If the patient lacks all "triad ventilatory muscles,"
ropathies, or incomplete SCls, may show a tendency to
they may be able to breathe using their upper acces
ward lateral breathing, or breathing that takes place pri
sory muscles only. Generally they will need mechani
marily in gravity-eliminated planes. For example, in
cal ventilation to augment their independent effort.
supine, patients with weakened chest muscles could not
694
PART VII
FIGURE 37-12
Intercostal retractions noted during inspiration.
FIGURE 37-13
A and B, patients with hemiplegia. Note asymmetry of trunk.
37
695
effectively oppose the force of gravity in the anterior
disorder with oximeter)' during sleep. Patients show
plane, thus they alter their breathing pattern to cause ex
ing deficiencies may need repositioning of their sleep
pansion in the lateral plane where gravity is eliminated.
postures, nighttime ventilation, oxygen support, or a
In sitting, these same patients would tend to breathe in
combination of these. Rigorous exercising or activities
feriorly where gravity would assist the movement.
of daily living (ADL) training may be more appropri
Likewise, in side lying, they would tend to breathe in
ately scheduled later in the day for these patients until
an anterior plane. Overall, these patients have the best
their sleep problems have been rectified.
prognosis for effective breathing retraining methods be

cause they have weakness, not complete paralysis.
The last breathing pattern to be discussed involves
CHANGES IN PULMONARY FUNCTIONS
patients with central nervous system deficits resulting
The abnormal breathing patterns discussed previously
in high tone, such as MS, Parkinson's disease, and
develop secondary to the patient's neurological
some head traumas. Their breathing patterns are altered
deficits. However, those new patterns then change the
not so much by muscle weakness as by the following:
patient's pulmonary function, which in turn affects
(1) chest immobility because of abnolmally high neuro
functional respiratory status. Specifically, changes in
muscular tone (spasticity, rigidity, tremors), which se

verely limits chest expansion in any plane,
(2) cerebel
respiratory rates (RR), tidal volume (TV), and vital

capacity (VC) are addressed here.
(3) improper sequencing because
Alveolar minute ventilation is the product of TV
of lesions in the brain, most commonly seen with
times RR. The optimal relationship between these
lar incoordination, or
medullary lesions. Breathing is usually symmetrical,
two parameters is those values that result in minimiz
shallow, sometimes asynchronous, and frequently
ing the mechanical work that the lungs must perform
25 breaths/minute).
with a particular breathing pattern. In other words, it
Initiation and follow-through of a volitional maximal
is the combination of RR and TV that requires the
tachypneic (respiratory rates over
inspiration is difficult or impossible for these patients.
body to put out the least muscular effort per breath.
This will markedly curtail the ability to produce an ef
Because most of the compensatory breathing patterns

that have been discussed thus far reduce the patient's
fective cough and to maintain bronchial hygiene.
TV, the only recourse this patient has is to increase

RR. Normal RR is between
SLEEP DISORDERS
12 to 20 breaths/minute;
however, for this neurological population, it is not
The patients described in this chapter frequently
uncommon to see RRs at least twice that figure.
need to use their accessory muscles cognitively, to ar
Although adjusting RR does bring the patient's res
rive at a work-efficient, ventilation-efficient, breathing
piratory system back to a state of equilibrium, it may
pattern. Because of this, they should be evaJuated for
not produce the most efficient pattern in the long run.
nighttime ventilatory assistance. Muscle weakness or
The idea of the oxygen cost of breathing in that pat
breathing inefficiency may cause a state of chronic
tern must be considered in its long-term functional
hypoventilation and/or sleep apnea episodes during
use. Ideally, TV at rest should be about
sleep. Drowsiness, lack of concentration, disturbed
actual Vc. At this level, the able-bodied person needs
sleep, and/or irritability are common complaints of
less than
this s t ate. In the c l i n i c a l setting, we see m a n y
to operate the respiratory mechanisms. When per
10% of one's
5% of the total oxygen available to the body
tetraplegic patients and other severely involved neuro
forming a normaJ physical task or low-level exercise,
logical patients who are lethargic after awakening.
this oxygen consumption rate increases slowly, never
Hospital staff may incorrectly label these patients as
quite reaching a point where the oxygen cost of oper
lazy or uncooperative. It should be assessed whether
ating the respirator), system outweighs the cost of per
this behavior is volitional or whether it is due to a
forming the activity. However, for patients with im
state of chronic nighttime hypoxemia. Assessments
paired chest functions, such as in this popUlation, the
can be made by screening high-risk patients for this
total oxygen consumption level of the respiratory
696
PART VII
muscles at rest can be as much as 4 to 10 times that
the work of breathing. If VC remains less than 60% of
amount. These patients may have TVIYC ratios that
the predicted value, most research indicates that these
are already in the 33% to 67% range at rest, indicating
patients will demonstrate inadequate coughs. Similarly,
inefficient breathing patterns, reduced VCs, inade
a FEV 1 less than 60% indicates lack of sufficient power
quate respiratory reserves, or both. When they attempt
behind the cough. When VC remains or decreases to
a mild exercise, they become quickly short of breath.
only 25% to 30% of the predicted nonn, then ventila
They do not have adequate oxygen reserves to supply
tion assistance usually becomes necessary.
the respiratory and the nonrespiratory muscles simul

taneously, thus severely limiting exercise tolerance.
Therefore although these patients may show adequate
ADVERSE MUSCULOSKELETAL CHANGES
maintenance of alveolar minute ventilation at rest, a
Neuromuscular wea kness and the compensatory
mild increase in activity level may magnify respira
breathing patterns may cause adverse musculoskele
tory insufficiencies.
tal changes over a prolonged period of time. Previous
An adequate VC is imperative in restoring a pa
discussion in this chapter revolved around the ad
tient's functional status. Without the ability to expand
verse effects that gravity can play on the skeleton if
the chest maximally under his or her own muscle
the body is unable to counteract its force. Pronounced
power, VC will decrease after a neurological insult. For
deformities are more prevalent in children, of course;
example, studies show that tetraplegia resulting from
however, both children and adults are effected. Sev
SCIs may reduce the patient's VC to 33% of the pre
eral examples of specific changes are presented.
dicted value, increasing the TVIYC ratio to 30%. For
A common musculoskeletal deformity secondary
SCIs, an adequate VC is generally considered to be
to muscle weakness is seen as a flattened anterior
66% of the expected value. This would restore the
c h e s t w all, as s e e n w i t h m a n y p a r a p legic and
TVIYC ratio to approximately 15%, thus decreasing
tetraplegic patients. (Figure 37-14) For the patient
FIGURE 37-14
Musculoskeletal changes in adult chest secondary to spinal cord injury
anterior chest wall and narrowing of the upper chest.
(SCi). Note
flattening of the
37
The Patient ith Neuromuscular or Musculoskeletal Dysfunction
697
with weak or paralyzed intercostal muscles, this t1at
Anterior or lateral t1aring of the lower rib cage
tening often occurs because of prolonged supine posi
may also be noted. This is usually a result of insuffi
tioning along with the significant resistance that ante
cient abdominal strength, thus the lower ribs are not
rior chest expansion meets from gravity.
stabilized and integrated into the abdominal area (see
Another common deformity is a pectus excuva
Figure 37-8, p. 687). In upright, this is seen as a
tum at the base of the xiphoid process. Patients who
marked delineation between the rib cage and abdom
have a strong diaphragm but no muscular support
inal area in the mid-trunk region (see Figures 37-3,
from the intercostals and abdominal muscles may
p. 683 and 37 -15).
develop this type of musculoskeletal deformity (see
Upper chest ad verse m uscu loskeletal changes
Figure 37-7, p. 686). It can result from the di
occur when the intercostal and/or other upper acces
aphragm pulling inward so hard that the sternum,
sory muscles are impaired. The diaphragm is not po
without intercostal muscle support, cannot maintain
sitioned to assist in expansion of this area. Therefore,
its neutral position. Over time, it caves in, resulting
without those accessory muscles, the anterior wall of
in a permanent deformity.
the upper chest wiII become flattened and appear
FIGURE 37-15
Independent upright posturing. Adult with tetraplegia. Kyphosis restricts chest movement for
respiration. Note folding at mid-trunk line.
698
PART VII
more narrow than that of the normal upper chest (see

Figure 37-14, p. 696), resembling the more primitive
triangular shaping of the chest seen in the newborn
(see Figure 37-4, p. 684).
Spinal curves are not spared deformities. In a
weakened, low-tone patient, scoliosis is common be
cause the patient cannot adequately maintain himself
or herself upright against gravity. Slowly, the spine
collapses on itself, seeking stability; therefore scolio
sis is developed. All types of patients with the neuro
logical diagnoses discussed in this chapter are at risk
for developing scoliosis. The second possible spinal
change, a lumbar and thoracic kyphosis, can occur as
well because of the force of gravity on a mobile spine
and lack of paraspinal muscle support. Secondary to
these kyphoses, many patients develop an excessive
cervical lordosis to maintain eye contact. In sitting
the patient hunches over his or her trunk, making eye
contact and head righting difficult (see Figures 37-3,
p. 683 and 37-15, p. 697).
These spinal changes affect the functioning of the
respiratory system adversely. With a kyphotic thorax
in an upright posture, expansion of the chest in all
three planes of ventilation will be impaired. The ribs
require a stable base from which to become properly
mobilized. A kyphotic, weak posterior support does
not provide the necessary stability for optimal rib
mobility and function. Therefore proper elevation and
angulation of the ribs becomes impossible. This lim
its overall chest expansion and vital capacity.
Musculoskeletal changes in children must be ad
dressed. They are in a state of habilitation rather than
rehabilitation. Because of this, the neurological
deficit affects their developing chests more severely.
Their rib cages remain more triangular in shape, since
the muscles of the upper chest never develop fully or
normally. The ribs also remain more horizontal than
in the normal adult, probably because of less upright
posturing and lack of intercostal and abdominal mus
cle contractions on the rib frames. Their necks and
shoulders do not mature developmentally, often be
cause of overuse of the neck accessory muscles. This
leads to a permanent shortening of the neck strap
muscles, making the child appear to lack a cervical
area (see Figures 37-7, p. 686, and 37-8, p. 687).
Proper elongation of the cervical spine cannot occur,

resulting in skeletal changes to that area. Scoliosis,
along with thoracic kyphosis, tends to be more pro
nounced than in the adult.
DECREASED COUGH EFFECTIVENESS
With decreased chest expansion, the presence of
compensatory breathing patterns, and the adverse
musculoskeletal changes, the patient's ability to
cough will be drastically reduced. Vital capacity will
be impaired as will the ability to build up sufficient
intraabdominal pressure, especially for patients with
weakened, flaccid, or uncoordinated abdominal mus
culature. For many patients with traumatic brain in
juries, Parkinson's disease, CP, and CVA, the inabil
ity to coordinate an effective cough will be
significantly impaired. This inability may be due to
cerebellar damage or to high neuromuscular tone
(spasticity, rigidity, tremors). Frequently, the quick
action required to produce an effective cough will be
the same action that will trigger a sudden increase in
the abnormal neuromuscular tone. Objectively, when
the patient can not expel at .Ieast 60% of his or her ac
tual vital capacity in 1 second (FEV d, he or she will
often be incapable of producing an effective cough
without some assistance or retraining.
MAINTAINING BRONCHIAL HYGIENE
All these changes in respiratory functioning lead to a
decreased ability of the neurologically impaired pa
tient to independently maintain bronchial hygiene.
Complete expansion of the chest in all three planes
of ventilation and in all postures is impaired, so the
ability to properly aerate all lung segments is im
paired. Thus the ability to perform independent
bronchial drainage will I ikewise be impaired. Ineffi
cient breathing patterns rl)ay cause them to remain in
a state of chronic hypoventilation. Inability to pro
duce an effective cough impairs the ability to clear
the lungs of secretions. Therefore most of these pa
tients will require some assistance, either physically
or through verbal instruction, to achieve adequate
bronchial hygiene.
37
TIle Patient with Neuromuscular or Musculoskeletal DysfWlction
IMPAIRED PHONATION
699
provided by the muscles of ventilation (Figure 37-16).
Aphasia, as a secondary impairment to neurological
When the respiratory muscles are malfunctioning, as
deficits, is generally recognized by all members of the
in the neurological diseases discussed, the patient's
medical team as a problem that necessitates speech
ability to regulate the flow of air out of the lungs may
therapy. However, many persons with neurological
be impaired. Good eccentric control of the inspiratory
impairments display serious deficits in communica
muscles (the ability to slowly release these muscle
tion that remain untreated and the deficits remain un
during exhalat ion) is needed to p r oduce normal
acknowledged. Primarily, that deficit is inadequate
lengths of phonation. Otherwise, the air may be ex
breath support for phonation; in other words the pa
pelled from the lungs too quickly because of the nat
tient's inability to control the force and duration of ex
ural elastic recoil of the diaphragm, rendering that
halation for the purpose of phonation. Duration of
volume of air useless for phonation. Therefore both a
phonation and voice intensity are regulated by a deli
decrease in tidal volume and a decrease in eccentric
cate balance between airway resistance, provided by
control of the respiratory muscles will lead to impair
the laryngeal muscles, and the force of exhalation,
ments in functional speech.
FIGURE 37-16
Relationship of air flow and vocal folds.
700
PART VII
The average adult breathes at a ratio of 1:1 or 1:2
Airtlow out of the lungs should be as impOitant to
(inhalation time: e x h alation time) d u ring quiet
clinicians as airflow into the lungs. An evaluation of
breathing. The average ratio during phonation be
expiratory eccentric control is nccessary for all neu
comes I :5, with 8 to 10 syllables per breath being a
rological patients regardless of diagnoses. All disci
comfortable speaking length. Clinically, many pa
plines should incorporate a phonation facilitation pro
tients are seen to struggle with two- to thee-syllable
gram into their rehabilitation program, especially for
phrases because of inadequate breath support. Often
those patients who would otherwise not receive any
these same patients are not referred to speech therapy
speech training.
for training because they are not diagnosed as having

a "speech" problem (e.g., many patients with SCIs,
MDs, polio, or spina bifida). Optimally, these pa
ticnts should be able to phonate (an "ah" or "oh"
GOALS OF A NEUROMUSCULAR OR
MUSCULOSKELETAL RESPIRATORY PROGRAM
sound) for at least I 0 to 12 seconds during a con
In conclusion, the combination of secondary cfJ'ects
trolled expired vital capacity. Many of their voices
that follow a neurological and/or musculoskeletal in
fade away after 3 to 4 seconds. Without the ability to
sult are responsible for leaving the person with residual
communicate with normal speaking lengths and nor
musculoskeletal or neuromuscular deficits at greater
mal voice intensities, these patients' successful reen
risk for developing respiratory complications long
try into society's mainstream becomes significantly
after their acute phases have subsided. The long-term
more difficult.
goal of any respiratory rehabilitation program for these
Another misconception about these patients is that
patients is obvious; reduce their risk for developing
they are mentally slow or retarded because they do
these complications. First and foremost is the need to
not use all the proper figures of speech. In reality,
increase or maintain chest expansion in all three planes
these patients may exclude figures of speech because
of ventilation. Second, educating the patient and/or
of the extended time it takes them to communicate
family in methods to maintain good bronchial hygiene
something. For them, it is more expedient to forego
must be emphasized to prevent infections. Logically,
their inclusion.
improving cough effectiveness will improve airway
A marked example of this was seen in our clinic.
clearance. Next, increasing the patient's vital capacity
A 3-year-old girl who sustained a complete C4 to C5

spinal cord lesion at birth and had not received prior
rehabilitation was seen. On initial examination, her
speech was choppy, brief, and grammatically incor
rect. She rarely initiated conversation and her voice
Respiratory Rehabilitation Goals
intensity was very low. It was suspected that she per

haps suffered some anoxic brain damage to account
with a physical rehabilitation program, her speech
changed drastically. She spoke fluently, with 8 to 10

syllables/breath, correct inclusion of grammar, and
louder and more varied voice intensities. Instead of
being quiet and more reserved as she had been before
treatment, the mother reported that the child was a
became understood that her cognitive skills were well
maintain chest expansion in all three
Educate the patient and/or family in methods for

Improve cough effectiveness
Inc r e a s e the patient's vital capacity and t idal
volume
Reduce high respiratory rates
Modify inadequate breathing pattern s
Improve eccentric control of the diaphragm and

other ventilatory muscles for improved phonation
regular chatterbox. Her new communication skills ap

peared to improve her self-esteem. At that point, it
or
maintaining good bronchial hygiene
for her developmentally delayed speech. After an in

tense breathing retraining program in conjunction
lncrease
pl anes of ventilation
skills
underestimated on initial screening.
Incorporate effective ventilatory strategies with all
motor tasks
37
and tidal volume, where indicated, will help to im

prove aeration of the lungs. If necessary, reducing high
respiratory rates to improve pulmonary functions will
be a goal. Other goals include modifying inadequate
breathing patterns, which could mean increasing or de
creasing the use of accessory muscles to achieve maxi
mal breathing efficiency, and improving eccentric con
trol of the diaphragm and other ventilatory muscles for
improved phonation skills. These concepts lead us to
realize the need for incorporating effective ventilatory
strategies with all motor tasks. These goals are summa
rized in the box on p. 700. When implementing this
program, it is necessary to recall that the patient's res
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701
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Cherniak, N.S.
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Why should a therapist be concerned about

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7.
7(2): 110-14.
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What symptoms would be noted in patients
6.
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velopment?
5.
offhe airways. New York: Marcel Dekker. 399-418.
Cartwright, R.D. (1984) Effect of sleep position on sleep apnea

Cherniak, R.M. Cherniak, L., Naimark, A. (1972). Respiration
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c h il d with acquired d e f i c its in u tero or

Which orthopedic and neurologic diagnoses
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Para
The Transplant Patient
Susan Scherer
KEY TERMS
Cardiac rehabilitation
Organ rejection
Denervation of the heart
Psychosocial
Immunosuppression
Pulmonary rehabilitation
Organ donation
Secretion management
HISTORY
BACKGROUND
The ability to transplant an organ from one individual
Early transplant experiments were carried out on ani
to another is a relatively new phenomenon. Early at
mals in the early 1900s, with success at maintaining
tempts at transplant were barely successful. New ad
life for 90 minutes to 8 days (Hosenpud, Cobanoglo
vances in surgical techniques and immunosuppres
Norman, Starr, 1 991). Medical advances in car
sive drugs, however, have made transplantation of
diopulmonary bypass and immunosuppressive med
solid organs a viable treatment option. The increased
ications provided the opportunity for successful
life expectancy of transplant patients means that
transplants. After many trials and failures, the first
physical therapists have many opportunities to treat
successful orthotopic heart transplant was performed
patients after transplant in various settings. Trends in
in 1967 by Barnard; the first successful lung trans
patient demographics indicate that a physical thera
plant was performed in 1963 by Hardy and Webb.
pist may see a transplant patient not only in a re
Improvements in surgical technique, detection of
gional medical center setting but also in outpatient
rejection, and immunosuppressive drugs means trans
and rural clinics. This chapter contains guidelines for
plants are increasing in number. Virtually every solid
treating patients with heart or lung transplants.
organ can be transplanted from one individual to an

703
704
PART VII
other of the same species if there are similarities in
National I-year survival rates are as follows:*
immune system markers. Kidney transplants are the

simplest and most common, whereas heart-lung block
Kidney
93 8%
transplants are uncommon.
Liver
76.7'k
82.6%
57%
68%
Heart
Heart-lung
Lung
Purpose of Transplants
Although transplants are considered an acceptable
treatment option, a solid organ transplant is usually
Organ Donation
considered a last-resort therapeutic intervention.
The major limitation of organ transplantation is a
Medical intervention for diseases, such as cardiomy
supply and demand issue. The number of patients
opathy and interstitial pUlmonary fibrosis, is limited.
who could benefit from transplant significantly ex
When conventional medical therapy has failed, a
ceeds the number of organs available. Media cover
transplant may be considered. Although a transplant
age assists with identifying the issues and may play a
offers a patient a second chance at life, the medical
role in increasing the number of donors. To become
management of a transplant causes a patient to re
an organ donor, check with your state about specific
quire medical intervention on a long-term basis.
requirements; often a driver's license has a space to

identify you as an organ donor. Make sure that you
discuss your wishes with your family. If you are hos
Availability of Transplants
pitalized, family members or close personal friends
The number of medical centers who perform trans
wil I often be approached about donating your organs.
plants has grown to approximately 175 worldwide
If your family is confident that you wished your or
in 1989 (Hosenpud et aI., 1990). Because of the suc
gans to be donated, they will more likely say "yes" to
cess rates, many types of transplants are no longer
organ donation.
considered experimental but are considered appro

priate treatment for organ failure. In 1994 approxi
mately 10,000 kidney transplants were performed
CURRENT TRANSPLANT ISSUES
and 2500 heart transplants were completed (Col
Transplant trends include early detection of rejection,
orado Organ Recovery Systems [CORS], Denver,
development of new immunosuppressive medica
Colorado 1994).
tions, and donor management. For donor organs to be

viable, the donor must be managed in a way that pre
serves organs. In the past, fluids were pushed to pre
Rejection Issues
serve kidney function for transplant. This extra fluid,
Although transplants are successful, some health pro
however, made the lungs unusable. New donor man
fessionals believe that patients are merely exchanging
agement techniques are increasing the viability of
one set of problems for another. For a transplant to be
multiple organs from the same donor.
successful, a patient must remain on powelful immuno

suppressive drugs for the remainder of his or her life.
Some of these medications have crippling side effects.
The effects of long-tenn prednisone are well known:
Ethical Considerations
Should a p e rson who h a s developed end-stage
osteoporosis, muscle weakness, and glucose intoler
chronic obstructive pulmonary disease (COPD) from
ance, whereas the long-term effects of cyclosporine and
smoking be allowed to receive a lung transplant?
azathioprine impact on the patient's ability to fight in
Should a heart transplant be given to someone who
fection. Patients also need to manage medication side
developed alcoholic cardiomyopathy? Should a pa
effects on a day to day basis. It is these medications,

however, that make for impressive survival rates.
'Source: CORSo Denver. 1994.
38
tient with cystic fibrosis receive a double-lung trans
705
transplant program. Because of these needs, most
plant even though the donor lungs could go to two
transplants are performed at large, regional medical
different individuals with pulmonary fibrosis? These
centers, often those associated with a medical school.
are some of the ethical issues with which transplant
Because donor organs are viable for only hours after
teams struggle. There are no easy answers nor is there
removal from the donor, patients waiting for trans
unanimous agreement on each case. Despite the diffi
plant are required to live within a several-hour radius
culty of making wise choices, each team carefully
of the transplant center. Some patients may arrange
considers each candidate for transplant. Criteria are
air transportation to the medical center, others may
used so that individual preferences of team members
relocate themselves and family to temporary housing
are not given priority. When and if health-care re
within the metropolitan area. Most patients are given
sources become more limited, the decisions may be
a beeper to maintain contact in a timely manner.
come more difficult. If transplant success improves

and donor organs increase in number, transplants
could become
mainstream of treatment.
Psychosocial Implications
A strong support system is considered an essential
Criteria for Being listed on a Transplant Waiting list
component of a successful transplant. Demands of

waiting and relocation to the transplant city put con
Virtually every medical center with a transplant
siderable stresses on the patient and significant others.
program has developed criteria for patient selec
The patient is torn between wanting to remain hopeful
tion. Although each center may set its own criteria,
that a transplant will provide new life and the reality
there are similarities among the medical centers
of knowing that death may come before the transplant.
(see box below).
Patients feel these oppositional forces continuously

and struggle to keep a balance between hope and real
ity. Therapists can assist patients by listening to feel
Waiting Time
ings, being supportive, and encouraging participation
The time spent waiting for a transplant can vary con
in support groups. Because most patients experience
siderably. Some patients wait less than a week; others
these feelings, support groups offer invaluable inter
wait up to 18 months. During the waiting period, pa
vention. Groups which include patients both before
tients struggle with the need to carry on their lives, all
and after transplant probably have the most to offcr in
the while knowing that at any moment they may be
terms of psychosocial support. Those patients who re
called to the hospital for transplant.
locate to transplant centers may have the most diffi
The number of transplant centers in the United
cult time psychologically, especially as they leave
States is limited. State of the art hospital facilities and
family and significant others behind. Feelings of
surgeons are neccssary components of a successful
being useless are common because patients waiting in

a foreign city must find something to do.
Spouses and significant others also benefit from
group support. The psychological stresses are some
what different on spouses. Spouses speak of the
Criteria for Transplant Waiting List
struggle to remain hopeful, yet plan for a future that

may not include their loved one. If the patient and
Age: under 65 (60 in some centers)

Terminal illness (expected life span less than I year
Nonsmoker
spouse move to a new city to wait for transplant, they

may find themselves with more time together than
they have ever spent before. ]n this forced retirement,
Adequate social support system
new stresses are added to relationships. Transplant
Disease free in other systems
teams usually include a psychologist or social worker

to whom patients may be referred for individual or
706
PART VII
family counseling if the stresses limit function or par
fort and function after surgery. The physical therapist
ticipation in pretransplant programs.
should be familiar with the surgical incisions and im
After transplant, patients struggle with conflicting
pact on rehabilitation.
feelings. Patients are often emotionally overwhelmed
Heart transplants are usually performed through a
with a feeling of gratefulness that they are alive and
median sternotomy incision and cardiopulmonary by
feel guilty that someone else's glief has given them a
pass is used. A midline incision from sternal notch
chance to rejoice. Psychological or spiritual support
distally allows the sternum to be accessed and split.
may be requested or s u g gested after transplant

(Craven, Bright, and Dear,
1990).
Although the native heart is excised, a portion of the

right atrium and the SA node is preserved. The donor
heart is sutured to the atrial cuff and the major ves
sels reattached. After surgery, the two halves of the
Patient Education
sternum are wired together, the new heart defibril
The waiting period time provides an ideal opportu
lated, bypass reversed, and the patient awakened.
nity for patient education. Nursing generally provides
Lung transplantation surgical incisions depend on
much of the education regarding preoperative proce
whether a single or double-lung transplant is to be
dures, postoperative course, and medication. Rehabil
performed. Single lung transplants are performed
itation teaching includes breathing training, airway
through a posterolateral thoracotomy incision, with
clearance techniques, and activity progression.
the patient side lying on the opposite side. To allow

visual access for the surgeon, the latissimus dorsi and
lower trapezius muscles are cut. The incision through
TRENDS IN TRANSPLANT CARE
the fourth or fifth intercostal space also means the in
Transplants are being made available to a broader
tercostal muscles at this level may be incised. If the
group of patients. Although transplants are only per
rib at the surgical level fractures, it is resected so that
formed in certain centers, patients from rural areas
the bone ends do not rub or puncture the lung. The
are being evaluated at regional centers. Because
serratus anterior muscle is preserved if at all possible,
transplant criteria differ slightly from center to center,
but the lateral portion of the rhomboid may be cut to
some patients may be evaluated at several centers.
allow more access for the surgeon. Postoperative pain
The increased availability of transplants and the relia
and impaired upper quarter movement patterns may
bility of air transportation means that even patients
present significant problems for patients.
from outlying geographical areas may be considered
Double-lung transplants are performed through an
for transplant. After transplant, improved medical
anterior incision sometimes described as a clamshell
care has led to shorter hospital stays. For the patient
approach. A horizontal incision above the level of the
who has relocated to the transplant city this means
diaphragm is performed, but the distance needed for
that he may be discharged to an apartment and return
adequate visualization means that the pectoralis
to the hospital several times a week for physician fol
major and minor may be incised bilaterally.
low-up and rehabilitation. Once medically stable, pa

tients may be allowed to return to their homes as
early as 2 to 3 months after transplant, if medical sup
PHYSICAL THERAPY CONSIDERATIONS

As important members of the transplant team, physi
port and rehabilitation needs can be met.
cal therapists need an understanding of the physiolog

ical components of both the pretranspJant disease and
SURGICAL PROCEDURES
posttransplant state, the influence of surgery or physi
The surgical approach for transplant is chosen to pro
ology on musculoskeletal structure and function, and
vide the surgeon the optimal working area and visual
how medical management may necessitate modifica
field. The choice of incision may affect patient com
tion of therapeutic interventions.
38
Physiology
707
c1es of respiration is reduced. The physical therapist
The cardiovascular and respiratory systems are criti
needs to optimize breathing in the preoperative pe
cal elements of functional ability, in areas of en
riod, yet prepare the chest and shoulder muscu
durance and movement. Adequate oxygenation and
loskeletal system for normal function.
circulation are needed to provide fuel to perform

daily activities. In the patient awaiting heart trans
plant, cardiac output is significantly compromised,
Medical Management
and hemodynamics may be unstable. Because of
Knowledge of medical management including med
these limitations, pretransplant exercise is inappropri
ications, ventilatory support, and hemodynamic mon
ate. Posttransplant. however. the main interventions
itoring assists the therapist in determining whether
will be to restore normal cardiac output. Knowledge
modifications are needed during rehabilitation. Table
of physiology allows the therapist to choose appropri
38-1 lists suggested areas to monitor during both be
ate interventions.
fore and after transplant rehabilitation. For example,
In patients with terminal lung disease. the primary
patients often complain of tremors during rest and ac
limitation is ventilation. Pulmonary rehabilitation has
tivities. Therapists should be knowledgeable enough
been beneficial in improving daily function (Toronto
to question other health professionals as to whether
Lung Transplant Group, 1988; Petty, 1980; Moser,
the tremors are a result of medications, such as cy
Bokinsky. Savage, Archibald, Hansen, 1980) and
c1osporine, a metabolic abnormality, a seizure disor
may be used in the pretransplant period. Supplemen
der, or muscle weakness.
tal oxygen can be lIsed during exercise to maintain

adequate oxygenation. The waiting period before
transplant is an ideal time to optimize muscle func
PHYSICAL THERAPY ASSESSMENT

The purpose of physical therapy before transplant is
tion and flexibility.
to identify baseline function and to screen for impair

ments that may limit rehabilitation goals. In some in
Musculoskeletal Considerations
stances, physical therapists will provide treatment in
The musculoskeletal problems of patients with pul
the pretransplant period; in other cases, the informa
monary disease are well documented (see Chapter 4).
tion gained from early assessment allows the thera
Patients undergoing lung transplants are unique in
pist to identify areas needing attention or modifica
that after transplant the musculoskeletal system re
tion after transplant. Physical therapy assessment in
turns to normal structure. The chest wall adapts in
the postoperative period addresses specific impair
size to the new lung. The need to use accessory mus-
ments and functional limitations of the individual.
TABLE 38-1
Recommended Monitoring
"
heart
x =
lung
BLOOD PRESSURE
Before exercise
-.J
HEART RATE
x
-.J
Sa02
RA TING OF PERCEIVED EXERTION
During exercise
-.J
-.J
After exercise
-.J
-.J
-.J
708
PART V[[
Guidelines for the Delivery of Cardiopulmonary Physical Therapy; Special Cases
PRETRANSPLANT REHABILITATION
Cardiac Patients
Pretransplant assessment of the cardiac patient in
cludes functional ambulation (6-minute walk) and
Heart Transplant
screening for deficits in muscle strength or range of
Because the patient awaiting heart transplant has sig
motion. Exercise training is not generally recom
nificantly compromised cardiac output and may be
mended pretransplant. Range of motion may be in
hemodynamically unstable, preoperative rehabilita
creased or specific muscle strengthening may be ac
tion is generally not recommended. Some patients
complished, however, if the need is determined to be
with moderate congestive heart failure may be able to
significant. All patients will be limited in functional
tolerate a mild level of exercise (Roubin, Anderson,
endurance, therefore the results of the 6-minute walk
et aI., 1990; Hillegass and Sadowsky, 1994). Most
is compared with posttransplant functional status.
patients, however, are unable to tolerate endurance

training.
Some patients may need musculoskeletal interven
Pulmonary Patients
tion for decreased range of motion, muscle weakness, or
Because rehabilitation in the pretransplant period is
general discomfort. If physical intervention is needed,
often indicated in patients waiting for lung transplant,
heart rate, blood pressure, and ECG monitoring is used
the physical therapy assessment information may be
to guide treatment. If heart rate or blood pressure de
used to design a more effective rehabilitation pro
creases during exercise, exercise should be stopped.
gram. Upper and lower extremity muscle strength
The main goal in the preoperative period is to pre
and range of motion is assessed, as well as posture,
vent losses of function. Maintenance of range of mo
shoulder and trunk mobility, breathing pattern, breath
tion, soft tissue extensibility, and muscle strength are
sounds, and functional mobility.
suggested goals.
Posttransplant Assessment
Lung Transplant
(Heart and Lung)
Although each patient is treated individually, there
After transplant, physical therapy assessment ad
are similarities among patients, resulting in a stan
dresses all areas of functional limitations and the cor
dard program for pretransplant rehabilitation (Figure
responding impairments. Patients should be evaluated
38-1). Pretransplant rehabiIi tation resembles pul
in the immediate postoperative phase, and reevalu
monary rehabilitation programs in existence for pa
ated on admission to the outpatient treatment phase.
tients with COPD, CF, and restrictive d i seases
Because of the surgical intervention, bed mobility,
(Toronto Lung Transplant Group, 1988; Conners and
ventilation, secretion management, range of motion,
Hilling, 1993; Malen and Boychuck, 1989).
and pain control are important areas to address.
General Considerations for Rehabilitation

REHABILITATION OF THE TRANSPLANT
Since the primary limitation in pulmonary disease is
PATIENT
ventilatory, oxygen needs are essential to monitor. A
To assist in treatment planning, rehabilitation is cate
pulse oximeter with finger or ear probe is mandatory
gorized into the following four phases: pretransplant,
in a pretransplant pulmonary rehabilitation program.
postoperative acute phase, postoperative outpatient
Oxygen saturation should be maintained above 88%
phase, and community- or home-based phase. Al
at all times. A source of supplemental oxygen is nec
though the ultimate goal of transplant rehabilitation is
essary, whether the patients bring their own oxygen
to improve the patient's function and quality of life,
or it is supplied by the center. In patients with severe
each phase of rehabilitation has its own emphasis.
disease, oxygen-conserving devices may need to be
38
709
loskeletal impairments to function. Using the waiting

time to maximize muscle strength and range of mo
tion means that less time is needed posttransplant to
return to functional activities. Pretransplant rehabilita
tion programs have been shown to decrease posttrans
plant hospital stay (Scherer, 1995). It is reasonable to
set goals to achieve normal muscle strength in lower
extremity musculature, increase upper extremity mus
cle strength, increase shoulder and chest wall range of
motion to normal or within functional limits, demon
strate coordinated diaphragmatic breathing with exer
cise and activities, and improve cardiovascular en
durance. An example of a preoperative pulmonary
rehabilitation program is in the box on p. 710.
Interventions
Deficits which are found in any of the above areas
may be addressed in the pulmonary rehabilitation
program, except in patients with primary pulmonary
hypertension or Eisenmenger's syndrome. In those
patients, exercise which increases cardiac workload
is contraindicated. However, if cardiac output is
monitored and the physician agrees, range of motion
exercises may be taught and light strengthening ex
ercises may be performed. For example, a 22-year
old female with primary pulmonary hypertension
was found to have injured her shoulder 4 weeks pre
FIGURE 38-1
viously, resulting in decreased range of motion in a
Pre-lung transplant rehabilitation.
capsular pattern. She has been on the lung transplant

waiting list for 3 months. The physician wants her
used. Patients with COPD should have blood gases

monitored for carbon dioxide retention, since increas
ing exercise often requires an increase in supplemen
tal oxygen. Several of our patients has carbon dioxide
levels in the 88 to 100 range. Although heart rate is
not a good measure of exercise intensity, patients
with lung disease may demonstrate signs of right
heart failure and should have heart rate and blood
pressure monitoring on a regular basis.
only to walk as necessary for her daily activities.

With consultation with the physician, joint mobi
lization, range of motion activities, and modalities
may be used with few precautions. Strengthening
exercises may be used cautiously, avoiding breath
holding and Valsalva maneuvers.
Other Transplants
Patients awaiting other organ transplants may also be
referred to physical therapy for treatment of muscu
loskeletal problems. Because of the level of meta
Goals
bolic abnormality in patients awaiting liver and kid
The overall goal of pretransplant pulmonary rehabili
ney transplants, endurance training is difficult to
tation is to maximize function and reduce all muscu
perform. Other physical therapy interventions, how
710
PART VII
Preoperative Pulmonary Rehabilitation

10 minute
Warm-up (group)
Active range of motion
Upper body
Lower body
Trunk
Light resistance (5 to 10 reps)
Individualized Endurance Program

Bike (Airdyne)
25 to 30 watts
Treadmill
0.8 to 1.5 mph

0% to 5% grade
10 to 30 minutes
Arm ergometer
0 to 25 watts
10 to 15 minutes forward and backward
10 to 20-minute intervals
15 to 20 minutes
Individualized Strength Program

Pulleys
Theraband
Latissimus pull-downs
Rhomboids
Diagonal arms
Shoulder extension rotation
Pectoral
Shoulder flexion
Latissimus
Triceps
Subscapularis
Lower Extremity
Quadriceps
Hip extensors
Hip abductors
10 minutes
Cool-down (group)
Stretching (full-body)
B reathing
Relaxation
ever, m a y be u s e d as appropriate (i.e., muscle
and increasing functional abilities in self-care and
strengthening, range of motion).
ambulation.
ACUTE PHASE REHABILITATION
Heart Transplant (Acute)
The acute phase of rehabilitation begins in the inten
Considerations
sive care unit and continues throughout the patient's
In the immediate postoperative period after heart
hospital stay. Interventions are focllsed on facilitat
transplant, cardiac output is compromised and hemo
ing normal cardiovascular and pulmonary function
dynamic responses slowed. A transplanted heart is
38
711
University Hospital Cardiovascular Rehabilitation Supervised Exercise/Activity Plan/Surgical Patients

DX
Physician
MEDS
Step/Date
Exercise
Activity
I ICU
-Active/Passive ROM, in bed
5 reps
-Partial self care

-Feed self
1/5 METS
-Use of bedside commode
-Teach hourly ROM exercise
-UP in chair for meals as

-Turn, cough, deep breathe & use incentive spriometer, q2-4
-Sitting bed bath
21CU
-Active ROM, sit on edge of bed
1.5-2.0 METS
-Teach Rating Perceived Exertion
5 reps
-Sit in chair as tol

-Partial/complete self care
-Up in chair for meals
-Turn, cough, deep breathe and use
incentive spriometer, q2-4
-Sitting bed bath
3 FLOOR
-Active ROM/warmups, standing
2.0 METS
-Walk 100 ft. slow pace
IO reps
-Sit in chair 2-3x/day (20 min)

-Complete self care
-Sitting bed bath
-Incentive spriometer indep, TID
4FLOOR
-Warmups, standing
2.5 METS
-Walk 150 ft, average pace
-Use of bathroom w/assist
-Teach pulse counting
-Walk around room
10 reps
-Complete self care
-May take warm shower after pacer

wire removed
-Incentive spriometer indep, TID
IO reps
5 FLOOR
-Warmups, standing
3METS
-Walk 300 ft, average pace
6 FLOOR
-Warmups. standing
3.5 METS
-Walk 500 ft. average pace
-Dressing indep
-May stand at sink for ADLs
10 reps
-As above
-Introduce to phase II
-Walk down flight of stairs

-Instruct in home exercise
7 FLOOR
-Warmups, standing
4METS
-Walk up flight stairs
-All self care indep
10 reps
-As above
-Walk 500 ft average pace

-Schedule sub max ETI
-Enroll in Phase II
Guidelines for Exercise

-Pt HR to be 50-120 bpm
-no significant anhythmias
-Exercise HR not more than 20 beats above rest
-SBP
-No worsening ST changes
-<
-RPE of IO or less
-no angina or other symptoms
<
200, DBP
<
120 during exercise
10-15 DBP drop during exercise
712
PART VII
stiff for several days, and the sympathetic nervous
the heart is denervated. Because of the lack of sym
system input to the heart is destroyed in the transplant
pathetic input, heart rate cannot increasc quickly and
process. To maintain cardiac output (HR x SV) in a
contracti I ity is not under sympathetic control. The
heart with decreased stroke volume a fixed rate pace
only mechanism by which heart rate can be increased
m a k e r is u s e d at a r a t e of a p p r o x i m a t e l y 120
is by circulating catecholamines, which take 10 to 15
beats/minute for several days. ECG readings may be
minutes to influence a response. Therapists working
normal because the donor heal1 has an intact conduc
with heart transplant patients should allow time for
tion system, although the atrial cuff left from the na
patients to adapt to changes in position and may want
tive heart may cause the ECG to have two P waves.
to use light active bed exercises as a warm-up activity
The therapist working with heart transplant patients
(Irwin and Tecklin, 1995 ).
in the ICU should be aware that heart rate cannot in

crease significantly, therefore blood pressure and pa
tient response should be monitored. Surgical cardiac
rehabilitation guidelines can be used to guide treat
Lung Transplant
Considerations
ment, with increases of 0.5 to I metabolic equivalent
After lung transplantation, patients are generally me
(MET) per day (see box on p. 711). Complications of
chanically ventilated for 24 to 72 hours. Often, para
heart transplant include sternum instability, infection
lytic agents are lIsed in this period so that ventilation
or pain, and potential nerve or circulatory damage to
can be optimized. Patients who received double-lung
the femoral area because of intraaortic balloon pump
transplants may be more hemodynamically compro
(lABP) cardiac assist. Acute rejection episodes are
mised if they were on bypass during surgery. Chest
characterized by flu-like symptoms including low
tubes are likely in place, and patients are medicated
grade fever and muscle achiness and is often accom
for pain. Infection control is imperative; isolation
panied by dysrhythmias. Rejection episodes can only
rooms with negative-pressure ventilation are used
be confirmed by tissue biopsy.
and medical personnel at minimum are required to

wash their hands and wear masks when in the pa
Goals
tient's room. Isolation or reverse-isolation procedures
Goals of the acute phase of rehabilitation include the
are followed (the patient wears the mask when leav
following: (I) regain normal postural cardiovascular
ing the room). The primary monitoring is oxygen sat
responses (no postural hypotension) and (2) increase
uration, followed by heart rate and blood pressure. A
functional activities. The former is primarily focused
common complication in the immediate postoperative
on the patient being able to tolerate changes in posi
period is pneumothorax.
tion, increase time in upright sitting, and transfer in

dependently. Upper and lower extremity range of
Goals
motion and strength need to be adequate to perform
In the immediate postoperative period the major goals
activities of daily living.
are to increase time out of bed, optimize ventilation

perfusion ratio, and increase active range of motion on
Exercise Guidelines
the surgical side (Malen and Boychuck, 1989). Major
Deconditioning and lack of sympathetic input to in

crease heart rate response contribute to the possibility
of hypotension. Because of the high incidence of pos
tural hypotension, patients need to change positions
problems and goals are listed in Table 38-2.
Interventions
The range of therapeutic interventions are many. In
slowly and be given time to adapt to the new posi
general an intervention may continue until an abnor
tion. Exercise may be continued during mild-to-mod
m a l exercise response is reached. Abnormal re
erate rejection episodes but is not performed during
sponses include a decrease in heart rate or blood pres
periods of severe rejection. The main consideration
sure with an increase in exercise, a decrease in
for exercise in patients with heart transplants is that
oxygen saturation below recommended levels (88%
38
713
TABLE 38-2
Problems and Goals for Acute Posttransplant Rehabilitation: Lung Transplant
PROBLEM
GOAL
Decreased secretion clearance
Independent secretion management
Because the lungs are denervated, there is decreased

sensation of secret ions.
Incisional pain
Pain management
Postoperative pain is related to the surgical incision
Pain medication
and decreased movement of muscles

Abnormal postural hemodynamic responses
Normalize hemodynamic response
(i.e., postural hypotension and fatigue)
(i. e. , no postural hypotension, normal heart rate, respiratory
Increased oxygen/venWatory requirements
Adequate oxygenation without supplemental (Sa02 94%
rate, and blood pressure response to exercise)

to 96% on room air)
Diaphragmatic breathing
Normal vital capacity
Decreased runctional mobility
Independent activities of daily living (dressing, hygiene,
Decreased shoulder range of motion
Need adequate shoulder range of motion to perform these
Decreased exercise tolerance
Independent transfers
shower, toilet)
activities
Out of bed most of day
Independent ambulation SOO ft
Bicycle 10 minutes, no resistance
Compromised nutrition
No supplemental feedings
to 90%), or symptoms of dizziness and diaphoresis.

Suggested treatments are shown in Table 38-3.
(IV)
Considerations
As mentioned before, transplanted hearts lack auto
nomic innervation. Implications for exercise response
are that heart rate increases can only be accom
POSTOPERATIVE OUTPATIENT REHABILITATION
plished, using circulating catecholamines. For the

phase II cardiac rehabilitation patient, this means that
Heart Transplant
the warm-up and cool-down portions of exercise
Once the patient leaves the hospital, rehabi litation
should be increased to 10 t o 15 minutes and pro
looks much like phase II cardiac rehabilitation. The
gressed slowly. Resting heart rates are close to the in
overall objective is to increase functional activity to
trinsic heart rate of 100, and heart rate should not be
within normal limits.
used as an indication of fitness nor to establish exer
Duration of this phase of rehabilitation generally
cise intensity. Rating of perceived exertion is a more
continues for 8 to 12 weeks, at which time the patient
appropriate indication of exercise intensity. Recom
is encouraged to continue exercise on his or her own
mended guidelines are 11 to 13 on the 20-point Borg
or at a fitness facility. Many heart transplant patients
scale (Irwin and Tecklin, 1995; Hosenpud et aI.,
return to predisease levels at this stage.
1990). Both endurance and strength exercise can be
714
PART VII
TABLE 38-3
Acute Rehabilitation Interventions
GOALS
INTERVENTIONS
Independent secretion management
Incentive spirometer
I
I
Secretion removal (positioning, percussion, and vibration)

Assisted cough or instruction
Active range of motion shoulder girdle
Pain management
Pain medication
Positioning
Mild heat
Massage/soft tissue techniques
Normalize hemodynamic response
Sitting on edge of bed
(i.e., no postural hypotension, normal heart rate,
Out of bed to chair day 1 or 2
respiratory rate, or blood pressure response to
Ambulation to bathroom day 2 or 3
exercise)
Adequate oxygenation without supplemental oxygen
Instruction of diaphragmatic breathing
Diaphragmatic breathing with activity
Facilitation of diaphragmatic breathing
Normal vital capacity
Lateral costa l expansion techniques (surgery side)
Independent activities of daily living (dressing,
Encourage and assist with activities of daily living
Incentive spirometry
hygiene, shower, toilet)
Active and active-assisted range of motion

All motions shoulder girdle
Need adequate shoulder range of motion to
Wand exercises
perform these activities
Side lying shoulder abduction

Independent transfers
Daily schedule
Out of bed most of day
Assisted ambulation in room initially, to hallway within
Independent ambulation 500 ft
2 to 3 days
Bicycle in room, 2 minutes initially, progress to 10 minutes
Bicycle 10 minutes, no resistance
Schedule rehabilitation around meals
No supplemental feedings (IV)
Medical management of nausea
performed in this rehabilitation stage, although upper
should be reported to the physician immediately. Re
extremity strengthening should only be started after
jection episodes are monitored by biopsy. Exercise
the sternum has healed. To protect the sternum, lift
can continue if the rejection episode is mild or mod
ing should be limited to Jess than 10 lbs for 6 to 8
erate as determined by biopsy. Summary guidelines
weeks. Treadmill, bike, arm ergometry, and indoor
for postoperative rehabilitation for heart transplant
cross-country ski equipment are all appropriate
are outlined in the box below.
choices.
Signs of Rejection
Lung Transplant
The primary signs and symptoms of rejection include
Because patients are discharged from the hospital as
flu-like symptoms including low-grade fever and
early as 8 days after transplant, much of their medical
muscle aches. Dysrhythmias and bradycardia below
management and rehabilitation occurs on an outpatient
60 or relative bradycardia (decreased compared with
basis. In the early stages of this postoperative outpa
patient's normal resting heart rate) are significant and
tient phase, patients are medically labile and need
38
715
portable oximeter at home and may report episodes
Summary Cardiac Guidelines
of desaturation. Rejection should be suspected and

reported if a decrease in Sa02 of 4% to 5% for the
Cardiac phase II protocols
same amount of activity is seen (Malen and Boy
Heart rate is not intens ity regulator
chuck, 1989).
Increase warm-up and cool-down to 10 to 15 minutes
RPE II to 13 (20-point Borg scale)
Goals
No exercise in severe rej ection ( b iops y )
Patients are generally excited about the improvement
Continue exercise in mild rejection
in shortness of breath and surprised at the level of

muscle weakness seen especially in the lower extrem
ities. Once ventilation is no longer a limiting factor in
function, other deficits emerge. In the initial stages of
Once- or twice-a-week monitoring of medical status.
outpatient rehabilitation, patients may have multiple
Rehabilitation should progrcss in this phase, but close
complaints about the side effects of medications and
communication with medical personnel is recom
often generally do not feel well. Rehabilitation
mended because of thc many medication changes.
should continue through these periods of malaise.
Blood levels of immunosuppressive drugs are moni
The overall objective of outpatient rehabilitation is to
tored and metabolic function (fluid and electrolyte lev
improve function to levels appropriate for the pa
els, kidney and liver function) are followed.
tient's age and interests. Generally, patients are

closely followed by the medical staff for 2 to 3
General Considerations
months after transplant, and rehabilitation 2 to 3
Patients in the outpatient phase of rehabilitation begin
times per week continues throughout this period.
at low levels of function and progress to having few
The most common impairments that limit func
functional limitations. Therapists need to adapt and
tion are decreased cardiopulmonary endurance, de
progress the rehabilitation program appropriately. If
creased muscle strength and endurance, range of mo
rehabilitation is not aggressive, patients may succumb
tion limitations, and abnormal movement patterns of
to the effects of prednisone and cyclosporine. Because
the shoulder or trunk. Impairments may be caused by
of the debilitating side effects of immunosuppressive
the surgical procedure itself or as a result of years of
medications, rehabilitation needs to be aggressive and
abnormal muscle mechanics, posture, and decreased
preventive in nature. Rehabilitation can occur in a
activity. Cardiopulmonary endurance training is em
group setting and/or on an individual basis.
phasized at this stage of rehabilitation, as is posture

reeducation, range of motion, and upper extremity
Monitoring
movement patterns. Lower extremity strengthening
The areas of emphasis in the lung transplant patient
can begin early, but upper extremity resistive train
follow from the physiology and surgery performed.
ing should be delayed until wound and tissue healing
The primary limitation pretransplant is ventilatory,
is complete, generally about 6 weeks because of the
with the surgery intended to improve ventilation.
delays in wound healing caused by prednisone.
Monitoring of ventilatory status should be the pri
Goals which specifically address impairments may
mary consideration of the therapist. Respiratory rate
include normal shoulder range of motion, normal
and oxygen saturation should be followed closely
muscle strength in all major muscle groups of upper
during exercise sessions.
and lower extremities, and normal thoracic mobility

(Figure 38-2).
Rejection
The primary symptoms of acute rejection are short
Interventions
ness of breath, exercise intolerance, and desaturation
To achieve the goals of rehabilitation and address im
at rest or with exercise. Patients generally have a
pairments, a pulmonary rehabilitation protocol may be
716
PART VII
Lung Transplant Guidelines

Keep S a0 2 above 90%
Add supplemental oxygen if necessary during
treated acute rejection episodes
Patient should wear mask when with people
Increase strength program during prednisone bursts
Return to home can occur at this point in time, whether

or not rehabilitation goals have been met. The major
goal of community-based rehabilitation is return to
normal function with minimal limitations. Many pa
tients feel so good after transplant that return to prior
FIGURE 38-2
level of function, including employment, is a natural
Post-single lung transplant inp atient.
phenomenon. Formal rehabilitation may only be neces

sary in complicated cases or after rejection episodes or
illness. Patients may also seek physical therapy advice
used, or the therapist may creatively design a rehabili
for musculoskeletal problems unrelated to the trans
tation program. Except for delaying upper extremity
plant. Therapists should be comfortable treating pa
strengthening for 6 weeks after surgery, no therapeutic
tients in many settings, addressing the common com
interventions are contraindicated. For endurance train
plications, and watching for signs of rejection.
ing, stationary bicycles, treadmills, arm ergo meters,

indoor nordic ski machines, rowers, and stair climbers
may be used. Pulleys, weight equipment, free weights,
Heart Transplant
resistive elastic bands, or gymnastic balls all may be
Ironically, the medications used to prevent rejection
appropriate for strengthening and facilitation of nor
in transplant patients may increase the incidence of
mal movement patterns. Because of the effects of
coronary artery disease. It is recommended that pa
prednisone, proximal muscle function must be ad
tients partici pate in a regular exercise program to
dressed, and strengthening programs should be ag
manage the effects of the medications and to prevent
gressive, keeping the repetitions to 10 or less. Once a
coronary artery disease complications. Hospital
patient has achieved a satisfactory level of function
based phase III cardiac rehabilitation programs are
(determined by the therapist and patient), formal reha
appropriate, or patients may elect to independently
bilitation may be discontinued.
exercise in a fitness facility. Some follow-up by the
The general considerations for lung transplant pa

tients are to monitor oxygen saturation and prevent
center is important to encourage compliance in exer

cise programs.
the patient from contracting respiratory infections. A

summary of lung transplant treatment guidelines are
listed in the box below.
lung Transplant
For patients who have left their home community to
COMMUNITY OR HOME-BASED REHABILITATION
wait for lung transplant, the transition to home fre

quently occurs at 3 months after transplant. Ideally,
Patients are generally followed at the transplant center
rehabilitation goals from the outpatient phase will
until the medical staff is satisfied with patient progress.
have been accomplished, and the patient will be able
38
717
and needed long-term therapy. A 55-year-old male

had a bowel obstruction after surgery, which length
ened his recovery time. If the patient is medically sta
ble but has rehabilitation needs, the patient may be
referred for physical therapy in his or her home town,
possibly away from the transplant center. Other pa
tients may have multiple episodes of rejection, which
are treated with high-dose steroids, and develop
steroid myopathy, requiring intensive and progressive
strength training.
Goals
Physical therapy assessment is critical to identify
problem areas and evaluate progress toward goals.
Goals at this stage should be primarily guided by spe
cific patient quality of life issues. Common long-term
impairments are chest wall soreness, abnormal upper
quarter movement patterns, and low back and knee
pain from overuse.
Influence of Medications on Treatment
FIGURE 38-3
Post-douhle lung transplant outpatient at approximately 3
months pust-surgery.
Patients are on a multitude of medications after trans

plant, and additional medications may be added to
decrease the side effects of the primary immunosup
pressive drugs (Miller, 1995). Prednisone, cy
closporine, and azathioprine (lmuran) are the main
stay of immunosuppression, with OKT 3 and FK 506
being additional options.
Prednisone
to return home to pursue his or her own interests.

Success stories are many. One patient returned home
and progressed to walking 5 miles a day, fishing 4 to
5 times/week, and bow hunting with a 50-lb bow.
One gentleman reported at a 6-month follow-up visit
that he was pleased to be riding around his ranch and
checking up on things. The therapist asked if he was
riding in the truck, and he replied, "no, on my horse."
A 21-year-old male (130 Ib) with cystic fibrosis re
sumed weight lifting and bench pressed 1 JO Ibs, 8
months after a double-lung transplant (Figure 38-3).
Other patients have more rehabilitation needs. For
example, a 40-year-old single-lung transplant patient
sustained a brachial plexus injury from the surgery
Because organ rejection is primarily an inflammatory

response, corticosteroids are usually used in trans
plant patients. Steroid therapy may be delayed until
primary wound closure is certain (1 to 2 weeks) at
which time the patient is begun on low-dose oral
steroids. Acute rejection episodes are treated with
oral or intravenous steroid pulses. Corticosteroids
work by immobilizing macrophages and decreasing
B and T lymphocytes.
Cyclosporine
Cyclosporine is a very powelful immunosuppressive
agent that works by inhibiting T lymphocyte growth
factor and T helper cells. Side effects are common
and annoying to patients. It is considered a peripheral
718
PART VII
Side Effects of Immunosuppressive Medications

Prednisone
Cyc1osporine
Hypertension
Tremors
Glucose intolerance
Hypertension
Osteoporosis
Increased cholesterol
Muscle weakness
Nephrotoxicity
ability to analyze movement and function allow reha

bilitation professionals to maximize a patient's qual
ity of life. The field of organ transplant is exciting
and growing. New advances in long-term manage
ment of transplant recipients means that rehabilitation
professionals need to continue to develop and evalu
Delayed wound healing
ate approaches to care.
REVIEW QUESTIONS
I.
What feelings do patients and family com

monly experience before and after an organ
nerve irritant. Therapists should watch for muscle

tremors and peripheral neuropathy.
transplant?
What is the role of pretransplant pulmonary
2.
rehabilitation?
Azathioprine
Azathioprine ({muran) is a powerful drug that inhibits
How does the surgical incision affect the
3.
musculoskeletal function of a posttransplant
RNA and DNA synthesis of most immune system

cells. Bone marrow suppression (leukopenia, anemia)
is common as are gastrointestinal symptoms of nau
patient?
4.
What are the signs of organ rejection in the

cardiac transplant patient? the lung trans
sea, vomiting, and anorexia.
plant patient?
How is the rehabilitation of the heart trans
5.
New Drugs
plant patient similar and different than tradi
Research has added drugs such as OKT 3 and FK 506

to the immunosuppression regimen. OKT 3 is a mon
oclonal antibody that is used for management of
tional cardiac rehabilitation')

How is the rehabilitation of the lung trans
6.
plant patient different than other forms of
acute rej ection and is not used on a daily basis. OKT

3 blocks all T lymphocyte functions for a short time
after administration and can help remove T cell
pulmonary rehabilitation?
How do immunosuppressive drugs affect a
7.
patient's neuromuscular function? Muscle
byproducts from the graft site. Because of its dra
strength? Cardiopulmonary endurance?
matic and potentially dangerous side effects, this

medication is given in a controlled setting where the
patient can be carefully monitored at 15 or 30
minute intervals. Pulmonary edema, bronchospasm,
fever, chills, and hypokalemia are common reactions.
Rehabilitation should not be given during ad
ministration of these medications. The box above
summarizes the effects of common immunosup
pressive medications.
References
Conners,
G., &
Hilling, L. (1993). AACVPR guidelines for pul
rnon{/l)' re/wiJililalion programs. Champaign.
111.:
Human
Ki
netics Publishers.
Craven, J.L., Bright,
J., &
Dear. C.L.
(J991).
Psychiatric, psy
chosocial, and rehabilitative aspects of lung transplantation.

Clinics Chesl Medicine,
E., &
Hillegass,
1/(2),247-57.
Sadowsky. S.A. (1994). Essenlials of cardiopul
monary rei1.aiJilirarion. Philadelphia: WB Saunders.
Hosenpud,
SUMMARY
.I .D.,
Cobanoglll,
A., et al. (199 I).
Cardiac rral/splanra
liol1. New York: Springer-Verlag.
Physical therapy has an important role in maintaining

and improving functional levels of patients both be
fore and after organ transplant. Knowledge of cardio
vascular and pulmonary physiology along with the
Irwin, S.,
&
Tecklin, 1.S. (1995). Cardiopulmol/ary physical rher
apy. St. Louis: Mosby.
Malen,
J.F., &
Boychllck. J.E. (1989). Nursing perspectives on
lung transplantation. Crilical Care Nursing Clinics of Norlh

America,
1(4),707-722.
38
Moser, K.M., Bokinsky, G.E., et al. (1990). Results of a compre

hensive rehabilitation program: physiologic and functional ef
fects on patients with chronic obstructive pulmonary disease.
Archives of Intemal Medicine 140( 12): 1596-1601.
719
Toronto Lung Transplant Group. (1988). Experience with Singlc
lung transplantation for pulmonary fibrosis. lAMA, 259(15),
2258-2262
Urliversill' Hospital surgical cardiac rehab ilitation proto col.
Scherer, S.A. (1995). Preoperative pulmonary rehabilitation re
(1994). Denver.
duces pot-operative length of hospita l stay after lung trans

plant. Denver: International Conference on Pulmonary Reha
bilitation and Home Ventilation; abstract.
The Patient in the Community
Donna Frownfelter
KEY TERMS
Assisted living
Outpatient
Continuity of care
Skilled nursing and rehabiliatation facilities
Home care
Subacute hospitals
Managed care
Transitional care units
INTRODUCTION
This chapter focuses on patients in the skilled
Physical therapy in the community may take on a
nursing home, home care, and alternative long-term
wide variety of forms. The practice has certainly
care settings. These concepts and ideas could easily
changed dramatically over the last few years. Diag
be used in an adult day care or outpatient setting,
nostic related groupings (DRGs) began the trend of
senior housing, or a transitional or an assisted liv
patients leaving the hospital earlier and often in a
ing facility. The settings described in this chapter
more acute stage of recovery. Subacute hospitals,
will be used only as examples on which to focus the
Medicare skilled nursing, and rehabilitation facili
discussion.
ties with transitional care units provide therapy and
Continuity of care is an essential component of qual
facilitate patient progression so that he or she will
ity health care in light of the trend toward earlier hospi
be back home within a short (perhaps a month) pe
tal discharge either to a skilled nursing/rehabilitation fa
riod of time. Managed care has had a significant
cility or to home with nursing and therapy support. A
impact on diagnoses and treatment authorization,
colleague in hospital practice recently commented that
which affects the type of diagnosis given to patients
she feels more like a triage therapist than a physical
and the number of therapy sessions authorized for
therapist. At times the absolute basics of therapy (i.e.,
given diagnoses or symptoms.
transfers and gait with an assistive device) are all that a

721
722
PART VII
Guidelines for the Delivery of Cardiopulmonary Physical Thempy: Special Cases
patient is able to receive before leaving the hospital set
live fuller and more salisfying lives even if they are
ting. An exercise sheet may accompany the patient
unable to return home aCLcr rehabilitation. Many
home but, in general, after discharge from the hospital,
nursing home chains have developed beautiful, hotel
most patients do not know their exercise programs. In
like atmospheres with a range of services. The resi
addition, they have poor endurance because they are
dents may live in independent apartments and, if a
generally still healing from the insults or injuries for
disease or trauma occurs, may return to the skilled
which they were hospitalized. In the geriatric popula
nursing area to receive rehabilitation services. When
tion the caregiver is often an elderly spouse who also
they are able, they transfer to an assisted living area
has medical problems and is limited in the ability to as
and continue to live there or will transfer back to
sist the patient.
their apartments when they are sufficiently recovered.
The types and diagnoses of patients seen in the com
Even after an acute incident (e.g., a cerebrovascu
munity may vary; often they are the very young and the
lar accident [eV AD, a patient may not be able to re
very old. With the medical community's ability to save
turn home in a month but may continue to make
premature, low-birth-weight infants we have had an in
gains up to a year or more as strength, balance, and
flux of ventilator-assisted, oxygen-dependent infants
endurance improve. Therapists can screen residents
with bronchopulmonary dysplasia (BPD). They may be
and continue to try to improve their physical status
slow to develop and need intervention to prevent pul
and to enable them to live to their fullest capacity.
monary infections and to improve in the natural devel

opmental sequence. Often they may have difficulty
swallowing, and nutritional issues may delay their
MANAGED CARE
physical gains, as well as their speech and language,
Managed care groups are having a significant impact
secondary to poor breath SUppOit.
on placement and case management of individuals
Specialty hospitals have been developed to care for
who are able to return home. We are seeing many pa
the medically fragile, ventilator-assisted (dependent)
tients in home care 5 days a week with caregivers pre
patient who is not stable enough to be at home or
sent around the clock. Significant cost savings may be
lacks the resources to be at home. Many patients, es
noted compared with an extended hospitalization or
pecially children on ventilators whose parents can
stay in a skilled nursing facility. Most managed care
provide some care and are assisted by nursing staff,
companies are willing to listen to suggestions that
are coming home successfully on ventilators. They in
save money and improve customer satisfaction.
tegrate into the community in school and recreation,

function well, and perceive a high quality of life.
When we think of these practice settings, it be

comes obvious that cardiopulmonary concerns are
Elderly patients will often try valiantly to remain
highlighted. From the very young to the very old, pri
at home and independent, amazing the most seasoned
mary and secondary cardiopulmonary issues are often
clinician with their inventiveness and family/friend
the limiting factor in a patient's rehabilitation progress.
supports. Others will recognize that they no longer
Before considering some specific differences in
are able to care for themselves and that the caregiver,
community settings, we will look at the commonalities
who is often also elderly (often a frail spouse), cannot
in the principles of exercise training and prescription.
continue in that role.

Nursing homes, long thought of as a place "to go
to die," have become centers of skilled nursing and
rehabilitation. The trend is moving toward "transi
tional care units" where a patient will go for approxi
mately I month to gain strength and practice activi
GENERAL PRINCIPLES OF EXERCISE

TRAINING AND PRESCRIPTION
Specificity of Training
ties of daily living, transfers, and gait and develop
Exercise programs are ind i viduall y developed to
endurance that will allow them to return home.
meet specific goals. To develop muscle strength, a
The focus of long-term care is to help residents
high-resistance, low-repetition program (i.e., weight
39
723
lifting) is prescribed. To develop muscle endurance, a
of resting. Even more troublesome were the results
low-resistance, high-repetition program (i.e., walk
that it took 10 to 50 days for the values to return to
ing, treadmill) is prescribed. The benefits of exercise
the level before resting (Saltin et aI., 1968).
depend on the targeted exercise. Strength training in
In normal individuals who received ventilatory
creases muscle fibers (white) and endurance training
muscle training followed by a month without train
increases the number of capillaries and mitochondrial
ing, the subjects lost the achieved training effect
content (Celli, 1994).
(Keens et aI., 1977).
It is noted that a weight lifter is usually not a long

term runner, and few runners are able to lift heavy
arm weights. In developing exercise programs, we
must keep in mind the goals for the individual. Gen
SPECIFIC CARDIOPULMONARY CONCERNS

IN THE COMMUNITY
erally, some form of both strength and endurance is
Patients in nursing homes, alternative long-term care
desired. However, programs often focus on one or the
and independent living facilities, and the home after

disease or trauma often have several problems in
other, not both.
common. They may have decreased independence,

mobility level, strength, and endurance, as well as
Intensity and Duration of Training
poor posture, and are at risk for falls 'if:condary to
Both intensity and duration have significant conse
poor balance and weakness. Often they are poorly
quences on the amount of training effect. Olympians
nourished, either from lack of appetite or dysphagia
often train at maximal or near maximal levels to
or as a result of depression brought on by their physi
achieve their "superstar" level of fitness. However, it
cal limitations and feelings of being overwhelmed
has been noted that middle-aged, nonathletic individ
with their situations. At times there is a sense of
uals benefit from lesser levels of exercise. Siegel et
hopelessness and a feeling that things will not be the
a!. (1970) demonstrated that training sessions of
30
same again. This depression is especially common
minutes about three times a week significantly im
when patients are placed in nursing homes when they
proved V021l1a, when the heart rate was raised over
wanted to go home but realized they could not take
80% of predicted maximal heart rate.

Casaburi et al. (1991) studied 19 COPD patients
who could achieve either 50% or 80% of maximal
care of themselves or their families insisted on the

placement.
exercise (anaerobic threshold). They found that pa
disease, such as asthma, emphysema, bronchitis,
tients who participated in the higher intensity training
coronary artery disease, prior myocardial infarction,
program benefited more than the lower intensity
hypertension, dysrhythmias, or congestive heart fail
training patients. However, significant training did
ure. In addition to those diagnoses, they often have
occur in the lower intensity group (Casaburi, 1991).

The number and length of treatments have a sig
Many patients have a preexisting cardiopulmonary
fractured hips, knee replacements, or CV A. The car

diopulmonary factors may in fact be the limiting con
nificant effect on endurance training. An intense pe
sideration to the progress with therapy. These con
riod of care followed by a maintenance or managed
cerns need to be dealt with so that the patient reaches
care period prevents the effects of stopping exercise
his or her full rehabilitation potential.
training. Carry-over and maintenance is extremely

important (Make, 1991).
IF YOU CANNOT BREATHE YOU CANNOT FUNCTION

Functioning depends on the ability to breathe. An ex
Deconditioning Effect
ample of this was seen in a patient that fell in the
Training effect can be lost after the exercise has
parking lot of a hospital while going to a pulmonary
stopped. Bed rest in normal individuals was shown to
rehabilitation program. She was in a long leg cast at
result in a significant decrease in Vo2max with 21 days
home and became very short of breath with sit-to
724
PART VII
stand transfers. Limited by severe shortness of breath,
dentures fit or is he or she not eating or chewing
she could barely ambulate across the room with her
food because of poor dentition or denture fit? Is he
pick-up walker. When observed using her bron

chodilator metered-dose inhaler (MDI), she was
or she aspirating? Does he or she have dysphagia?
Is the patient sleeping? Many patients after
found to be using it improperly. After she was in
surgery, trauma, or a CVA are left supine or in a
structed on how to use it properly, she used the bron
side-lying position to sleep. They may not have
chodilator before transfer and gait and was like a dif
ever slept in that position before. However, they
f e r e n t patient. She was able to coordinate h e r
do not recognize that may be the reason they are
breathing pattern with control t o match her activity
not sleeping. If the patient states he or she cannot
and her endurance was remarkably improved.
sleep ask him or her about previous sleep posi
With these principles in mind, we can look at
tions and try to work with the nursing aide staff
some of the considerations in nursing home and

home health settings.
on positioning for sleep.
Follow-through of methods of working with

the patient should be consistent so as not to
confuse the patient. For example, breathing ex
lONG-TERM CARE FACILITIES
ercises in conjunction with activities should be
AND NURSING HOMES
consistent. If the patient is taught in therapy to
As mentioned previously, with the changes in health
inspire when extending the trunk, that should
care, much rehabilitation is now taking place in transi
be communicated to other caregivers and con
tional care units, Medicare skilled nursing homes, and
sistently encouraged. If the goal is for the pa
assisted living facilities.
tient to walk to meals, a coordinated effort
The following are special considerations when
should be made to try to have the patient ac
working in a long-term care setting.
complish this as a transition plan. For example,
There are several layers of care from geriatric
when the therapist talks with the aide and a
specialist nurse consultants to head nurses to
care plan is established, the patient can start
general floor nurses to aides.
walking to one meal or as far as he or she can
Most patient care is given by aides.
toward the dining room. When that is accom
Communication and cooperation are the keys to
plished, the goal will be to walk to two meals,
achieving patient goals and success.
and so on. Then additional goals can be added
Input and involvement of the patient and family or
to walk to activities, social settings, out to the
significant others is essential in developing goals.
car to meet the family, and other functional,
Clear and achievable goals need to be devel

oped and revisited as the patient progresses or
appropriate goals.
In-services to reinforce the therapy techniques and
regresses in therapy. Is the goal to transition to
goals should be done individually and in formal
home, to assisted living, or to living at the
classes. Classes are helpful, on a one time basis, to
nursing home?
discuss and instruct on a particular topic. How
Quality of life issues need to be taken into con
ever, an ongoing one-on-one therapist/aide pa
sideration. How mobile is the patient? Is he or
tient-specific mini-in-service is essential. The
she independent? Is he or she a morning person?
classes need to be repeated on a regular basis for
When is therapy going to be most efficient time
new staff and as a refresher for some aides who
wise? Will it conflict with his or her other inter
have not used or practiced the techniques. The
ests and activities, which may give him or her
aides may at first feel they are "too busy and un
moral support or act as a distractor and provide
able to do the job," but you can convince them
real recreation?
that it will be of benefit to dle aide, as well as the
Nutritional concerns need to be taken seriously. Is
patients. The patient will be able to do more and
the patient losing or gaining weight? Do his or her
in the long run, the aide will have less work. In ad
39
dition, the family members will be pleased and re
markable in their patient care follow-through for

therapy goals. Be on the look out for ways to
also benefit the nursing home because it will be
praise and thank them in a sincere manner. They
care, which will make the director of nursing and
will be more willing to help in the future.
the administrator pleased. Most aides would like
Sponsor open house times in the therapy depart

ment so that the staff come in and can see the ther
to do the best for their. patients and provide the
apists. You can provide educational material for
best care they can render.
the staff (and food). Welcome their input and sug
Try to get other programs and nursing home ac
gestions for patients who may benefit from ther
tivity groups to follow-through with therapeutic

goals. Talk with the activity department if pa
725
gard the work of the aide more highly. This will

known for its individualized, excellent patient
apy but are not on the physical therapy caseload.

Prepare a bulletin board to show the accom
tients need extra encouragement or help with
plishments of patients in pictures and descrip
oxygen to participate. If patients need to drink
tion. We all love success stories and being part
more water for increased hydration, ask them to
of the success. Show pictures of aides, as well as
remind the patient and provide water.
therapists, helping the patients.
As a therapist, be willing to pitch in and help

whenever you are able, even if it "isn't in your
In addition to chart reviews and talking about pa

tients with the nurses, screen patients in the din
job description." Your willingness to be a
ing rooms and activity sessions and walking in
team player will be noticed. If an aide is off
the hall. The aides will be a terrific source of pa
sick and you are available at lunch and see
tient referrals; they are with the patients more
there is a problem passing out trays, offer to
than anyone else.
help. The next time you ask an aide for help

there will probably be more willingness. If
there is a patient that is difficult to transfer,
offer to help in getting the patient up for phys
ical therapy. This will serve as both a teaching
MONITORING CARDIOPULMONARY STATUS

IN THE LONG-TERM CARE FACILITY
With the increase in patient acuity, it is more impor
opportunity and as a help to the aide. Look for
tant than ever to monitor the patient's response to
ways of blending your therapy with the needs
mobilization and exercise. Many long-lerm care and
of the nursing staff.
subacute facilities are purchasing pulse oximctcrs and
Give recognition to aides who have been re
portable ECG monitors because they have more
FIGURE 39-1
Pulse oximeter.
726
PART VII
unstable patients (Figure 39-1). In addition, all thera
oxygen in the arterial blood) or to relieve the myocar
pists should be competent in blood pressure monitor
dial work, such as in a patient with a severe myocardial
ing and taking pulse rates; auscultation training is
infarction or other cardiac dysfunction (see Chapters 4
highly recommended (see Chapter 14).
and 27).
During the initial evaluation the vital signs and
It is important to note that the arterial blood gas
oximetry should be taken. The readings should be
is drawn at rest with no patient activity unless
taken at rest in a supine or semi-Fowler's position for
specifically noted otherwise (such as an exercise
a baseline. Readings should then be taken in sitting
test blood gas). Generally the Medicare guidelines
and standing positions. It is helpful to take the blood
require that the patient has a P02 of 55 mm Hg
pressure on both arms to see if there is a difference in
(Torr) to be placed on oxygen. This is on the steep
the readings.
part of the oxyhemoglobin dissociation curve (see
When the patient begins treatment, vital signs and
Chapter 3).
oximetry should be performed before and after the
When the patient exercises he or she consumes
mobilization or gait activity. A normal exercise re
more oxygen than at rest. Consequently if a patient
sponse would be that the blood pressure and pulse
is on oxygen at rest and the P02 is 55 or 60 mm Hg
would increase in relation to the activity. An increase
he or she may desaturate during exercise. This
of 20% to 30% might be expected and would be
means that the red blood cell Hg will give up more
within normal limits. The time the vital signs take to
oxygen to supply the exercising muscle. However,
return to normal (recovery time) should be within 5
it is enough oxygen for exercise and the patient will
to 10 minutes.
experience i n c reased s h o r tness of b r eath, the
Many patients who are not considered cardiopul
oximeter will note a drop below 90%, and the blood
monary patients have an abnormal response to exer
pressure and heart rate may initially increase be
cise. If we are not observing and measuring objec
cause of the stress and later drop as the heart cannot
tively, we will not know the cardiopulmonary response
compensate for the decrease in oxygen level.
is abnormal, and deleterious effects may occur.
The pulse oximetry reading of normals is 97.5%
An example of this was seen in a patient one
oxygen saturation. It is clinically acceptable to main
month after a CV A. The patient was very fatigued
tain oxygen saturation at 90% or above. This satura
and complained that his knees felt like they were
tion corresponds with keeping the P02 generally at
going to buckle. This patient had been doing quite
above 55 mm Hg. When the P02 drops below 55 mm
well and was not being monitored. However, after the
Hg, a dramatic drop in oxygen saturation will occur
patient ex pressed the feeling of weakness the thera
for a small drop in P02.
pist took the vital signs after the patient rested and
If the nursing home does not have an oximeter, the
walked again. The blood pressure and heart rate
durable medical equipment company that supplies the
dropped during the exercise. The doctor was in
oxygen may be called and will bring an oximeter
formed and ordered a blood test that revealed the pa
when they check the oxygen. However, any patient
tient did not have an appropriate blood level of digi
on oxygen at rest should be tested for desaturation.
talis. The medication was increased and the patient
Another option is to call the patient's doctor to re
improved. Had the therapist not checked the vital
quest an increase in oxygen during exercise. For ex
signs and continued to push the patient, there could
ample, a patient on I Llmin at rest can have a pre
have been serious consequences.
scription written for I Llmin at rest and 2 or 3 I/min

during exercise. The increase in oxygen is no prob
lem as long as the oxygen is decreased back to the
SPECIAL MONITORING CONSIDERATIONS

FOR PATIENTS ON OXYGEN
resting amount as soon as the patient recovers back to
Patients receiving oxygen therapy have usually been
ers whose oxygen is carefully titrated to prevent tak
placed on oxygen because of hypoxemia (low levels of
ing away the hypoxic drive to breathe.
baseline. This is even true for carbon dioxide retain
39
727
DOCUMENTATION
CARDIOPULMONARY CONCERNS IN HOME CARE
Functional outcomes are key to documentation. As
Home care takes the practice setting one step further
we evaluate patients and write care plans, we set
from the hospital. Managed care is having major im
goals that are both short and long tenn. Each goal
pacts on changes in this area of therapy and nursing
should be linked to functional outcomes that enable
care. Cost effective yet excellent therapy is the goal
the patient to be more mobile, safe, as independent as
of managed care. There is a great deal of creativity;
possible, and functional in. the care setting in which
deals can be made if a provider group can demon
he or she lives.
strate that the patient will benefit and a cost savings
Documentation needs to show progress toward
to the managed care group will occur. We are seeing
the functional outcomes the therapist has developed
coalitions form between' contract service therapy
with the patient. Goals should be attainable and real
agencies, durable medical equipment companies,
istic. If there is poor or slow progress to a goal, there
nursing agencies, and enteral feeding companies to
needs to be documentation and explanation in the
provide "one-stop shopping" groups. The managed
notes of what has occurred and how the treatment
care companies prefer to make one call that will pro
program will be modified or how the goals need to
vide them with nursing service, therapists, and home
be changed.
medical equipment, such as walkers, canes, tub seats,
When the functional outcomes have been met, the

patient is reasscssed to see if they can accomplish more
raised toilet seats, oxygen, IVs, and enteral feeding.

Home care involves not only seeing more acutely
ill patients but also seeing some interesting cardiopul
or if the patient should

.
a maintenance program. A screening date should be set
monary situations. For example, in working with
to check back and monitor the patient to ensure mainte
major medical centers who perform transplant surgery
nance, improvement, or decline in condition. At times
the therapist works with patients before and after heart
patients who have "plateaued" will improve and may
and lung and other transplant surgeries. It has been
be picked up on a screening to request a doctor's order
demonstrated that patients, even as seriously ill as pre
to have additional therapy with specific increased goals
transplant patients, can improve their functional abili
defined. If a patient's condition has declined, the pa
ties, strength, and endurance to be better candidates
tient can be reevaluated to see if the patient's former
for surgery. Postoperative care is also improved when
status can be resumed or maintained.
the patient is in better physical condition before
It shou ld be remembered that third party payors
surgery. Other diagnoses are also being treated effec
are reading the notes to understand what the evalua
tively before and after surgery. It makes sense to
tion and treatment plan for the patient is and how
begin preoperative orthopedic consults to evaluate pa
the patient has progressed in meeting functional out
tients and teach them the exercises they will be doing
comes. Because the patient is receiving long-term
after surgery. In addition, any patient facing abdomi
therapy, the more therapy the patient needs, the
nal or thoracic surgery could benefit from a preopera
more documentation is necessary to tell the story to
tive visit if coming to the hospital presents difficulty.
the third party payor or the managed care group. A
Consequently, therapists who never thought they
good quote to remember is, "If it wasn't written, it
would be required to work with cardiopulmonary pa
wasn't done!"
tients are needing to increase their knowledge bases to
In summary, every patient in a long-term facility
treat these patients appropriately.
is a patient with cardiopulmonary concerns. The car
In the home-care setting the therapist is alone with
diopulmonary system needs to be optimized for full
supports through the nursing and home-care agencies.
rehabilitation to occur. Cooperation with the nurses
However, in the home they usually must be prepared to
and aides, as well as special activities staff, is essen
evaluate patients and their progress with very little su
tial for follow-through of treatment programs and pa
pervision or consultation. In addition, they must be able
tient success. Teamwork is the key, and communica
to handle emergencies and crisis situations. AU home
tion and documentation are vital.
care therapists must have a basic CPR certification
728
PART VII
renewed annually. Policies and procedures dealing with
friends, or a caretakers smokers? Signs need to be
how to handle emergencies, infection control, and
posted to warn of danger of smoking and flames
safety are essential for any therapist in the home.

Therapists need to know how to obtain necessary
around oxygen. Patients who are smokers need to

have this reinforced very clearly.
information and equipment for the patient. They need
Does the patient have stairs? I s the bedroom up
to be creative in adapting equipment and be innova
stairs? Is there a first floor bathroom? If the bathroom
tive if the patient cannot afford to purchase medical
is on the second floor can the patient get up the stairs
equipment. This is not the setting for new graduates,
safely and in a timely manner, or does a commode on
but rather for the experienced therapists.
the lower level seem more appropriate?

Is the bed the proper height? Are there handrails? I s
i t difficult for the patient to transfer into bed? Is a de
HOME SETTING
vice needed to help the patient transfer independently?
In the hospital or outpatient center the patient comes to
The question of the bed arose with one home-care
your place of business. They come where you work.
patients who had a fractured pelvis. When I first vis
With long-term care and home care, you go to work
ited her, I asked how she had broken her pelvis and
where they live. A certain etiquette is required when
she replied, "Hopping into bed." I questioned what
going into a patient's residence. Pennission needs to be
she meant and she said, "I' JI show you." I followed
requested to enter the residence, alter their living space,
her to her bedroom watching her gait with her walker.
put in grab bars, remove scatter rugs and telephone
When we got to her bedroom, it was quickly noted
cords that are seen as a safety hazard, or rearrange
that this very short patient had
rooms that you may consider too cluttered and unsafe.
mattress was between her iliac Crest and waist when
very tall bed. The
The therapist must remember that this is the patient's
she backed up to the bed. She stated, "I used to have a
home and must be tactful in the way recommendations
stool that I climbed into bed on, but my son thought it
are made. The cluttered room may hold treasures that
wasn't safe and took it away. Now I have to hop up
have been accumulated over a lifetime. They may sur
into bed!" She had returned home to do the same ac
round themselves with items that are all they have left to
tivity that had put her in the hospital with a fractured
remember. It may be true that a path needs to be made
pelvis. Looking at the bed, I noted that there were 3-
for safe walker ambulation, but how this is communi
inch rolling casters and a caster pad under the hed.
cated may make all the difference in developing good
The son was called and the casters and pads removed.
rapport between a home-care therapist and the patient.

I nitially, an evaluation of the patient's home needs
The patient was quite pleased that the bed was 4

inches lower and she could transfer in quite easily.
to be made. What equipment do they have, is it in
Is there family support or a caretaker if the patient
working order, do they know how to use it? Often a
is not independent? If the spouse needs to work or go
patient borrows "grandpa's cane" and does not real
out, how long can the patient be safely left alone?
ize that he or she is eight inches shorter than grandpa.
Does the patient know how to obtain a caretaker? Are
Modifications may need to be made so that existing
they able to financially afford the support?
equipment fits properly and is functional.
Most home-care agencies have social worker sup
Safety is a primary consideration. Are there cords
port to help patients discover resources available to
across the floor? Are scatter rugs loose or tacked down
them. A physician's referral is needed and the service
with carpet tape? Can the patient pick up his or her foot
is generally covered under Medicare.
sufficiently to walk over the scatter rug without trip

ping? Are there pieces of kitchen linoleum that have
come up and might trip the patient? Are the kitchen
chairs on rollers and the patient's balance poor?
COMMUNICATION AND CROSS REFERRALS

TO OTHER DISCIPLINES
Is the patient on oxygen and you discover that he
It is essential that communication take place between
or she h a s a gas stove? Are the close relatives,
the members of the home-care team. Communication
39
729
is difficult because everyone is on the road and travel
and is having difficulty swallowing may benefit from
ing to patients' homes. Generally, pager numbers of
speech and occupational therapists working on seating
therapists and nurses are exchanged and compliance
systems and feeding. The interaction and communica
with answering pages is good. However, considera
tion between therapists facilitates ideas for both thera
tion needs to be given to the realization that we do not
pists, provides continuity and follow-through, and
like to be interrupted frequently when seeing patients.
helps to optimize patient care.
Generally a system of timing the calls or pages is wel

comed. A 91 I can be placed after the page number to
identify an urgent call if the call is very impOltant or
information needs to be given immediately.
Physical therapy is the most common therapy. How
MONITORING CARDIOPULMONARY
STATUS AT HOME
Cardiopulmonary status at home is similar to that in a
ever, at times another therapy will be indicated but not
long-term care facility. However, at home there is not
made when the patient is discharged. When a patient
usually an oximeter available. This is unfortunate, since
expresses a problem that could be handled better or
many more patients are coming home on oxygen and
could provide increased service to a patient, a cross re
ventilators. This trend should change and home-care
ferral should be made by calling the home-care agency
therapists should have oximeters available for evaluation
or the patient's nurse case manager. Identify the prob
of patient status and exercise desaturation. The durable
lem and why you feel the additional therapy is indi
medical equipment company has oximeters and the ther
cated. The physician will be called and the order gener
apist may reqnest an oximetry study done with a physi
ally obtained. It would then be helpful for the refelTing
cian referral. It is helpful to make an appointment and
therapist to call the new therapist and update rum or her
meet the therapist to see the results and to try to reenact
on the patient and reason for the referral. This commu
the therapy to see if the patient de saturates with exercise.
nication should be documented to show the necessary

communication between the therapists and nurses.
An example of this was seen in
The same blood pressure and pulse monitoring

should be done at rest on both arms and in sitting,
patient that I re
ceived a refelTal on for home care that had been on a
standing, and before and after exercise as mentioned

previously in this chapter.
ventilator for a month in the hospital. She had been intu

bated, was very hoarse, and complained that she was
having trouble swallowing and eating. Liquids espe
HOME OXYGEN
cially were going down the wrong way. The home-care
Home oxygen may be supplied by an oxygen concen
referral said that the patient had a swallowing study in
trator, by tanks or as a liquid oxygen system (Figure
the hospital that demonstrated she was aspirating. A
39-2) (Chapter 41). One consistent problem that must
speech language pathologist had been working with her
be dealt with in exercise with patients at home on oxy
on swallowing in the hospital. However, speech therapy
gen is the incredibly long oxygen tubing needed to
had not been ordered at home. Nothing had changed on
allow patients t o go to the bathroom, out to the
the day the patient had been discharged. Since the pa
kitchen, and to the living room (Figure 39-3). Often 60
tient was still aspirating, a speech consult was requested.
to 90 feet of tubing must be used. The question often
At times it is helpful to do a joint treatment session
arises, "Does the patient get the right amount of oxy
with another discipline. This can be done to coordinate
gen with such long tubing?" The answer is yes because
therapy and provide focus and continuity of goals. It
the flow meter is a compensated one, which means it
will also lead to success for the patient. For example, a
reads what really is occurring. If more tubing is added
physical therapist and a speech language therapist may
and a lesser flow was occurring, the flow meter would
meet to focus on a patient with poor posture who lacks
drop to indicate that had happened. Then it would be
breath support for phonation. Another patient who is
readjusted to the proper liter flow as ordered.
having difficulty feeding because of trunk weakness
It has been found that the portable oxygen systems,
and is sitting in flexion with a forward head and neck
in particular the demand oxygen system, do not always
730
PART VII
"1
jf
r-;- .
--
-f .
FIGURE 39-2
FIGURE 39-3
Oxygen concentrator.
Oxygen tubing presents a significant safely hazard.
deliver the exact amount expected (Figure
39-4). It is
Be compliant with medications and health
Learn preventative care (i.e., prevent pulmonary
precautions.
necessary to use oximetry to determine whether the pa

tient has an appropriate oxygen saturation reading.
Patients need to be taught either to coil the tubing or
infections and not increase salt/water intake if
to develop a means to make sure that they do not trip

over the tubing because it creates a safety hazard.
on cardiac precautions or taking steroids).
Some patients have more than one tank or concentrator

in the home to prevent having long lengths of tubing.
Learn ventilatory strategies to increase comfort

and function (see Chapter
pending trouble
change in mucus, decreased urine Olltput, or

rapid weight gain) (Figure
monary dysfunction need to:
(i.e., increased shortness of
breath, swelling in ankles, productive cough,
THERAPEUTIC GOALS FOR HOME-CARE PATIENTS

WITH CARDIOPULMONARY DYSFUNCTION
To be independent at home, patients with cardiopul
00).
Learn to monitor themselves for signs of im
39-5).
Train to pace activity and use energy conserva

tion techniques and rest periods to accomplish
more with less stress.
Understand the dysfunction or disease.
39
731
FIGURE 39-4
Portable demand oxygen system.
FIGURE 39-5
Patient monitoring oximeter
with exercise.
732
PART VII
FIGURE 39-6
Nasal CPAP unit.
Maintain proper nutrition and hydration.
Develop a support network to help when needed
patients at home. As health-care practitioners, we
and to check on the patient occasionally.
offer helpful suggestions for modification of the pa
Maintain walking program and general exercise
tient's home environment and life style. However, we
tion are essential in the progress and maintenance of
to continue functional gains.
cannot force a patient to comply or accept what we
Some patients may need noctural nasal continu
have proposed. The patient in the home setting is in
39-6).
dependent in his or her judgments and activities. We
ous positive airway pressure (CPAP) (Fig.
This may be ordered to treat sleep apnea or to rest
need to respect that and at the same time provide our
the patient and assist with ventilation. A Bt-PAP
experience and therapeutic judgment and expertise.
unit allows the patient to rest and let the machine as
This setting is often the most rewarding a therapist
sist ventilation by providing pressure support on in
can have, although at times it also may be the most
spiration and exhalation. Often at first, the patient
frustrating. One thing is certain, if you ask a patient
may have difficulty adjusting to the nasal CPAP, but
where they want to be, the answer sounds like,
in time, the patient will adapt to the assistance and
"There's no place like home'"
feel it is beneficial.
REVIEW QUESTIONS
SUMMARY
I. What are some common problems patients in the
Education, self-monitoring, compliance to medica

tion, reduction of risk factors, nutrition, and hydra
community have in common?

2. What role does a preexisting cardiopulmonary
39
condition play in a new diagnosis or trauma (e.g.,
Jackson,
D.E., &
Wilhoire, M.J. (1985). Home health physical
therapy, considerations for the provision of care.
CV A, hip fracture)?
3. What are some uniques situations or concerns
about patient care being delivered in a nursing
home, assisted living center, home care?
agement in
Physical Therapy,
Clinical Mun
5: I O.
May, B.1., ( 1 993 ) . Home health and rehabilitation,
Ca re,
733
Conce pis of
Philadelphia. F.A. Davis.
May, B.J. (1990). Principles of exercise for the elderly, In Ba5ma
4. What role can a physical therapist play in opti

mizing the patient's care in the above settings?
5. How can cardiopulmonary function be monitored
outside the hospital?
jian, J.V.
&
Wolf, S.L. (Eds.). (1990). Therapeutic exercise,
& Wilkins. 1990.

exe rc ise inslrllClion sheets: Home exercise
fo r rehabili/{llion therapy skill b uilders. Tucson.
(5th ed.). Baltimore: Williams
Pfau, J. (1989). Adull
Polich, C. (1990). The provision of home health care services
6. What special considerations should be taken with
through health maintenance organizations: Conflicting roles for
Home He alth Care Quarterly, II: 17.

J. & Adam, L. (1986). Geriatric exercise booklet, Cli nical
Manageme nt in Physical Therapy. 6:32, 1986.
Schaefer, K. & Lewis, C. Marketing geriatric programs-A home
care example, Clinit'al Management in Physical The rap y ,
HMOs.
a patient on oxygen')
Sallade,
References
Emlet,
c.,
Cragtree, J., Condon,
V., &
Tremel, L. (1995).
In - ho me
aHessmenl of older aduil.\', an inlerdisciplinary approach.
G ithersburg, Md.: Aspen Publishers.

Harrington, J. (1983). The case for home heallh
6: \1-17,1986.
Vassif, J.A. (1985).
Harper
specialization.
Clillical Mallagemenl in Physical Therapy, 3: 17.
&
The
Home Health Care Solution, New York:
Row.
Zola. I.K. (1990). Aging, disability and the home care revolution,
Archives of Physical Med icine and Rehabilitation, 71:93.
Jackson. B.N. (1984). Home health care and the elderly in the
1980's. Am erican Journal of OccupalirJII(l1 Therapy. 38:717.
PART
VIII
Related Aspects of
Cardiopulmonary
Physical Therapy
Body Mechanics-The Art of

Positioning and Moving Patients
Mary Massery
Donna Frownfelter
KEY TERMS
Body mechanics
Ventilation related to:
Dependent patients
Supine
Lifting and moving
Sidelying
Upright
Upright
Neutral alignment of trunk, head

and shoulders
INTRODUCTION
who can move independently and assume any given
Body mechanics may be defined as the efficient use of
position with ease. In this chapter, the principles of
one's body as a machine and a locomotive entity. In
body positioning and moving dependent patients are
working with critically ill or chronically dependent pa
discussed.
tients, it is essential that optimal body positioning is ac

complished to facilitate maximal ventilatory potential.
Therapists and nurses attempting to position or move
POSITIONING FOR OPTIMAL VENTILATION
dependent patients must understand and use proper
Because of the three-dimensional nature of breathing,
body mechanics (Neil, 1959; Fuerst and Wolff, 1969).
the therapist's goal is to facilitate chest excursion in
This is necessary to reduce stress and trauma and to
all three planes of ventilation-anterior-posterior, su
promote success for both the patient and the nurse or
perior-inferior, and lateral (Massery, 1994). This can
therapist. Positioning and moving dependent patients is
be accomplished by improving the length-tension re
an art that is quite different than working with a patient
lationships of the muscles used in inspiration (Crosbie

737
738
PART VIII
Related Aspects of Cardiopulmonary Physical Therapy
1985; Kendall, 1993). Massery reasons
Upper chest expansion can be increased by remov
that the success of proper positioning to enhance in
ing pillows under the patient's head to increase tho
and Myles;
spiratory muscles will do the following:
racic extension. This will increase the length-tension
I. Improve the length-tension relationship of the
relationship of the neck accessory muscles (scalene
accessory ventilatory muscles involved in that
and sternocleidomastoid muscles). Increased move
posture
ment will be noted in the upper chest in a superior
2. Incorporate a passive stretch of the chest wall

3. Use the natural coordination of the trunk-chest
and anterior plane. Further anterior expansion can be

achieved by using a towel roll placed longitudinally
wall movement with inspiration and exhalation
at the vertebral spine to open the anterior chest of a
patterns to maximize movement
patient who tends toward excessive flexion of the
The following are some common improvements that

can be incorporated into normal positioning.
trunk (Figure
40-1).
If the patient needs some support under his or her

head to achieve a neutral chin tuck to protect his or her
swallowing ability, then
Supine Position
thin pillow or horizontal
towel roll under the occiput, may be used (Figure 40-2).
37, all activity is performed
External rotation of the shoulders with the scapula
in the field of gravity. Patients in a supine position
in a neutral or retracted position will place the pec
As mentioned in Chapter
may find breathing difficult because they must over
toral is and intercostal muscles on stretch. This will
come gravity to move the chest wall with each
improve lateral and anterior chest wall movement
1993). If a patient has full range of motion
breath. Using towel rolls or pillows to facilitate a bet
(Kendall
ter position may significantly improve the patient's
(ROM) and is comfortable with the arms placed over
opportunity for improved respiration.
head or in full flexion/abduction/external rotation for
"
//
,'\
\
'.t
FIGURE 40-1
Placement of vertical towel roll.
40
Body Mechanics-The Art of Positioning and Moving Patients
FIGURE 40-2
Increased openness of anterior chest wall with the vertical thoracic towel roll and the occipital
towel roll combined.
FIGURE 40-3
Buttertly position with thoracic towel rolllO open anterior chest.
739
740
PART VIII
maximal stretch, this is the optimal po ition for full

excursion of the anterior chest wall (Figure 40-3). If
there are significant shoulder limitations, moderate
shoulder abduction with forearm supination lUay be
the best position available to facilitate chest excur
sion. Whenever significant limitations are found, the
therapist should try to modify the position to accom
modate the patient and achieve optimal ventilation.
Sidelying Position
Side lying is an optimal position for improving breath
ing pattell1s. Gravity is elimi. nated
sion and the diaphragm moves freely. In addition side
lying is a reflex-inhibiting posture, and some high-tone
patients will be able to relax and breathe more freely.
It is impoltant to consider the shunt effects if a patient
has lung pathology. For example, if a patient has right
lower lobe pneumonia or atelectasis, sidelying on the
good side will improve oxygenation. Conversely, side
lying with the affected side down will cause a decrease
in oxygenation (differential shunt) because a poorly
ventilated patient receives more perfusion to the down
lung and more shunting will occur. The patient's hip
and knee joints should be flexed and supported for
comfOlt. The upper extremities can be moved up and
away from the body to allow for
free movement of the
upper chest wall. A pillow can be used to support the

upper arm anteriorly, or the patient can be placed in a
three-quarter supine position and
back to support the uppermost arm.
pillow behind the
If the patient has
full range of motion and is comfortable,
FIGURE 40-4
Unsupported upright position of patient with Tl paraplegia.
NOTE: Posterior plevic tilt and excessive thoracic khyphosis

with resulting collapse of anterior chest wall.
butterfly po
sition of the anns can be used. This will automatically

open up the rib cage and facilitate inspiration.
(Woodhall-McNeal,
and Gee,
Upright Postures
1992; Borello-France, Burdett,

1988). The anterior tilt of the pelvis will im
prove upper-extremity ROM and ventilation poten
Upright postures create new challenges to breathing
tial. Attending to this one consideration may be all
by adding the component of balance and an unsup
that is necessary to improve the breathing capacity in
ported spinal column. Pelvic alignment is a key com
some patients, allowing them to continue to advance
ponent. An anteriorly tilted pelvis in healthy flexible
in their exercise programs or rehabilitation courses.
adults will tend to do the following:

kyphotic curve in the thoracic spine,
(I) reduce the

(2) adduct the
tilt in sitting is to have the patient lean forward over
One simple means of attaining an anterior pelvic
scapula toward a neutral position, (3) produce a more
his or her legs, then slide a towel roll horizontally just
neutral or externally rotated upper-extremity position,
behind the ischial tuberosities, which will prevent the
and (4) pull the head back into a neutral chin tuck
pelvis from rolling back into a posterior tilt (Johnson,
40
741
and head back into a more neutral alignment. The an

terior chest wall will also be more open with this
technique.
A neutral head and neck position is important for
patients with impaired speech volume or endurance
and for patients with swallowing or aspiration dys
function. A neutral chin tuck will optimize the
length-tension relationship of the vocal folds, mini
mize vocal strain, and improve protective airway re
flexes (Massery, 1994).
It is also vital to evaluate the patient's shoulder
positioning. Internal rotation of the shoulders and
scapular protraction tends to block the upper chest
from reaching its full expansion potential. Alter
n a tely, external rotation of the s h o u l ders will
markedly increase upper chest wall movements and
thoracic extension. Clinically, improved lung vol
umes will be noted when these positioning considera
tions are taken into consideration. Often these smail,
seemingly insignificant changes will position the pa
tient for success with other therapeutic activities. If
unattended, these small factors can impede patient
progress. Positioning has everything to do with in
creasing ventilation and functional skills.
LIFTING AND MOVING DEPENDENT PATIENTS

There has been a change from earlier concepts and
FIGURE 40-5
Ischial towel roll to support pelvis in anterior tilt in patient
principles of lifting. As discussed, the body has
with Tl parapkgiJ. NmL: ch enges in the thoracic spine and
been thought of as a machine. It was believed that
open anterior chest wall as well as improved head and neck
improper mechanics of lifting would result in

tremendous loads on the disks. The key components
alignment..
of lifting were to "keep it close," "bend knees," "lift

with the legs." Later the spinal posture was the cen
ter of attention during lifting (Physical Therapy
1989) (Figures 40-4 and 40-5). This is well tolerated
Forum, 1985).
for many patients with intact sensation and a pelvis
During observation, lifting seemed to occur "natu
that is at least minimally mobile. For neurological pa
rally" from slightly bent knees and then, during the
tients with impaired sensation or less pelvic mobility,
raise lift butt-end first, with the patient rearing back
a wedge may be substituted; however, caution must
ward at the start as the therapist started to extend the
be used because some sliding may occur.
knees before lifting. The predominance of injuries

seems to occur with the back in flexion. There is a ra
tionale for strengthening abdominal muscles to pro
Neutral Alignment of the Head and Shoulders
mote safer lifting. Abdominal strength is necessary to
A vertical or horizontal towel roll may also be used
support a pelvic tilt during lifting. Many commer
with wheelchair positioning to bring the shoulders
cially available lumbar and abdominal elastic velcro
742
PART VIII
supports are now available and widely accepted.
factors, such as limited space (i.e., small hospital
They provide additional abdominal wall support.
rooms), clothing, or degenerative knee joints.
Another current school of thought advocates lift
The first consideration in body mechanics is the
ing with the lordotic lumbar curve intact. This is the
need for maintenance of proper posture and balance
technique used by weight lifters. When these individ
(body stability). Consideration should he paid to the
uals are questioned about backaches, they usually
relationship between gravity, posture, and body sta
deny any problems.
bility (Figure 40-6). It is commonly known that grav
The lifting technique may be modified by other
itational force is always exerted in a vertical direction

toward the center of the emth. In addition, that point
in a patient or object at which all of its mass is cen
tered is called the (crller or gravity (the point at
whieh the patient's maximum weight is concen
;"
trated). In the standing position the human body's

center of gravity is approximately SSG;!., of the body's
e
0'
gm"",
total height and in the pelvic cavity, slightly anterior

to the upper part of the sacrum. The lower the center
of gravity, the greater the hody stability. Conse
quently, when the human body is used as a machine
to lift an object, muscular cffort great enough to
maintain stability and to lift against the force of grav
ity is necessary, especially when the patient's center
of gravity is fUlthcr removed from your own. There
fore one way to conserve energy and maintain stabil
Center of gravity
ity is to carry the weight of the patient (or object) as

close to one's own centcr of gravity as possible. This
allows maximal conccntration of onc's own energy
toward movement of the patient, with minimal stress
or injury to oneself. To help accomplish this, the bed
I
)
I.
should be adjusted so the therapist or nurse can reach

the patient comfortably. Usually adjusting the bed to
one's hip level is adequate. This makes the patient
close to the therapist's center of gravity.
The majority of lifting should be done with the
legs (knees) and not by straining to lift with the arms
and back (Figure 40-7). Whenever there is a question
about one's ability to lift a patient alone, generally it
should not be done, and assistance should be obtained
(Rantz & Courtial, 1977).
Another point to consider is the base of support
while lifting. The base of support is defined as the
- Base of support
area between the feet that provides the body's stabil

ity. It is easily appreciated that the wider the base of
support, the greater the body's stability. To enlarge on
this concept, one also needs to define the line of grav
FIGURE 40-6
The line of gravity passes through the center of gravity and
ity and its relationship to body stability. The line of
the base of support to maintain body stability.
gravity is an imaginary line passing through the center
40
of gravity of an object and perpendicular to the sur
743
places the center of gravity in the direction of
face on which the object (body) rests (see Figure 40-
the weight being lifted. To conserve energy and
6). The closer the line of gravity passes to the center
maintain stability, carry the weight as close to
of the base of support, the greater the body's (ob
your own center of gravity as possible. Lower
ject's) stability. Increased muscular effort needs to be
your hips to the level of the surface supporting
exerted in proportion to the distance the line of gravity
the weight you plan to lift by flexing your hips
shifts away from the base of support (Rauch, 1971).
and knees. Adjust the bed up as high or down
To summarize and apply these concepts, one can
as low as you need for comfortable and effi

cient work.
list the following guidelines:

1. The lower the center of gravity, the wider the
3. The effort to petform a given activity depends on
base of support, and the nearer the line of grav
the weight of the object to be lifted. Know your
ity falls to the center of the base of support, the
limits. Do not attempt to lift alone if YOLl have
greater the body's (object's) stability. When
any doubts about your ability to do so. Don't be a
lifting, stand with feet well apart, knees slightly
hero in a back brace. Obtain assistance for the
tlexed, and one foot forward. Keep head and
sake of both the patient and yourself.
trunk in proper alignment.

2. When our bodies are used as machines, the ex
ternal weight on which we are working dis-
4. Other general tips for lifting are as follows

(Figure 40-7):

Lift with your legs. Keep legs in a position

that permits them to supply most of the force
for shifting your trunk.
Do not attempt to lift with your arms and back.

W hen lifting, avoid rotation of the spine.
Shift feet into position for weight shift when
moving or lifting patient.
Stabilize your body against a stationary ob
For best efficiency, coordinate the move by a
ject whenever possible.

synchronized verbal expression understood
by therapists and patient, such as "1-2-3 lift."
One additional consideration mLlst be noted
moving against the resistance of friction. Friction is
defined as a force that opposes the movement of one
object over the SUlface of another. Friction is reduced
as the amount of surface area contact between two
objects is reduced.
W hen moving a patient side to side or up and
down in bed, the therapist or nurse attempts to reduce
the contact of the patient's body sutface with the bed.
This can be accomplished by several maneuvers
use a turning sheet (placed just above the patient's
shoulders to just below the patient's hips), cross the
patient's arms over the chest or abdomen, flex the pa
FIGURE 40-7
Reach work level by bending the knees and hips rather than
tient's knees and hips, and ask the patient to flex his
the back. Lift with the legs! This can also be done with a
or her neck and raise the head as he or she is lifted (if
full double knee squat similar to techniques by
the patient is unable to do this, the therapist or nurse
weightl ifters.
will assist) (Figure 40-8).
744
PART VIII
Related Aspects of Cardiopulmonary Physical Thel'apy
MOVING DEPENDENT PATIENTS

r.
Moving the patient up or down (Roper, 1973;

Lewis, 1976; Neil, J 976).
A. Using a turning sheet (Figures 40-9 to 40-11).
I. Sheet should cover from shoulders to hips.

2. Gather material as close to the patient's
body as possible.
3. Hold at shoulders and hips, with a flexion

pattern (see Figure 40-10).
4. Cross patient's arms over chest, flex knees

and hips.
5. Ask patient to raise head if possibl e.
6. Synchronize action by counting"1 2 3 lift."

-
7. Shift weight from one leg to the other

rather than lifting up and pulling on back.
B. Without turning sheet (up or down), two people.
I. Follow basic procedurc-cross arms, lift
head, tlex knees and hips.
2. The therapist places his or her hands and
forearms under the patient's shoulders and
hips.
-0.
3. If patient is extremely hea vy or tall, an

other person can bend knees and assist.
FIGURE 40-8
The patient should be prepared for a position chenge: knees
bent, arms crossed over chest and head lefted up to reduce
friction between the patient's body and the bed.
GIfJ "\
FIGURE 40-9
To insert the drawsheet, the patient is tumed to
his side and the half-rolled drawsheet is tucked
under him (from just above the shoulders to
just below the hips). He rolls over the
drawsheet and it is pulled out behind him.
40
745
FIGURE 40-10
The drawsheet should be rolled close to the patient's body.
A flexion hand grip at the patient's shoulders and hip is

most efficient.
FIGURE 40-11
Moving the patient toward the head of the bed. The patient
is prepared. The therapist is positioned to move toward the
II. Moving the patient to the side of the bed.
head of the bed in order to shift his body weight to move
A. With turning sheet.
the patient.
I. Cross arms, and other body parts, toward

the side to w hich the patient is to be
moved.
2. Therapist's hands at patient's hips and
shoulder on material close to patient's
body.
2. Bring right arm to the side at a 90-degree
3. One therapist pushes, the other pulls.
angle up and away from body.

3. Place left arm across chest.
B. Without turning sheet.

I. Both persons stand on the desired side.
4. Place left leg over right leg.
2. One therapist's forearms under patient's

shoulder, the others under patient's hips.
3. Synchronize action by counting "1-2-3
5. Pull sheet at patient's back to turn.

B. Without turning sheet (to right side).
I. Move to opposite side (therapist's hands
pull."
and forearms under patient's shoulders
III. Turning the patient to his side.
and hips).
A. With turning sheet (to right side) (Figures 40-
2. Same steps as 2, 3, and 4 above.

3. Roll to right side using left shoulder and
12 and 40-13).
l. Move patient supine to opposite side of
turn (e.g., if turning to right side, move
patient to left side of bed).
left hip to push or pull.

IV. Turning the patient prone (e.g., roll to right side)
(Figure 40-14).
746
PART VIII
' ------ J
FIGURE 40-12
Preparation for the patient to turn to his left side: move
patient to the right side of the bed, position his left arm up
to the side at a 90-degree angle, cross the right leg and arm
over his body and turn the patient's head to the left.
)
FIGURE 40-13
A one-person turn to the right side using a drawsheet. The
patient's body position is the same as for the turn to the side.
The therapist is positioned with one foot forward, the other
back. He pulls the sheet with his hands positioned at the hips
and shoulders of the patient.
k!-
"@::
40
747
physical therapy. It is so often taken for granted and

pelformed with little thought or planning. Therapists
and nurses need to analyze beforehand their physi
cal activities in relation to the principles of efficient
movement and the proper application of body me
chanics. A "tube index", counting and identifying
each technical attachment, (e.g., IV, Foley cather,
arterial blood gas stint, or chest tubes) should be
done before moving a patient. Extra care needs to be
taken to prevent dislodging important medical
equipment. This could prove life threatening if ven
tilator tubing was pulled and a patient was extu
bated. The practical application of body mechanics
will not only conserve energy and preserve muscles
and joints but will also allow the patient to be
moved with a minimum amount of pain and discom
fort, with greater safety.
REVIEW QUESTIONS
I. Why is it important to utilize efficient body me
chanics when positioning and moving dependent
patients?
2.
FIGURE 40-14
Positioning pa tient prone
How can changing a patient's position affect

ventilation?
3. How can therapist use towel rolls and easily ac
(EXM"IPLE: Rolling to the right
side). The patient's right arm is tucked in at his side with
cessible equipment to improve a patient's posi
the left arm and leg crossed ove r.
tion and potential for improved ventilation?

4. What ventilation/perfusion changes occur when a
patient is turned from the "bad" side down to the
"good" side down?
S. Can positioning alone be considered therapeutic
when it accomplishes the plan of treatment goal?
A. With or without turning sheet.

l . Move patient to opposite side of bed from
side toward which he or she is turning.
References
2. Cross left arm and left leg over body.

3. Right hand and arm at body side tucked in
B orello-France, D.P., Burdett, R.G.,
&
(1988). Modifi
using seat
68(l), 68-7l.
Gee, Z.L.,
cation of silting posture of patients with hemiplegia
as close as possible.
boards and backboards, Physical Therapy,
4. Use hips and shoulders to turn.

S. Free both arms, do not allow patient to lie
on arm or hand.
6. May want pillow under hips and lower

legs to bend knee and relieve back strain
at lumbar spine.
To summarize, we find patient positioning and
movement is a necessary and integral function of
(1985). An investigation into the effect

on some aspects of normal pulmonary
function. Physiolherap)" 7,(7),311-314.
Fuerst, E., & Wolff, L. (J 959). Fundamel1lals of nursing (4th ed)
Philadelphia: 18 Lippincott.
[s there a right way to lift') ([985). Physical Therapy Forum, 4, 23.
Johnson, G. (1989). Functional Orlhopedics I. San Ansellmo,
Crosbie, W.J.,
&
Myles, S.
of postural modification
Calif: Institute of Physical Art. Chicago: Course presentation

June
8-11,1989.
748
PART VIII
Kendall, FP., McCreary, E.K., & Provance. P.G. (1993). Muscles

lesling am/ flUlellOll. Baltimore: Williams & Wilkins.
Lewis. L (1976). FUlldamellfai skills in patient care Philadelphia:

.
Lijiing, moving and
ferring
Irans
paliellls: a manual, S . . Louis, Mosby.
Rauch, B. (J 971 L Kinesiology alld app/red allatomy, Philadelphia:

Lea & Febiger.
JB LippincotL
Masscry. M. (1994). What's positioning got to do with it? Neuml

Report, /8 (3). 11-14.
Roper, N. (1973). Principles of
(2nd ed). New
Neil, C. (1959). Body management in nursing. Nursing Times,

55,163.
Rantz. M. & Comiial, D.
Woodhall-McNeal, A. P. (19')2). Changes

with age, Aging, 4 (3), 219-225.
1I1
posture and balance
Respiratory Care Practice Review
Michael Wade Baskin
KEY
TERMS
Aerosol
Humidity
Oxygen
Oxygen delivery
rntermittent positive pressure

breathing
(IPPB)
INTRODUCTION
OXYGEN THERAPY
Proper care of the pulmonary patient involves a multi
The atmosphere around us contains 20.95/'1 oxygen,
disciplinary approach, and all professionals involved
one of the most essential elements needed to sustain
should have a working knowledge of each individual
human life. Oxygen exerts
profession's scope of care. As respiratory therapists,
mm Hg at sea level (dry air) and approximately 97
partial pressure of 159.6
physical therapists, occupational therapists, and nurses
mm Hg in arterial blood. The normal range as mea
apply their expertise in providing care for pulmonary
sured by arterial blood gas analysis is
patienls, it becomes ev ident that coordi nated team
Hg. Under normal circumstances, this molecule trav
80
to 100 mm
work is essential 10 ensure errective treatment pro
els from the atmosphere to the mitochondria at the
gramming. The purpose of this chapter is to provide
cellular level where it is used to produce ATP in a
nonrespiratory therapist health-care professionals with
process called aerobic metabolism. The pathway in
an overview of respiratory care principles and modali
volves the lungs, blood, circulation, and the muscle
ties frequently encountered in the various settings. It
tissue where the mitochondria reside. Any process
is also the intention of this chapter to eliminate the
that inhibits the transport of oxygen from the atmos
anxiety experienced by professionals because of the
phere to the cellular level can cause tissue hypoxia
plethora of attachments to the cardiopulmonary pa
and ultimately death.
tient. Interaction with the various modalities and

pieces of equipment is also discussed.
One of the most common drugs that a respiratory

therapist uses is oxygen. Patients with cardiopul
749
750
PART VIII
monary problems frequently need oxygen supple
The nasal cannula, also called nasal hi-prongs, is
mentation. Respiratory therapists and the nursing
one of the most common low now devices encoun
staff are generally responsible for administration of
tered because of its low expense and high patient
this drug under a physician's order. There are several
compliance (Figure 4 1-]). This device supplies be
different methods a therapist may choose to deliver
tween 24% and 40% oxygen with flow rates from I
oxygen in the most effective way.
Llmin to 6 Llmin. Flow rates above 6 Llmin can
The purpose of oxygen therapy is to treat and to
cause nasal mucosa irritation and drying. The approx
prevent hypoxemia, excessive work of breathing, and
imate liter flow and resultant Flo2 values are shown
excessive myocardial work (Kacmarek, Mack, and
in Table 41-1.
Dimas, 1 990). Although individual oxygen appli
Nasal canulas deliver 100% oxygen, however, this
ances offer suggested guidelines regarding oxygen
percentage significantly lessens as the oxygen mixes
administration, the only way to ensure effective de
with inspired air from the room. The amount of oxy
livery from a given device is blood gas monitoring of
gen delivered depends on the now rate and the venti
Pao2, partial pressure of oxygen in the arterial blood
latory pattern of the patient. A larger minute volume
or by monitoring hemoglobin saturation by oximetry.
(TV
Oxygen therapy can be administered by one of two
rate causing a greater decrease in the percentage de
methods-low-flow and high-flow systems.
livered to the lungs. In other words, the faster and
RR) would dilute the oxygen at any given flow
deeper a patient breathes, the more diluted the oxy

gen will become. On the other hand, if a patient has a
Low-Flow Systems
low minute volume, the oxygen percentage delivered
A low-flow oxygen system is that which does not in
will increase (Kacmarek et aI., 1990). If precise con
tend to meet the total inspiratory requirements of the
trol of Flo2 is needed, the nasal cannula should not be
patient. This method of oxygen delivery is not used
used (Bazuaye, Stone, Corris, and Gibson, 1992).
when a specific concentration of oxygen is needed

(Burton, Hodgkin, and Ward, 1991).
Mouth breathing by patients on a nasal cannula

typically causes the attending health-care provider to
switch the patient to a mask; however, this may be un
necessary. If the nasal passages are unobstructed, then
oxygen is able to collect in the oral and nasal cavity
(anatomical reservoir). On inspiration, the oxygen col
lected in this area is drawn into the airway system. If a
patient with a nasal cannula is mouth breathing, the
practitioner should ensure the nasal passages are un
obstructed. If there is concern that the patient is not
TABLE 41-1
Approximate liter flow Hod resultant Fl02 values.
FIGURE 41-1
Oxygen cannula.
FLOW (Llmin)
Flo2(%)
I
2
3
4
5
6
24
28
32
36
40
44
41
751
receiving adequate oxygen, an oxygen saturation mea
cheal oxygen catheters are more efficient than nasal
surement should be obtained. If this is not feasible, or
cannulas, and they have a high patient acceptance
if the patient is unable to breathe through the nose, it
rate with low complications (Kent, et a!., 1987). Be
would be appropriate to switch the patient to a mask.
cause the oxygen is administered directly into the tra
Breathing through the nosc should be encouraged
chea, 50% less oxygen is needed (Kacmarek et a!.,
to receive maximum benefil from the nasal cannula;
(990). For people who use portable oxygen systems,
however, mouth breathing does not mean the patient
and for those who require high oxygen flow rates,
is not receiving oxygen (Dunlevy & Tyl, 1992).
tracheal oxygen catheters may be beneficial (Jackson,
The simple mask, or open-face mask, is another
King, Wells, and Shneerson, 1992). The catheter can
low-flow oxygen delivery device commonly used. It
be covered by the patient's clothing, therefore, it is
can deliver from 40% to 60('>(; oxygen, depending on
cosmetically appealing.
the flow rate and the patient's ventilatory pattern.

This device requires a flow rate of 5 to 6 Llmin to
prevent rebreathing and excessive respiratory work
(Jensen, Johnson, and Sandstedt, 1991). As with the
HIGH-FLOW SYSTEMS
A high-flow oxygen delivery system is that which de
nasal cannula, this type of oxygen delivery method
livers a specific oxygen concentration despite the pa
should not be used if precise control of oxygen con
tient's ventilatory pattern. If it is found that a patient

requires oxygen delivered at an FIo2 of 50% to keep
centration (FI02) is required.

The partial rebreathing mask is basically a mask
with a reservoir bag attached. The oxygen source
the oxygen saturation at a safe level, then a high-flow

system would be the method of choice.
supplics the bag with 100% oxygen where it mixes
This type of system is also used when there is fear
with exhaled anatomical dead-space-air that has not
of administering too much oxygen to a hypercapneic
taken place in gas exchange. This exhaled air is rich
patient. The respiratory drive to breath could be re
in oxygen. The exhaled air that has taken place in gas
duced and possibly result in apnea. Precise control of
exchange and contains CO2 is vented through the
low-concentration oxygen is warranted in such cases.
open ports on each side of the mask. This mask can

deliver oxygen concentrations from 70% to more
than 80%, and it requires flows between 7 and 10
Llmin to keep the bag from fully collapsing during
inspiration (Kacmarek et a!., (990).
The nonrebreathing mask is another low-flow de
livery device that also contains a bag reservoir, but it
can deliver up to 100% oxygen. This mask contains
valves at the reservoir bag and the side vents to pre
vent ambient air mixing on inspiration and exhaled air
mixing on expiration. In order for this mask to operate
effectively, a good seal between the patient's face and
the mask should be achieved. The bag should partially
deflate during inspiration (Figure 41-2).
Another interesting form of low-flow oxygen de
livery is the transtracheal oxygen calheter. This
method has gradually gained wider acceptance as a
long-term oxygen delivery device. It is surgically
FIGURE 41-2
placed into the trachea via a small incision between
Left to right,
the second and third tracheal rings. Generally, these
nonbreathing bag.
devices are seen in home-oxygen patients. Transtra
junction between the mask and bag.
mask without bag, partial rebreathing bag,

NOTE:
the valves on the mask and at the
752
PART VIH
The Venturi mask is a common method of deliver

ing high-flow oxygen concentrations from 24% to
50%. This mask operates via the Venturi principle,

which provides for a mixing of 100% oxygen and en
trained ambient air. The oxygen flows though a nar
row orifice at a high velocity causing a subatmos
pheric pressure. This drop in pressure is what causes
the ambient air to be entrained through a port. The
size of the port determines the amount of air to be en
trained and thus the percentage of oxygen delivered.
The Venturi mask has a rotating air entrainment port
that allows the health-care provider to "dial in" the
desired FI02 (Figure 4 1-3).
Mechanical aerosol systems also operate via air en

trai nment, but the mask is connected to the aerosol
unit by large-bore tubing to allow a specific FI02 to be
FIGURE 41-3
delivered with high humidity (Figure 41 -4). Although
Venturi mask.
drainage bags are usually attached to the tubing to col

lect condensation, the tubing must be monitored for
possible pooling of water causing flow obstruction to
the patient. If pattial obstruction occurs, a mild back
pressure results in the tubing, causing less air entrain
ment. This means that a higher concentration of oxy
gen will result and possibly deliver a higher dosage of
oxygen to the patient than desired.
FIGURE 41-4
A, Heated aerosol. B, Nebulizers.
41
HOME AND PORTABLE OXYGEN
753
Smaller tanks are used for portability and can provide
As health care continues to move out of the hospital set
up to 3 hours of use. They can be refilled by transfer
ting and into the home, more health-care practitioners
ring gas from the larger reservoir tank.
will be providing care to oxygen patients in their homes.
Liquid oxygen is a low-pressure oxygen delivery
Oxygen is most commonly delivered in the home for
method, and it tends to be more convenient than
those needing long-term oxygen, usually chronic ob
using the high-pressure tanks, especially for the ac
stl1lctive pulmonary disease (COP D) patients. Generally
tive oxygen patient. The canisters are lightweight and
I to 2 Llmin is prescribed via nasal cannula, but the
allow patients to be away from the home reservoir for
flow rate will depend on the patient's need.
up to 8 hours. The down side is that liquid oxygen
Home oxygen-delivery systems can be divided
costs more, and the reservoirs need to be filled up to
into three categories: high-pressure oxygen cylinders,
twice a week with continuous use. If high flows are
low-pressure liquid oxygen, and oxygen concentra
needed, these units are not recommended.
tors (Burton et aI., 1991).
Oxygen concentrators are commonly seen in the
High-pressure oxygen tanks come in various sizes.
home health setting, especially since Medicare offers
The larger ones such as the H and K sizes are used as
coverage for these devices (Figure 4 I -5). Generally,
a base unit or reservoir. Long oxygen tubing con
they tend to be expensive initially but are actually
nected to these tanks allows for patient mobility.
less expensive for long-term use. They are electri

cally powered and create oxygen by drawing ambient
air across a semipermeable membrane, separating
oxygen from nitrogen. They generally operate at 2
Llmin and provide 90% oxygen. Long oxygen tubing,
up to 50 ft, allows patients extra mobility. Patients
using concentrators should have a back-up device,
such as a pOJ1abie tank, in case of a power outage.
RESPIRATORY MODALITIES
Intermittent Positive Pressure Breathing
Intermittent positive pressure breathing (lPPB) is
mentioned here not to educate the reader about its use
but to inform the reader about its declining use. Al
though this particular modality continues to be used
in some hospital settings, there is little evidence to
supports its efficacy.
This particular technology was developed during
World War II to assist pilots breathing in unpressur
ized cabins at high altitudes. IPPB subsequently be
came a very popular respiratory therapy device in the
1960s and I970s (Figure 41 -6). However, its use
began to decline in the 1980s. In 1983 the National
Heart, Lung, and Blood Institute reported that IPPB
has limited therapeutic benefit. This clinical trial is
only one of several studies that show IPPB is an out
moded medical technology. In fact, research dating
FIGURE 41-5
back to the 19 50s questions the efficacy of this de
Oxygen concentrator.
vice (Duffy and Farley, 1992).
754
PART VIII
Related Aspects of Cal'diopulmonary Physical Therapy
FIGURE 41-6
Left, Bird Mark and righI, Bennett AP-S IPPB machines.
FIGURE 41-7
Incentive spirometry device in use,
41
The purpose of the IPPB machine is to increase
755
rina. This humidification process is important to mu
alveolar ventilation, to improve the ventilation-pelfu
COlIS
sion ratio, to mobilize and facilitate expectoration of
ratory tract. When this normal humidification process
thick secretions, to decrease the work of breathing,
is interferred with, other methods of adding moisture
and to deliver aerosolized medications. It is a pres
to the respiratory system must be employed.
sure-cycled ventilator that, when triggered by a pa
production, ciliary activity, and a healthy respi
Humidification is the addition of water vapor in its
tient's inhalation, delivers ambient air or oxygen to
molecular form to a gas. When a dry gas is being ad
the patient until a preset pressure is rcached. It is ba
ministered to a patient (e.g., via a nasal cannula),
sically a lung expansion device that helps deliver an
some type of humidification appliance would be used
increased tidal volume. IPPB is used for a variety of
to prevent unneccssary complications. Flows of 2
pulmonary conditions, and treatment scssions usually

last
Llmin or less may not require humidification when

using a nasal cannula. Humidification therapy is also
10 to 15 minutes.
This modality comes into question in the clinical
indicated in the presence of thick tenacious secretions
setting because it has not shown to provide benefits
and when an artificial airway is in place. Artificial
over that of other simpler respiratory treatment meth
airways, such as endotracheal and tracheostomy
ods. It also introduces potential complications and
tubes, bypass the normal humidification system (the
hazards that the other treatments do not. Typically,
upper airway); therefore, supplementation is essential
IPPB has been used to treat asthma, COPO, and post
(Frownfelter,
operative atelectasis; however, other therapies, such
1987).
There are basically two types of humidifiers. Bub
as incentive spirometry (IS), postural drainage, and
ble-through humidifiers are those which are generally
aerosol therapy, tend to prevai I as the treatment of
used with simple oxygen appliances. The pass-over
choice over IPPB.
type of humidifier is usually found in conjuction with
Although IPPB is questionable regarding its clini
a mechanical ventilator. Both bubble-through and
cal efficacy, it may be a beneficial form of treatment
pass-over humidifiers are available for ventilators,
in acute asthma or COPO that is refractory to stan
and they are usually heated to warm the humidified
dard therapy, atelectasis that has not responded to
air to body temperature before entering the airway
simpler therapy, and the prevention of respiratory
(Kacmarek et ai., 1991).
failure in patients with kyphoscoliosis and neuromus

cular disorders (Handelsman,
199 I).
Aerosol Therapy
An aerosol is created when a suspension of liquid or
INCENTIVE SPIROMETRY
solid particles exists in a gas. Today, the two most
Incentive spirometry (IS), also called sustained maxi
common forms of medication aerosol delivery in the
mum inspiration (SMI), is simply a visual and/or
clinical setting are the small.
audio feedback device that encourages slow, deep in
and the metered dose inhaler (MOl). A bland aerosol
spiration (Figure
41-7). Generally, this treatment is
performed frequently, up to every hour, and its pur

pose is to treat and prevent atelectasis, especially in
postoperative thoracic and abdominal patients.
is administration of water or saline solution to the pa

tient's lungs.
In general the goals of aerosol therapy are to hy
drate dried retained secretions, to improve cough effi
ciency, to restore and maintain function of the mu
cociliary elevator, to deliver medications, and to
HUMIDITY AND AEROSOL THERAPY
humidify gases delivered through artificial airways.
Humidity Therapy
The MOl is strictly used for medication delivery.
Under normal circumstances, when inhalation takes
Other forms of aerosol delivery are the spinning
100(;'(; saturated with water vapor
disk, such as in a room humidifier or mist tent, and
before entering the lower airway tracts below the ca
the ultrasonic nebulizer. Both of these are electri
place, air becomes
756
PART VIII
ble while taking slow, deep breaths with a short 3- to

4-second inspiratory hold. Mouth breathing is en
couraged if aerosol therapy is delivered by mask.
Nasal breathing may filter out particles of optimal
size. Of course, not all patients will be able to
achieve this position and ventilatory pattern, and the
therapist must modify accordingly.
In comparing SVN with MOl's ability to deliver
medications, it is found that the MOl is either equal
in efficacy or outperforms nebulizers. Significant cost
savings are also realized by those institutions who
recog nize M O l usage as an effec tive means of
aerosol medication delivery over SVN (Orens,
Kester, Fergus, and Stoller, 1991).
To further enhance the efficacy of the MOl treat
ment, a spacer or holding chamber may be attached
to trap the aerosol particles before inhalation. This
device allows greater drug particle deposition to the
FIGURE 41-8
airways and reduces oropharyngeal deposition (Ash
Commonly used spacer device.
worth, Wilson, Sims, Wotton, and Hardy, 1991).

Ventilator patients that are receiving drug aerosol
therapy also receive greater benefit from an in-line
MOl with a holding chamber as compared with a jet
nebulizer (Fuller, Oolvich, Posmituck, Pack, and
cally powered as opposed to the SVN, which is
Newhouse, 1990).
pneumatically powered (Figure 41-8) (Branson and

Seger, 1988).
A key element in aerosol delivery is particle size.
Aerosol-Therapy Precautions
The size of the aerosol particle will determine its abil
It should be mentioned that there are hazards associ
ity to penetrate into the airway before depositing or
ated with aerosol therapy. Bronchospasm may occur
raining out. The therapeutic range is considered I 11
as the smooth muscle of the bronchial passages
with the smaller range of paJticles having the greatest
react to foreign particles entering the lung. Short
penetrating ability. The larger particles deposit sooner.
ness of breath and respiratory distress may also
If they are greater than 5 11 then the chances of entry
o c c u r as a r e s u l t of d r i e d retained secretions
into the airway are less. The particles may deposit in
swelling and occluding portions of the lung. Cross
the nose and proximal airway. The greatest amount of
contamination is a concern in that aerosol devices
alveolar deposition (95% to 100%) occurs in the I to
may harbor organisms that can be transmitted to pa
2 11 range. On the other hand, aerosol particles smaller
tients. Frequent equipment changes and proper ster
than I 11 are so stable that they may not deposit at all
ilization and cleaning techniques are key in prevent
(Kacmarek et aI., 1991).
ing this occurrence.
Although particle size is important in determining

appropriate deposition, a patient's ventilatory pattern
is probably more important in that it is the more vari
MECHANICAL VENTILATION
able and controllable of the two. Gravity also plays a
The subject of mechanical ventilation is vast and
factor, and it too can be used to benefit particle depo
highly technical. The purpose of this section is to give
sition. Patients should be sitting up as much as possi
the reader a concise overview of mechanical venti la
41
757
FIGURE 41-9
A, Puritan Bennett 7200a microprocessor driven ventilator. B, Bennett MA-I ventilator-bellows
system driven by an electric compressor.
tion and provide a foundation from which to make ap
tive pressure breaths to a patient. Positive pressure
propriate decisions when working in this environment.
ventilation is opposite of normal physiological venti
Many disease states that lead to cardiac and/or res
lation in that normal ventilation occurs when negative
piratory failure will require mechanical ventilation to
pressure, created by contraction of the diaphragm,
support the patient's effort to ventilate and oxygenate
causes air to enter the lungs. Whereas normal inspira
41-9). Today, patients receiving mechanical
tion occurs by "pulling" air into the lungs, ventilators
(Figure
ventilator support can be found in both the hospital
"push" air into the lungs. This is important in that the
and the home. Acute exacerbations of disorders such
thoracic cavity becomes an area of higher pressure,
as emphysema, COPD, and chronic hronchitis com
which may create adverse cardiovascular and hemo
monly require mechanical ventilation and are gener
dynamic events.
ally seen in hospital rcus. Disorders requiring long

term ventilation, such as spinal cord injury, brain
injury, and certain neuromusculoskeletal diseases,
Modes of Mechanical Ventilation
may be found receiving mechanical ventilation in the
The physician and respiratory therapist have a nev
home or long-term care facility.
erending sea of choices in which to choose the most
Today, mechanical ventilator assistance is pro
appropriate method of ventilation. This area some
vided primarily by machines that deliver preset posi
times presents confusing terminology and a lack of
758
PART VIII
consistency. In fact, choosing the appropriate mode
breaths with the patient's spontaneous breaths. In
of ventilation may be considered more of an art than
IMV the machine may cycle a breath before the
a science. Before describing the modes of ventilation,
patient can completely exhale a spontaneous
the following terms should be defined:
breath. If no inspiratory effort is present, the ma
1. Trigger-Variable that causes a breath to be

delivered by the ventilator. A patient may inhale
chine delivers the mandatory breaths.

causing the ventilator circuit pressure to drop to
Continuous positive airway pressure (CPAP).

The patient spontaneously breathes and a preset
a preset number (i.e., less than 1 or 2 em H20).
level of pressure is constantly maintained. This
This is called a pressure trigger. Some ventila
method of ventilation can also be achieved
tors are volume and flow triggered.
through use of commercially available pneumati
2. Flowrate-The speed at which the ventilator
cally powered units that hook directly into the
breath is deli vered. This parameter is usually
oxygen wall outlet. A tight fitting mask is secured
measured in liters per minute.
around the patient's mouth and nose, and a preset
3. Frequency-R e fers to the number of breaths

delivered over time (e.g., 10 breaths per minute).
pressure and oxygen percentage is delivered.
4. Spontaneous breath-Breathing through the
Airway pressure release ventilation (APRV).

The patient is allowed to spontaneously breathe
ventilator circuit without assistance.
with a set amount of CP AP. If additional ventila
The following is a descri ption of common current
tion is required, the CPAP will be dropped period
ventilator modes:
ically, releasing the pressure, causing the patient
Controlled mechanical ventilation (CMV). The
to exhale. When the exhalation is complete, CPAP
control mode is a lesser used method of ventilation
is restored. Proponents of this mode claim that by
and generally requires the patient be sedated and
allowing the patient control, patient comfort and
paralyzed. The ventilator delivers all breaths at a
compliance are high.
p r e s e t f re q uency, volume or p r e s sure, a n d
Pressure support ventilation (PSV). In using

pressure support the patient is allowed to breathe
breaths or trigger the machine.
spontaneously and receives a preset amount of
Assist control (AC). The patient receives a preset
inspiratory support until the fIowrate reaches a
pressure or volume, f requency or number of
minimal level. The patient controls the fre
breaths, and fIowrate. In between machine-cycled
quency, tidal volume, inspiratory time. This
breaths, the patient can trigger the machine to de
mode is often used in conjuntion with SIMV.
li ver another breath at the preset parameters. All
This mode is also popular due to high patient
breaths are machine delivered. No spontaneous
compliance.
breathing can occur.

flowrate. T h e patient cannot take spontaneous
Mandatory minute ventilation (MMV). The pa
Assisted mechanical ventilation. This mode is
tient is allowed to breathe spontaneously; how
similar to AC, however, there is no set frequency.
ever, a minimal level of minute ventilation will be
The patient triggers the machine at will to deli ver
achieved through ventilator-assisted breaths. This
a set pressure or volume at a set fIowrate.
is usually accomplished by using PSV.
Intermittent mandatory ventilation (lMV). As
Volume-assured pressure support (V APS).
the ventilator delivers a set mandatory frequency
This is one of the newest modes of ventilation. It
and volume or pressure, the patient is allowed to
allows the patient to breathe spontaneously in the
take spontaneous breaths between cycles. This is a
PSV mode and monitors each breath's tidal vol
former popular mode.
ume. If the breath is not going to reach the set
Synchronized intermittent mandatory ventila
volume, the ventilator will hold the fIowrate con
tion (SIMV). This mode improves on that of IMV
stant and increase the pressure until the desired
in that it synchronizes the machine delivered
volume is reached (Branson and Chatburn, 1992).
41
Alarm Management and Precautions
759
or excessive water buildup (Figure 41-10). Low
When working around ventilators, it is inevitable that
pressure may signify a leak in the ventilator circuitry
alarms will sound. Alarms are important indicators of a
or a bad patient connection.
patient's condition or machine malfunction. All alarms
If you are unfamiliar with a particular ventilator
should be recognized and valued as excellent sources
and an alarm sounds that you are unable to identify
of information. If alarms are silenced or ignored with
and/or remedy, first ensure the patient is not in any
out interpretation, patient fatalities may result.
extra distress. Assess the overall appearance and,
The most common alarms are those which moni
most of all, rise and fall of the chest as the ventilator
tor high and low pressurc. FI02, apnea, disconnec
cycles. If the patient does not appear to be receiving
tion, and volume. Generally, if the high-pressure
breaths, immediate action should be taken to remove
alarm continucs to sound, the patient should be
the ventilator from the patient and to begin manual
checked for secretion buildup. Suctioning can rem
ventilation with a self-inflating bag. The respiratory
edy this problem. The ventilator tubing should also
care practioner should be called to rectify the situa
be checked for possibJe occlusion from compression
tion. When the problem is resolved, the patient

should be returned to the mechanical ventilator.
One primary precaution to keep in mind when
working with a ventilator patient is to watch for con
densation in the tubing that could accidentally be
poured directly into the patients lungs. When moving
a ventilator patient, plan ahead by securing aJl lines,
wires, and tubing. Follow the appropriate procedure
for emptying any water from the ventilator tubing be
fore moving the patient. Aspiration of water from
ventilator tubing can be fatal.
SUMMARY
Physical therapists need to understand the basic
equipment and principles of respiratory care in order
to optimize functional outcomes of their patients.
REVIEW QUESTIONS
I. If precise control of oxygen percentage to a pa
tient is wananted, what type of delivery system
is indicated?
2. Does mouth breathing by a patient on a nasal
cannula indicate that he is receiving no oxygen?
3. Why do low-flow oxygen masks require a certain
minimum liter flow, that is,S to 6 Llmin for a
simple mask?
4. Why is IPPB come into question as an effective

FIGURE 41-10
Condensation build-up in ventilator tubing-a potential
hazard.
modality?
5. What are two concerns regarding condensation
collecting in mechanical ventilator tubing?
760
PART VIII
References
Fuller, H.D., Dolovich, M.B., Posmituck, G., Pack, W.W.,
Ashworth, HL, Wilson, CG., Sims, E.E., Wotton, P.K.,
& Hlirdy,
& New
house, M.T. (1990). Pressuril.ed aerosol versus jet aerosol de
lG. (1991). Delivery of propellant soluble drug from a metered
livery to mechanically ventilated patients. Comparison of dose
dose inhaler. Thorax, 46(4),245-247.
to the lungs. American
Barharash, R.A., Smith, L.A., GOdwin, J .E.,
& Sahn, SA (1990).
Mechanical ventilation. DICP, The Annals of Pharmacother

apy.
24, 959-970.
of Respiratory Disease. 141(2),
>f' Handelsman, H. (1991). Intermittent positive pressure breathing

(IPPB) therapy. Health Technology Assessment Reports.
Bazuaye, E.A . , Stone, T.N , Corris, P.A.,
& Gibson, GJ. (1992)
Variability of inspired oxygen concentration with nasal cannu
4 7(8 ) , 609-611.
ranson, R.D., & Seger, S.M. (1988). Bronchial hygiene tech
niques. In R.M. Kacmarek, & 1.K. Stoller. C urren l respiralory
las. Thorax,
care (pp. 24-28). Philadelphia: B.e. Decker.
Branson, R.D.,
Rel'iew
440-444.
1. 1-9.
-J Hodgkin, J.E., Connors, G.L., & Bell, e.w. (1993). Pulmonary re

habilitation guidlines to success (2nd ed.). Philadelphia: JB
Lippincotl.
Jackson, M., King, M.A., Wells, F.e.,
& Shneerson, J.M. (1992).
Clnical experience and physiologic resulls with an implantable

intratracheal oxygen catheter. Chest, 102(5), 1413-8.
& Chatburn, R.L. (1992). Technical description and
Jensen, A.G., Johnson, A.,
& Sandstedt, S. (1991). Rebreathing
classification of modes of ventilator operation. Respiralory
during oxygen treatment with face mask. The effect of oxygen
Care, 37(9),1026-1044.
flow rates on ventilation. Acta Anaesthesiologica Scandinal'
-*' Burns, S.M. (1990). Advances in ventilatory therapy: high-fre

quency, pressure support, and nocturnal nasal positive pressure
ventilation. Focus on Critical Care. 17(3),227-237.
f Burton, G.G., Hodgkin, J . E., & Ward, J.J. (1991). Respiratory care
a
guide to
clinical
practice (3rd ed.) (pp. 524-525). Philadel
phia: J.B. Lippincott.

Duffy S.Q.,
& Farley, D.E. (1992). The protracted demise of med
ica, 35(4),289-292.
Kacmarek, R.M., Mack, e.W.,
& Dimas, S. (1990).
The essentials
o{respiratory care (3rd ed.). SI. Louis: Mosby.
Kent, e., et a!. (1987). A program for transtracheal oxygen deliv

ery: Assessment of safety and efficacy. Annals of Internal
Medicine, 107,802-808.
Orens, K.D., Kester, L., Fergus L.e., & Stoller, J.K. (1991). Cost
ical technology: the case of intermittent positive pressure
impact of metered dose inhalers vs small volume m:huli/.crs in
breathing. Medical Care, 30(8),718-734.
hospitalized patients: the cleveland clinic experience. Resp ira
..( Dunlevy, e.L., & Tyl, S.E. (1992). The effect of oral versus nasal
breathing on oxygen concentrations received from nasal cannu
las. Respiratory Care, 37(4),357-60.
tory Care, 36( I 0), 1099-1104.
Pilbeam, S.P. (1992). Mechanical ventilatioll physiological alld

clinical applirllliol1s. St. Louis: Mosby.
Frownfelter, D.L. (1987). Chest physical therapy and pulmanary

rehabilitation an interdisciplinary approach (2nd ed.). St
",*, .zadai, e.e. (1992). Pulmonary manogclllcnt in phvsical therapy.

New York: Churchill Livingstone.
Louis: Mosby.
Care of the Patient With

an Artificial Airway
Lisa Sigg Mendelson
KEY TERMS
Airway clearance
Tracheostomy
Artificial airway
Tracheostomy tube/cuff
Suctioning
HISTORICAL PERSPECTIVE
purposes:
An artificial airway is a tube inserted in the trachea
(I) to bypass upper airway obstruction,
(2) to assist or control respirations over prolonged pe
(3) to facilitate the care of chronic respiratory

(4) to prevent aspiration of oral
either through the mouth or nose or by a surgical in
riods,
cision. Artificial airways have been known to med
tract infections, and
ical science for
3000 years. George Washington ulti
and gastric secretions. Multiple disease processes and
mately died of upper airway obstruction because his
traumatic problems can require an artificial airway,
p h ysicians could not agree on t h e use of tra
but each situation, simple or complex, can fit into one
cheostomy. It was not until
1909, when Chevalier
or several of these categories (see box on p. 762).
Jackson published his classical paper on tracheotomy,

that this procedure gained some acceptance. The pro
cedure did not become a highly specialized technique

in patient care until the invention of modern tra
INDICATIONS OF NEED-OBSERVATION
The respiratory care team can play a vital role in rec
cheostomy tubes and the development of intermittent
ognizing patient need for a tracheostomy from physi
positive-pressure ventilators. In today's clinical prac
ological changes that indicate respiratory distress.
tice, artificial airways have the following four basic
Cardinal signs of dangerous airway obstruction are

761
762
PART VIII
Disease Processes that CouLd Require all ArtificiaL Airway because of Respiratory Illsufficiency
I. Primary lung disease (e.g.. emphysema. chronic bronchitis, pulmonary fibrosis. cystic fibrosis,
severe
pneumonia,
burned lung, and toxic inhalation).
2. Systemic disease with secondary lung involvement (e.g.. cardiac failure, renal failure (fluid overload), and Illulti
organ system failure).
3. Neuromuscular disease (e.g., polio, Guillain-Barre syndrome, my asthenia gravis usc of muscle relaxants. and
,
tetanus).
4. Central nervous system depression (e.g.. drugs, postanesthesia, metabolical coma. cerebrovascular accident,
meningitis. and central nervous system tumors).
5. Trauma (e.g.. head/necklchest surgery or injuries).

6. Diseases complicated by extremes of age (e.g., premature infant or elderly).
7. Mechanical obstmction (e.g., upper airway infection. laryngeal paralysis, tumor. edema. bleeding. foreign body,
and thyroid malignancy).
8. Recurrent aspiration (e.g .. glottic incompetence, occlusive diseases of the esophagus, and swallowing disorders of
various causes).
From Selecky PA: Tracheostomy-a review of present day i ndicat ions complications and
,
care,
!-Iellrt Lung 3: 272-283, 1974.
stridor and chest wall retractions. Early clinical signs
long-term intubation. The nasal tube is more efficient
may include restlessness, agitation, tachycardia, con
in that it is better secured, the patient may eat, it is
fusion, motor dysfunction, and decreased oxygen sat
easier to suction, and it is generally more comfortable
uration on pulse oximetry. These signs may be ac
for the patient.
c o m p a n i e d by h e a d a ch e , f l a p p i n g t r e m o r, a n d
There are certain complications with nasotracheal
diaphoresis. Cyanosis from impaired oxygenation of
tubes. Among these are sinus blockage and pain,
the blood is a late, ominous sign.
vocal cord damage, or pressure necrosis to the carti
In children, restlessness must be due to lack of
laginous structure of the nose. To reduce these com
oxygen unless another factor (e.g., thirst) is clearly
plications, the airway should be evaluated daily. The
evident. Extreme fatigue and an inability to sleep in
tube should be removed as quickly as possible when
dicate impending danger. Apprehension, restlessness,
the indication for intubation is reversed. However, if
and mental confusion at any age may be taken as
there appears to be a need for a more long-term air

way, a tracheostomy should be considered. The pro
early signs of hypoxia.
cedure should not be taken lightly because many ad

ditional complications may occur.
Complications of Tracheostomy
Complications of tracheostomy can be surgical,
The selection of the appropriate airway is made by
postoperative, or physiological. Complications that
the following factors:
(I) What is the best means of

(2) Is it an emergency or a
controlled, determined situation? (3) Will the airway
occur at the time of the operation are more frequently
accomplishing the goal?
direct results of the surgical procedure itself. Delayed
be needed for long-term care? In general, oral endo
surgery, from postoperative care, or from the abrupt
tracheal tubes are inserted in emergencies. They are
physiological changes resulting from tracheostomy.
complications may result directly or indirectly from
the quickest and easiest tubes to insert even for rela
Nursing objectives in caring for the patient after a tra
tively untrained personnel. A nasotracheal tube will
cheostomy are to maintain patency of the tube, clean
generally replace the oral endotracheal tube for a
liness of the wound site, and good aeration and to ob
42
serve any changes in the patient's vital signs and oxy
Care or the Patient With an Artificial Airway
763
A patient with an artificial airway is understand
ably apprehensive and has special communication
genation by pulse oximetry.

In patients with artificial airways the normal phys
needs. He or she should also be reminded that the in
iological mechanism for adding moisture to the air
ability to phonate is only temporary. The patient must
via the nasal mucosa obviously is bypassed. There
be reassured that he or she will be attended to con
fore supplemental humidification is extremely impor
stantly and will be able to trust and depend fully on
tant to protect the mucosa from drying and crusting,
the nursing staff to attend to his or her needs. If alert,
which results in obstruction.
the patient must be equipped with a signal light or
The dressing under the tracheostomy tube and tra

cheostomy ties should be changed when they become
bell, paper and pencil, magic slate, or picture board

for communication.
soiled because dried blood and other secretions near
Airway obstruction is the foremost complication that
the incision can encourage bacterial growth. The inci
exists for the postoperative tracheostomy patient. Tra
sion should be checked frequently for bleeding. The
cheal secretions are the major source of obstruction,
skin may be cleaned with half-strength hydrogen per
particularly if they are excessive or viscous. When
oxide and sterile saline when a new dressing is ap
using cuffed tube, acute obstruction might occur from
plied. The dressing should be folded into place
overinflating the cuff, which would allow it to balloon
never cut. This eliminates the possibility of lint or
over the end of the tube. Other causes of obstruction are
frayed threads being aspirated. Commercially pre
dislodgement of the tube into a false tract anterior to the
pared dressings best meet these criteria.
tube tracheal opening, occlusion by an overinflated
When changing the tapes that hold the tube in
cuff, and kinking of softened plastic cannula.
place, it is best to have one nurse hold the tube in
Tracheobronchitis, inflammation of the trachea and
place while another replaces the old tapes. An angle
bronchus, is a complication resulting primarily from ir
is cut at the end of the tape to facilitate its placement
ritation resulting from incorrect suctioning technique.
through the flange of one side of the tube. The tape is
Crusting is a common and complex problem that
then threaded through the back of the tracheostomy
may result from inadequate humidification of inspired
tube and through the other flanged opening and tied
air or may result from dehydration. In many instances,
securely with a square knot placed on one side of the
ulceration of the tracheal mucosa results from irrita
patient's neck. One finger should be placed under the
tion by the airway or incorrect suctioning. This ulcer
twill tape while tying to prevent the tape from being
ated area becomes infected with various organisms
tied too tight.
and is virtually covered by crust. Further suctioning
Pneumothorax can occur immediately after tra
removes the crust, causing discharge of serum and
cheostomy because of laceration of the mediastinal
bleeding. The discharge produces a wet eschar that is
24 hours (arises
covered with mucus. Because of the drying effect of
often in children and patients with chronic obstructive
air passing over this mass, a hard crust can form. This
pleura at the time of surgery or within
lung disease). Other problems include air embolism,
process can compound the difficulty because the de
aspiration, and subcutaneous and mediastinal emphy
velopment of this crust in the trachea might eventually
sema. Recurrent laryngeal nerve damage or posterior
produce a mass large enough to completely plug the
tracheal penetration may occur but is uncommon.
tracheal cannula and almost completely obstruct the

trachea. Cases have been cited where an entire cast of
the tracheobronchial tree has been removed.
Postoperative Physiological Complications
Other physiological complications may be related
(1) hypoxia developing before or
Attentive nursing care is the single most essential
to the following:
factor in postoperative management. A ratio of one
during the procedure and resulting in an uncontrol
nurse for each patient is the ideal; however, since this
lable patient, cardiac arrest, and increased myocardial
is not often possible, increased vigilance by the entire
sensitivity to adrenalin;
respiratory care team is of vital importance.
rapid carbon dioxide wash-out after establishment of
(2) alkalosis developing from
764
PART VIII
the airway, resulting in myocardial fibrillation and
tube can be replaced by the nurse on written order of
apnea; (3) cardiac fa i lure resulting in profuse bron
the physician.
chorrhea caused by pulmonary edema and shock.

Other chronjc complications cited by Dailey, Simon,
Young, and Stewalt (1992) include the following:
(1) in
fection at the surgical site, (2) aspiration, (3) aerophagia,

(4) persistent stoma, and (5) tracheal stenosis.
TRACHEOSTOMY TUBES
Metal Tubes
Tracheostomy tubes are of two basic types-metal
and polyvinyl chloride (hard and soft). Metal tubes
Postoperative Mechanical Complications
can be made of either stainless steel or sterling silver
Dislocation of the tube may result from unsatisfactory
and composed of the following three parts: (I) an
nursing care, poor attention to the airway during posi
outer cannula that fits into the tracheal incision,
tioning, or ventilator tubing pulling on the airway. If
(2) an inner cannula that fits into the outer cannula,
the tracheostomy tube tapes are not kept tight and tied
and (3) an obturator. Before the outer cannula is in
with a square knot or if they become loose as a result
serted into the tracheal incision, the obturator is
of cervical emphysema or edema, the tube may be
placed inside. The lower end of the obturator pro
coughed out of the trachea and become lodged in the
trudes from the end of the outer cannula and facili
tissues of the neck and obstruct the airway.
tates its insertion into the trachea. This is the only
Stay sutures are useful in tracheostomy patients
purpose of the obturator. The protruding end of the
when there is the possibility of tube displacement.
obturator obstructs the lumen of the outer cannula.
These sutures are valuable during recannulization of
When the obturator is removed, immediately replace
the tube if it comes dislodged before a tract has been
it with the inner cannula. When dealing with metal
well established. Stay sutures will prevent entry into
tubes, the parts of each set are not interchangeable
a false tract. Advantages of this technique include the
and fit only one particular set. If one part is lost or
following:
(I) blockage or displaced tubes can be
damaged, the entire set is useless. Therefore each
rapidly replaced, (2) exposure of the trachea at surgi
part, including obturator, is accounted for carefully.
cal intervention is improved, (3) firm anchoring of
Plastic tubes generally have interchangeable parts.
the trachea at the moment of incision, (4) decreased
Care should be exercised in handling sterling silver
trauma associated with extubation, and (5) uniform
tubes, since silver is easily dented.
tracheostomy technique for aJJ ages.
Mucus that has dried inside the inner cannula can
Dislodgement of the outer cannula or required re
not be cleaned by merely rinsing in water. The can
moval before a tract has been well established (usu
nula should be soaked in hydrogen peroxide and
ally 5 to 10 days) again requires diligence and quick
scrubbed with a tracheostomy brush and rinsed with
action by the nurse. No attempt at reinsertion should
saline to be sure aJJ secretions have been removed. If
be made without adequate light, satisfactory tissue re
a silver inner cannula becomes discolored, it may be
traction, tracheal hook, and a Trousseau's dilator. A
cleaned with silver polish.
Trousseau's dilator and tracheal hook should be read
The inner cannula should always be inspected to
ily available. A spare tracheostomy tube of the cor
be sure it is clean and clear of secretions before it is
rect size should be kept at the patient's bedside at all

times. Then, should the tube be coughed out, the
reinserted. Be sure to lock the inner cannula in posi

.
tion after reinsertion.
nurse uses the Trousseau's dilator to hold the wound

apart while summoning the physician. Tragedies have
occurred from inserting the tube into the soft tissues
of the neck or mediastinum because of a dislodged
Polyvinyl Chloride (Plastic) Disposable

Tubes and Cuff Inflation
cannula and the frantic efforts to replace it. Once the
The development of plastic tracheostomy tubes came
tracheostomy tract has been firmly established, the
about for the following three important reasons:
42
Care or the Patient With an Artificial Airway
765
(1) application of silicone to the inner sUliace of the
fore insertion of the tube into the trachea to be certain
plastic tube minimizes crusting and adherence of se
that there are no leaks. The Luer valve inflation port
cretions; (2) there is greater ease in attaching a safe,
to the pilot balloon is self-sealing. Some Luer valves
dependable, permanent inflatable cuff to the plastic
have a relief valve when pressure exceeds 25 mm Hg.
tube that cannot slip off and occlude the tracheal

opening; and (3) lower costs allow the tube to be dis
posable. Plastic tubes come with and without cuffs.
The cuffed tracheostomy tube is primarily used in
Cuff Inflation
There are two commonly used methods of cuff infla
conjunction with a positive-pressure ventilator to
tion. These are the minimal air leak, in which a small
form a closed system (Figure 42-1). It is also used to
amount of air escapes on inspiration, and minimal oc
reduce the possibility of aspiration because of absent,
clusive volume, in which just enough air is placed in
protective laryngeal, and pharyngeal reflexes. The in
the cuff to stop air from escaping on inspiration. Ac
flatable cuff is located around the lower portion of
cording to Crabtree Goodnough (1988), the minimal
the tube and, when inflated, seals the trachea from
leak cuff technique may produce less injury than the
most airtlow except through the tube itself (see Fig
minimal occlusive volume inflation technique. Re
ure 42-1). The cuff, usually made of pliable plastic, is
gardless of which technique is used, the pressure of
inflated by injecting air into the fine-bore tubing. A
the cuff should be checked every 4 to 8 hours and the
small pilot balloon is located proximally in the tubing
pressures documented. With continued research and
and indicates that the cuff is inflated. The nurse must
monitoring of tracheal cuff pressures, potential tra
check the inflation end of the cuff and the balloon be
cheal injury can be prevented.
FIGURE 42-1
A, Cuffed adult tracheostomy tubes, uncuffed pediatric tracheostomy tube (far left). B, Cuffed adult
endotracheal tubes, uncuffed pediatric endotracheal tube (far left).
766
PART VIII
Once the cuff is inflated, the only route for air ex
ideall y every 8 hours but at least once every
24
hours.
change is through the patient's tracheostomy tube;
The Communitrache I is a tracheostomy tube that
therefore careful observation of the patient by the
permits the removal of secretions above the inflation
nurse is essential. If the patient is on mechanical ven
cuff without nasotracheal suctioning. The other plus
tilation, observation is essential if there is ventilator
factor to this tracheostomy tube is the patient's ability
failure because asphyxiation may occur. Alarms are
to communicate, especially while on a ventilator.
always in the "on" position when a patient is being
When the patient is weaned from the ventilator, a
mechanically ventilated. Some means of resuscita
fenestrated tube may be used. Fenestrated comes
jenesfre,
tion, such as a manual resuscitating bag with mask,
from the French word
must be available at the bedside to ventilate the pa
There is a window (fenestration) in the outer cannula.
meaning window.
is
tient in case the tracheostomy tube comes out or is
When the tube is used for speaking the cuff
dislodged.
the inner cannula removed, and an external plug is in
down,
Considerable emphasis has been given to the inci
serted to cap the tracheostomy tube to allow the pa
dence of tracheal ischemia and resulting stenosis
tient to speak. The cuff must be deflated when the
from the use of a cuffed tube. This ischemia results
cap is in place. If the cuff was inflated, the patient
from the pressure of the cuffed tube against the tra
would be unable to breathe air into the lungs. The pa
cheal wall, which heals with scar formation, resulting
tient exhibits immediate distress if this mistake is
in subsequent stenosis. This complication can be re
made. If a patient with fenestrated tube needs to be
duced or eliminated by minimal air leak or minimal
suctioned, the inner cannula must be placed so that
occlusive volume. For the minimal occlusive volume,
the suction catheter does not enter the fenestration
the cuff must be inflated to eliminate any air leak on
and cause injury to the tracheal wal.l mucosa.
inspiration. Cuff pressures should be monitored and

documented every
to 8 hours to prevent tracheal in
jury. The recommended cuff pressure is I S to
2S
mm
Other Airway Devices
Hg. Inflate the cuff until there is no air leak between
The Olympic tracheostomy button is used as an in
the wall of the trachea and the cuff, and then release a
terim airway after tracheostomy tube removal (Figure
small amount of air to allow only a slight air leak be
42-2).
tween the walls of the trachea and the cuff. This re
patient from tracheostomy tube but still maintaining
duces the pressure of the cuff, still allows the ventila
the stoma should a tracheostomy be again needed.
This method is another example of weaning a
tor to function properly, and reduces the likelihood of
The patient that benefited most from the procedure
tracheal ischemia. Any difficullY in properly inflating
was the COPD patient. This was one method used to
the cuffed tracheostomy tube should be immediately
facilitate secretion removal after hospitalization when
reported to the physician.
it became necessary because of the disease proces?
If the tracheotomized patient is conscious, he or
The Olympic tracheostomy button allowed the tra
she may attempt to speak. If the cuff is properly in
cheostomy patient the opportunity to reestablish an
flated, he or she will be aphonic, since no air can pass
unobstructed airway and at the same time allowed the
over the vocal cords. If he or she needs to speak, the
patient to speak.
cuff can be deflated, and the patient may be given a
The Passy-Muir valve is used for patients with
sterile dressing to hold over the tube. This will allow
upper airway obstruclion, and with difficult decannu
him or her to speak and also simulate a cough by
lation (Figure
rapid exhalation to clear secretions.
valve, allowing inspiration only and forcing exhala
Inspired air must be continuously and adequately
42-3).
The Passy-Muir is a one-way
tion through the upper airway. By using the valve the
humidified by means of nebulizing equipment to pre
upper airway muscles gradually recover, allowing for
vent the formation of crusts. The equipment used for
transition to a fenestrated tube or a smaller size tra
this purpose can be a possible source of infection.
cheostomy tube and preparing the patient for eventual
Therefore the nebulizer and tubing should be changed
decannulation (Pierson and Kacmarek,
1992).
42
Basic length 27-40
Care of the Patient With an Artificial Airway
mm
-I
FIGURE 42-2
Dimensions and actual positiorung of an Olympic tracheostomy button. (From Pierson OJ and Kacmarek
RM: Foundations of respiratory care, Churchill Livingstone, 1992, Edinburgh David 1. Pierson.)
FIGURE 42-3
The Passy Muir Valve. This valve attaches to a standard lS-mm tracheostomy adapter. It allows
inspriation A, via the valve, but exhilation 8, must occur via the upper airway. (From Pierson OJ
and Kacmarek RM: Foundations of respiratory care, Churchill Livingstone, 1992, Edinburgh
David J. Pierson.)
767
768
PART VIII
Airway Care
Normally, the mucociliary escalator and the cough
reflex provide ajrway clearance. When these mecha
nisms fail, suctioning of the airways is indicated.
Suctioning does have potential hazards, but it should
be a safe procedure with proper guidance and care.
Suclioning
Proper explanation of the suctioning technique to the
patient helps allay apprehension and enhance cooper
ation. Medicate your postoperative patient before
suctioning to decrease the pain of coughing. Always
maintain a calm and reassuring manner.
Maintain aseptic technique throughout the entire
procedure. Use sterile gloves and a sterile disposable
catheter for each suctioning.
Position the patient properly unless contraindi
cated. Nasotracheal and/or pharyngeal suctioning
should be done with the patient in Fowler, 60 to 70
degrees, or semi-Fowler position, approximately 45
degrees, with the neck hyperextended (Figure 42-5).
FIGURE 42-4
The Montgomery T-tube. (Reprinted with permission from
Montgomery WW: Manual care of the Montgovery silicone
tracheal T-tube. The annals of olOlogy rhinology &
lQ/yngology (supplement 73) 89(4): 3,1980.)
The supine position is best for the patient with tra

cheostomy or endotracheal tubes (Figure 42-6).
Pharyngeal suctioning may be necessary before de
flating the cuffed tracheostomy tube. The nurse should
not suction the pharynx and then the trachea with the
same catheter, but the trachea may be suctioned first
and then the pharynx with the same catheter.
Duration of suctioning is of extreme importance.
Each suctioning procedure should last no longer than
The management of major airway obstruction
5 to 10 seconds to avoid hypoxia.
by tracheal tumor, external compression, or tra
Prolonged suctioning may result in precipitating a
cheal disease below the thoracic inlet still present
dysrhythmia or cardiac arrest. A good way to judge
difficult problems. The Montgomery T tube is a bi
the elapsed time is to hold one's
furcated silicone rubber stent designed to preserve
guided by the development of discomfort. This is
patency of the airways in a patient with injury to
most important for the patient who depends on venti
the trachea or main bronchi (Figure 42-4). When
latory assistance.
OWIl
breath and be
the T tube is in place, the patient breathes normally
The lowest possible vacuum settings are to be llsed
through nose and mouth and can speak. The T tube
(below 120 mm Hg) that will still support suctioning
is a method in which secretions can be removed if
the tracheostomy tube. The higher the setting is
necessary and is helpful in long-term therapy to al
raised, the greater the risk of trauma to the tracheal
l e v i a t e o b s t r u c t i o n or d u r i n g r e c o n s t r uctive
mucosa. Caution should be exercised to avoid kinking
surgery. This device does not cause any adverse
the suction tubing or catheter. When negative pressure
tissue reaction on a long-term basis, according to
is excessive and released suddenly, inadvertent re
Montgomery.
moval of portions of tracheal mucosa may occur.
42
. t With
.
an Artificial Airway
Care 0 f the Pahen
Fowler 60-70 degrees
Seml-Fowler 10- 12"

.
FIGURE 42-5
A, Fowler ' s an
, dB, Semi-Fowler's positions.
FIGURE 42 6
Supine posillon,
769
770
PART VIII
)(
FIGURE 42-7
The catheter will simulate coughing when it contacts the carina (in a patient with cough reflex).
FIGURE 42-8
The catheter is withdrawn I cm after it reaches the carina, before applying suction.
42
771
Insertion of the suction catheter should be done
Right main-stem bronchus aspiration is the usual
gently, using aseptic technique and sterile gloves.
case because of the more direct alignment of this
Goggles are used as part of universal precautions if
bronchus with the trachea. This can be carried out al
there is any danger of coughed-ollt secretions. The
most always with a straight tracheal catheter.
catheter should first be moistened in sterile saline or
Excessive suctioning can be harmful. Use judg
with a water-soluble gel. Suction is not applied while
ment to determine just how often a patient requires
the catheter is passed down into the trachea. Proper
suctioning. Auscultation by stethoscope should be
insertion of the catheter will stimulate coughing when
used to determine the thoroughness of suctioning.
it contacts the carina (Figure 42-7). It is then immedi
Suction only when it is needed (Carroll, 1994). Allow
ately withdrawn I cm before suction is applied (Fig
the patient to rest and breathe between each insertion
lire 42-8). Do not force the catheter lip and down
of the suction catheter and, if necessary, ventilate him
while suctioning. Suction is applied only while the
or her for few minutes before further suctioning. Re
catheter is being wi thdrawn. Rotating the catheter
member each suctioning attempt removes air as well
during withdrawal results in suctioning a larger area
as secretions. Hyperoxygenation and hyperinflation
and increases the surface contact of the trachea and
with 100% oxygen has been suggested with better re
tracheostomy tube (Figure 42-9).
sults and fewer complications. Complications from
Left main-stem bronchus aspiration is more diffi
tracheal suctioning include the following: (l) hypox
cult because of the anatomical arrangement of the
emia, (2) cardiac dysrhythmia, (3) bronchospasm,
bronchus. It was formerly thought that left bronchial
and (4) infection. Suctioning can lead to hypoxemia
aspiration was facilitated by turning the patient's
because oxygen is removed from the airways, and
head to the right. Studies by Kirimli et al. (1970) and
this could lead to tissue hypoxia. To minimize this
Panacek et II. (1989) indicate that left bronchial aspi
problem, preoxygenation is recommended. This can
ration is best accomplished by using a Coude tip
be done by hyperinflating the patient with Ilf2 times
catheter. After its insertion into the trachea. the
their normal tidal volume on a ventilator and hy
curved tip should be positioned to point toward the
perox-genating with 100% oxygen for 3 to 5 breaths.
left main-stem bronchus. Even so, insertion is diffi
Cardiac dysrhythmias, such as premature ventricular
cult, and auscultation by stethoscope is necessary to
contractures, bradycardia, and tachycardia, can be di
thoroughly access the suctioning.
minished by hyperinflating and hyperoxygenating the
To suction unit
Connection
Detall
Air vent I
Catheter
FIGURE 42-9
The catheter is rotated during withdrawal in order to suction a larger surface area.
772
PART VIII
patient with 100% oxygen. If any dysrhythmias occur
18. Discard used equipment and remove gloves.
on the monitor, the suctioning procedure should be
19. Wash your hands.
discontinued. Bronchospasm may be effectively pre

vented by a few puffs of a bronchodilator, such as al
buterol, to the tracheostomy tube before suctioning.
Nasopharyngeal Airways
Infection can be decreased by maintaining sterile
When frequent, aggressive nasopharyngeal suction
technique with sterile gloves and sterile catheters
ing is indicated in a semicomatose patient, a nasopha
when suctioning.
ryngeal airway (NPA) will lessen the trauma of fre

quent passage of the catheter. The NPA is a soft latex
material that provides easy access to the trachea for
Suctioning Artificial Airway

Nasotracheal, Endotracheal, and Tracheostomy
I. Check equipment, be sure you have all necessary
equipment and maintain sterile field.
nasopharyngeal suctioning. The nasal and pharyngeal

mucosa are protected and the procedure thus becomes
more co mfortable to the patient. In addition, a
fiberoptic bronchoscope may be passed through the
2. Check monitors.
airway if the procedure is indicated.
3. Wash your hands.

4. Inform patient of the procedure.
5. Hyperoxygenate with 100% oxygen for three to
five breaths with manual resuscitation bag.
Endotracheal or Tracheostomy Suctioning

The procedures are the same except sterile technique
6. Place patient's neck in extension.
is followed and no lubrication is usually necessary,
7. Put on sterile gloves.
although it may be used if there is difficulty passing
8. Lubricate catheter with sterile saline or water
the catheter.
soluble gel.
9. Place catheter (without suction) upward and
backward in short increments. Continue until an
obstruction (the carina) is reached.
Sterile Suctioning
The technique for correct sterile suctioning of artifi
10. When the carina is stimulated, the patient will
cial airways is perhaps the most important and vital
generally cough un less his or her reflexes are
segment of care for the patient because it removes se
obtunded.
cretions that would otherwise obstruct the airway. If
11. The catheter should be pulled back slightly, from

the carina, then suction applied with no more
than 120 mm Hg pressure as catheter is with
drawn in a rotating motion.
suctioning is not performed properly, it can cause

physiological or psychological trauma to the patient.
The equipment necessary for proper sterile suc
tioning includes proper mechanical apparatus, con
12. The aspiration time should be within 10 to 15 sec
necting tubing, sterile gloves, sterile saline, suction
onds total. (A good guideline is for the therapist to
catheters, dressings, and goggles as indicated with
hold his or her breath during suctioning as the pa
universal precautions. While suctioning the patient, it
tient is also not breathing. This gives the therapist a
should be remembered that the patient's only air pas
better sensitivity for what the patient experiences.)

13. The patient should be allowed to rest for several
seconds and again be preoxygenated.
sage is being partially occluded. Thus the suction

catheter should never be larger than one half the di
ameter of the tube opening; if it is larger, it may com
14. Check the patient's breath sounds and repeat the

procedure if necessary to remove more secretions.
15. Suction pharynx.
pletely occlude the patient's air passage.

One method of determining the size of the catheter
used for suctioning is to double the size of the tra
16. The monitor is to be watched for any dysrhytlunias.
cheostomy tube in place and add two. For example, if
17. Pulse oximetry is to be used for indications of
the patient has a #6 tube, the calculation would be as
desaturation.
follows: 6 + 6
12 + 2
14. Therefore a 14-fr catheter
42
773
the trachea or large bronchi is usually indicated by
TABLE 42-1
coarse rattling sounds. Fine bubbling sounds usually
The Pediatric Trach Card

TRACHEOSTOMY SIZE
suggest fluid located more peripherally (i.e., in the

alveolar spaces). If accumulated secretions are not
RECOMMENDED
CATHETER SIZE
cleared, they can cause respiratory and cardiac rates

to increase; effective oxygen and carbon dioxide
Pediatric Tubes
transfer is impaired causing cyanosis to appear and
6.S FR
6.S FR
8FR
8FR
10 FR
IOFR
OOPT
OPT
I PT
2 PT
3 PT
4 PT
low-grade fever to develop.
Extubalion/Decannulalion
Extubation or decannulation is the removal of the ar
Neonatal Tubes
tificial airway. The patient is helped to gradually re
00 NT
ONT
I NT
learn normal breathing through his or her upper respi
6.S FR
6.S FR
6.S FR
ratory tract before the tube is removed. This can be a

time of considerable fear and anxiety for patients be
cause they have learned they can breathe safely
SCT-Single Cannula Tracheostomy Tubes
S seT
6 seT
7 seT
8 seT
through their tracheostomy, and they may become
10 FR
12 FR
14 FR
14 FR
apprehensive when asked to breathe in a normal man

ner. The relearning process can be accomplished
under the physician's direction by reducing the lumen
of the tube for a day or two or by partially obstructing
Reprinted with permission of Janetti Publications, Inc., publisher
Pediatric Nursing,
Volume
20,
Number
2,
(March-April,
1994).
the tube's outer opening for increasing lengths of

time. Eventually, the patient is able to tolerate the
complete occlusion of the tracheostomy opening.
This is sometimes difficult and similar to breathing
through a straw.
would be the largest catheter that could be used to suc
When occluding the tracheostomy opening with a
tion the #6 tracheostomy. See Table 42-1 for a correla
cuffed tube, the cuff must be deflated first. Failure to
tion of tracheostomy sizes to catheter sizes.
do this will result in total obstruction of the patient's
The catheter used for pharyngeal suctioning
airway as the tube opening is occluded.
should never be used for subsequent suctioning of the
Fenestrated tubes have also been excellent for
artificial airway, but using an artificial airway suction
weaning the patient from the tracheostomy tube. Ac
catheter for pharyngeal suction is acceptable. Aseptic
tually, they do not increase the airway resistance as in
technique is absolutely necessary to minimize the risk
the above method and are probably more effective.
of infection and, ideally, only disposable catheters
They also allow the patient to talk and attempt to

cough to mobilize secretions. Other methods used in
should be used.
Suctioning may be necessary every few minutes
decannulation include the Olympic tracheostomy but
when the patient initially returns from surgery be
ton and the Passy-Muir valve. The Olympic tra
cause there is an increase in secretions, which usually
cheostomy button allows the airway to remain patent
results from irritation of the endotracheal tube plus a
for suctioning and reinsertion of a tracheostomy tube
reflex mechanism initiated by the surgical trauma.
should it become necessary. The Passy-Muir valve
Usually by paying attention to the patient's color, res
allows for normal recovery of the upper airway mus
piratory rate, lung sounds, and oxygen saturation on
cle, making it possible to reduce the size of tra
pulse oximetry, the nurse or therapist can determine
cheostomy tube leading to eventually plugging and
the amount of secretions present. Excessive mucus in
decannulating. Careful observation and documenta
774
PART VIII
tion of the patient's ability to ventilate must be done

when either of these devices are used in the decannu
lating process.
Goodwell, EW. (1':)34). The story of
trach"ostolll)'.
Srilish .Iour
l1al of ('hildren '.\' iJi.l'l'{/se.l', 31(367-36')),167-176.

Goodwell, E.W. (1934). The story of tracheostomy. Srilish Jour
nal of Children's Diseases, 31(370-372),253-27 I.
Close supervision should continue after extuba
Jackson,
tion. After a tracheostomy tube is removed, the skin
Jackson,
C (1909). Tracheostomy. Laryngoscope, 18,285-290.

C (1921). High tracheostomy and other errors. The chief
edges are usually taped together with butterfly strips
causes of chronic laryngeal atenosis. Surgery, CynecoIOfi.Y, Ob
for a few days until the wound heals. While healing,
slelrics, 32, 392-395
air will escape through the wound and reduce the ef

fectiveness of the patient's cough. The patient should
be instructed that the noise from the partially closed
trachea is normal and small secretions should be re
moved from this area. The patient should be taught to
hold a sterile dressing firmly over the incision when
coughing until the opening healed.
&
Jackson, D.,
Albamonte, S. (1994). Enhancing communication
with the Passy-Muir valve. Pedialric Nursing, 20,(2),149-153.
J .A. (1980).
Kirchner,
Tracheostomy and its problems. Surgical
Clinics ofNorih America, 60,(5), 1093-1104.
lE., &
Kirimli, B., King,
Pfaeffle, H.H. (1970). Evaluation of tra
cheobronchial suction technique. Journal of Thoracic and Car
59, 340-344.
OJ., & Tyler, ML (1993).
diovascular Surge!)"
Lull,
J.M,
Pierson,
Methods of Air
way Maintenance. In Inlellsive respiralOry care. Philadelphia:

WB Saunders.
S., &
Mocaluso,
REVIEW QUESTIONS
I. What physiological changes occur with surgical
placement of tracheostomy tube?
with a tracheostomy.
List information that you would include in a
teaching plan for the tracheostomized patient.
4.
How does the patient care team prepare the tra
silicone tracheal T-tube. Annals of OlOlof!)" Rhinology and

Montanari,
1., &
Spearing,
C (1986).
Of measuring tracheal curf
pressure. Nursing, 86(7),46-49.

Noll, M.L., Hix, CD"
&
Scott, G. (1990). Closed tracheal suction
systems: effectiveness and nursing implications. In ArlCN clin

ical issues in crilical care nursing. Philadelphia: JB Lippincott.
Panacek, E.A., Albertson, T.E., Rutherford, W.F., Fisher,
C.J., &
Foulke, G.E. (1989). Selections left endobronchial suctioning
cheostomized patient for self care?

Compare emergency care, acute care, and long
5.
Montgomery, W.W. (1989). Manual of care or the Montgomery

La!)'ngology (Supp. 73),89(4),3.
2. Discuss possible psycosocial concerns of patients

3.
Roman, M. (1994). Managing post-intubation in
juries. Medsurg Nursing, 3(3),192-202.
term care for a patient with upper airway ob

struction and tracheostomy placement.
of the intubated patient. Chesl, 95,885-87.
C (1991).
Patton,
Reviews for Ihe

Pierson,
OJ., &
The critical airway classic problems. CurrenI
p(1S! Aneslhesia Care NI/rses, 13(5),33-40.
Kacmarek, R.M. (1992). In Foundalions of respi
ralory care. New York: Churchill Livingstone.

Roberts,
References
J.T. (1994).
In Clinical Management of the Airway,
Selecky, P. (1974). TraCheostomy-a review of present day indica
Carroll, P. (1994). Safe suctioning PRN. RN, May. 32-37.

Class, P. (1992). Nursing considerations for airway management in
the PAC U . Currenl Reviews for POSI Aneslhesia Care Nurses.
14(1),1-8.
tion, complications and care. Hearl Lung, 3. 272.

Tr acheoslomy lUbe a d u l l homecare guide. (1993). Irvine:
MaLlinckrodt Medical TPT.
Traver,
Crabtree Goodnough, S.K. (1988). Reducing tracheal injury and

aspiration. Dimension of Crilical Care Nursing, 7(6),324-331.
Dailey, R.H., Simon. B., Young, G.P.,
&
Stewart, R.D. (1992).
l.A.,
Mitchell, IT.,
&
Flodquist-Priestly,
Gaithersberg, Md.: Aspen Publishers.

Traver,
J.A.,
Mitchell,
IT, &
Flodquist-Priestly, G. (1991). Suc
Airway maneuvers. In The airway emergency management. St.
lioning. In RespiraIO!), care: a
Louis: Mosby.
Md.: Aspen Publishers.
Frost,
E.A. (1976). Tracing

85, 618-624.
the tracheostomy. Annals of OlOlaryn
Warnoch,
C, &
clinical approach.
Gaithersberg,
Porpora, K. (1994). A pediatric tmche card: trans
fonning research into practice. Pediatric Nursing, 20(2), 186-188.
gology,
Funllll, N.D, Dutcher, P.O.,
d. (1991). Artifi
cial airway care. In RespiralOry care: a clinical approach.
&
Roberts,
J.K. (1993).
The safety and
Weilitz, P.B.,
&
Dertenrneier,
P.A. (1994).
Back to basics test your
efficacy of bedside tracheostomy. OlOlaryngology-Head alld
knowledge of tracheostomy tubes. American Journal of Nurs
Neck Surgery, (109),707-711.
ing, 94(2),46-50.
Respiratory and Cardiovascular

Drug Actions
Arthur V. Prancan
KEY TERMS
Adrenergic drugs
Corticosteroids
Antihistamines
Functional reflex
Cardiovascular reflex
Metered dose inhalers
Carotid baroreceptors
Mucolytics and expectorants
Cholinergic blocking drugs
Sympathomimetic drugs
Cholinergic drugs
Xanthines
INTRODUCTION
Before a drug can be used effectively, the system
The respiratory and cardiovascular systems have
it is to modify must be understood. How the mecha
many built-in mechanisms for controlling their func
nism of the drug action relates to the biological sys
tions during health and disease. In healthy individu
tem must be clear before an effect can be predicted.
als, both systems act quickly and positively to main
This chapter describes much of the basic respira
tain proper functioning under the most complicated
tory and cardiovascular physiology that underlies the
conditions. Even during trauma or disease, these sys
action of the drugs presented. Hopefully, the relation
tems often overcome distress and regain normal func
ship between basic physiology and the drug mecha
tion. The physiology of respiration or circulation is
nism of action is also evident.
sometimes altered by a disease so that the homeosta
All pharmacological interventions for the respi
tic mechanisms are no longer effective. In such a
ratory and cardiovascular systems are not covered.
case, a drug with the appropriate action becomes nec
Certainly no attempt has been made to describe the
essary to restore normal physiological function.
pharmacology of other systems or disease states.

775
776
PART VIII
For further study, one of the books listed in the ref
tagonistic action of the two components of the auto
erence section at the end of the chapter is highly
nomic nervous systcm.

Some organs, however, have only one innervation.
recommended.
Much of the arterial blood vessel network is con

trolled only by sympathetic nerves. Also, gastric se
AUTONOMIC PHARMACOLOGY
cretion and gastric motility are primarily regulated by
This section introduces the basic aspects of drug action
one system-the parasympathetic.
related to both components of the autonomic nervous

system-the sympathetic and parasympathetic nervous
systems. For both systems, synthesis, storage, and re
lease of the chemical neurotransmitter are described to
SYMPATHETIC NEUROTRANSMISSION
Sympathetic nerves transport impulses from the vaso
emphasize the places in the metabolical scheme where
motor center in the medulla of the brain through the
drugs can intervene. The sites of action for the adrener
spinal cord and out to the smooth muscle, heart mus
gic (sympathetic) and cholinergic (parasympathetic)
cle, and secretory cells. These tissues have receptor
transmitters and blockers is also described.
sites that will accept the norepinephrine released
The autonomic nervous system controls all of the
from the nerve ending. Norepinephrine, also called
bodily functions over which you have no voluntary
noradrenalin. is synthesized in the nerve ending only
control, and perhaps which you might not control as
in the sympathetic neurons. It is stored in the terminal
well if you had the opportunity. The functions in
until an electric impulse reaches the terminal, then it
clude regulation of respiratory airway diameter, res
is released into the synapse.
piratory secretions, blood vessel diameter, heart rate,
The norepinephrine molecule attaches to a recep
intestinal motility, pupil size, and many others. It is
tor molecule on a cell sUlface in the immediate vicin
easy to see that it might take more than the talents of
ity of its release. This drug-receptor combination
a well-trained expert to keep an active person func
causes a biological change, such as stimulation of the
tioning day and night.
pacemaker cells in the heart to fire more frequently
The sympathetic nervous system is the half of the
(increased heart rate). The effect is terminated when
autonomic system that takes a dominant role in the
the norepinephrine is reabsorbed into the nerve termi
cardiovascular and respiratory systems when some
nal. About 90% of the released norepinephrine is
sort of bodily activity is necessary. This includes ac
taken back into the neuron. There, it is either restored
tions such as increasing ventilation capacity, elevat
into granules for future release or it is destroyed by
ing blood pressure, and shunting blood flow to the
the enzyme monoamine oxidase (MAO).
skeletal muscles. Classically, the sympathetic compo
There are two types of sympathetic receptors
nent of the autonomic nervous system has been called
alpha and beta. The alpha-receptor is found in the
the fight-or-t1ight system. The other half of the auto
arterioles, and the beta-receptor is found in the arte
nomic system is called the parasympathetic nervous
rioles, heart, and bronchioles. Stimulation of the
system. It is most important in maintaining the less
alpha-receptor in the arteriole causes vasoconstric
exciting functions of the body like digestion, saliva
tion that results in increased blood pressure. The
tion, and urination. In some organs the two systems
beta-receptor in the arterioles causes vasodilation
work against each other to provide very fast and very
and a lowered blood pressure. Some drugs stimu
fine control. For example, the size of the pupil re
late both receptors, and in those cases the effect
sponds quickly to a change in light intensity. The
will be determined by the degree of alpha or beta
parasympathetic system actively functions to de
activity of the drug. An example is norepinephrine.
crease the size of the opening while the sympathetic
It has 90% alpha activity and 10% beta activity, and
system relaxes, thereby causing a quick decrease in
it always causes vasoconstriction. Epinephrine is
pupil size. If the light is turned down, the opposite
50% alpha and 50% beta and may cause a rise or
occurs just as fast. This is a good example of the an
drop in blood pressure.
43
Stimulation of the beta-receptor in the heart results

in increased heart rate (beats per minute) and in
Respiratory and Cardiovascular Drug Actions
777
Epinephrine (Adrenalin)
Epinephrine (Adrenalin) is also a mixed activity drug
creascd stroke volume (number of milliliters of blood
(50% alpha, 50% beta). It is naturally produced in the
the left ventricle pumps out into the aorta every time
adrenal medulla and can be released during sympa
it contracts). Incidentally, the combination of these
thetic nervous system activation. When this occurs, it
two changes (heart rate [HR] x stroke volume [SV])
acts as a circulating hormone, stimulating both alpha
is another way of saying cardiac output (CO) (milli
and beta-receptors. This drug wi II increase heart rate
liter of blood pumped per minute):
and stroke volume and may slightly increase or de
beats/min(HR) x mllbeat(SV)
crease total peripheral resistance at the arterioles. In
mllmin(CO)
any case, cardiac output always goes up; blood pres
This expression, cardiac output, is a common one

and it constitutes half of the blood pressure regulation
equation: CO x TPR
BP, where CO is cardiac out
sure may go up or down slightly.

In the bronchioles, epinephrine exerts a dramatic
dilating effect that is mediated by the beta-receptor.
put, TPR is total peripheral resistance, and BP is
Epinephrine can be administered by inhalant aerosol
blood pressure. Total peripheral resistance is deter
to reverse a bronchoconstrictive episode. It is also
mined by vasoconstriction or vasodilation in the arte
administered intramuscularly and subcutaneously to
rioles. Vasoconstriction increases resistance so TPR
treat asthma, anaphylactic reactions to an allcrgic re
and BP goes up.
sponse, cardiac arrest, heart block, and as a mild
Stimulation of smooth muscle beta-receptors will

relax these tissues wherever they are found. Respiratory
airway smooth muscle will decrease tension when the
beta-receptor is activated by beta-acting drugs like epi
vasoconstriction to keep local anesthetics at the in

jection siteo
Isoproterenol (Isuprel)
nephrine or isoproterenol. The functional result will be
Isoproterenol (lsuprel) is a synthetic compound that
an increase in air flow because of a larger airway diam
has 100% beta activity. This means that it can in
eter. Likewisc, blood vessels respond to beta-acting
crease heart rate and stroke volume to produce a great
drugs by increasing in diameter, allowing a greater rate
rise in cardiac output, and it stimulates the beta-recep
of flow. In this case, TPR has decreased and blood
tor on the arterioles to effect a profound vasodilation.
pressure will drop.
The final result can be a high cardiac output with low

blood pressure. This drug improves blood circulation
in shock patients by increasing local blood flow (va
Adrenergic Drugs
sodilation) and elevating cardiac output. Isoproterenol

is considered very useful for treating acute asthmatic
Norepinephrine (Levarterenol, Levophed)

As
mentioned
previously,
conditions because of its bronchodilating action.
n o repinephrine
(Levarterenol, Levophed) is a mixed-activity drug
(90% alpha, 10% beta). It stimulates beta-receptors in

the heart, which results in an increase of heart rate
Phenylephrine (Isophrin, Neo-Synephrine)

and Metaraminol
Both phenylephrine (lsophrin, Neo-Synephrine) and
and stroke volume (increased cardiac output). In the
metaraminol are powerful and prolonged stimulators
arterioles, norepinephrine causes vasoconstriction via
of alpha-receptors. The action is directly on the re
the alpha-receptor, resulting in increased total periph
ceptor site itself. The response to the administration
eral resistance. The total effect, of course, is an in
of either of these drugs is a rise in blood pressure be
crease in blood pressure. Norepinephrine has little ef
cause of vasoconstriction accompanied by a reflex
fect on the bronchioles. This drug is given only
bradycardia, which causes a decrease in cardiac out
intravenously, and it can be used clinically to raise
put. Reflex alterations of cardiovascular function are
blood pressure. The natural sympathetic compounds
explained later in this chapter. The primary useful
are known as catecholamines.
ness of these drugs is in various hypotensive states.
778
PART VIII
Phenyle phrine is used as a nasal decongestant and
asthma. The drugs are metaproterenol (Alupent,
mydriatic and for the relief of paroxysmal atrial
Metaprel), terbutaline (Brethine, Bricanyl), albuterol
tachycardia. Phenylephrine affords relief from the
(P r o v e n t il, Ven t o l i n ), i s o e t h ar ine ( B r on kosol,
tachycardia because it increases blood pressure and
Bronkometer), and salmeterol (Servant).
evokes the cardiovascular reflex that is marked by

high vagal tone and bradycardia.
Alpha-Adrenergic Blocking Drugs
Ephedrine
Phentolamine (Regitine)
Ephedrine has both alpha and beta activity as direct
Phentolamine (Regitine) is a competitive alpha-receptor
effects and it also causes release of epinephrine and
blocker. Its action is reversible. This drug prevents the
norepinephrine. Its pharmacological actions are simi
hypertensive effect of norepinephrine, and it reverses
lar to epinephrine, with the main exception that dura
the blood pressure elevating effect of epinephrine (epi
tion of action of ephedrine is longer. Ephedrine in
nephrine reversal). Epinephrine reversal looks like an
creases cardiac o utput and vascular resistance,
isoproterenol effect with high cardiac output and low
resulting in increased blood pressure. Ephedrine also
blood pressure. Phentolamine may be used clinically as
causes bronchial muscle relaxation, which is less po
a vasodilator. It is also useful as a clinical diagnostic
tent than that of epinephrine but has a longer duration.
agent in evaluating hypertensive patients who may
This drug is useful in controlling milder cases of bron
have pheochromocytoma, which is a tumor that grows
choconstriction that require long-term drug therapy.
in the gastrointestinal chromaffin tissue. The tumor pro
Amphetamine (Dextroamphetamine, Dexedrine)

Amphetamine (Dextroamphetamine, Dexedrine) drug
has pharmacological properties related to the cate
cholamines because it causes release of norepinephrine
duces epinepJu'ine and norepinephrine and may be re

sponsible for one aspect of a clinical hypeltension.
Phenoxybenzamine (Dibenzyline)
Phenoxybenzamine (Dibenzyline) is also an alpha
from the nerve terminal. Amphetamine has both alpha
adrenergic blocki ng agent. It has effects similar to
and beta-receptor activity, although indirectly, through
phentolamine in the cardiovascular system but it is
its release of norepinephrine. The usual cardiovascular
less reversible. This drug is gaining some usefulness
response is an increase in blood pressure often accom
in the treatment of shock syndromes characterized by
panied by a reflex bradycardia. Amphetamine also has
high vascular tone.
potent central nervous system (CNS) activity. It is a

stimulant of the medullary respiratory center, and it
can antagonize drug-related central nervous system de
Prazosin (Minipress), Doxazosin (Cardura), and

Terazosin (Hytrin)
pression. Respiratory depression often accompanies
Prazosin (Minipress), doxazosin (Cardura), and tera
overdoses of CNS depressant drugs and this effect may
zosin (Hytrin) are selective for arterioles and venules
be overcome by amphetamine. This drug is usually
and are the most useful against hypertension of the
used for its central nervous system effects and not for
drugs in this class. Although they act by vasodilation,
peripheral cardiovascular or respiratory effects.
these drugs exert minimal reflex tachycardia because

they do not potentiate the vasomotor center and the
BetarReceptors Stimulants
increased venous capacitance reduces venous return
There are several drugs that act primarily at the beta2
and cardiac output.
smooth muscle receptor site, causing selective actions

in the bronchioles and arterioles but not in the heart.
Thcse drugs will produce a bronchodilation without
increasing cardiac output. This particular lack of car
Beta-Adrenergic Blocking Drugs
Propranolol (/nderal)
diovascular effect makes them safer than isopro
Propranolol (Inderal) is a beta-adrenergic blocker. This
terenol or epinephrine in treatment of bronchial
drug occupies the beta-receptor sites of the heart, the
43
blood vessels, and the bronchioles. It prevents the beta
779
crease in catecholamine response to sympathetic stim
adrenergic effect usually seen with drugs like epineph
ulation. Blood pressure in humans does not drop dra
rine, norepinephrine, and isoproterenol. In the arteri
matically with therapeutic doses of reserpine, but when
oles, when epinephrine is given after propranolol, the
reserpine is used in combination with diuretics or other
usual mixed alpha and beta effect is eliminated, leav
antihypertensive agents, a significant antihypertensive
ing only an alpha-adrenergic action. This causes pro
effect is obtained. Reserpine is used in this way to treat
found vasoconstriction, allowing greater increase in
essential hypertension. One serious side effect related
blood pressure than is normally seen with epinephrine
to reserpine use is the behavioral modification that can
alone. In the heart the beta-receptors are blocked and,
result in severe depression and suicide.
since there are no alpha-adrenergic receptors in this

organ, all effects of catecholamine drugs on the heart
Guanethidine (Ismelin)
are effectively eliminated, allowing the vagal influence
Guanethidine (Ismelin) is an adrenergic neuron
on the heaJ1 to predominate. Propranolol decreases the
blocking agent that works by replacing norepineph
heart's requirement for oxygen because it blocks the
rine in the nerve terminal. Norepinephrine is usually
cardiac stimulant action of norepinephrine. In the res
taken up by the nerve terminal after its discharge and
piratory system the administration of propranolol re
i s r e u s e d to m a i n t ain g r a n u l e c o n c e n t r a t i o n s .
sults in bronchoconstriction. This effect is increased
Guanethidine takes the place o f norepinephrine i n the
dramatically in patients who are susceptible to asthma.
granules and prevents the reuptake of norepinephrine,
The main use for propranolol is in conditions related to
thereby causing its metabolism outside of the neuron
hypertension and tachycardia, where a decrease in car
and its eventual depletion. The result on the cardio
diac output is beneficial.
vascular system of this action is postural hypoten
Metoprolol (Lopressor) and Atenolol (Tenormin)
sion. The patient is unable to control blood pressure

by sympathetic activity. This drug is used in treat
Metopolol (Lopressor) and atenolol (Tenormin) are
ment of severe hypertension, usually after diuretics
beta-adrenergic antagonists that have been designed
and reserpine are shown to be ineffective.
to be cardioselcctive. This offers an advantage in

safety when a beta-blocker must be used in asthmatic
patients, in whom this disease would be aggravated if
Methyldopa (Aldomet) and Clonidine (Catapress)

Methyldopa (Aldomet) and c10nidine (Catapress) de
respiratory beta-receptors were blocked. The natural
crease the activity of the sympathetic nervous system
beta-adrenergic agonist, epinephrine, is bronchodilat
at its control center in the brain. The consequence is a
ing, and an important class of bronchodilating drugs
total decrease in sympathetic activity in the heart and
acts at bronchiolar beta-adrenergic receptors.
blood vessels leading to a reduction in blood pressure.
SympatholytiC Drugs
PARASYMPATHETIC NEUROTRANSMISSION
Reserpine
The center for parasympathetic control is the vagal
Reserpine is an alkaloid of Rauwolfia serpentina, also
nucleus in the medull a . T h e vagus nerves p a s s
known as the Indian snake root plant. There are many
through t h e spinal c o r d a n d out to t h e heart, the
commercial preparations of this compound, but it is
smooth m u s c l e , and e x o c r i n e g l a n d s ( s a l i v a r y
widely sold as the simple plant extract. This compound
glands and pancreas). In all of these tissues, acetyl
depletes norepinephrine from the nerve endings in the
choline is released from the nerve terminals and
various tissues of the body that produce and store nor
combines with receptor sites to cause an effect such
epinephrine, including the brain. The depletion takes
as bradycardia (slowing of the heart) or an increas
several days to accomplish, and it may take several
ing gastric motility. Acetylcholine is found in many
weeks to restore catecholamine levels to normal after
parts of the central and peri pheral nervous system.
therapy is discontinued. During this time, there is a de
Acetylcholine is the only transmitter used in the
780
PART VIII
Related Aspects or Cardiopulmonary Physical Therapy
parasympathetic system. It is used to transmit im
acid and choline. The acetic acid is washed away for
pulses from the nerve that comes out of the spinal
further metabolism, and the choline is reabsorbed into
cord to the nerve that finally reaches the cells in the
the nerve terminal for resynthesis to acetylcholine.
organ being affected. This connection is called a gan

glion and exists in both sympathetic and parasympa
thetic systems. Acetylcholine is also the neurotrans
m i t t e r t h a t m a k e s t h e c o n n e c t i o n b e t w e e n the
voluntary (somatic) nerves and the skeletal muscle.
There are two types of receptors in these systems.
Cholinergic Drugs
AcetylchOline
Acetylcholine is the endogenous cholinergic trans
mitter that accounts for nicotinic and muscarinic ac
Acetylcholine affects both, but some drugs affect only
tions within the autonomic nervous system. It is
one and not the other. The two types of receptors are
rapidly hydrolyzed by acetylcholinesterase and the
called nicotinic and muscarinic. They are named after
nonspecific cholinesterase and therefore has a short
the drugs that selectively stimulate them. Nicotine
duration of action if administered parenterally. This
stimulates only those receptors in the ganglia and at
makes acetylcholine (ACh) a poor drug. Nicotinic ef
(I) stimulation of parasym
the neuromuscular junction. The muscarinic receptor
fects of acetylcholine are
site is found everywhere a parasympathetic nerve ter
pathetic ganglia, causing occurrence of all muscarinic
(2) stimulation of sympathetic ganglia, caus
mjnal synapses at a tissue. The biological effects usu
effects,
ally attributed to the parasympathetic nervous system,
ing increase in vascular resistance and cardiac output
such as bradycardia, salivation, and bronchoconstric
to produce hypertension, and (3) stimulation of the
tion, for example, are produced when the muscarinic
neuromuscular junction (NMJ) at the skeletal muscle
receptors are stimulated. Of course, it is also possible
(muscle contraction and movement). Muscarinic ef
to stimulate muscarinic receptors indirectly with a
fects of acetylcholine are bradycardia, salivation, pin
nicotinic drug by activating the parasympathetic gan
point pupils, bronchial constriction, gastric and in
glia. In fact, in a sirilliar way, it is possible to stimulate
testinal hypermotility, increased gastric acid and
the entire sympathetic nervous system. The neuro
mucous secretion, and facilitated urination. Toxic ef
transmitter at the sympathetic ganglia is acetylcholine
fects of cholinergic stimulation include diarrhea, uri
and it affects nicotinic receptor sites there. One of the
nary incontinence, bradycardia, bronchoconstriction,
toxic effects of acetylcholine and drugs that act like it
excessive salivation, CNS excitement, and respiratory
is hypertension with tachycardia because of stimula
collapse. In all of these toxic effects, atropine, a com
tion of the sympathetic postganglionic fibers.
petitive muscarinic blocker, is the antidote of choice.
To better understand the action of acetylcholine

and related drugs, let us consider the synthesis, re
lease, and inactivation of this transmitter. Acetyl
Bethanecol (Urecholine)
Bethanecol (Urecholine) is a synthetic choline ester
choline is synthesized inside the nerve terminal from
that is not destroyed as easily as acetylcholine by
acetyl-CoA and choline. The acetylcholine is then
cholinesterase enzymes. It is useful in treating patients
stored in granules and is released out into the synapse
with urinary retention and paralytic ileus, and it is ad
when an action potential reaches the terminal. The
ministered orally or subcutaneously. The side effects
acetylcholine molecule attaches to a receptor site,
and toxicities for this drug are exactly those for ACh.
muscarinic or nicotinic, or to the enzyme that breaks it
However, since the drug is not given intravenously,
apart. Combination with the receptor site results in bi
cardiac and respiratory effects are minimized.
ological action, and coupling with the enzyme ends in

destruction. The enzyme, acetylcholinesterase, is
Carbachol (Carcholin)
found at all cholinergic synaptic sites. A nonspecific
Carbachol (Carcholin) is a mixed nicotinic and mus
variety of the enzyme is also prevalent in many other
carinic drug because it releases acetylcholine from the
tissues. It too will break down acetylcholine. The final
nerve ending, producing the expected cholinergic ef
action of either enzyme is the production of acetic
fects at all receptor sites. The drug is useful for treat
43
781
ment of glaucoma (applied topically), paralytic ileus,
cholinesterase, such as diisopropy lfluorophosphate
and urinary retention (orally and subcutaneously).
(DFP) or sarin, is ingested, inhaled, or absorbed

across the skin, a great variety of toxic cholinergic ef
Pilocarpine
fects are seen. The first effects seen after exposure to
Pilocarpine is a cholinomimetic that is useful in oph
an anticholinesterase are often ocular and respiratory
thalmology as an antiglaucoma agent. Cholinergic
effects. In the eyes, marked miosis is produced
compounds decrease intraocular pressure by relieving
quickly. In the respiratory system, bronchoconstric
the obstruction to the canal of Schlemm, a drainage
tion and bronchial secretions combine to produce
circuit for the eye. Miosis (pinpoint pupils) is one
tightness in the chest and wheezing. Gastrointestinal
feature of cholinergic therapy and may be beneficial
symptoms include nausea, vomiting, cramps, and di
to glaucoma treatment because the muscular base of
anhea. Other muscarinic effects are severe salivation,
the relaxed iris may contribute to the drainage block.
involuntary defecation and uri nation, swea ting,
Another use of pilocarpine is to promote salivary
lacrimation, bradycardia, and hypotension.
flow in patients with a ganglionic blockade.
Further effects are related to nicotinic functions of

acetylcholine. These include skeletal muscle twitch
ing, weakness, and paralysis. CNS effects include de
Anticholinesterases
Before proceeding to sp
pression of the respiratory and cardiovascular control

ific anticholinesterase drugs,
centers, leading to respiratory collapse. At the time of
it is important to understand the basic mechanism of
death, respiratory paralysis is evident and it is because
action for these compounds. Acetylcholinesterase is
of a combination of bronchoconstriction, bronchose
the enzyme responsible for destroying acetylcholine at
cretions, respiratory muscle paralysis from overstimu
the various nerve junctions where it is released. The
lation, and CNS and control depression. The treatment
class of drugs that intetfere with this function is called
of this toxicity is closely related to preserving respira
anticholinesterascs. These drugs attach to the enzyme
tory function. Administration of atropine, a mus
and thereby block the enzymatic hydrolysis of ACh,
carinic blocker, will effectively decrease bronchocon
causing ACh to accumulate outside of the nerve end
striction and secretion. Another drug, pralidoxime
ing. This results in a greater response than normal to
(Pr o t o p am), is u s e d to re a c t i v a t e the a c e t y l
any cholinergic nerve stimulation. Some of these anti
cholinesterase. I t i s most effective shortly after expo
cholinesterases are relatively short-acting compounds
sure to the toxic agent because it breaks down the an
and are therapeutically impot1ant, whereas others are
ticholinesterase so it can be removed from the enzyme
ext.remely long-lasting and potent compounds that are
site. Additional measures are related to physiological
important only as poisons. The long-acting compounds
suppOt1 of the patient. Maintenance of an airway, arti
have been used as insecticides and as nerve gases in
ficial respiration, and oxygen administration are im
chemical warfare. The therapeutically useful anti
portant therapeutic applications for these patients.
cholinesterases are beneficial in problems related to

the eye, intestine, and the skeletal neuromuscular junc
Physostigmine (Eserine)
tion (NMJ). In these applications, these drugs increase
Physostigmine (Eserine) is useful in glaucoma and in
the amount of ACh available for activity, an effect that
selected therapeutic measures where a cholinergic ef
is es
ially impOt1ant in cascs where the synthesis or
release of acetylcholine is lower than normal, as in

myasthenia gravis.
There is also great medical interest in the toxicol
ogy of the anticholinesterases, especially the ex
fect is beneficial. It functions as an indirect choli

nomimetic by blocking the acetylcholinesterase.
Neostigmine (Prostigmine)
Neostigmine (Prostigmine) is useful in patients with
tremely potent irreversible anticholinesterases. Toxic
nonobstructive paralytic ileus to increase tone and
ity because of these compounds is not uncommon
motility of the small and large intestines. It is also
and is often severe. When a toxic irreversible anti
useful for stimulating skeletal NMJ. Neostigmine is
782
PART VIII
used for treating
gravis because it indi
increases acetylcholine at the NMJ and it acts

directly at the nicotinic receptor site itself. The dis
and does not counteract the nicotinic 2:aufllionic ef

fects or the nicotinic effects at the NMJ.
Because heart rate is controlled
resulting i n skeletal muscle weakness.
parasympathetic effect on the heart,
temporarily restores muscle Nrpncrth
the sym
system to increase heart rate and stroke vol

ume to cause an increase in cardiac output. In
Edrophonium (Tensilson)
This a very
both sympathetic
and parasympathetic tone, atropine will eliminate the
ease is marked by subnormal response t o
may occur after atropine administration. In
anticholinesterase. It is pri
marily useful as a diagnostic agent in
cases where
exists because of high vagal
tone, atropine can be used to reverse this depression.
to reveal, for a few minutes, if the dose of

w o u ld risk a serious c holinergic
In the
tract,
is a bronchodila
tor. It is also possible to
is appropriate. A longer-acting
if t h e
neostigmine dose was alreadv at the therapeutic limit.
respiratory depression
associated with
tranquilizing, and anti
cholinesterase drugs
atropine, either as a
agent or as an antidote
tion to
is a transmitter. There are

for each type of acetylcholine
blocks all cholinergic action right
at the muscarinic receptor site on smooth muscle, ex

and myocardium. Another cholinergic
curare, works only at the neuromuscular
the antidote of choice for all cholinergic toxicities.

One of the most important clinical uses for at
type of nicotinic blocker is the
blocker,
which blocks both sympathetic and

occupvinfl the
acts to de
in the OI tract so that other antiulcer
crease
and it is possible that it also decreases acid se

cretion, Other
related to hypermotility of
the OJ tract are treated with atropine,
to de
muscle activity during treatment of
conditions such as cramping and diarrhea.

tone needs to be
In ophthalmology,
decreased. It is possible to selectively inhibit cholin

effects in the body to produce a desired effect or
to eliminate an undesirable effect. Because of this se
is useful for
dilation. It is contraindi
which is
cated in glaucoma
an acute attack.
Atropine itself is also capable of producing toxic
have
use in many areas of medicine.
dry
effects. These are mydriasis,
and urinary retention, Effects related to
Atropine
the central nervous
ladonna, also known as the deadly
An
and hallucinations,
other plant extract, scopolamine, has action similar to

works by establishing a
atropine,
at the muscarinic receptor
the effector at all tissues innervated

nervous
are also apparent, and
these include sedation initially, followed by delirium
Atropine is an extract from the
tive
agent. This
cer and
crease
choline receptor there. These
lectiveness,
(Ol) tract as an antiul
ropine is in the
in paralysis of skeletal muscle. Still another
ever sympathetic or
A more general med
ical use for atropine exists as an emergency tool. It is
agents can remain in contact with the OI mucosa
to block the nicotinic effect of
parasympathetic ganglia
bronchiolar secretions and laryngeal
spasm, as well as
antagonists block the various
receptor.
medica
Atropine is used widely as
Cholinergic Blocking Drugs
respiratory
which is
lead to a coma, In severe

convulses and
severe
which may be the final course.

and
Anticholinesterase drugs, such as
the parasym
are effective antidotes for atropine be
This blockade is selective
cause they increase the amount of acetylcholine that
for the tissue effect of the parasympathetic system
will compete with atropine for the
rl
43
-------- -----
Homatropine (Novatrin) and
783
.----
some way this reflex is i
Cyelopentolate (Cyelogyf)
a condition
known as orthostatic hypotension will exist. A com

mon manifestation of this condition is fainting on
( Novatrin) and cyclopentolate

gyl) are anticholinergic
ropine.
------
because of inadequate blood flow to the
related in action to at
brain. This section is devoted to the functional as
are useful in ophthalmology to
of the retlex after a change in blood pressure.
mydriasis.
Dicyelomine (Bentyl)
Dicyclomine (Bentyl) is considered very useful in the
gastrointestinal tract to decrease secretions and motU
that fire electrical im
These are stretch
rr;hexyphenidyl HCL (Artane) and
pulses at a rate
Benztropine Mesylate (CogenUn)
related to the blood pressure,
As the pressure in the
and
me
sylate (Cogentin) are antiparkinson
that enter
the CNS to reverse the imbalance between the cholin

and
Neuronal elements, known as baroreceptors, exist in

the sinus of the carotid arteries supplying the brain.
It is sometimes called a chemical vagotomy,
Trihexyphenidyl HCL
The Carotid Baroreceptors
systems in this disease, They
(and
the receptor firing rate. Conversely, a decrease in

blood pressure results in a decrease in stretch receptor
is sent directly to
firing rate. This firing rate

the
have some of the same side effects as
the ves:-;el wall
stretches, causing an increase in
where the vasomotor center and
nu
cleus respond to it.
Penlolinium (Ansolysen) and

Hexamethonium (Methium)
Pentolinium (Ansolysen) and hexamethonium (Me
block the
thium) are nicotinic
acetylcholine receptor site in the ganglia in both the
The Functional Reflex

To create an
experienced a loss of
blood pressure. The carotid
sympathetic and
are used to control
to a
slow their
hypotension. They will also decrease
cholinergic effects at the parasympathetic effector

sites because
block the
of mouth, and
by in
sympathetic nerve activity, This control al

ways
to information
If the pressure had
would have increased their
as well. This means

blurred vision, dryness
as well as other atropine
blood pres
of the
sure in the carotid artery by doing the
for the entire
nervous
that a patient may
shorten and
This message is then delivered to
the brain, and the vasomotor center
tonc, Because of their
action at the sympathetic ganglion, these drugs pro

duce a
this
let us assume we have
the barore
rate and the
vasomotor center would have responded by slowing

the sympathetic nerve
rate. Since the blood
pressure in this example is
like peripheral effects.
increases
nerve
in in
creased release of norepinephrine from the nerves
THE CARDIOVASCULAR REflEX
that reach the heart and arterioles. Norepinephrine in
The cardiovascular reflex involves many of the com
creases the heart rate and stroke volume, thereby pro
ponents of the autonomic nervous system to maintain
ducing an increase in cardiac output. In the
a normal blood pressure. This mechanism is impor

tant for
blood pressure within certain

of physical
from a
Even the
position
stimulates the
ducing
"rt"rlrllp
pro
which results in increased
resistance result in raised blood pressure. A third

component of the sympathetic nervous system can be
by this reflex system, If in
involved
activation.
784
PART VIII
released from the adrenal medulla also increases car
creasing release of histamine, and in a broader ap

proach, the general stabilization of cells that can re
diac output.
Meanwhile, the vagal nucleus is responding to the
decreased baroreceptor firing by decreasing its own ac
lease mediators of the disease, thereby lowering the

severity of the disease.
tivity. The vagus nerve to the heart will release less

acetylcholine, allowing the sympathetic effect to pre
dominate. The total effect becomes an increase in
blood pressure, which is the response required to re
turn the systemic pressure to normal. If the original
pressure alteration had been an increase above normal,
Sympathomimetic Drugs
Isoproterenol (Isuprel) and
Epinephrine (Adrenalin)
The muscle relaxant bronchodilator effect attributed to
the opposite reflexive actions would have occurred to
the beta-adrenergic sympathomimetic compounds is
return pressure to a normal range. In this case the pre
most commonly required for asthmatic or allergic
dominant effect would have been an increase in vagal
emergencies. Isoproterenol (Isuprel) is often self-ad
nerve tone, releasing high amounts of acetylcholine at
ministered by inhalation to reverse mild-to-moderate
the heart, causing a dramatic slowing of heaJ1 rate, ac
obstructive episodes. However, during a severe acute
companied by a decrease in stroke volume. This com
obstruction, the airway is unable to pass the drug to the
bination produces a decrease in cardiac output. The
alveoli, and the intramuscular or subcutaneous routes
sympathetic system would have responded to the in
for epinephrine (adrenaline) and isoproterenol are
creased baroreceptor firing by decreasing firing in all
used. Isoproterenol is a purely beta compound. Epi
sympathetic nerves, thereby decreasing norepinephrine
nephrine has 50% beta-adrenergic activity and also ex
and epinephrine release. All of these factors combine
erts a great bronchodilating effect. Both of these agents
to decrease blood pressure to normal.
are useful when given parenterally or by inhalation.

The most common side effects of isoproterenol are
DRUGS USED IN AIRWAY OBSTRUCTIVE DISEASE
flushing of the skin, headache, palpitation, and tachy

cardia. Epinephrine may cause an anxiety reaction in a
Patients suffering from asthma, emphysema, and
patient along with headache, palpitations, and respira
chronic bronchitis may have an obstructed airway for
tory difficulty. Both drugs can cause serious cardiac
several reasons. Acute asthmatic obstruction and
reactions (dysrhythmias), which have resulted in death.
some chronic airway obstruction are due to bronchial

smooth muscle contraction, resulting in a smaller di
ameter airway. Inflamed passageways, wh ich are
swollen because of edema, may also constitute an air
Metaproterenol (Alupent), Isoetharine

(with Phenylephrine, Bronkosol-2),
and Salmeterol (Servant)
way obstruction. A further complication seen in
Metaproterenol (Alupent), isoetharine (with Phenyle
many respiratory diseases is the thickening and col
phrine, Bronkosol-2), and salmeterol (Servant) are
lection of secretions that cannot be eliminated from
isoproterenol analogs that exert most of their action
the respiratory tree and subsequently block the air
on respiratory or vascular smooth muscle but have lit
way. In this section the various drugs that can reverse
tle effect on the heart. They are useful compounds for
smooth muscle contraction, inflammatory edema, and
selectively relaxing bronchial smooth muscles without
collection of secretions are presented.
directly affecting the heart. The major advantage of
A variety of therapeutic mechanisms are useful
these drugs is that their action on the heart is minimal
against this collection of obstructive conditions. The
or absent, and their potential for inducing cardiac toxi
single most effective mechanism for relief of smooth
cities is correspondingly reduced. However, because
muscle spasm is the beta2 activity that is available in
vascular smooth muscle responds much like respira
some of the adrenergic agents. Other useful mecha
tory smooth muscle to these drugs, arterial resistance
nisms aim at potentiating the beta activity of adrener
can be decreased, leading to a drop in blood pressure
gic agents, decongesting the inflamed airway, de
and a reflexive tachycardia. The beta agonists are
43
-... --.---
785
------------------.-----
inhalation, which minimizes their sys
often
temic absorption and potential for side effects,

variety of antiinflammatory pOltenCle:s.
Ephedrine
of corticosteroids in
from
and
the symp
on the ability of these
is a sympathomimetic that acts by liberat
toms of inflamed tissue. The mechanism of action for
sites in addition to having a possible direct effect on
the drugs, however, has not clearly been defined. Some
receptors. Its usefulness and side effects
specific effects of corticosteroids that relate to the anti
<>,""c> ,,,'
<tT,r
are similar to those of epinephrine. One beneficial
dilation
inflammatory action are decreased

and stabilization of
factor in ephedrine use is that it can be administered
and
orally for convenient
branes in white blood cells, In
I"Q.-'Q(";,<n"
that can
pounds decrease the synthesis of

nr"<n,rot.,
Xanthines
broncho-obstl11ctive disease- prostaglandins

use of the corticos
and ieukotrienes. The
XanthineI' have effects similar to the catecholamines in
teroids is recommended
the respiratory and cardiovascular systems. This simi
The reason for this caution is that they produce serious

side effects and permanent
in effect may be due to the elevation of

AMP. Both the catecholamines and xanthines are
elevated
known to
AMP levels in the tis
if used for 2 weeks
After I week of corticosteroid therapy, be
or
havioral
ulcers may be ob
and acute
is instituted and
sues they stimulate. The catecholamines activate
served. However, when
ate cyclase, the enzyme that converts A TP to
adrenal suppression occurs, the patient requires supple
AMP. The
formed cyclic AMP exelts its effects
on the local tissue (e.g., bronchial muscle relaxation)
until normal adrenal cor
mental corticosteroid
tex function is restored. This state of
and is inactivated by the enzyme
last for as long as several months after
The xanthines inhibit
Most
promoting its effects. Addi
AMP and
tional actions of xanthines may be direct smooth muscle
who receive corticosteroids for long-term

syn
therapy develop a condition called
of muscles be
drome. It is characterized by
relaxation that cou Id increase
cause of the breakdown of
tagonism of adenosine, which is brC)fIctlo(;on
of fat from the extremities to the face and the trunk,

Eventually these patients develop osteoporosis and dia
Theophylline and Aminophylline
betes. Other serious complications are
Theophylline and aminophylline are structurally very

similar to caffeine. They are llsed to control asthma
when given
or
is
intercranial
aminophylline is the treatment of acute asthmatic air

to epinephrine alone. Intravenous administration of this
and
retardation. The time to onset of side effects can

applying dosing
antiin
benefit in the
at low systemic doses.
m!m"t",I"V
COiticosteroids can be
administration or
in cases that do not
ulcers,
be prolonged and the
often used orally for long-term maintenance of mild-to

moderate disease. One of the most common uses for
way obstruction,
redistribution
at low doses in alternate
can be
inhalation in
a form that is not systemically absorbed.
drug increases the opportunity for serious side

which are hypotension and cardiac dysrhythmias,
Antihistamine
Cromolyn Sodium (intal) and
Nedocromil Sodium (Ti/ade)
Corticosteroids
The antiinflammatory steroids are related to the natu
glucocorticoid, cortisol (Prednisone,
Cromolyn sodium (Intal) and nedocromil sodium

have limited usefulness
with the
786
PART VIII
other drugs presented here-they can only prevent an
torants that are usually used in mixtures or adminis
asthmatic episode. The mechanism of action is proba
tered as cough syrups are ammonium chloride, syrup
bly the stabilization of the mast cell that synthesizes,
of ipecac, and glyceryl guaiacolate. These are useful
stores, and releases histamine. Since histamine can
for patients who cannot tolerate the iodide salts.
precipitate broncho-obstructive reactions, these drugs

are useful by preventing its release. They are admin
istered by inhalation.
DRUG INHALATION DEVICES

Most drugs given by inhalation in respiratory disease
are deli vered by pressurized metered-dose inhalers
Mucolytics and Expectorants
(MDI). These devices rely on pressurized chlo
Acetylcysteine (Mucomyst) and
roflurocarbon propellants to deliver very small drug
Pancreatic Dornase (Dornavac)
particles (less than
Acetylcysteine (Mucomyst) and pancreatic dornase
5 micron diameter) into the air
way. Each activation of the metered valve allows an
(Dornavac) act by breaking the chemical bonds that
accurately determined volume (dose) of propellant
hold together the large protein structure that con
and drug mixture to be released at a high velocity.
tributes to the viscosity of mucus. Mucolytics are in
The delivery of drugs to the site of action in the
haled to liquify mucus so that it can be moved out of
airway by any type of inhalation is inefficient, and
the bronchial tract to prevent airway obstruction. Side
therefore, correct technique in use of the MDI is an
effects associated with these drugs are bronchospasm,
important concern. The MDI will allow delivery of
nausea, and vomiting. Acetylcysteine also inactivates
20% of the metered drug to the airway if the pa
the penicillin antibiotics and is contraindicated in
tient correctly coordinates the proper rate of inhala
their presence.
tion with activation of the device and then ade

quately holds the breath before exhalation. It is
Trypsin (Tryptar)
estimated that
50% or fewer patients manage the
Trypsin (Tryptar) is a proteolytic enzyme that may
drug delivery correctly. In response, patient educa
also be useful for liquefying respiratory secretions. It
tion on correct MDI technique is an important part
can be administered by inhalation, although it can
of therapy, and additional devices, called spacers,
cause irritation to the eyes, nose, and throat. An addi
have been developed to allow success with varia
tional problem with this drug is a possible anaphylac
tions in technique. The spacers come in various
tic reaction in sensitized patients. There is a variety
configurations, but they all provide a chamber be
of other enzymes with specific actions on protein that
tween the patient and the MDI, which can be
may be useful in liquefying secretions.
charged with the drug-propellant mixture that is

then inhaled without concern for critical timing.
Sodium Iodide and Potassium Iodide
Patients with poor MDI technique should benefit
Sodium iodide and potassium iodide are expectorants
from the addition of a spacer.
that act by increasing the amount of respiratory secre
An alternative to the MDI, in patients who have
tion so that is relatively less viscous and can be more
difficulty with inhalation technique, is the single-dose
easily removed. The iodide salts are often used in late
or multi-dose powder inhaler. This device offers a
bronchitis, bronchiectasis, and asthma, and they break
drug compounded into a fine powder, which is deliv
up especially tough bronchial secretions by attracting
ered from a container on simple inhalation by the pa
fluid to the respiratory tract. Characteristic side effects
tient. Coordination of drug delivery is simple and not
with these compounds are gastric irritation, nausea,
a pl'Oblem, because only inspiration by the patient
and vomiting. More serious complications occasion
drives powder delivery to the airway. The method of
ally involve the respiratory tract. These patients
fers the same or lower efficacy of drug delivery
wheeze and experience bronchial spasm. Other expec
to
20%), compared with MDI.
(69'c
43
787
References
REVIEW QUESTIONS
1. Why is it important to have an understanding of
Clark, TJ.H., Godfrey,
S., & Lee, T.H., (Eds.). (1992). Asthm({.
London: Chapman and Hall.
the system a drug is to modify?

2. What are the primary and secondary effects of
the commonly used bronchodilators, Ventolin

and Alupent?
Hardman,
J., Gilman, A.G., Limbird, L., & Rail, T.W., (Eds.).
(1995). The pharmacological basis of therapeutics. New York:

McGraw-HilI.
Kaliner, M.A. (1993). How the current understanding of the patho
3. What is the cardiovascular reflex and why is it
physiology of asthma influences our approach to therapy. .lour1101 afAllergy and Clinical Immunology,
important to physical therapists?

4. What is the pharmacologic rationale for treat
ment of patients with chronic obstructive airways

disease. (COPD)?
92( I pI. 2), 144-147.
Katzung, B.G., (Ed.). (1995). Basic and clinical pharmacology.

East Norwalk, CT: Appleton
& Lange.
O'Brien-Ladner, A. (1994). Asthma: new insights in the manage

ment of older patients. Geriatrics,
5. Why is patient compliance with their medica
tions a concern of the physical therapist?
Powell,
C.Y. (1993).
49( 11),20-25,30-32.
Management
of ac ute
asthma
in
ch ildhood.British .lournal ( fHospil{/1 Medicine, 50(5),272-275.

Whelan, A.M.,
& Hahn, N.W. (1991). Optimizing drug delivery
from metered-dose inhalers. Drug Intelligence and Clinical

Pharmacology,
25, 638-645.
GLOSSARY
Acid-base balance:
a condition existing when the net
rate at which the body produces acids or bases equals

the net rate at which acids or bases are excreted. The
surgery, gram-negative sepsis, multiple blood

transfusions, oxygen toxicity, trauma, pneumonia, or
other respiratory infection.
result of acid-base balance is a stable concentration
Aerosol:
of hydrogen ions in body fluids. The amount of acid
Airway clearance:
or base in the arterial blood is measured by pH.
Acidosis:
the removal of mucus and foreign
material from the airways.
Airway-clearance deficits:
a process causing acidemia, which is a
blood pH of less than 7.38.
deficits in the ability to
remove mucus and foreign material from the airways.
Acute exacerbation of chronic airflow

limitation:
nebulized particles suspended in a gas or air.
Alveolar proteinosis:
an increase in the severity of the signs
a disorder marked by the
accumulation of plasma proteins, lipoproteins, and
and symptoms of chronic airflow limitation usually
other blood components in the alveoli of the lungs.
triggered by infection, inflammation, or increased
The cause is unknown and clinical symptoms vary,
sputum production.
although only the lungs are affected. Some patients
Acute lung injury:
injury to the lung characterized by
a clinical spectrum of parenchymal lung dysfunction
are asymptomatic, whereas others show dyspnea and

an unproductive cough.
Alveolar ventilation:
resulting from multiple etiologies and leading to

alveolar capillary membrane leaking (high protein
the volume of inspired air that
reaches the alveolar level and participates in gas

exchange, measured by Peo2.
content). Mild-to-moderate lung injury results in

noncardiogenic edema and severe injury results in
adult respiratory distress syndrome. The hallmarks of
Alveolitis:
an allergic pulmonary reaction to the
inhalation of antigenic substances characterized by
worsening lung injury include refractory hypoxemia,
acute episodes of dyspnea, cough, sweating, fever,
right-to-left shunt, and reduced lung compliance.
weakness, and pain in the joints and mnscles
Adult respiratory distress syndrome (ARDS):
lasting from 12 to 18 hours. Recurrent episodes
respiratory syndrome characterized by respiratory
may lead to chronic obstructive lung disease with
insufficiency and hypoxemia. Triggers include
weight loss, increasing exertional dyspnea, and
aspiration of a foreign body, cardiopulmonary bypass
interstitial fibrosis.
G-1
G-2
Glossary
Anesthesia:
the absence of normal sensation, especially
sensitivity to pain, as induced by an anesthetic

substance or by hypnosis or as occurs with traumatic
or pathophysiological damage to nerve tissue.
Angina:
angina pectoris, the paroxysmal chest pain
an abnormal condition characterized by
Atelectasis:
the collapse of lung tissue, preventing the respiratory

exchange of carbon dioxide and oxygen. Symptoms
may include diminished breath sounds, a mediastinal
caused by anoxia of the myocardium.

a paroxysmal thoracic pain caused
Angina pectoris:
bronchodilators, beta-adrenergic drugs,

methylxanthines, and sh0l1-term use of corticosteroids.
most often by myocardial anoxia as a result of

atherosclerosis of the coronary arteries. The pain
shift toward the side of the collapse, fever, and

increasing dyspnea.
a common arterial disorder
Atherosclerosis:
usuall.y radiates down the inner aspect of the left arm
characterized by yellowish plaques of cholesterol,
and is frequently accompanied by a feeling of
lipids, and cellular debris in the inner layers of the
suffocation and impending death. Attacks of angina
walls of large and medium-sized arteries. The vessel
pectoris are often related to exertion, emotional
walls become thick, fibrotic, and calcified, and the
stress, and exposure to intense cold.
lumen narrows, resulting in reduced blood flow to
Ankylosing spondylitis:
a chronic inflammatory
organs normally supplied by the artery.
disease of unknown origin, first affecting the spine
Antilipidemic agents do not reverse atherosclerosis,
and adjacent structures and commonly progressing to
but a diet low in cholesterol, calories, and saturated
eventual fusion (ankylosis) of the involved joints. In
fats, adequate exercise, and the avoidance of
addition to the spine the joints of the hip, shoulder,
smoking and stress may help prevent the disorder.
neck, ribs, and jaw are often involved. Physical

therapy aids in keeping the spine as erect as possible
to prevent flexion contractures. In advanced cases,
Blood:
the liquid pumped by the heart through all the
arteries, veins, and capillaries. The blood is
surgery may be performed to straighten a badly
composed of a clear yellow tluid, called plasma, and
deformed spine.
the formed elements, and a series of cell types with
Arrhythmia:
an abnormal heart rhythm represented
different functions. The major function of the blood
by an irregularity of the timing or the appearance of
is to transport oxygen and nutrients to the cells and to
the ECG tracing. This term is often used
remove from the cells carbon dioxide and other

waste products for detoxification and elimination.
synonymously with dysrhythmia.

Arterial blood gas:
a test to evaluate the acid-base
balance and panial pressures of oxygen and carbon
the difference between the oxygen
breaths per minute.

Bronchiectasis:
an abnormal condition of the
bronchial tree, characterized by irreversible dilatation
blood.
Artifact:
an abnormally slow heart rate.

a decreased respiratory rate under 10
Bradypnea:
content of arterial blood and the amount in venous
using one's body effectively to
prevent injury.
Bradycardia:
dioxide in the anerial blood.

Arteriovenous-oxygen difference (a-vo2
difference):
Body mechanics:
extraneous detlection of the ECG waveform
and destruction of the bronchial walls. Symptoms of
caused by movement or electrical interference.
bronchiectasis include a constant cough productive
Artifact may be mistaken for a dysrhythmia.
of copious purulent sputum, hemoptysis, chronic
Artificial airway:
a plastic or rubber device that can
sinusitis, clubbing of fingers, and persistent moist,
be inserted into the upper or lower respiratory tract to
coarse rales. Treatment includes mobilization,
facilitate ventilation or the removal of secretions.
frequent postural drainage, antibiotics, and, rarely,
Assessment:
an evaluation or appraisal of a condition.
Assisted cough:
the physical assistance of a cough,
an acute viral infection of the lower
respiratory tract that occurs primarily in infants under
either by the patient or an assistant.

Asthma:
surgical resection of the affected part of the lungs.

Bronchiolitis:
a respiratory disorder characterized by
recurring episodes of paroxysmal dyspnea, wheezing

on expiration/inspiration because of constriction of the
bronchi, coughing, and viscous mucoid bronchial
18 months of age, characterized by expiratory

wheezing, respiratory distres , inflammation, and
obstruction at the level of the bronchioles.
Bronchitis:
an acute or chronic inflammation of the
secretions. Treatment may include elimination of the
mucous membranes of the tracheobronchial tree.
causative agent, hyposensitization, aerosol or oral
Acute bronchitis is characterized by a productive
Glossary
G-3
cough, fever, hypertrophy of mucous-secreting
present at birth or shortly thereafter. Early
structures, and back pain. Most common in adults, it
identification of the disorder facilitates the handling
is uften a complication of cystic fibrosis in children.
of infants with cerebral palsy and the initiation of an
Treatment includes the cessation of cigarette
exercise and training program. Treatment is
smoking, avoidance of airway irritants, the use of
individualized and may include the use of braces,
expectorants, and postural drainage. Currently,
surgical correction of deformities, speech therapy,
prophylactic antibiotics, steroids, and desensitization
and various indicated drugs, such as muscle rel.
therapy are not recummended.
Bronchopulmonary dysplasia:
and anticonvulsants.
an iatrogenic condition
Childhood asthma:
reversible airway hyperreactivity
observed in neonates that resembles chronic airflow
and edema affecting children that is often triggered
limitation and is associated with positive pressure
by dust or animals; hallmarked by narrowing of the
mechanical ventilation and oxygen therapy.
airways, wheezing, shortness of breath, accessory
Burns:
an injury to tissues of the body caused by heat,
electricity, chemicals, radiation, or gases in which the

extent of the injury is determined by the amount of
exposure of the cell to the agent and to the nature of
the agent. The treatment of burns includes pain relief,
muscle use, and impaired oxygenation.

a lung condition characterized
Chronic bronchitis:
by the presence of a chronic productive cough for at

least 3 months in each of 2 successive years.
impaired function of the
Chronic renal insufficiency:
careful asepsis, prevention of infection, maintenance
kidneys manifested by impaired blood urea nitrogen,
of the balance in the body of fluids and electrolytes,
creatinine clearance, and reduced urinary output.
and good nutrition. Severe bUllls of any origin may

cause shock, which is treated before the wound.
Renal insufficiency may precipitate renal failure.
Chronic airflow limitation:
a more precise term for
chronic obstructive pulmonary disease (e.g., chronic
Cardiac output (Q):
bronchitis and emphysema).
the amount of blood ejected
from the heart into the aona each minute.
Clinical decision making:
the process of making
decisions based on a thorough history, assessment,
a supervised program of
Cardiac rehabilitation:
integration of the results of laboratory tests and
progressive exercise, psychological support, and

education or training to enable a myocardial
investigations, and the patient's needs and wants.
infarction patient to resume the activities of daily
Complications with coughing:
living on an independent basis. Special training may
Complications
associated with an impaired cough (e.g., impaired
be needed to adapt the patient to a new occupation
mucociliary transport, mucous accumulation,
and lifestyle.
pulmonary aspiration, and increased risk of infection).
Cardiopulmonary failure:
progressive insufficiency
Congestive heart failure (CHF):
an abnormal
of cardiopulmonary function resulting in significant
condition that reflects impaired cardiac pumping,
impairment of cardiac output and/or ventilation that
caused by myocardial infarction, ischemic heart
cannot be adequately compensated without
disease, or cardiomyopathy. Failure of the ventricle to
ventilatory support.
eject blood efficiently results in volume overload,
Cardiopulmonary function:
the integrated function
of the heart and lungs.
Retrograde transmission of increased hydrostatic
Cardiopulmonary physical therapy: see p. ix.

Cardiopulmonary unit: the heart and lungs, which
function interdependently as a unit.
Catabolic:
congestion; elevated right heart pressure causes
Connective tissue dysfunction:
relating to catabolism, which is the
impaired function of
connective tissue observed in connective tissue and
compounds into simpler ones, often accompanied by

the liberation uf energy.
vascular collagen conditions.
Continuity of care:
the processes involved with
the provision of continuous care
from one setting to another (e.g., inpatient to
cellular metabolism, including energy transfer,
outpatient facilities).
oxygen utilization, and carbon dioxide production.
Cerebral palsy:
pressure from the left heart causes pulmonary

systemic venous congestion and peripheral edema.
breaking down in the body of complex chemical
Cellular respiration:
chamber dilatation, and elevated intracardiac pressure.
a motor function disorder caused by
a permanent, nonprogrcssive brain defect or lesion
Controlled breathing:
teaching a patient ventilatory
strategies to exert cognitive control over ineffective

breathing patterns.
G-4
Glossary
Control of breathing:
the central and peripheral
regulation and control mechanisms of breathing.
Control of the heart:
the central and peripheral
regulation and control mechanisms of the heart.
Coronary artery disease:
any one of the abnonual
conditions that may affect the arteries of the heart
constituents of saliva, and overactivity of the

autonomic nervous system. The glands most affected
are those in the pancreas, the respiratory system, and
the sweat glands. Because there is no known cure,
treatment is directed at the prevention of respiratory
infections, which are the most frequent cause of
and produce various pathological effects, especially
death. Mucolytic agents and bronchodilators are used
the reduced flow of oxygen and nutrients to the
to help liquefy the thick, tenacious mucus. Physical
myocardium. Any of the coronary artery diseases,
therapy measures, such
such as coronary atherosclerosis, coronary arteritis,
drainage, and breathing exercises, can also dislodge
or fibromuscular hyperplasia of the coronary arteries,
secretions. Life expectancy in cystic fibrosis has
as
exercise, postural
may produce the common characteristic symptom of
improved markedly over the past several decades,
angina pectoris. Studies over the last 30 years
and with early diagnosis and treatment, most patients
confirm that coronary atherosclerosis occurs most
can be expected to reach adulthood.
frequently in populations with regular diets high in

calories, total fat, saturated fat, cholesterol, and
refined carbohydrates. Other risk factors include
Dead space:
the amount of lung in contact with
ventilating gases but not in contact with pulmonary
cigarette smoking, hypertension, serum cholesterol
blood tlow. Alveolar dead space refers to alveoli
levels, coffee intake, alcohol intake, deficiencies of
that are ventilated by the pulmonary circulation but
vitamins C and E, water hardness, hypoxia, carbon
are not perfused. The condition may exist when
monoxide, social overcrowding, heredity, climate,
pulmonary circulation is obstructed, as by a
and viruses.
thromboembol.us. Anatomical dead space is an area
Cough:
a sudden, audible expulsion of air from the
in the trachea, bronchi, and air passages containing
lungs. Coughing is preceded by inspiration, the
air that does not reach the alveoli during respiration.
glottis is partially closed, and the accessory muscles
As a general rule the volume of air in the
of expiration contract to expel the air forcibly from
anatomical dead space in millimeters is
the respiratory passages. Coughing is an essential
approximately equal to the weight in pounds of the
protective response that serves to clear the lungs,
involved individual. Certain lung disorders, such as
bronchi, or trachea of irritants and secretions or to
emphysema, increase the amount of anatomical
prevent aspiration of foreign material into the lungs.
dead space. Physiological dead space is an area in
It is a common symptom of diseases of the chest and
the respiratory system that includes the anatomical
larynx. Because the function of coughing is to clear
dead space together with the space in the alveoli
the respiratory tract of secretions, it is important that
occupied by air that does not contribute to the
the cough bring out accumulated debris. Where it
oxygen-carbon dioxide exchange.
does not, because of weakness or inhibition of the
Denervation of heart:
the transplanted heart initially
force of the cough caused by pain, instruction and
loses its innervation (i.e., it is deriervated and relies
assistance in effective coughing and deep-breathing
on exogenous catecholamines for cardiac
exercises are required.
Cough pump:
acceleration and deceleration).
the integrated thoracic and abdominal
mechanisms involved in cough resulting in forced

expiration and evacuation and clearance of the airways.
Cough stages:
the stages of cough include maximal
inspiration, closure of the glottis, increased

intraabdominal pressure, opening of the glottis, and
forced expiration.
Cystic fibrosis:
Dependent patients:
patients unable to help
themselves.
Depolarization:
the changes in ionic concentrations
across muscle cell membranes leading to contraction

of the cell.
Diabetes:
a clinical condition characterized by the
excessive excretion of urine. The excess may be
an inherited disorder of the exocrine
caused by a deficiency of antidiuretic hormone
glands, causing those glands to produce abnormally
(ADH), as in diabetes insipidus, or it may be the
thick secretions of mucus, elevation of sweat
polyuria resulting from the hyperglycemia OCCUlTing
electrolytes, increased organic and enzymatic
in diabetes mellitus.
Glossary
Diaphragmatic breathing pattern:
involves teaching
the function of the endocrine
Endocrine function:
glands responsible for normal physiological function.
patients with CO PO how to relax the accessory

muscles and to pelform controlled diaphragmatic
Evidence-based practice:
practice based on evidence
from the physiologic and scientific literature.
breathing.
the process in which solid, particulate
Diflusion:
G-5
Exercise:
(I) The petformance of any physical
activity for the purpose of conditioning the body,
matter in a t1uid moves from an area of higher

concentration to an area of lower concentration,
improving health, or maintaining fitness or as a
resulting in an even distribution of the particles in the
means of therapy for correcting a deformity or
fluid. No energy is required.
restoring the organs and bodily functions to a state of
Documentation:
written material associated with the
history, the compilation of laboratory reports and
health. (2) Any action, skill, or maneuver that exerts

the muscles and is performed repeatedly in order to
investigations, and the results of the clinical
develop or strengthen the body or any of its parts.
assessment.
(3) To use a muscle or part of the body in a repetitive
Dyspnea:
way to maintain or develop its strength. The physical
the sensation of difficulty in breathing.
therapist constantly assesses the patient's needs and

ECG monitoring:
electrocardiographic monitoring
involving electrode placement on the chest wall and
provides the proper type and amount of exercise,

taking into account the patient's physical or mental
on the limbs for a 12-lead ECG; such monitoring
limitations. Exercise has a beneficial effect on each
provides a tracing of the electrical activity of the
of the body systems, although in excess it can lead to

the breakdown of tissue and cause injury.
heart.
evaluation of cardiac structure
Echocardiography:
Quantitative and qualitative measurements can be

dimensional, Doppler, and transesophageal echoes.
a measure of myocardial function,
it is the amount of ventricular volume ejected with

each heart beat. Expressed as a percent, the ejection
volume)
Expiratory reserve volume (ERV):
the maximum
volume of gas that can be expired from the resting

expiratory level.
factors related to the patient's care
that contribute to cardiopulmonary dysfunction and
100 end-diastolic volume.
Electrocardiogram (ECG):
the physical stress imposed by
movement (i.e., mobilization and exercise.)
Extrinsic factors:
(end-diastolic volume - end-systolic
exercise on oxygen transport.

Exercise stress:
derived. The most common types include two
fraction
blood gases taken before,
during, and after exercise to determine the effect of
and function by using the properties of sound.
Ejection fraction:
Exercise blood gases:
the tracing produced by
impaired gas exchange.
the sequential depolarization and repolarization of

myocardial cells as detected by sutface electrodes
Electromechanical coupling:
cardiac output.
effect on electrolytes.
Forced expiratory volume in one second (FEV I):
the
amount of air expired in I second during a forced
electromyography is the
process of recording the electrical activity of muscle
exhalation after a maximal inhalation.

Forced vital capacity (FVC):
on a cathode-ray oscilloscope. The

electromyographic (EMG) power spectrum is the full
the total amount of air
exhaled during a forced exhalation after a maximal

inhalation.
range of electrical activity of the muscle.

Emphysema:
the status of blood
balance in the body; fluid balance often has a direct
the coupling of
electrical and mechanical events of the heart to effect

EMG power spectrum:
Fluid and electrolyte status:
volume and distribution, and the status of electrolyte
placed on the skin.
a lung condition characterized by an
Functional residual capacity:
the volume of gas in
abnormal permanent enlargement of the air spaces
the lungs at the end of a normal expiration. The
distal to the terminal bronchioles, accompanied by
functional residual capacity is equal to the residual
destruction of their walls.

Endocardial cushion defect:
volume plus the expiratory reserve volume.

any cardiac defect
Function optimization:
optimal functioning of the
resulting from the failure of the endocardial cushions in
patient as a whole person based on optimal
the embryonic heart to fuse and form the atrial septum.
physiological functioning at an organ system level.
G-6
Glossary
Gas exchange:
the movement of oxygen and carbon
temperature. The percentage is usually represented in
dioxide between the pulmonary capillary blood and
terms of relative humidity, with 100% being the
the alveolar tissue and between the systemic capillary
point of air saturation or the level at which the air can

absorb no additional water.
blood and peripheral tissue cells.
Gastrointestinal dysfunction:
abnormal function of
the gastrointestinal system.
Gravitational stress:
disease of the newborn,
characterized by airless alveoli, inelastic lungs, more
stress imposed on the human
body by gravity and its physiological effects.
Gravity:
Hyaline membrane disease:
the heaviness or weight of an object resulting
from the universal effect of the attraction between any
than 60 respirations a minute, nasal flaring,

intercostal and subcostal retractions, grunting on
expiration, and peripheral edema. The condition
occurs most often in premature babies. The disease is
body of matter and any planetary body. The force of
self-limited; the infant dies in 3 to 5 days or
the attraction depends on the relative masses of the
completely recovers with no after-effects. Treatment
bodies and on the distance between them.
includes measures to corTect shock, acidosis, and

hypoxemia and use of positive airway pressure to
Head injury:
any traumatic damage to the head
resulting from blunt or penetrating trauma of the

skull. Blood vessels, nerves, and meninges can be
torn; bleeding, edema, and ischemia may result.
Health behavior:
an action taken by a person to
maintain, attain, or regain good health and to prevent
prevent alveolar collapse. This is also called
respiratory distress syndrome (RDS) olthe newborn.

Hypercapnia:
the presence of an abnormally large
amount of carbon dioxide in the circulating blood.
Hyperpnea:
Hypertension:
rapid shallow breathing.

a common, often asymptomatic
illness. Health behavior reflects a person's health
disorder characterized by elevated blood pressure
beliefs. Some common health behaviors are
persistently exceeding 140/90 mm Hg. Patients with
exercising regularly, eating a balanced diet, and
high blood pressure are advised to follow a low
obtaining necessary inoculations.
sodium, low-saturated-fat diet, to reduce calories to
Heart:
the muscular, cone-shaped organ, about the
size of a clenched fist, that pumps blood throughout

the body and beats normally about 70 times per
minute by coordinated nerve impulses and muscular
control obesity, to exercise, to avoid stress, and to

take adequate rest.
Hypoxemia:
a low level of oxygen in the blood, often
characterized by a Pa02 of less than 80 mm Hg.
contractions. Enclosed in pericardium, the heart rests

on the diaphragm between the lower borders of the
lungs, occupying the middle of the mediastinum. The
sinoatrial node of the heartbeat sets the rate. Other
factors affecting the heartbeat are emotion, exercise,
hormones, temperature, pain, and stress.
Heart-lung interdependence:
the heart and lung are
paralysis of one side of the body.

status of the heart and its
capacity to effect blood movement to perfuse the

tissues of the body.
Hibernating myocardium:
abnormal function of
Immunosuppression:
of or peI1.aining to a suhstance or
procedure that lessens or prevents an immune response.

the maximum volume of
gas that can be inhaled from the resting expiratory

level. Equal to the sum of the tidal volume and the
inspiratory reserve volume, it is measured with a
spirometer.
contractile dysfunction of
the myocardium as a result of prolonged ischemia,

appearing as a regional wall motion abnormality.
Home care:
immunological protection.
Immunological dysfunction:
Inspiratory capacity (Ie):
a cardiopulmonary unit.
Hemodynamic status:
function of the immunological
system and its components in effecting optimal
the immunological system.
structurally and functionally interdependent and form
Hemiplegia:
Immune function:
a health service provided in the patient's
place of residence for the purposes of promoting,
Inspiratory muscle training:
resistance ventilatory
training designed to increase the strength and

endurance of the inspiratory muscles.
Inspiratory resistance breathing:
a method of
respiratory muscle training that includes normal
maintaining, or restoring health or minimizing the
ventilation with added external threshold loading
effects of illness and disability.
on inspiration consisting of 15 to 30 minutes of
Humidity:
pertaining to the level of moisture in the
atmosphere, the amount varying with the
training 5 days per week. External loading is

increased from 30% of maximal inspiratory pressure
Glossary
G-7
to 60% of maximal inspiratory pressure as patient's
nephrons. All the blood in the body passes through
tolerance increases.
the kidneys about 20 times every hour but only about
Inspiratory reserve volume:
The maximum volume
one fifth of the plasma is filtered by the nephrons
of gas that can be inspired from the end-tidal
during that period. The kidneys remove water as
inspiratory level.
urine and return water that has been filtered to the
Intermittent positive pressure breathing (IPPB):
form of assistive or controll.ed respiration produced
blood plasma, thus helping to maintain the water

baJance of the body. Hormone, especially the
by a ventilatory apparatus in which compressed gas
antidiuretic hormone (ADH), produced by the
is delivered under positive pressure into the person's
pituitary gland, control the function of the kidneys in
airways unti I a preset pressure is reached. Passi ve

exhalation is allowed through a valve, and the cycle
regulating the water content of the body.

an abnormal condition characterized
Kyphoscoliosis:
begins again as the flow of gas is triggered by
by an anteroposterior curvature and a lateral
inhalation. This is also called i11lermillent positive
curvature of the spine. It occurs in children and
pressure ventilation (IPPV).
adults and can be associated with cor pulmonale.
Interstitial pulmonary fibrosis:
a classification of
restrictive lung disease including conditions that

result in a final common pathway of bouts of chronic
the late effects of
poliomyelitis that may occur in poliomyelitis

survivors 30 to 35 years after onset. These effects
lung infection and irreversible fibrosis.
Intraaortic balloon counter pulsation:
Late sequelae of poliomyelitis:
procedure for
include disproportionate fatigue, weakness, pain,
assisting left ventricular function and coronary
reduced endurance, choking and swallowing
petfusion involving the insertion of a balloon in the
problems, altered temperature sensitivity, and
femoral artery. The inflation and deflation of the

balloon is synchronized with the ECG such that it
inflates during diastole and deflates during systole.
pressures within the
Intracardiac pressures:
psychological problems.
Learning theory:
a group of concepts and principles
that attempts to explain the learning process. One

concept, Guthrie's contiguous conditioning premise,
chambers of the heart. Optimal movement of blood
postulates that each response becomes permanently
through the heart depends on pressure gradients
linked with stimuli present at the time so that
throughoLlt the heart. Normal pressures within each
contiguity rather than reinforcement is a part of the
heart chamber are within a restricted range.
Intracranial pressure monitoring:
learning process.
invasive
Liver:
monitoring instituted to measure changes in cranial
the largest gland of the body and one of its
most complex organs. More than 500 of its functions
pressure usually resulting from increased volume of
have been identified. It is divided into four lobes,
the brain because of injury. bleeding, fluid
contains as many as 100,000 lobules, and is served
accumulation, or an intracranial mass.
Isocapnic hyperpnea:
by two distinct blood supplies. Some of the major
a method of respiratory muscle
training that includes high ventilation with low
functions performed by the liver are the production

of bile by hepatic cells, the secretion of glucose,
external loading consisting of sustained periods of
proteins, vitamins, fats, and most of the other
hyperpnea lasting 15 to 30 minutes daily for several
compounds used by the body, the processing of
weeks with the addition of carbon dioxide to
hemoglobin for vital use of its iron content, and the
maintain a normal level.
conversion of poisonous ammonia to area.
Lung cancer:
Jacobsen's progressive relaxation exercise:
a pulmonary malignancy attributable to
cigarette smoking in 50% of cases. Lung cancer
technique involving contraction followed by
develops most often in scalTed or chronically diseased
relaxation to progressively relax muscle groups.
lungs and is usual.

because metastases may precede the detection of the
Kidneys:
a pair of bean-shaped urinary organs in the
dorsal part of the abdomen, one on each side of the
primary lesion in the lung. Symptoms of lung cancer

include persistent cough, dyspnea, purulent or blood
vertebral column. The kidneys produce and eliminate
streaked sputum, chest pain, and repeated attacks of
urine through a complex filtration network and
bronchitis or pneumonia. Surgery is the most
reabsorption system comprising more than 2 million
effective treatment, but only one half of cases are
G-8
Glossary
operahle at the time of diagnosis and of these 50% are
Metabolical demand fluctuates depending on the
not resectable. Thoracotomy is contraindicated if
activity level of the individual, the presence of illness
metastases are found in contralateral or scalene lymph
and increascd temperature, and the requirements of
nodes. In"adiation is used to treat localized lesions and

unresectable intrathoracic tumors and as palliative
therapy for metastatic lesions. Radiotherapy may also
be administered after surgery to destroy remaining
tumor cells and may be combined with chemotherapy.
Lung capacities:
lung volumes that consist of two or
more of the four primary nonoveriapping volumes.

Functional residual capacity is the sum of residual
volume and expiratory reserve volume. Inspiratory
capacity is the sum of the tidal volume and
healing and repair.
Method:
a technique or procedure for producing a
desired effect, such as a surgical procedure, a

laboratory test, or a diagnostic technique.
Minute ventilation (VE):
the amount of air inspired
in I minute. It is the product of tidal volume and

respiratory rate.
the total expired volume of air
Minute ventilation:
per minute.
Mobilization:
the therapeutic and prescriptive
inspiratory reserve volume. Vital capacity is the sum
application of low-intensity exercise in the
of the expiratory reserve volume, the tidal volume,
management of cardiopulmonary dysfunction usually
and the inspiratory reserve volume. Total lung
in acutely ill patients. The primary goal of
capacity, at the end of maximal inspiration, is the
mobilization is to exploit the acute eflects or exercise
sum of the functional residual capacity and the

inspiratory capacity.
Lung compliance:
the volume change per unit of
pressure change in the lungs.
Lungs:
to optimize oxygen transport.
Morbid obesity:
an excess of body fat that threatens
normal body functions, such as respiration.
Mucous blanket:
a pair of light, spongy organs in the thorax,
the normal layer of mucous lining
the bronchopulmonary tree. This blanket provides a
constituting the main component of the respiratory
medium through which foreign material and bacteria
system. The two highly elastic lungs are the main
can be wafted centrally by the cilia for eventual
mechanisms in the body for inspiring air from which

oxygen is extracted for the arterial blood system and
removal by coughing or swallowing.
Multiple sclerosis (MS):
a progressi ve discase
for exhaling carbon dioxide dispersed from the
characterized by disscminated demyelination of
venous system.
nerve fibers of the brain and spinal cord. It begins
Lung volume:
the volume of the lungs that may be
slowly, usually in young adulthood, and continues
compartmentalized into component volumes and
throughout life with periods of exacerbation and
capacities.
remission. As the disease progresses, the intervals

between exacerbations grow shorter and disabil ity
Malnutrition:
any disorder of nutrition. It may result
from an unbalanced, insufficient, or excessive diet or
becomes greater. There is no specific treatment for

the diseasc; corticosteroids and other drugs are
from the impaired absorption, assimilation, or use of
used to treat the symptoms accompanying acute
foods.
episodes. Physical therapy may help to postpone
Managed care:
a health care system in which there is
or prevent specific disabilities. The patient is
administrative control over primary health care
encouraged to live as normal and active a life
services in a medical group practice. Redundant
as possible.
facilities and services are eliminated and costs are

reduced. Health education and preventive medicine
Multisystem assessment: the assessment of

multiple organ systems based on clinical examination
are emphasized. Patients may pay a flat fee for basic
and investigative laboratory reports. Such assessment
family care but may be charged additional fees for
helps identify all factors that contribute to deficits in
secondary care services of specialists.
Measurement:
oxygen transport.
the determination, expressed
numerically, of the extent or quantity of a substance,

the use of artificial
the maximum force that a muscle
can develop with maximal stimulation.
mechanical means to support ventilation.
Metabolical demand:
the ability to sustain repetitive
contraction against a given load.
Muscle strength:
energy, or time.
Mechanical ventilation:
Muscle endurance:
Muscular dystrophy (MD):
the energy and oxygen
demands of the body required to support metabolism.
a group of genetically
transmitted diseases characterized by progressive

atrophy of symmetrical groups of skeletal muscles
Glossary
without evidence of involvement or degeneration of

neural tissue. [n all forms of muscular dystrophy,
there is an insidious loss of strength with increasing
disability and deformity, although each type differs
Oxygen (02):
G-9
a tasteless, odorless, colorless gas
essential for human respiration.
Oxygen consumption (Vo2):
the difference between
oxygen that is inspired and the amount of oxygen
in the groups of muscles affected, the age of onset,
exhaJed. The difference between inspired and expired
the rate of progression, and the mode of genetic
oxygen is a primary measure of aerobic fitness.
inheritance. The basic cause is unknown but appears

to be an inborn error of metabolism. Treatment of the
muscular dystrophies consists primarily of supportive
measures, such as physical therapy and orthopedic
procedures to minimize deformity.
Myocardial infarction:
Oxygen delivery (Do2):
the delivery of oxygen to the
tissues of the body. an essential component of

oxygen transport.
Oxygen desaturation:
the desaturation of oxygen
from the hemoglobin molecule in the blood in
necrosis of a portion of
response to a reduction of tissue oxygen levels.
cardiac muscle caused by obstruction in a coronary
Oxygen transport:
the process by which oxygen is
artery from either atherosclerosis or an embolus.
absorbed in the lungs by the hemoglobin in
Also called a heart attack.
circulating deoxygenated red cells and carried to the

peripheral tissues. The process is made possible
Needs assessment:
assessment of the patient's specific
physical, functional, and psychological needs.
Nocturnal ventilation:
because hemoglobin has the ability to combine with

oxygen present at a high concentration, such as in the
the selective use of
lungs, and to release this oxygen when the
mcchanical ventilation during the night. Patients with

cardiopulmonary dysfunction are at greater risk
concentration is low, such as in the peripheral tissues.
Oxygen transport pathway:
during the night when they are recumbent and the

respiratory drive is depressed.
the pathway for oxygcn
delivery to the tissues from the ambient air, through

the airways and lungs, across the alveolar capillary
membrane, into the pulmonary circulation through
Obesity:
an abnormal increase in the proportion of fat
cells. mainly in the viscera and subcutaneous tissues
the chambers of the heart, via the peripheral and

regional circulation to the tissues and the
of the body. Obesity may be exogenous or
mitochondria where oxygen is used in cellular
endogenous. Hyperplastic obesity is caused by an
respiration.
incrcase in the number of fat cells in the increased

adipose tissue mass. Hypertrophic obesity results
from an increase in the size of the fat cells in the
(I) A goal. (2) Of or pertaining to a
phenomenon
or
a measurement of the amount of
oxygen attached to a hemoglobin molecule.
Oxyhemoglobin dissociation:
the dissociation of
oxygen from the hemoglobin molecule in peripheral
increase adipose tissue mass.
Objective:
Oxygen saturation:
tissues when the concentration of oxygen is low.
clinical finding that is observed; not
subjective. An objective finding is often described in

health care as a sign, as distinguished from a
the tissue of an organ as distinguished
from supporting or connective tissue.
symptom, which is a subjcctive finding.
Obstructive lung disease:
Parenchyma:
Parkinson's disease:
a classification of lung
a slowly progressive,
degenerative, neurological disorder characterized by
disease referring to airflow limitation secondary to
resting tremor, pill rolling of the fingers, a masklike
obstruction and increased airway resistance (e.g.,
expression, shuffling gait, forward flexion of the
chronic bronchitis and emphysema).
trunk, loss of postural reflexes, and muscle rigidity
Osteoporosis:
a disorder characterized by abnormal
and weakness. It is usually an idiopathic disease of
rarefaction of bone, occurring most frequently in
people over 60 years of age, although it may occur in
postmenopausal women, in sedentary or immobilized
younger people, especially after acute encephalitis or
individuals, and in patients on long-term steroid
carbon monoxide or metallic poisoning, particularly
therapy. The disorder may cause pain, especially in

the lower back, pathological fractures, loss of stature,
and various deformities.
Outpatient:
facility.
the pressure exerted by an
individual gas, a percent of the total pressure of gases.
patient, not hospitalized, who is being
treated in an olTiec, clinic,
by reserpine or phenothiazine drugs.
Partial pressure of gases:
or
other ambulatory care
Patent ductus arteriosus (PDA):
an abnormal
opening between the pulmonary artery and the aorta

caused by failure of the fetal ductus arteriosus to
G-10
Glossary
close after birth. The defect, which is seen primarily

in premature infants, allows blood from the aorta to
flow into the pulmonary artery and to recirculate
through the lungs, where it is reoxygenated and
returned to the left atrium and left ventricle, causing
an increased workload on the left side of the heart
and increased pulmonary vascular congestion and
resistance.
Prevention:
any action directed toward preventing
illness and promoting health to avoid the need for

secondary or tertiary health care.
Primary cardiopulmonary dysfunction:
cardiopulmonary dysfunction resulting from a primary
condition of the heart, lungs, or both.
Pulmonary rehabilitation:
rehabilitation of
cardiopulmonary dysfunction including the acute,
Pediatric cardiac rehabilitation:
specialized cardiac
subacute, and chronic phases of the disease or after
rehabilitation for children instituted in the chronic
thoracic surgery. The long-term management
stage of heart disease or after cardiovascular surgery
includes a comprehensive program of exercise,

ventilatory support, additional airway clearance
when the patient is through the acute phase.

Pediatric pulmonary rehabilitation:
specialized
pulmonary rehabilitation for children instituted in the
interventions as needed, nutrition, stress reduction,

smoking cessation, pacing and energy
subacute or chronic stages of lung disease or after
conservation, vocational rehabilitation, sexual
thoracic surgery when the patient is through the acute
rehabilitation, and education.
phase.
Perfusion:
Pulmonary development:
the passage of a fluid through a specific
organ or an area of the body.

Perioperative complications:
system during nom1al growth and development.

complications before,
during, and after surgery.

Peripheral circulation:
the anatomical and
physiological development of the cardiopulmonary

Pulmonary circulation:
the blood flow through a
network of vessels between the heart and the lungs
the systemic circulation,
which excludes the circulation to the heart and lungs
for the oxygenation of blood and removal of carbon

dioxide.
(the central circulation).

Peripheral vascular disease:
any abnormal condition
that affects the blood vessels outside the heart and
Quality care:
the provision of holistic care in which
the needs and wants of the patient are considered.
the lymphatic vessels.

Pneumonia:
an acute inflammation of the lungs,
usually caused by inhaled pneumococci of the
Recumbency:
species Streptococcus pneumoniae. The alveoli and
Reflex cough:
bronchioles of the lungs become plugged with a
Reliability:
fibrous exudate. Pneumonia may be caused by
the state of lying down or leaning
against something.
a cough stimulated reflexively.
the extent to which a test measurement or
a device produces the same results with different
other bacteria, as well as by viruses, rickettsiae,
investigators, observers, or administration of the test
and fungi.
over time. If repeated use of the same measurement
Positron emission scans:
tomographic scans using
positron emitting radionuclides. The tracers used are

often taken up in the metabolical pathways of the
tissues being studied (e.g., oxygen metabolism or
gluclose metabolism).
Prescription:
tool on the same sample produces the same consistent

results, the measurement is considered reliable.
Residual volume:
Resources:
an order for medication, therapy, or a
therapeutic device given by a properly authorized

person to a person properly authorized to dispense or
perform the order. A prescription is usually in written
form and includes the name and address of the
patient, the date, the [4]+ symbol (superscription),
the volume of air remaining in the
lung after a maximal expiration.

services, personnel, and treatment options
that can be drawn on to maximize treatment delivery

and effectiveness.
Respiratory muscle fatigue:
a loss in the capacity of
a muscle underload to develop force or velocity that

is reversible by rest.
Respiratory muscles:
the muscles that produce
the medication prescribed (inscription), directions to
volume changes of the thorax during breathing. The
the pharmacist or other dispenser (subscription),
inspiratory muscles include the hemidiaphragms,
directions to the patient that must appear on the label,
external intercostals, scaleni, sternomastoids,
the prescriber's signature, and, in some instances, an
trapezius, pectoralis major, pectoralis minor,
identifying number.
subclavius, latissimus dorsi, serratus anterior, and
Glossary
muscles that extend the back. The expiratory muscles
Sclerodenna:
G-11
a relatively rare autoiuunune disease
are the external intercostals, abdominals, and the
affecting the blood vessels and connective tissue. The
muscles that flex the back.
disease is chaJ'acterized by fibrous degeneration of lhe
Respirator), muscle weakness:
a chronic loss in the
Respiratory mechanics:
the physical properties of
the lung including resistance and compliance
Scleroderma is most common in middle-aged women.

Secretion management:
management of airway
secretions.
characteristics.
Respiratory failure:
connective tissue of the skin, lungs, and intemal organs,

especially the esophagus, digestive tract, and kidneys.
capacity of a rested muscle to generate force.
the inability of the cardiac and
Sedation:
an induced state of quiet, calmness, or sleep,
as by means of a sedative or hypnotic medication.
pulmonary systems to maintain an adequate

exchange of oxygen and carbon dioxide in the lungs.
Sepsis and multiorgan system failure:
overwhelming
systemic infection and pathogens leading to failure
Respiratory failure may be oxygenation or
within multiple organ systems.
hypcrcapniac. Treatment of respiratory fai lure

includes maximizing ventilation, clearing the airways
by suction, bronchodilators, or tracheostomy,
Shock:
an abnormal condition of inadequate blood
flow to the body s peripheral tissues, with life
antibiotics for infections usually present,
threatening cellular dysfunction, hypotension, and
anticoagulants for pulmonary thromboemboli, and
oliguria. The condition is usually associated with
electrolyte replacement in fluid imbalance. Oxygen
inadequate cardiac output, changes in peripheral
may be administered in some cases; in others it may
blood flow resistance and distribution, and tissue
further decrease the respiratory reflex by removing
damage. Causal factors include hemorrhage,
the stimulus of a decreased elevated level of oxygen.

Restrictive lung disease:
a category of lung disease
involving restriction of the lung parenchyma and
vomiting, diarrhea, inadequate fluid intake, or

excessive renal loss, resulting in hypovolemia.
Skilled nursing and rehabilitation facilities:
an
characterized by stiffness (reduced compliance) and
institution or part of an institution that meets criteria
reduced lung volume.
for accreditation established by the sections of the
Rheumatoid arthritis:
a chronic, destructive, sometimes
Social Security Act that determine the basis for
deforming collagen disease that has an autoimmune
Medicaid and Medicare reimbursement for skilled
component. Rheumatoid aJthritis is characterized by
nursing care, including rehabilitation and various
symmetric inflammation of the synovium and increased

synovial exudate, leading to thickening of the synovium
and swelling of the joint. Rheumatoid arthritis usually
medical and nursing procedures.

Spinal cord injury:
any one of the traumatic
disruptions of the spinal cord, often associated with
first appears in early middle age, between 36 and 50
extensive musculoskeletal involvement. Common
years of age, and most commonly in women. The
spinal cord injuries are vertebral fractures and
course of the disease is variable but is frequently
dislocations, such as those commonly suffered by
marked by remissions and exacerbation.
individuals involved in car accidents, airplane
Risk factors:
factors that cause a person or a group of
crashes, or other violent impacts. Such trauma may
people to be particularly vulnerable to an unwanted,
cause varying degrees of paraplegia and
unpleasant, or unhealthful event, such as
quadriplegia. Treatment of spinal cord injuries varies
immunosuppression, which increases the incidence
considerably and involves numerous approaches,
and severity of infection, or cigarette smoking, which
such as exercise, ambulatory techniques, and special
increases the risk of developing a respiratory or
physical and psychological therapy.
cardiovascular disease.
Routine body positioning:
Stable angina:
the routine use of body
positioning in the management of patients to
anginal pain that is well-controlled,
medically stable, and has a predictable

activity/exercise threshold.
minimize the negative effects of static positioning
Status asthmaticus:
an acute, severe, and prolonged
and maximize comfort. The purposes of routine body
asthma attack. Hypoxia, cyanosis, and
positioning are distinct from the specific goals of
unconsciousness may follow. Treatment includes
prescriptive body positioning, which are related to
bronchodilators given intravenously or by aerosol
optimizing particular components of
inhalation, corticosteroids, controlled positive
cardiopulmonary function and gas exchange.
pressure ventilation, sedation, frequent therapy,
G-12
Glossary
and emotional support. A bronchodilator may be
myocardium based on perfusion of the area. This
given by aerosol inhalation from a ventilator.
agent can be used for rest studies, exercise stress
Stroke volume (SV):
the amount of blood ejected
Stunned myocardium:
contractile dysfunction of the
myocardium as a result of an acute episode of

ischemia that persists even after perfusion has
hospitals that specialize in the
the diaphragm, and associated muscles.
Thoracic surgery:
the branch of medicine that deals
manipulative and operative methods.
Throat clearing:
management of nonacute conditions.
Subjective:
the cavity enclosed by the ribs, the
thoracic portion of the vertebral column, the sternum,
with disease and injuries of the thoracic area by
returned to normal.
Subacute hospitals:
studies, and pharmacological stress studies.
Thoracic cavity:
from the ventricles during systole.
the spontaneous elicitation of a
(I) Pertaining to the essential nature of an
coughlike maneuver to clear secretions or an
object as perceived in the mind rather than to a thing
obstruction from the oropharynx that may be
(2) Existing only in the mind. (3) That
in itself.
which arises within or is perceived by the individual,
threatening the upper airway.
Tidal volume (TV):
the amount of air inhaled and
as contrasted with something that is modified by
exhaled during normal ventilation. Inspiratory
external circumstances or something that may be
reserve volume, expiratory reserve volume, and tidal
evaluated by objective standards.
Suctioning:
volume make up vital capacity.
the use of mechanical airway suctioning
that uses a catheter and negative pressure to remove

oropharyngeal or airway secretions when the patient
is unable to spontaneously or voluntarily take deep
breaths and cough effectively.
Supraventricular:
pertaining to a feature or event
the branch of medicine concerned with
diseases and trauma requiring operative procedures.
Syncytium:
the volume of gas in the
lungs at the end of a maximum inspiration. It equals

the vital capacity plus the residual capacity.
Tracheobronchial tree (TBT):
an anatomic complex
that includes the trachea, the bronchi, and the
occurring superior to the ventricles of the heart.
Surgery:
Total lung capacity (TLC):
the arrangement of cells, as in the
myocardium, such that stimulation of one cell causes
bronchial tubes. It conveys air to and from the lungs.
Tracheostomy:
an opening through the neck into the
trachea through which an indwelling tube may be

inserted.
Tracheostomy tube/cuff:
a tube/cuff that is
positioned directly through the trachea in the neck to
stimulation of adjacent cells, thus causing an action
provide a functioning airway that bypasses the nares
potential to spread from the initial focus.
and oropharynx.
Systemic disease:
dysfunction or condition affecting
one or more systems.
Systemic lupus erythematosus (SLE):
Transitional care units:
settings that specialize in
providing care between the acute, subacute, and

a chronic
inflammatory disease affecting many systems of the

body. The pathophysiology of the disease includes
severe vasculitis, renal involvement, and lesions of
the skin and nervous system. The primary cause of
long-term stages of a patient's illness.
Transitional circulation:
a transition from one type
of blood vessel to another on moving peripherally

through the circulation.
Treatment selection and prioritization:
the process
the disease has not been determined; viral infection
of selecting treatments and then prioriti7.ing the order
or dysfunction of the immune system has been
in which these treatments are administered. This
suggested. Adverse reaction to certain drugs also
process is based on the relati ve contribution of the
may cause a lupus like syndrome. SLE occurs four
pathogenesis that each treatment addresses with
times more often in women than in men.
respect to oxygen transport deficiencies.
Trunk-ventilation interaction:
Tachycardia: an abnormally rapid heart rate.
Tachypnea: an increased respiratory rate over 20
breaths per minute.
Thallium-20l scan:
the interrelationship of
the shape and movement of the trunk or chest wall on

alveolar ventilation. Trunk and ventilation interaction
depends on body positioning and movement.
a radionuclide scan that evaluates
myocardial perfusion. The tracer is taken up in the
Tuberculosis:
callsed by
an
a chromic granulomatous infection

acid-fast baci Ilus, mycobacterium
Glossary
tuberculosis, generally transmilled by the inhalation

or ingestion or infected droplets and usually affecting
the lungs, although infection of multiple organ
systems occurs
Type I fibers: a type of skeletal muscle fiber that is
also called slow-twitch and is suitable for sustained
.
tonic activity (e.g., the maintenance of posture or

breathing, which require resistance to fatigue).
Type IlA fibers: a type of skeletal muscle fiber that is
also called fast-twitch; this type of fiber is used for
short-term, fast, powerful activity in which
endurance to fatigue is not required.
Validity:
the extent to which a test measurement or
other kind of device measures what il is intended

to measure.
G-13
with high, intermediate, or low probability of

pulmonary embolus.
Ventilation and perfusion matching: the matching
of ventilation and perfusion in the lungs. Optimal
ventilation and perfusion matching occurs in the
mid zones of the upright lung where the ratio is
0.8 to 1.0.
a measurement of the amount of

air that can be expelled at the normal rate of
exhalation after a maximum inspiration, representing
the greatest possible breathing capacity. The vital
capacity equals the inspiratory reserve volume plus
the tidal volume plus the expiratory reserve volume.
Vital capacity (Ve):
The average normal values of 4000 to 5000 ml are

affected by age, physical dimensions of the chest
cage, posture, and gender. The vital capacity may be
an acquired or congenital
disorder of a cardiac valve, characterized by stenosis
reduced by a decrease in functioning lung tissue,
and obstructed blood flow or by valvular
pneumonia, pulmonary resection, or tumors; by

limited chest expansion, resulting from ascites, chest
deformity neuromuscular disease, pneumothorax, or
pregnancy; or by airway obstruction.
Valvular heart disease:
degeneration and regurgitation of blood.

the process by which gases are moved
into and out of the lungs.
Ventilatory strategies: teaching patients to control
breathing with the utilization of ventilatory patterns
(e.g., combining inspiration with trunk extension and
Ventilation:
exhalation with trunk l1exion).

two scans which are
used to assess patients for the presence of
pulmonary emboli. Criteria (BIELLO or PIOPED)
are used to determine if matched defects present
Ventilation-perfusion scan:
resulting from atelectasis, edema, fibrosis,
the total amount of effort

required to expand and contract the lungs; the
physiological "cost" of breathing. Generally, quiet
Work of breathing:
breathing consumes 2% to 3% of the oxygen

consumption and requires 10% of the vital capacity.
If a greater amount is used, one would say the work
of breathing is increased.
I N D E X
bronchiOlitis, 477
bronchitis, 476--477
Abscesses
chronic airflow limitation, 478--481
radiography of, 164, 164
chronic bronchitis, 476--477
respiratory failure and, 579,580t, 581
cystic fibrosis, 483--486
AC; see Assisted control (AC)
ACB;
see
emphysema, 478--481
Active cycle of breathing (ACB)
hypertension, 488
Acetylcholine, pharmacology of, 780
Acetylcysteine (Mucomyst), pharmacology of, 786
Acid base balance
in arterial blood
gases, 153,154
tuberculosis, 487--488
Acute surgical conditions, primary dysfunction secondruy to, 495-508
respiratory failure and, 619
cardiovascular surgery, 501-502
symptoms of, 236t
extrinsic factors, 500
Acidosis, anaerobic metabolism and, 6
Acquired immunodeficiency syndrome (AIDS); see AIDS

sec
Airway clearance
techniques (ACT)
Acute dyspnea, patient history and, 130
Acute heart failure, pathophysiology of, 93
Acute medical conditions, primary dysfunction secondary to,
469-492
alveolitis, 477-478
angina, 488-490
asthma, 481-483
atelectasis, 470--472,471
pathophysiology, 500
postoperative management, 502,502-505, 506, 507
in airway clearance, 325-326
clinical applications of, :149-352, 350, 35 I
intrinsic factors, 500
mobility/recumbency, 500
perioperative course, 496, 496-500, 498
Active cycle of breathing (ACB)
alveolar proteinosis, 478
myocardial infarction, 490-491
pneumonias, 472--476
ICU, and, 236, 2361
Active assistivc cough techniques;
interstitial pulmonary fibrosis, 486
preoperative management, 502
surgical effects, 500
surgical prep, 499
thoracic, 500--502
AD; see Autogenic drainage (AD)
Adenosine, for stress testing, 199
Adenosine triphosphate (ATP)
nuclear imaging and, 203
in oxygen transport, 4, 6-11,13,18
Adenosinetriphosphatase pump, tha lium 20 I'and, "200--20 I
1-1
1-2
Index
Adolescents, myelomeningocele in, 646, 646
anterior chest compression, 375, 375
Adrenal runetion
co stoph renic, 373, 373-374
cardiopulmonary effects of, 109-110, 110
counter rotation, 375, 376,377
laboratory tests in,193t, 194
hands-knees rocking,38 I -382
Adrenergic drugs, pharmacology of,777-778
Heimlich, 374, 374-375
Adult respiratory distress syndrome (ARDS); see also Respiratory
long silting self, 379, 379-380, 380
distress syndrome (RDS)
prone on elbows, 378, 378-379
management of, 625, 625--627
self, 377-382
Adventitious breath sounds, patient assessments and,219-220
associated with eating/drinking, 368
Aerobic capacity, cardiac aging changes and, 671,671--674,673,673t
complications, 368-369
Aerobic metabolism, in oxygen transport, 6-8, 10-11
evaluations, 369-371
Aerosol therapy
infants, 653, 657
defined, 755-756, 756
patient instruction, 371-372
for oxygen transport treatment, 259-260,260
pumps, 368
precautions in, 756
stages of, 369-371
Afterload
physiology and, 321-334
cardiopulmonary physiology of. 65
active cycle of breathing, 325-326
oxygen transport and, 13
assessments,334
Aging changes
autogenic drainage,326-327
cardiac, 670, 670-671
contraindications. 330, 330-334
aerobic capacity, 671,671--674,673, 673t
exercise, 329-330
vascular/autonomic, 673, 673-675, 674t
factors affecting, 332, 332-334
pulmonary, 674--677, 675, 675t
The Flutter"", 328
high frequency chest compression. 328-329
exercise, 675-677, 677, 677t
AIDS; see also HIV
indications, 322-323
cardiopu Imonary effects of, 110
manual hyperventilation, 325
galliu III scintigraphy for, 206
percussion, 323-324
Air, ambient; see Ambient air
positive expiratory pressure,327-328
Air-conditioned environments, oxygen transport and, 16
postural drainage, 323, 324
Air flow measurements
shaking, 325
airway closure volume, 149,149-150
vibration, 324-325
flow volume curve, 147, 148,149
Airway closure volume tests, 149, 149-150
forced expiration, 147
Airway obstructive diseases,drugs for, 784-785
Airway p re s sure release v e ntila t i o n (APR V), defined, 758
Airway clearance techniques (ACT)

clinical applications of, 339-365,365t
Airway resistance,physiology of,58-59, 59
active cycle breathing,349-352, 350, 35 I
Airways, al1ificial; see Artificial airways
assessments, 364
Akinesia, nuclear imaging of, 200
autogenic drainage, 352-354, 355
Albumin
costs,363
laboratory tests of, 190, 191t
dynamic air therapy bed,363-364
in oxygen transport, 15
effectiveness, 362
for plasma volume, 234
exercise,359-361, 361t
Albulerol (Proventil, Ventolin), pharmacology of, 778
future trends, 363
Alkaline phosphatase, laboratory teSls and, 194, 194t
high frequency chest compression, 358. 358-359
Alkalosis, intensive care of, 579, 580t, 581
intrapulmonary percussive ventilator, 363,364
Allergies, treatment of, 784
manual hyperinflation, 348, 348-349
Alpha-adrenergic blocking drugs, pharmacology of, 778-779
percussion, 344-346,345
Alternative long-term care facilities; see Long-term care facilities
positive expiratory pressure, 354-358,355
Alveolar diseases,radiography of, 162, 162
postural drainage, 340, 340-344, 341,342
Alveolar ducts, anatomy of, 42t, 44
selection of,361,361
Alveolar proteinosis
support, 362-363
management of, 478
utilization of,340
pathophysiology of,86, 86-87,478
vibration/shaking,346-349, 347, 348
cough/suction for, 367-382
active assistive, 373-382
Alveolitis
management of,478
pathophysiology of, 477-478
Index
chronic secondary dysfunction and
Ambient air, oxygen transport and, 15-16
management of, 558
threats/treatment, 261
Aminoglycusides, intensive care and, 579,580t,581

Aminophylline, pharmacology of, 785
Anorexia nervosa, cardiopulmonary effects
Amphctnminc (Dextroilmphetamine, Dexedrine), pharmacology
ANS; see Automatic nervous system (ANS)
0 1',
1 10-11 1 , II I
Anterior chest compression, 375, 375
uL 77R
Amylase, lahoratory tcsts of, 193t, 193-194, 194t
Antianginal agents, for reus, 572-573
Anaerobic Illcwh"lism. in oxygen transport, 6-8, 10-11. 13
Anticholinesterases, pharmacology of, 781
Analgesic
Antihistamines, corticosteroids and, 785-786
for leUs, 572-573

fur oxygen transport treatment 259-260, 260
Anaphylactic rcactions. trcatment of.777
Anatomy
Antiinflammatory agents
for oxygen transport treatment, 259-260, 260
treatment with, 784
Anxiety, oxygen transport threats and, 255
bronchopulmonary segment, 4 I, 42t, 43. 44
Aortic volume, cardiopulmonary physiology of, 66, 66
canliupulmonary.2-'-50
Apnea
circulation. 48--50
heart. 44-4R,45,46,47,48
fetal,6Je)
cardiopulmonary effects of, 109

patient asseSSlnents for, 216
respiratory failure and, 579, 580t, 581
lungs.40-A4. 41. 42t, 43
Appearance, patient assessments and, 212-213
lymphatic circulation, 50
APRY; see Airway pressure release ventilation CAPRY)
muscle" 26--40
Arrhythmias
diaphragm, 26, 2li28. 27, 28

erector spi nac 30. 3 I
,
expiration, 27. 31-32

inspiration, 26
intercostal>. 2R, 29
electrocardiograms and, 177, 178, [79-184,179-184

supraventricular. 177, 178, 179,179,180,181
ventricular, 180-184, 182, [83, 184
intensive care of, 236, 236t, 239
larynx. 35. 1536
Arsenic, respiratory failure and, 579, 580t,581
lower airways. 36--40, 37,39t
Arterial blood gase s 153-157

,
nose, 32-34, 33, 34
acid base balance and, 153- [54
pectoralis major, 29, 30
assessment purpose in, 153, 157
pe<:toralis minor, 30
chemoreceptorslhypoxemia response and, [55
pharynx, 33, 34-35
excess/deficit in, 154
ribs. 24-25, 25y
factors affecting, 156-157
scalenes, 29, 29
hemoglobin and, 155
serratus antcrior. 29-30
interpretation of, 155-156
sternocleidomastoid, 28-29.29
normal values in, 154
trapezius. 30. 30
partial pressure of, 154-155
nerve system, 47,47--48. 48
renal buffering and, 154
patient assessments and, 210-211, 21 I, 212, 213
pediatric, 1,36-637
thorax, 23-25. 24, 25
Anesthetics
in secondary dysfunction, 427

Arteritis, cardiopulmonary effects of, 102-103, 103
Artificial airways,761-774
cpinephrine and, 777
care of, 768
respiratory failurc and, 579. 580t, 581
endotracheal,772
extubationldecannulation and, 773-774
Angina
chronic primary
history of, 76 I
management of, 525-526
Montgomery T tubes and, 768
pathophysiolugy of, 525
nasopharyngeal,772
management of, 489--490

pathophysiology of. 90-91. 488--489
Angiography
cardiovascular, 20 [t, 205
respiratory, 206
cardiopu lmonary effects of. 102-103, [03
Olympic tracheostomy buttons and, 766, 767,768, 768

Passy-Muir valves and, 766, 767,768, 768
postoperative complications of, 763-764
mechanical, 764
suctioning of, 768,769-771,77 1 ,772, 773, 773t
tracheostomy tubes and,764-766, 765,767-771, 768,
77 [-774, 773t
1-3
1-4
Index
use of, 761-764, 762
Aspiration
Bacterial pneumonias
GI dysfunction and, 107
infant aspiration pneumonia in, 642
meonium aspiration syndrome (MAS), management of,
641-642
Aspiration pneumonia, pediatric, 642
Assessments;
see also
specific value being tested, e.g., Blood
gases, arterial
multisystem laboratory,
Barbiturates, respiratory failure and, 579, 580t,581
Baroreceptors, defined, 783
Barrel chest, patient assessments for, 214-2 I 6,216
J 89-195
Basal metabolic rate (BMR), in oxygen transport, 19
Assisted control (AC), defined, 758
Beclomethasone, pharmacology of, 785
Assisted mechanical ventilation, defined, 758
Bed rest
Asthma
alternatives to, 293-294
chronic primary
hazards of, 293
management of, 5 I 9-520
pathophysiology of,S I 9
indications for, 294
as therapy, 291-292
pathophysiology of, 77-80, 78, 79, 80,481-483
Benztropine mesylate (Cogent in), pharmacology of, 783
pediatric, 642-M3
exercise for, 660--66 I
Beta-adrenergic blocking drugs, pharmacology of, 778-779
Beta-blocking agents, for ICUs, 572-573
primary, management of, 483
primary/ICU, 589-59 I
Bagging, obstructive lung disease and, primary/lCU, 587
Beta2-receptor stimulants, pharmacology of, 778
Bethanechol (Urccholine), pharmacology of, 780
Blood
pathophysiology of, 589
complete count, 190--192, 191t
treatment of, 777,784
desaturated, 19
beta2-receptors stimulants for, 778
laboratory tests of, 190-- I 92, 191t
Asymmetrical dysfunction, facilitation and, 405-406
oxygen transport and,
Atelectasis
differential diagnosis of, 227t
flow, 12, IS
management of, 472
hematocrit, 14
pathophysiology of, 470-472,471
hemoglobin, 11-12,14-15,155
radiography of, 164-165, 165,166
respiratory failure and, 579, 580t, 58 I
plasma, 11-12,15
Atenolol (Tenormin), pharmacology of, 779
viscosity, 14
Atherosclerosis, pathophysiology of, 89-90
volume, 13-15
Atmospheric air content, oxygen transpol1 and, 15-16
Blood gases, arterial, 153-157
ATP; see Adenosine triphosphate (ATP)
acid/base balance of, 153-154
ATPase pump, thallium 201 and, 200--201
assessments of, 153, 157
Atrial pressure, left, ICU measurement of, 24 I -243
Atrioventricular (A V) conduction, electrocardiograms and, 170-172
Atropa belladonna, extract of, 782
hemoglobin in, 155
Auscultation, 217,217-221, 2J8, 219
ICUs and, 236-237
breath sounds, 218-220, 219
interpretation of, 155-156
chest sounds, 217-218
normal values in, 154
heart sounds, 221-222
partial pressure of, 154-155
secondary dysfunction and, 427
renal buffering and, 154
stethoscope use in, 2 I 7,217
techniques for, 217, 218
Blood loss, dextran for, 234
Blood pressure, oxygen transport threats and, 254
Blood urea nitrogen (BUN), laboratory tests of, 192, 192t
clinical applications and, 352-354, 355
Automatic nervous system (ANS), oxygen transport and, 19
Autonomic nervous system, systemic disease effects on, 106-107
A V conduction; see Atrioventricular (AV) conduction
base excess/deficit of, 154
chellloreceptors/hypoxemia responses in, 155
factors affecting, 156-157
AU'opine, pharmacology of, 782
Azathioprine, for organ transplants, 718
I 1-15
cardiopulmonary physiology of, 67-68,68
BMR; see Basal metabolic rate (BMR)

Body mechanics; see Positioning, body mechanics
Body positioning; see Positioning
BPD; see Bronchopulmonary dysplasia (BPD)
Bradydysrhythmias, intensive care of, 239, 240t-241 t
Index
Bradypnea, patient assessments for, 216
future trends in, 363
Breath sounds, patient assessments and, 218-220, 219
high frequency chest compression, 358, 358-359
abnormal, 219
intrapulmonary percussive venti lators, 363, 364
adventitious. 219-220
manual hyperinflation, 348,348-349
bronchial, 218
percussion, 344-346, 345
bronchovesitular,218
positive expiratory pressure,354-358, 355
extrapulmonary,220
postural drainage, 340, 340-344, 341, 342
vesicular, 218-219
selection of,361, 361
voice. 220
support, 362-363
Breathing
utiliwtion of, 340
control in, 53-55,54
vibration/shaking, 346-349. 347,348

cough/suction, 367-382
exercise testing/training in
primary dysfunction, 420, 420-421
seconoary dysfunction,435-436
complications of, 368-369
glossopharyngeal, 410-412,412
costophrenic, 373,373-374
laterRI costal facilitation of, 396, 397, 399, 399
counter rotation,375, 376, 377
mechanical function 01',56-59,57,58,59
eating/drinking type, 368
oxygen transport treatment and, 261
evaluation of, 369-371
patient assessments and, 216
hands-knees rocking,381-382
patterns
Heimlich, 374, 374-375
musculoSKeletal/neuromuscular disorders,689, 691-693,

692,693,694,695
long sitting, 379, 379-380, 380

patient instruction and, 371-372
paced,435-436
paradoxical. 438-439
pumps, 368
physiology of, 321-334

active cycle of breathing,325-326
assessments in, 334
self, 377-382
stages of, 369-371
Bronchi, radiography of, 162, 162
autogenic drainage, 326-327
Bronchial breath sounds, patient assessments and,218
contraindications for,330,330-334
Bronchial muscle relaxants
exercise, 329-330
factors affecting, 332,332-334
The F1utterT", 328
high frequency chest compression, 328-329
indications for, 322-323
manual hyperventilation and, 325
percussion and, 323-324
positive expiralOry pressure, 327-328
postural drainage and, 323, 324
ephedrine as, 778

inhaler treatment and,784, 785
Bronchiectasis
chronic primary
pathophysiology of, 80, 80-83, 81
mdiography of, 162, 163, 164
Bronchiolitis
shaking and, 325
acute medical conditions, primary secondary to, 477
vibration and, 324-325
repattcrning in, 393
management of, 477
secondary dysfunction
pathophysiology of,477
exercise testing/training and, 435-436

paced,435-436
systemic disease effects on, 104
Breathing clearance techniques
airway (ACT), 339-365, 365t
active cycle breathing, 349-352, 350,351
assessments of, 364
autogenic drainage, 352-354, 355
Bronchitis
chronic
differential diagnosis of,227t
pathophysiology of, 72-73,76-77, 514-515
chronic primary
Bronchodilators
costs, 363
betarreceptors stimulants as, 778, 779
dynamic air therapy bcd, 363-364
for leUs, 572-573
effectiveness of, 362
metered-dose inhalers, 723-724
exercise, 359-361, 361t
1-5
Index
1-6
Bronchograms,radiography of,162, 162
arrhythmias,91-92
Bronchopulmonary dysplasia (BPD),preterm infants and,641
chronic hean failure,93-94
Bronchopulmonary segments, anatomy of,41,42t, 43,44
compensated/decompensated heart failure, 94
Bronchovesicular bn:ath sounds, patient assessments and,218
congestive heart failure, 93
Buildings,health issues and,16
coronary artery disease, 89-90, 91-94
Burns
respiratory failure and, 579,580t,581
patient classification and,133
secondary dysfunction and
patient history and, 133
pediatric,639t,639-640
management of,613-615
pathophysiology of, 612--{)13
respiratory failure and,620
BUlleLfly techniques,ventilation facilitation and,408,409,410
systemic, 100-101
fluid balancc effects of,101
ischemic, 109
II C acetate,for cardiovascular testing,201t,203
Cardiac function
CAD; see Coronary artery disease (CAD)
afterload in,13
Cameras, for nuclear imaging,198-202
aortic volume and,66, 66
Capillary function,in oxygen transport,18
cardiopulmonary physiology of, 65,65-67,66, 67t
Carbachol (Carcholin),pharmacology of,780-781
electrocardiograms and, 169-187
Carbohydrates,laboratory tests of,194, 194t
arrhythmias, 177,178,179-184,179-184
Carbon dioxide
conduction, 170-172,171
blocks, 184--186, 185, 186
ambient air/oxygen transport and,15-16
transport physiology of,68-69
evaluation of, 174, 174--177,175,176,177
Carbonic anhydrase,in C02/H02 reactions, 14
myocardial infarction, 186-187, 187
Cardiac aging changes
rate, 174, 174-176, 175, 176
aerobic capacity,671, 671-674, 673,673t
recording, 172, 172-174,17,1
defined,670, 670-671
rhythms, 176- 177, 177
use of, 169-170
vascular/autonomic, 673, 673-675, 674t
heartbeat physiology and, 66
Cardiac arrest, treatment of, 777
left atrial pressure, 241-243
Cardiac aLThythmias
electrocardiograms and, 177, 178, 179-184, 179-184
supraventricular, 177,178, 179, 179, 180, 181
myocardial contractility in, 13
myocardial viability and, 202-203
myocardial workload reduction and,592, 59l-594, 596
ventricular, 180-184, 182, 183, 184
intensive care of, 236, 236t,219
nuclear imaging of,200
output in, 11,12,14,17,636
patient assessments in,220-221
respiratory failure and,619-620
preload, Il
Cardiac development
anatomy of,44-48,45,46,47,48
septal defects/ICU and,245
fetal, 636
ventricular
diastole/systole,66
neonatal,636
left assist devices/lCU,245
Cardiac disorders
dyspnea/patient history and,134
left ejection fraction, 200
exercise testing/training in, primary dysfunction,419
left end diastolic volume, 13
fluid balance effects of,101
left fetal anatomy of,636
functional/therapeutic classification of, 133
left output,636
ischemic,109
left pressure/ICU, 241-243, 245
left ventricular assist devLces,245
right ejection fraction, 200
right pressure/1CU,241-243
chronic primary dysfunction and,526-528
Cardiac sounds,patient assessments and,221-222
Cardiac surgery
pathophysiology of,91-93,490
myocardial ischemia,245
oxygen transport threats and,254
treatment,261
pathophysiology of
acute heart failure, 93
ICUs and, 245
open heart, 595,596
CaJdiac transplants
acute phase care in,710-7 I 1,714
assessments in,708
considerations jn
Index
availability. 704
lCUs and
ethical. 704-705
monitoring systems, 229-246
organ donation, 704
patient management, 565-577
organ preservation, 704
primary dysfunction, 579-596
patient education, 706
incentive spirometry and, 754, 755
p ychosocial impl icat ions, 705-706
intermittent positive pressure breathing and, 753-755
purpose of. 704
laboratory assessment and, 189-195
trcnds in. 706
lung injury and, 625, 626
waiting list criteria. 705. 705
measurements and, I 17-123
waiting time. 705
mechanical ventilation and, 756-759
when to
musculoskeletal/neuromuscular disorders and. 679-701
lise,
704
equipmcnt/monitoring in, 708-709
neonatal, 635--{i63
cxercise guidelines in. 712
nuclear imaging/radiopharmaceuticals and. 197-207
facility vs. home based rehabilitation in, 716-718
organ failure and, 628t, 628--{i29
goals in. 712
oxygen thera py and, 749-753
history of. 704
oxygen transport in, 3-20
interventions in. 710-711, 714
pathophysiology of, 71-95, 251-263
medication in. 716-718
patient assessments in. 209-228
other tr lI1splants and, 709-710
patient education and, 453-463
outpatient care in, 713-714, 714
patient history in, 127-142
pos t-transplant care in , 70S
pediatric, 635-663
pre-transplant care in. 70H
physical therapy role in, 3-20
rej ec tion signs in, 714, 715, 716
physiology in, 53--{i9
surgery and, 706
positioning and, 299-318, 737-747
therapy in
postoperative complications and, 621, 621-624, 622
assessments, 707-708
primary dysfunction and
tlefined, 708-709, 710. 710-713
acute medical conditions and, 469-492
medical management. 707, 707t
acute surgical conditions and. 495-508
musculoskeletal considerations, 707, 709-710
chronic, 513-535
physiology and, 707
ex e rcise testing/training in,417-423

rcus and, 579-596
therapist rt' quiremcnts, 706

Cardiogenic shock. ICUs and, 245
pulmonary aging changes and, 674-677
Cardiopulmonary failure, primary. intensive care of, 579, 580t, 581
pulmonary function tests and, 145-151
Cardiopulmonary function
respiratory failure and, 617--{i30
acute medical conditions and, 469-492
respiratory muscle fatigue and, exercise training,443-451
acute surgical conditions and, 495-508
secondary dysfunction in
aerosol therapy and, 755-756, 756
chronic, 537-561
airway clearance techniques and, 339-365, 365t
exercise testing/training in, 425-441
cough/suction, 367-382
physiology,321-334
lCUs, 599-615
sepsi:; and, 628t, 628-629
anatomy in. 23-50
shock and, 627--{i28
arterial blood gases in, 153-157
systemic diseases and, 99-112
artificial airways and, 761-774
transplant patients and, 703-718
cardiac aging changes and. 671--{i74
treatment in, 256-263, 257,258-259,260,261,262
chronic primary dysfunction and. 513-535
ventilation facilitation and, 383-415, 756-759
chronic secondary dy sfunction and, 537-561
x-ray interpretation, 159-167
documentation and, 12:1-126
Cardiovascular disease, chronic primary
drug and,775-7R6
exercise/mobility and. 265-296
exercise testing/training in
pri mary dysfunction. 417-423

secondary dysfunction,425-441
Cardiovascular reflex, defined, 783-784

Cardio va:;cular su rgery , p rimary dysfunction secondary to,
501-502
horne-based/facility care and, 721-732
Carotid barorece ptors, defined. 783
humidity therapy and, 755
Carrying, primary dysfunction and, 4 I 9-420
1-7
1-8
Index
Cascade oxygen, defined, 12, 12
ventilation facilitation and,392
Case studies
Chest tubes, in ICUs, 235, 235-236
exercise testing/training in, secondary dysfunction, 437--440.
438,439
Chest walls
oxygen transport and, 16-17
patient assessments and, 225-228
patient assessments and, 214-216, 216
Catecholamines, laboratory tests of,194
restriction effects on, 102-103, 103
Catheters,in (CUs
Chloroflurocarbon propellants, for metered-dose inhalers, 786
Swan Ganz,233,241-243, 243
Cholesterol,laboratory tests of, 191, 191 t
two-lumen, 241-242
Cholinergic blocking drugs,pharmacology of, 782
CBC; see Complete blood count (CBC)
Cholinergic drugs,pharmacology of,780-781
Cellular respiration
Chronic airflow limitation
oxygen transport and, 3, 4-8, 10
management of, 481
oxyhemoglobin dissociation and, 15
pathophysiology of, 478--480.514
Cellular responses, exercise and. 269-270
Chronic airway obstruction disease (COA), pathophysiology of,
Central chemoreceptors, cardiopulmonary physiology of,54
71-72
Chronic bronchitis
Central nervous system (CNS)
amphetamines and,778
treatment of, 261
pathophysiology of, 72-73,76-77,514-515
systemic disease effects on, 103,105-106
primary
Central venous pressure (CYP), ICUs and,243-244
Cerebral palsy
pathophysiology of,476--47 7
Chronic heart failure (CHF),pathophysiology of, 93-94
Chronic obstructive airway di se a se (COAO), pathophysiology of,
71-72
Chronic obstructive lung disease (COLD), 71-72
Cerebrospinal fluid (CSF), cardiopulmonary physiology of, 54
CF; see Cystic fLbrosis (CF)
patient assessments in, 214-2 J 5,222,224
Chemical vagotomy, defined, 783
Chemoreceptors
respiratory failure and, 579, 580t.581
cardiopulmonary physiology of
Chronic primary dysfunction
central, 54
angina,525-526
peripheral, 54-55
asthma,519-520
response to hypoxemia and, 155
bronchiectasis, 520-521
Chest development, in musculoskeletaVneuromuscular disorders,
682-689,684-689,686t
Chest pain, patient history and, 137-138
esophageal, 139
Chronic obstructive pulmonary disease (COPO)
chronic airflow limitation, 514
chronic bronchitis, 514-516
cystic fibrosis, 521-522
diabetes mellitus, 533-535
pericardial,139
emphysema, 516-518
pleuritic,138
hypertension, 531-533
pulmonary hypertension, 139
interstitial lung disease, 522-523
Chest radiographs, lateral, 159-160
lung cancer,523-524
Chest sounds, patient asse ssments and, 217-218
myocardial infarction,526-528
Chest therapy
obstructive patterns in, 514-522
child, 657-660, 658
peripheral vascular disease,529-531
positional rotation, 658-659,659, 660
primary cardiovascular disease, 525-535
pre/postoperative, 659-660
restrictive patterns in, 522-523
compression
anterior, 375, 375
valvular disease, 528-529
Chronic renal insufficiency, chronic secondary dysfunction and
high freq uenc y, 358, 358-359
infant
airway suctioning, 653, 657
Chronic secondary dysfunction
percussion, 652---{i53, 657
ankylosing spondylitis and, 557-558
positional rotation, 649,649,650-651
cerebral pal sy and, 546-547
postural drainage, 652,653t, 654---{i56
chronic renal insufficiency and, 560-561
Index
L ollagen v<ls u"lIkonn ctivc tissue diseases and, 555-556

'
ischemic heart disease and, 109
hemiplegia and. 541-543
Intc sequelae or poliomyd itis and. 550-552
pleural effusions and, 101
lllltitirk sL'icrosis and, 544-546
primary/lCU, 594, 594, 596
l11usL'lIlar dystrophy and, 5]8-5]9
radiography of, 164 165, 166,167

,
osteoporosis and, 553-555
Connective tissue disorders

P<lrkinson's disease and, 543-544

rheum atoid arthrilis and, 558-560
scleroderma <Ind. 556-557
spinal L'Ilrd injury and. 54t\-550
systemic, cardiopulmonary effects of, 103, 103
systemic lupus erythematosus ancl. 555-556
Consumption, oxygen; see Oxygen, consumption
thoracic JdUllllitics and, 552-553
Content, oxygen; see Oxygen,content

Continuous positive airway pressure (CPAP)
Circul'ltion
anatomy in. 40-49
defined, 758
fetal. 636
neo nata l, 636-6]7
Controlled mechanical ventilation (CMV), defined, 758
peripheral
Contused lung, respiratory failure, 579, 580t, 581
anatomy in. 4R-49
COPD; see Chronic obstructive pulmonary disease (COPD)
in oxygen tJ'ansrort, 18
Coronary artery disease (CAD)
physiology of, fl7, 67t
associated conditions of, 90-94
threats/trealment,262
cholesterol and, 191, 191 t
pulmonary. threats/treatment, 261
pathophysiology of, 71,89-90,91-94
Clol1idine (Catarrcss), pharmacology of, 779
primary/lCU
Closing volumL'fairway closure, pulmonary function tests and, 149,

1 49 150
Closure of ductus arterimus, pediatric anatomy and, 636---63 7

Closure or' foramen ovale, pediatric anatomy and,636---637
single photon emission tomography (SPECT) for, 199

transplant medication and, 716
Clubbing
Corticosteroids
Crohn's disease and, 214, 214
Cushing's syndrome and, 785
hepatic fibrosis and. 214, 214
pharmacology of, 785

Costophrenic assist techniques, 373, 373-374
patient assessments for, 214, 214

CMY; see Controlled mechanical ventilation (CMY)
Costs, airway clearance techniques and, 363
CNS; see Central nervous system (CNS)
Cough
COA; see Chronic airway obstruction disease (COA)
COAD; see Chronic obstructive airway disease (COAD)
Co gulation, laboratory tests and, 190, 191t
costophrenic, 373, 373-374
Cognition, oxygen trans port threats and, 255
counter rotation, 375, 376, 377
COLD; see Chronic obstructive lung disease (COLD)
hands-knees rocking, 381-382
Collagen vascular/connective tissue diseases. chronic secondary

dysfunction and
Heimlich, 374, 374-375

long sitting self, 379, 379-380, 380
pathorhysiology of, 555
self, 377-382
Collimatol.s. Jcfined, 19R
complications of, 368-369
Combined ventriL'ular output (CVO), fetal anatomy of, 636
eating/drinking and, 368
Community concerns. home-based/facility care, 721-7]2
evaluation of,369-371
Complete blood count (CBC), laboratory tests and, 190-192 191t

,
in museuloskeletalfneuromuscular disorders, 698
Comrliance, cardiopulmonary physiology or. 56-57, 57
obstructive lung disease and, primary/lCU, 588
Computerized tomography (CT), for respiratory use, 206-207
patient history and, 135, 136t, 137
Conduction, ck troeardiograrns and, 1 70- 172 171

,
blocks, 184-186, 1 5, 186

CongenitaJ. IKart disC'asc
neonate s and, 6.\9-640
patent ductus arterio>lIs and, 639-640
Congestive hemt failure (CHF)
intensive carc or. 2]5, 245
patient instruction and, 371-372

pumps and, 368
reflex physiology of, 55
stages of,369-371
suction and, 367-382
Counter rotation
assist techniques,375, 376, 377
1-9
Index
1-10
chronic primary dysfullction and
for ventilation, 407-408. 409
CP; see Creatine phosphate (CP)

CPAP;
see
Continuous positive airway pressure (CPAP)
Diaphragm
Crackles,defined, 219-220
Craniosacral therapies, secondary dysfunction and, 437
anatomy of. 26,26-28, 27, 28
Creatine phosphate (CP), in energy transfer, 8
contractilit y and, 444-448
Creatinine, laboratory tests of,
1 92t.
movement and, 222, 223
192-193
ventilation facilitation and
Crepitus, defined, 223
Cricoarytenoid arthritis. respiratory failure and, 579. 580t, 581
breathing, 389, 390, 391,392.394,394, .105, 396, 396
Critically ill patients
inhibition, 402-405, 404. 405
Diastole, ventricular physiology of. 66
acidosis/anaerobic metabolism in, 6
arterial blood gases in, 156
Dicyc10mine (Bentyl), pharmacology or, 783
oxygen consumption in, 13
Di fferential diagnosis, patient assessments and. 227t
oxygen transport in, 3
Diffuse interstitial pneUillonitis, cardiopulmonary effects of,
102-103, 103
Crohn's disease, clubbing and, 214, 214
Diffuse interstitial pulmonary fibrosis, pathophysiology of, 83-85
Cromolyn sodium (Intal), pharmacology of, 785-786
Diffusion
cardiopulmonary physiology of, 60, 60-61
Cross-referrals, in home-based care, 728-729
oxygen transport and,5. 12, 17
Crystal cameras, for Duclear imaging, 198
Diphosphoglycerate (DPG), in oxygen transport, 15
CSF; see Ccr\!brospinal fluid (CSF)

CT; sec Computerized tomography (CT)
Dipyridamole, for pharmacologic stress testing. 199
Curariform drugs,respiratory failure and, 579, 580t, 581
Discharge, from ICUs, 574
Cushing's syndrome, corticosteroids and, 785
Disseminated intravascular coagulation, pulmonary hemorrhage
and, 108
Cyanosis
intensive care of, 240
Disseminated intravascular coagulation (DIC), laboratory tcsts of,

190,191t
patient assessments and, 214
Cyclopentolate (Cyclogyl), pharmacology of, 783
D02; see Oxygen, delivery
Cyclosporin, for organ transplants, 717-7 J 8
Documentation, 123-126
side effects of. 718
Cystic fibrosis (CF)
assessments and. 1 25- J 26
content for, 124
management of, 484-486. 521-522
exercise testing/training and, secondary dysfunction,426-432
pathophysiology of, 483-484, 521
in homellong-term care facilities, 727
patient assessments and. 225. 227
objective. 125
pediatric
plans and. 126
exercise for. 661
pur'pose of, 123
recording electrocardiograms and. 172, 172-174, 173
Pseudomonas aeruginosa and, 643--&14
subjective, '124-125
respiratory failure and. 579, 580t, 581
types of, 123-124
Doppler echocardiography, defined, 20 It, 204
Down syndrome
2D echocardiography, defined, 201t. 203-204. 205
cardiology of, 639t
Dead space. defined,145-146
managcment of. 645t, 646--647. 647
Death
Doxazosin (Cardura), pharmacology of, 778
exercise and dying patients, 576-577, 577
DPG; see Diphosphoglycerate (DPG)
ICUs and, 576-577, 577
Dressing techniques, ventilation Lrcilitation and, 389
patient fear in, 577, 577
Drinking, coughs associated with, 368
Debt. oxygen; see Oxygen, debt
Drugs, 775-786
Deep vein thrombosis, management of, 623-624
for airway obstructive disease,784-785
Delivery, oxygen; see Oxygen,delivery
autonomic pharmacology of, 776
Demand, oxygen; see Oxygen. demand
rcus and, 572-573
Desaturated blood/C02, oxygen transport and, 19
immunosuppressive,717-718, 718
Dextran, for blood loss, 234
in intensive care, 572-573
Diabetes mellitus
pharmacology of
adrenergic agents,777-778
Index
anticholineSterascs.781
antihistamines, 785-786
Eating. coughs associated with, 368
antiinflammatory agents, 784
Eccentric resistance techniques. ventilation facilitation and. 414
beta- Ad rene rg ic blocking dru!!s. 778-779
ECD; sec Endocardial cushion defects (ECD)
bet32-receptors stimul ants, 77
ECG; see Electrocardiograms; Elect r ocardiograms (ECG)
bronchial muscle re l a x ants. 778
Echocardiography
bronchodilators. 778, 779
defined, 20 I t, 203-205
cholinerg i c blockin g drugs, 782
M -mode, 20 I t, 203-204, 205
d rugs. 78{}-78 I
cort icos tcroi C\s . 785
cholinergic
Edem a
patient assessments and. 223
cxpeetor'lnts. 785, 786
patient history and, 14{}-141
inhalers. 777, 786
r adiogra phy of, 165, 166
mucolytics, 786
Edrophonium (Tensilson), pharmacology of, 782
sympaiholytic drugs. 779
Education, patient, 453-463
sympathomimctic drugs, 7R4-7X5
defined, 454-456
vasa Iilators, 777. 778
Down syndrome, 645t, 646-647, 647
xanthines. 785
effectiveness in, 461-462
rcspiratorylcardiovascular systems and. 775-776
fundamentals of, 454-456
sympathetic ncurotransmission of, 776
interdisciplinary care and, 463
for trans plant pa tients
leaming needs assessments and, 457, 459
cardiac, 716-- 718
,Ireas, 457,457.459
pulmonary . 717-718
findings, 459
Dry environments. oxygen transport and, 16
goals, 459
DTPA (Tel; see Tcchnetium-99M-diethylcne triamine penta-acetic

(DTPA) aerosol
needs-based, 456
patient adherence and, 462
management oj', 647--648
teacher-learner relationship and, 462
Dynamic activitics, ventilation facilitation and, 388-389
Edward's syndr o m e, cardiology of, 639t
Dynamic a ir therapy bed. clinical applications of, 363-364
beLl. clinical a p p l ications and. 363-364
Dys func tion; see speci fic typcs, e.g . . Primary dysfun ction.
Secondary dysfunction
patient history and. 128-130. 129. 134-135
acute, UO
in cardiac patient s . 134
in
lCUs, 238. 239-241, 240t-241t
myocardial int'arction and, 186-187. 187
recording of, 172, 172- I 74, 173
use
exercise limiting, 1 31t

on exertion. 13{}-131. 131t. 132, 132t. 133.133, 134
fu nc tio n al, 135
of, 169-170
Electroencephalo grams (EEG), in IC U s, 246
Electrolyte abnormalities, respiratory failure and, 6 I 9
El ect rolyte balance
onhopnea. 134
ICUs and, 23{}-231, 234t, 234-235
paroxysmal noctumal. 134-135
laborato r y tests and, 191t, 191-192
platypnea. 135
trcpoplH:a. 135
Elevations, high; see High elevation environments
Dysrhyt h mias
Embolism. pulmonary, differential diagnosis of, 227t
ca rd iopulmona r y effects or. 101
electrocardiograms and. 177, 17X. 179-184. 179-184
pathophysiology oc. 91-92
arrhythmias and. 177, 178, 179-184, 179-184
evaluation of, 174. 174-177, 175, 176, 177
pat ient assessments and. 216
ventricular. 180-184. 182, 183. 184
Elect r oc ardiograms (ECG), 169-187
blocks, 184--186, 185, 186
Dyspnea
i nte n si vc care or. 236, 236t. 239
EEG; see Electroenc e phalograms (EEG)
conduction and, 170-172, 171
Dyskinesia. nucie,lr imaging of. 200
supraventricular . 177. 178. 179. 179,
tools. 457
methods in, 459-461, 460t, 461
D uchcn ne ' s musc ular dystrop hy

card io logy of. 639t
Dynamic ail ther a py l "
1-11
ISO, 181
Emotional stress
fight/f1ighUfright and, 20
Emphyse ma
chronic primary
management of. 517-518
1-12
Index
dyspnea and
pathophysiology of, 5 16-5 17
on exertion, 130- 13 1. 13lt. 132. 132t,133. 133, 134
limiting, J3 l t
intensity/duration of, 723
pathophysiology of, 73,73-77,74. 75,76,77,478-48 1
long term respons s of. 278-280,279
radiography of. 162, 163
monitoring and, 275, 285-286, 288, 289, 290. 29 1-292
Endocardial cushion defects
(ECD), management of, 640
multisystem effects of. 278-280, 279
oxygen transport and. 8. 10- 12, 13. 19
Endocrine disorders
cardiopulmonary effects of, 109- 1 10, 110
oxygen transporUmetabolic demand and. 267-268,268. 270
pathophysiological conditions and. 270-271. 27 I
laboratory tests and, 193, 193t
for pediatric asthma. 660-661
Endotracheal artificial airways, 772
Energy transfer, oxygen transport and, 4. 6--8,8, II
prescription for, 266--267. 268, 270-276. 273. 274t. 276. 278t
Enhancement ratio, oxygen; see Oxygen, enhancement ratio
preventive effects of. 291-292. 295
Environment
pulmonary aging changes and, 675-677,677. 677t
ICU, 576, 576y
stimulus in. 277-278, 278
oxygen transport and. 15- 16
stress and. 20
testing/training and
Eosinophilia, pulmonary, pathophysiology of, 85
Eosinophilic granulomas, pathophysiology of, 85-86
prescriptions in, 274,274. 276--277,280-285,281. 282t,
283t. 284--286, 290,290-29 1
Ephedrine, pharmacology of, 778, 785
Epiglottitis, respiratory failure and, 579,580t,58 1
breathing, 420,420-421
Epinephrine
laboratory tests and. 194
guidelines, 42 1-422
pharmacology of, 777. 778, 784
heart disease. 419
reversal of. 778
lung disease, 4 17-4 18
Eq uipment
for active cycle breathing
traditional, 422-423
(ACB), 349-352. 350, 351
upper/lower extremity, 4 19-420
for autogenic drainage, 352
secondary dysfunction, 425-441
for exercise airway clearance, 359-361, 36 1 t
breathing training, 435-436
for high frequency chest compression, 358,358-359
case studies, 437-440. 438. 439
for manual hyperinflation, 348. 348-349
evaluation, 426-432
for percussion, 344
patient history. 428,428. 429, 430
for positive expiratory pressure, 354--355
patient management. 432-433. 435
for postural drainage, 340,340-344,34 1,342
psychological factors. 425-426,426
for shaking, 346--349. 347, 348
testing guidelines, 430-43 I
for transplant patients
therapeutic options, 436-437
training guidelines. 43 1-432,432
cardiac, 708-709
training and prescription for, 722-723
pulmonary, 708-709, 7 15
for transplant patients,cardiac, 7 I 2
for vibration. 346--349, 347, 348
Erector spinae. anatomy of, 30, 3 1
Exercise stress testing, nuclear/cardiovascular. 199
Ergometers, for oxygen transport treatment. 259-260. 260
Expectorants, pharmacology of. 785. 786
Erythrocyte disorders. cardiopulmonary effects of, 108
Expiration
Escherichia coli, in bacterial pneumonias, 474-475
forced. 147
Esophageal chest pain, patient history and. 139
muscle anatomy in. 27, 31-32
Ethical considerations. transplant patients and. 704-705
ventilation facilitation and, 388
Eupnea. patient assessments and. 2 1 6
External thorax manipUlation, contraindications for,331, 331-332
Exercise. 8 , 10- 12. 1 3 , 1 9
Extrapulmonary breath sounds, patient assessments and, 220
acute responses to. 270-271. 27 1. 272. 273, 274. 274t
airway clearance teChniques and. 329-330. 359-36 1. 361 t
assessment of. 295-296
18F-f1uoro-deoxyglucose (FOG), for cardiovascular testing. 20 1t. 203
bed rest and. 291. 29 1-295
Facility-based care
cardiac aging changes and. 671, 67 I -674,673. 673t
concerns in, 723
cellular responses to. 269-270
documentation in, 727
deconditioning effects and, 723
monitoring in
defined. 265-266
cardiopulmonary, 725. 725-726
dying patients and, 576--577. 577
oxygen, 726--727
Index
1-13
Friedreich's ataxia, cardiology of. 639t
cardiac, 716--718
Fright/flight/fight reactions; see Fight or flight syslCms
pulmonary, 716--718
Function optimization, defined, 570, 571
work consideratIons in, 724-725
Functional reflex, defined. 783-784
FAD; see Flavin adenine dll1uclcotide (FAD)
Family history, patients and, 142
Gallium scintigraphy, for respiratory testing,206
Fatigue. patient history and, 140
FDG; sec 18F-fluoro-deoxyglucose (FDG)
Gallops, patient assessments and, 221
Fear
Gamma cameras,defmed, 198
dying patients and, 577, 577
Ganglionic blockade,defined,781
oxygen transport threats and, 255
Gas exchange
FET; see Forced expiratory techniques (FET)
cardiopulmonary physiology of
Fetal alcohol syndrome (FAS), cardiology of, 639t
diffusion, 60, 6
Fetal development, circulatory, 636
perfusion, 6 J -65,62, 63,64
61
exercise testing/training in,primary dysfunction, 418
Fetal disorders
in oxygen transport, 5,16
fetal alcohol syndrome, 639t
diffusion,5,12, 17
meconium aspiration syndrome,641-642
perfusion, 17
Fibrinogen, oxygen transport and, 15
ox ygen transport threats and, 254
Fibrobullous disease, cardiopulmonary effects of, 102-103, 103
Gaseous vapors, environmental effects of, 16
Fibrosis
Gases, arterial blood; see Arterial blood gases
diffuse interstitial pulmonary, pathophysiology of, 83-85
Gastrointestinal disorders
Fight or flight systems
systemic effects and, 107, 107
Glaucoma,treatment of, 78
parasympathetic system and, 776
781
Glossopharyngeal breathing, ventilation facilitation and,
First pass radionuclide testing, cardiovascular, 199, 20 It
410--412,412
Fixed position radiographs. interpretation of, 159-160
FK 506, for organ transplants, 718
Goals
Flail chest, patient assessments and, 214-216, 216
for home-based care,73
Flavin adenine dinucleotide (FAD), in energy transfer, 8
for lCU patient management, 568-572,570
732, 731, 732
for musculoskeletal/neuromuscular disorders, 70
Flight or fight systems
70 I
for transplant care, 709,712, 713t, 715
ox ygen transport and, 2 0
parasympathetic system and. 776
Gravitational flow, physiology of, 61-65, 62, 63, 64
Flow
Gravitational stress, oxygen transport and, 19-20
Gravity
blood in oxygen transport,12, 15
gravitational, 61-65, 62,63, 64
body positioning and,300-301, 301
volume curve, 147, 148, 149
in musculoskeletal/neuromuscular disorders, 68
Fluid balance
687,
682-687,686t
cardiac effects on, 101
Guanethidine (lsmelin), phalmacology of, 779
cardiopulmonary physiology of, 67,67t
Guillain-Barre syndrome, respiratory failure and,579, 580t, 581
hematologic conditions and, 108
ICUs and, 230-231, 234t, 234-235
oxygen transpol1 and, 13-14, 17
Hands-knees rocking assist techniques, 381-382
plasma protein disorders and, 109
Hct; see Hematocrit (Hct)
HDL; see High-density lipoproteins (HDL)
systemic disease effects on, 101-102
Head down body positioning,312
Head injuries, secondary dysfunctionlICU
Fluid collection, in ICUs, 235, 235-236
Fluid volume, oxygen transport threats and, 255
management of, 606-609, 608
FluLlerrM, for airway clearance, 328
pathophysiology of, 606--609, 607
Flutter valves, for oxygen transport treatment, 259-260, 260
Health issues, oxygen transport and, 16
Forced expiration, pulmonary function tests and, 147
Heart anatomy, 44--48, 45,46, 47,48
Forced expiratory techniques (FET), active cycle breathing and,

349-352,350,351
Heart block, treatment for, 777
Heart disorders
Fractures, secondary dysfunctionllCU and, 605-606
exercise testing/training in, primary dysfunction,419
Friction rub, defined, 220
fluid balance effects of, 101
1-14
Index
ischemic. 109
left ejection fraction,200
myocardial dysfunctionlrespiratory failure and, 620
left end diastolic volume, 13
left output, 636
chronic primary dysfunction and,526-528
left pressure, 241-243
management of,490-49 j
Heart sounds,patient assessments and, 221-222
pathophysiology of, 91-93,490,526
Heart surgery
myocardial ischemia,245
ICUs and,245
myocardial perfusion, 202-203
open,595,596
oxygen transport threats and. 254
Heart transplants
treatment,261
acute phase care in. 7 J07 ll, 714
pathophysiology of
assessments in, 708
acute heart failure,93
considerations in
arrhythmias. 91-92
availability, 704
chronic heart failure, 93-94
ethical, 704-705
compensated/decompensated heart failure, 94
organ donation,704
congestive heart failure, 93
organ preservation, 704
patient classifIcation and, 133
psychosocial implications,70S-706
patient history and,1:l3
purpose of,704
Heart failure
trends in, 70G
acute,pathophysiology of,93
waiting list criteria, 70S,70S
compensated/decompensated. pathophysiology of, 94
waiting time,705
congestive
when to use,704
intensive care of,235,245
equipment/monitoring in,70S-709
ischemic heart disease and,109
exercise guidelines in, 712
facility vs. home based rehabilitation in,716-718
pleural effusions and,101
goals in. 712
primary/lCU, 594,594,596
history of, 704
radiography of,164, 165, 166, 167
interventions in, 7 J0 711, 7 I 4
respiratory failure and,579, 580t,58 I
Heart function
medication in,716-718
other transplants and,709-710
afterload in,13
anatomy and, 44-48, 45, 46, 47, 48
post-transplant care in,708
aortic volume and,66,66
pre-transplant care in, 70S
cardiopulmonary physiology of, 65,65-67, 66, 67t
rejection signs in,714, 715, 716
surgery and, 70G
arrhythmias, J 77,178, 179-184,179-184
therapy in
conduction,170-172, 171
assessments,707 -70S
blocks,184-186,185, 186
defined,70S-709, 710,710--713
evaluation of. 174, 174-177. 175, 176,177
medical management, 707,707t
myocardial infarction, 186-187. 187
musculoskeletal considerations,707,709-710
rate, 174,174-176, 175, 176
physiology and,707
recording,172, 172- t 74,173
rhythms, 176-177, 177
use of, 169-170
heartbeat physiology and,66
left atrial pressure,241-243
myocardial contractility and,13
myocardial viability and, 202-203
therapist requirements, 706
Heartbeat, cardiopulmonary physiology and, 66
Heimlich assist techniques,374. 374-375
Hematocrit (Hct)
laboratory tests of,190-192, J 9 J t
Hematologic disorders,cardiopulmonary effects of
myocardial workload reduction, 592, 593-594, 596
malignant. 109
output in, I I, 12, 14,17,636
systemic, !O8-109, J09
preload,13
Hematology,oxygen transport and,S
ventricular
Hemiplegia,chronic secondary dysfunction and
diastole physiology,66
fetal anatomy of, 636
Index
Hemoglobin (Hgb)
1-15
respiratolY failure and, 579, 580t,581
ancri 1 blood gases and,155
Hyperglycemia, respiratory failure and,579, 580t, 581
laboratory tests of,190-192,191 t
Hyperinflation, manual, 348,348-349
in oxygen transport, 11-12, 14-15
Hyperoxia, ICUs and, 238
Hemophilia,pulmonary hemorrhage and, 108
Hypertension
chronic primary dysfunction and management of, 531-533
Henull,hilis il(/ll/enlOe, pneumonia in neonates, 642
Hemophilus inj7uelllOe, in bactcrial pneumonias, 474--475
management of,488
Hemoptysis, patient history and, 140
Hemorrhages
preterm infants and, 637-638, 638t
anticoagulants and, 108
disseminated intravascular coagulation. 108
treatment of,777, 778, 779
electrolyte balance and,230
Hyperrhyroidism, cardiopulmon8lY effects of, 109-1 10, I 10
hepatic failure and,108
Hyperventilation, manual airway clearance and, 325
Hcmosiderosis. pathophysiology of, 87
Hypocalcemia, respiratory failure and, 579, 5801., 581
Hemostasis, laboratory tests in, 190,191t
Hypocapnia, ICUs and, 238-239
Hemothorax, secondary dysfunctionllCU and, 605
Hypokinesia, nuclear imaging of, 200
Hepatic fibrosis,clubbing and, 214, 214
Hypomagncsemia, respiratory failure and, 579,580t, 581
Hering-Breuer reflex, cardiopulmonary physiology of, 55
Hyponatremia, respiratory failure and, 579, 5801, 581
Hexamethonium (Methium), pharmacology of,783
Hypophosphatemia, respiratory failure and, 579, 580t, 581
HFCC; sec High frequency chest compression (HFCC)
Hypothyroidism, cardiopulmonary effects of, 109-110, 110
Hgb; see Hemoglobin (Hgb)
Hypoxemia
High-dcnsity lipoproteins (HOL), cholesterol and, 191, 191t
cardiopulmonary cl'fects of,
High elevation environments, oxygen transport and, 16
ICUs and,237t, 237-238
High frcljuency chest comprcssion (HFCC), 328-329, 358, 358-359
management of,621
High-resolution computerized tomography (HRCT), for respiratory
101
symptoms of, 236t

Hypoxia, critical facts relating to, 252
tcsting, 206-- 207
Hip mobilization, secondary dysfullction and, 436
History
IABP; see Intraaortic balloon counter pulsation (IABP)
of artificial airways. 761
of organ transplants, 704
[CP; see Intracranial pressure (ICP)
of patients/family, 142
ICS; see Intercostal space (ICS)

ICUs; see Intensive care units (ICUs)
HIY; see also AIDS

associated cardiology of,639t
Idiopathic pulmonary hemosiderosis, pathophysiology of, 87
Immobility/recumbency,intensive care units and, 568
HMO; see Hyaline membrane disease (HMO)
Immunological disorders, systemic,cardiopulmonary effects of, I 10
Hoarseness, patient history and, 141
Immunological function, laboratOIY tests in, [94t, 194-195
Hodgkin's disease, cardiopulmonary effects of, 109
Immunosuppressive drugs
Homatropine (Novatrin),pharmacology of, 783
for organ transplants, 717-718
Home-based care
side effects of, 7J 8
concerns in, 727-728
IMT; see Inspiratory muscle training
goals for, 730-732, 731, 732
IMY; see Intermittent mandatory ventilation (IMY)
management of,722
Incentive spirometry (IS), defined, 754, 755
monitoring in, 729
Indices/measures, oxygen transport and, 5
oxygen, 729-730, 730
Indirect percussion; see Mediate percussion
III antimyosin, for cardiovascular testing,201t, 203
setting requirements in, 728
Indium
team communication in,728-729
Individualized education plan (lEP), Oowo syndrome and, 645t,
646--647,647
cardiac, 716--718
Indoor environments,oxygen transport and, 16
pulmonary, 716--718
Infants
airway clearance techniques (ACT) for, 653, 657
Home environments, oxygen transport and, 16
Human immunodeficiency virus (HIY); see
HIY
aspiration pneumonia in, 642
Humidity therapy, defined, 755
chest therapy for
Hyaline membrane disease (HMO), preterm infants and, 640-641
airway suctioning, 653,657
Hypercapnia
percussion/vibration,652---653, 657
ICUs and,239
pOsitional rotation, 649, 649, 650-651
Index
1-16
Swan Ganz catheter. 233, 241-243, 243
postural drainage,652, 653t, 654-656
patient management in. 565-577
intubation tracheostomy and, 644
assessments,572
myelomeningocele in,646, 646
Infarct avid scans,defined. 20 I t. 202
death, 576-577,577
Infection
discharge, 574
ICUs and,574
environment, 576. 576y
function optimization,570,571
Inflammatory bowel disease,cardiopulmonary effects of. 107
goals, 568-572,570
Information, ICU patients and, 571-572,572
immobility/recumbency, 568
Inhaled materials, toxic. 16
infection, 574
Inhalers
monitoring,572,572
patient information,571-572,572
metered-dose. 777,778
bronchodilators,723-724
personal recognition,574--575
defined,755-756,756
pharmacological agents,572-573
for oxygen transport treatment,259-260,260
preventive care,571-572
pharmacology of,777. 786
team work,574, 575
precautions in. 756
therapist expertise, 568,569
spacers for, 786
treatment in. 569-571, 570, 572-574
powder,pharmacology of,786
upright to supine position,570
Injuries
primary dysfunction and,579-596
head, secondary dysfunctionllCU and
asthma, 589-591
management of,606-609, 608
cardiopulmonary failure,579,580t, 581
pathophysiology of,606-609. 607
congestive heart failure,594,594,596
respiratory failure and,579,580t. 58 I
coronary artery disease,592-596
Inspiration
myocardial workload reduction, 592, 593-594,596
exercise for fatigue in. 444--448, 448-450, 450
obstructive lung disease, 581-589, 589
muscle anatomy in,26
open heart surgery,595,596
positioning and. 387-388
restrictive lung disease, 590-592
secondary dysfunction and,599--615
sustained maximum, 754, 755
Inspiratory muscle training (lMT), fatigue and, 444-448,
burns, 612--615
448-450.450
fractures, 604--606
lnspired air
head injuries, 606-609, 607,608
in ambient air, 15-16
hemothorax.605
in oxygen transport,5, 15-16
musculoskeletal trauma,603-604,694
Instillation therapy, obstructive lung disease and,primary
neuromuscular disease,600--602
dysfunction/lCU,587
obesity, 602--603
Insulin production,laboratory tests of. 193,193t
pneumothorax,605
Intensive care units (ICUs)
respiratory muscle training,610--612,6 I 1,612
monitoring systems for. 229-246, 572. 572t
rib fractures, 604--605
acid base balance. 236.236t
spinal cord injuries, 609--612
blood gases, 236-237
trauma, 605
central venous pressure. 243-244
Intercostal muscles, anatomy of, 28,29
chest tubeslfluid collection, 235.235-236
Intercostal space (lCS). defined, 220
description of,229-230, 230,231,232.233
Intermittent mandatory ventilation (IMY), defined, 758
ECG, 238, 239-24 I, 240t-24 I t
Intermittent positive pressure breathing (IPPB),defined.753, 754,755
EEG,246
Interstitial lung disease
fluid/electrolyte balance, 230-231, 234t, 234-235
gallium scintigraphy for, 206 .
hypercapnia. 239
management of, 486-487, 523
hyperoxia.238
pathophysiology of, 486, 522-523
hypocapnia, 238-239
radiography of, 162,163
hypoxemia,237t, 237-238
respiratory failure and,579, 580t. 581
intra-arterial I ines,24 I. 242
Interviews
intraaortic balloon counter pulsation, 244, 244-245
intracranial pressure, 245-246
intravenous lines. 243
patient assessments and,209-210
for patient history, 127-128
Intra-arterial lines, in ICUs, 241,242
Index
Intraaortic balloon counter pulsation (IABP), in ICUs, 244, 244-245
liver, 194, 194t
Intracranial pressure (ICP), ICU monitoring of,245-246
multisystem, 190- I 95
Intrapulmonary percllssive ventilators (IPV), 363, 364
pancreatic, 193,193t
Intravascular echocardiography, 204
peripheral vascular, 192, 192t
Intravenous lines. in ICUs, 243
thyroid,193t, 194
1-17
Lactic aci d. laboratory tests of, 190, 19 I t
Invasive cardiac testing. 205-207
Iodine, laboratory tests of. 194
Laryngeal edema, respiratory failure and, 579, 580t. 581
IPPB; see Inte.rmiltent positive pressure breathing (JPPB)
Larynx, anatomy of, 35, 35-36
IPV; see Intrapulmonary percussive ventilators (IPV)
Late sequelae of poliomyelitis, chronic secondary dysfunction and
IS; see Incentive spirometry (IS)
Ischemia, myocardial; see Myocardial infarction
Isocapnic hyperpnea, for respiratory muscle fatigue. 450-451
Lateral chest radiographs, interpretation of, 159-160
Isocapnic hyperventilation, for respiratory muscle fatigue, 449-450
Lateral costal breathing, ventilation facilitation and, 396, 397, 399
lsoetharine (Bronkosol, Bronkometer, Servant), pharmacology of,
LOL; see Low-density lipoproteins (LOL)
Left atrial pressure (LAP), ICU measurement of, 241-243
778,784-785
Isoproterenol (Isuprel), pharmacology of,777,784
Left ventricular assist devices, ICUs and, 245
Left ventricular end diastolic volume (LVEOV), oxygen transport
Left ventricular ejection fraction (LVEF), nuclear imaging of, 200
and, 13
.IRA; see Juvenile rheumatoid arthritis (JRA)

Jugular venous distension (1VO), patient assessments and,214
Left ventri cu l ar output (LVO), fetal anatomy of, 636
Jugular venous pressure,electrolyte balance and. 231
Left ventricular pressure (LVP), intensive care units measurement
Jugular venous pulse, patient assessments and, 214
of,241-243
Leukemia, cardiopulmonary effects of, 109
Juvenile rheumatoid arthritis (1RA)

cardiology of, 639t
Lifting, primary dysfunction and, 419-420
management of. 648
Lipoprotei ns, cholesterol and, 191, 191 t
JVO; see Jugular venous distension (1VO)
Listening skills, secondary dysfunction and,428,429, 430 428
Liver disorders, systemic, cardiopulmonary effects of, 107-108, 108
Liver function, laboratory tests in, 194, 194t
Kidney disorders
Long sitting self assist techniques. 379, 379-380, 380
Long-term care facilities
acid base imbalances and, 154
concerns in, 723
cardiopulmonary effects of, 108, 108
chronic secondary dysfunction and, 560-561
documentation in, 727
effects of systemic types of, 108, 108
monitoring in
organ damage and, 108
cardiopulmonary, 725, 725-726
oxygen, 726-727
work considerations in, 724-725
Low-density lipoproteins (LOL), cholesterol and, 191, 19 I t
Kidney function
arterial blood gases and, 154
Low elevation environments, oxygen transport and,16
laboratory tests in, 192t,192- I 93
Lower airways, anatomy of, 36-40, 37, 39t
Knees-hands rocking assist techniques, 381-382
Lower/upper extremity exercise. testing/training in, primary
Krebs cycle, in aerobic transport, 8-9, 18
dysfunction, 419-420
Kyphoscoliosis
Lung anatomy,40-44, 41, 42t, 43
patient asscssments and, 216, 216
Lung cancer,chronic primary dysfunction and management of, 524
poliomyelitis and, exercise training for, 437-440, 438, 439
radiography of, 167, 167
Kyphosis, respiratory failure and, 579, 580t, 581
Lung disorders
contused, respiratory failure and, 579, 580t, 581
exercise testing/training in, primary dysfunction, 417-418
Laboratory assessments, 189-195
adrenal,193t,194
treatment, 261
Lung function
blood, 190-192, 191t
endocrine, 193, 193t
pulmonary function tests and, 146, 146-147
immunological, 194t,194-195
Lung injury, management of, 625. 626
insulin production, 193, 193t
Lung transplants
kidney,192t, 192-193
1-18
Index
cardiology of, 639t
assessments in, 708
pediatric management of, 648
considerations in
availability, 704
MAS; see Meconium aspiration syndrome (MAS)
ethical, 704--705
Maximal voluntary ventilation, pulmonary function tests and, 149,
149-150
organ donation,704
organ preservation, 704--706
MOl; see Metered-dose inhalers (MOl)
patient education,706
Mean oxygen pressure, defined,12
psychosocial implications,705-706
Mean oxygen tension, defined, 12
rejection,704
Measurements, I 17-123
trends, 706
characteristics of, I 18-122
waiting list criteria, 705, 705
documentation and, 123-126
waiting time, 705
when to, 704
interpreting, 122-123
I 19
equipment/monitoring in, 708-709, 715
interval,
facility vs. home based rehabilitation in, 716--718
nominal, 118
goals in, 709, 712, 713t, 715
nuclear-derived,199-200
history of, 704
objective/subjective, 121, 121-122
interventions in, 709,712-713, 713t, 7 I 5-716,716
ordinal, 118-119
medication for, 7 I 7-718
performing, 122
other transplants and,709-710
ratio,119
outpatient care in, 714--7 I 6, 716
reliability and, I 19-120
post-transplant care and, 708, 7 I 2-7 I 3, 7 I 3t
selecting, 122
validity and, 120-121
pre-transplant care and, 708-709, 710
rejection signs in, 7 I 5
Measures/indices, oxygen transport and, 5
surgery and,706
Mechanical body positioning, 316
therapy in
Mechanical breathing function, cardiopulmonary physiology in,

56--59,57,58,59
assGssments,707-708
defined, 708-709, 710, 710-7 I 3
medical management,707, 7071
assisted, 758
musculoskeletal considerations, 707, 709-7 I 0
controlled, 758
physiology, 707
Meconium aspiration syndrome (MAS), management of, 641-642
pre/post assessments, 707-708
Mediate percussion, patient assessments and, 222
therapist req uirement s , 706
diaphragmatic movement,222, 223
techniq ues, 222
Lupus erythematosus,systemic (SLE)
Medical conditions
chronic primary dysfunction and
LVEOV;
sec
angina,525-526
Left ventricular end diastolic volume (LYEOV)
LYEF; see Left ventricular ejection fraction (L YEF)
asthma,5 I 9-520
Lymphatic circulation
bronchiectasis,520-521
chronic airflow I imitation,5 I 4
anatomy of, 50
in oxygen transport,16-17
chronic bronchitis,514--5 I 6
systemic disorders and, fluid imbalance,101
cystic fibrosis, 521 -522

diabetes mellitus, 533-535
emphysema, 516-518
M-mode echocardiography, defined, 201t, 203-204,205
hypertension, 531-533
MAB scans, defined, 20 I 1,206
interstitial lung disease, 522-523
Magnetic resonance imaging (MRI),defined, 207
I ung
Malignancies
cancer, 523-524
hematologic, cardiopulmonary effects of,109
obstructive pallerns in, 514--522
lung, chronic primary dysfunction and, management of,524
peripheral vascular disease, 529-531
radiography of,163, 165,166
primary cardiovascular disease, 525-535
restrictive pallerns in, 522-523
Managed ca re , defined, 722
Mandatory minute ventilation (MMY), defined, 758
valvular disease,528-529
chronic secondary dysfunction in
Marfan syndrome
ankylosing spondylitis, 557-558
Index
cer ebral palsy , 546--547
bronchodi lators, 723-724
chronic renal insufficil'llcy, 560--561
defined, 755-756, 756
collagen vascular/connective tissue diseases, 555-556
hemiplegia, 541-54
pharmacology of, 777, 786
latc sC4udae of poliomyditis, 550--552
precautions in, 756
multiple sclerosis, 544-546
1-19
spacers for, 786
muscular dystrophy, 538-539
Methyldopa ( Aldome t) , pharmac ology of, 779
os teoporos is, 551-555
Methylprednisolone, pharmacology of, 785
Parkinson's disease, 543-544
Metoprolol (Lopressor), pharmacology of, 779
rheumatoid "rthritis, 558-560
MI; see Myocardial infarction
scleroderma, 556-557
M ic rocircu lation
spinal cord inj ury, 548-550
cardiopulmonary physiology and, 67, 67t
systemi c lu pus erythematosus, 555-556
thoracic deformities, 552-553
MMV; see Mandatory minute ventilation (MMV)
primary dysfu nction secondary to, 469-492
Mobility
alveolar protcinosis, 478
acute responses to, 270-- 271, 271, 272, 273, 274, 274t
alvcolitis, 477-478
assessment of, 295-296
angina, 488-490
bed rest and, 291, 291-295
asthma, 481-483
cellular response to, 269-270
atelectasis, 470-472, 471
defined, 265-266
bronchiolitis, 477
long term responses of, 278-280, 279
chronic airflow limitation, 478-481
monitoring of, 275,285-286,288,289,290, 291-292
motor t h erapy, pediatric, 661-663, 662
cy stic fihrosis, 48 -4R6
mu ltisystem effects of, 278-280, 279
emphysema, 478-481
obstructive lun g disease and, primary dysfunction/ICU,

584-585
hypertension, 488
intcrstitial pulmonary fibrosis, 486
oxygen transportfmetabol ic demand and, 267-268, 268, 270
oxygen transport threats and, 256, 256
pneu monias, 472-476
pathophysiological conditions and, 270--271, 271
tuberculosis, 487-488
prescription for, 266-- 267, 270--276, 273, 274t, 278t
Medical su rgical con d itions, primary dysfunction secondary to,
preventive effects of, 291-292, 295
secon dary dysfunction and, 436
495-508
stimulus in, 277-278, 278
extrinsic factors , 500
surgery and, 500
testing/training and, 274, 274, 276--277, 280-285, 281, 282t,
mObilitylrecumbency,500
283t, 284, 285, 286,290, 290-291
Monitoring
of body positioning, 317-3 I 8
perio[Xrative course, 496, 496--500, 498
postoperative management, 502, 502-505, 506, 507
exercise and, 275, 285-286, 288, 289, 290, 291-292
in fa cility-based care
su rgical effects, 500
cardiopu lmonary, 725, 725-726
oxygen, 726-727
surgical prep, 499
in home-based care
thoracic, 500--502
cardiopulmonary, 729
Medication; see Drugs

Med ullary respiratory center, cardiopulmonary physiology of, 54
oxygen, 729-730, 730
Men ingitis, re spirato ry failure and, 579, 580t, 581
in ICUs, 572, 572
Metabolic acidosis, intensive care of, 236, 236t
in transplant patients
Metabolic alkalosis, intensive care of, 236, 236t
cardiac, 708-709
Metabolic disorders
pulmonary, 708-709, 715
Monoamine oxidase (MAO), 776
respiratory failure and, 580t, 617-618
Montgomery T tubes, 768
Metabolism, muscle, 10--11
Motion radiographs, interpretation of, 159-160
Metaproterenol (Alupent), pharmacol ogy of, 778, 784-785
Motor neuron disease, respiratory failure and, 579, 580t, 581
Metaraminol, pharmacology of, 777-778
Motor therapy, pedi atric, 661-663, 662
Metered-dose inhalers (MOl)
MS; see M u ltiple sclerosis (MS)
Index
1-20
99mTcOTPA; see Technetium-99M-diethylene triamine penta
chest development in,682-689, 684---{i89,686t
acetic COTPA) aerosol
compensatory breathing patterns in,689,691---{i93,692,

693,694,695
Mucolytic agents
for intensive care units, 572-573
di agno sis in, 680
for oxygen transpOlt treatment, 259-260, 260
gravity in, 680---{i87,682---{i87,686t
pharmacology of,786
impaired
MUGA; see Multiple uptake gated scans (MUGA)
chest expansion, 689
Multicrystal cameras,for nuclear imaging, 198
cough effectiveness, 698
Multiple fractures,secondary dysfunctionllCU, 605-606
function,689
Multiple sclerosis (MS)
phonation, 699-700
cardiopulmonary effects of,104
muscle/tonal effects in, 687-689,688, 689
planes of ventilation and, 680
program goals for, 700--701
pulmonary changes in,695-696

systemic,cardiopulmonary effects of,102,102-103
transplant patients and,707,709-710
Multiple trauma,secondary dysfunction/ICU and, 605

Multiple uptake gated scans (MUGA), defined, 199,20 I t
Musculoskeletal trauma, secondary dysfunction/ICU and,

603-606,604
Muhisystem assessment, laboratory,189-195
management of,604
Murmurs,patient assessments and,221

Muscarinic blockers, defined, 779-781
pathophysiology of, 603-604,604

Myasthenia gravis
Muscarinic receptors, defined, 780

Muscle contraction
respiratory failure and,579,5801,581
emotional stress and,20
treatment of, 781-782
oxygen lranspolt and, 9,10, 10--1 2
Myelomeningocele, pediatric management of, 646,646
Muscle fatigue, exercise test i ng/traini ng in, primar y dysfunction,

418-419
Muscles
Myocardial contractility, oxygen transport and, 13
Myocardial dysfunction,respiratory failure and,620

in respiration anatomy
diaphragms,26,26-28, 27, 28
erector spinae, 30, 3 I
electrocardiograms and,186-187, 187
expiration,27,31-32
pathophysiology of,91-93, 490
inspiration,26
intercostals,28,29
Myocardial ischemia,ICUs and,245
pectoralis major, 29, 30
Myocardial perfusion
pectoralis minor, 30
nuclear imaging for,202-203
scalenes, 29, 29
serratus anterior, 29-30
Myocardial viability, testing for,202-203
sternocleidomastoid, 28-29, 29
Myocardial workload reduction, primary dysfunctionllCU and,
trapezius, 30,30
592,593-594,596
in secondary dysfunction, 427-428,432-433, 435
Myoglobin, in oxygen transport, 18
ventilation facilitation and, 401-405,402, 404,405
Myxedema,respiratory failure and, 579, 580t, 581
Muscular dystrophy
cardiology of, 639t

N
NAO; see Nicotinamide adenine dinucleotide
Narcotics
for ICUs, 572-573
respiratory failure and,579,580t,581
pediatric management of,647-648
Nasopharyngeal suctioning,772
respiratory failure and,579,580t, 581
NOT; see Neurodevelopmental (NOT) treatment
Musculoskeletal conditions
chronic secondary dysfunction and,552-555
neuromuscular disorders and, 679-701
adverse changes in, 696,696-698, 697

bronchial hygiene and,698
Nebulizers,for oxygen transport treatment, 259-260,260

Neck
mobilization in secondary dysfunction and,436
patient assessments and,214,215
Nedocromil sodium (Tilade),pharmacology of,785-786
Index
Neonates
1-21
phonation, 699-700
chest therapy fo r
muscle/tonal effects in, 687-689, 688,689
airway suctioning, 653, 657
planes of vemilation and, 680
chest percussion/vibration,652-653,657
program goals for, 700-701
positional rotation, 649, 649, 650-651
pulmonary changes in,695-696
secondary dysfunction and,436
postural drainage, 652,653t, 654--656
chronic,538-543
development in
ca rd iac, 636-637
ICU,600-602
prelenn respiration,637, 1i38, 6381
management of. 600-60 I
pulmonary, 637-63tl
endocardial cushion defects in,640
Neuromuscular ju ncti on (NMJ), defined, 780-781
intubation tracheostomy in,644
Neurotransmission, drugs and, 776-777,778, 779-784
meconium aspiration syndrome in, 641-642
Nicotinamide adenine dinucleotide (NAO), in energy transfer, 8
myelomeningocele in, 646, 646
Nicotinic receptors, defined, 780
patent ductus arteriosus in, 639--640
Nitrogen, ambient air co ntent of, 15-16
pneumonia in, 642
NMJ;
preterm
Nocturnal ventilation, secondary dysfunction and,432-433, 435
sce
Neuromuscular junction (NMJ)
associated cardiology of, 639t
Noncardiogenic pulmonary edema, management of,625, 625
bronchopulmonary dysplasia in, 641
N onsmoking, environments, 16
Noonan's syndromc, cardiology or. 6391
chest therapy for
Noradrenalin, in neurotransmission, 776
airway suctioning,653, 657
Norepinephrine,laboratory tests of,194
postural drainage, 652,6531, 654-656
dysfunction factors in, 638t
Norepinephrine (Leval1erenol, Levophed),pharmacology of', 777
hyaline membrane disease in,640--641
Normal blood gas values, 154
patent ductus arteriosus in,639-640
Nose,anatomy of,32-34, 33, 34
respiration in, 637-638, 638t
Nuclear imaging
for cardiovascular t"sting, 199-204,20 I t
tetmlogy of fallot in, 640
angiography, 205
transient tachypnea of the new born in, 641
echocardiography, 197, 203-205
Neoplasms,respiratory failure and, 579, 580t, 581
Neostigmine (Prostigminc),pharmacology of,781-782
with exercise stress,199
Nervous systems
18F-fluoro-deoxyglucose (FOG), 203
gatedlungnted,199
drug interaction and,776-777
in heart anatomy, 47,47-48, 48
Indium II I antimyosin, 203
systemic, 103-107,104
in vasi ve, 205-207
Neurodevclopmental (NOT) treatment, pediatric motor therapy
myocardial viability, 202-203
noninvasive, 199-205
and, 661-663,662
nuclear-derived measurements,199-200
Neurological disorders
respiratory failure and,620-621
perfusion, 199-200
with pharmacologic stress, 199
systemic,103-107, 104
autonomic nervous system, 106-107
Technetium-99M-pyrophosphate, 203
central nervous system,103,105-106
Technetium-99M-sestamibi,202
peripheral nervous system,106
Technetium-99M-teboroxime,202
Thallium 201, 200-202, 20lt
Neuromuscular disorders
musculoskeletal,679-70 I
planar, 198-199
respiratory,205-207
advcrse changes in, 696,696-698,697
angiography,206
bronchial hygiene and,698
chest development in, 682-689,684-689,686t
computerized tomography,206-207
compensatory breathing patterns in,689,691-693, 692,
gallium scintigraphy,206
693,694,695
diagnosis in,680
gravity in,680-687, 682-687,686t
impaired
magnetic resonance imaging, 207
ventilation-perfusion lung scan,206
tomographic/SPECT,198-199
Nursing homes
chest expansion, 689
concerns in,723
cough effectiveness, 698
documentation in,727
function,689
monitoring in
Index
1-22
cardiopulmonary, 725, 725-726
content,11-12
oxygen, 726-727
debt,13
delivery, 4, 6, II, 12. 13,14, 14. 19
work considerations in,724-725
demand,4, 13
Nutrition
obstructive lung disease and, primary dysfunctionflCU, 583
enhancement ratio,4, 6, 13
gravitational stress. 19-20
Nutritional disorders, systemic, cardiopulmonary effects of.
hyperoxia and, 238
110-111,111
mean pre.,sure defined, 12
mean tension defined, 12
myocardial function, 17-18
Obesity
cardiopulmonary effects of. 110-111,III
tissue extraction, 18-19
respiratory failure and, 579, 580t,581
transport, 3-20,4,5, 6
airways, 16
secondary dysfunction/ICU,602-603
desaturated blood/C02, 19
diffusion,S, 12,17
inspired/ambient,S, 15-16
Obstructive lung diseases

COPO patient assessments and, 214-215, 222, 224
lungs/chest walls,16-17
pathophysiology of,71-72
measures/indices. 5
primary/le U
perfusion, 17
bagging,587
peripheral circulation, 18
body positioning, 585-586
Oxygen therapy
breathing,588
basics of, 749,750, 750t, 751,752
coughing, 588
high-flow systems in, 750, 751-752
home/portab le,751, 753
mobilization, 584-585
low-flow systems in,750. 750. 750t,751
nutrition,583
obstructive lung disease and. primary dysfullctionlICU, 5g6
oxygen, 586
Oxygen transport
airways, 16
secretion ckarance,587-588
threats,253
selective instillation, 587
treatment, 261
analysis schematic of. 129
ventilator withdrawal, 588, 588-589, 589
pulmonary function tests and, diagnosis, 150, 150-151
cardiopulmonary physiology or. blood, 67-68, 68
Obstructive sleep apnea, respiratory failure and,579,580t, 581
exercise/metabolic demand and, 267-268. 268. 270
Occupational history,patient,141
mobilization and,270
OER; sec Oxygen, enhancement ratio
OKT 3, for organ transplants, 718
critical problem-solving Sleps, 252,252
Olympic tracheostomy buttons, 766, 767, 768, 768
deficits/threats, 253-255,256
Open heart surgery, primary dysfunction/ICU and, 595. 596
extrinsic, 256
Organ damage, renal conditions and, 108
fundamental knowledge, 252, 252
Organ donation, 704-706
indirect dclicits,255,256
Organ failure, management of,628t, 628-629
problem list, 252, 253, 254, 255
Orthopnea,dyspnea/patient history and,134
restricted mobilitylrecumbency,256
Orthostatic hypotension,defined,783
treatment,256-263,257, 258-259, 260,261.
Osteoporosis, chronic secondary dysfunction and management of,

553-555
Oxyhemoglobin dissociation, cellular respiration and, 15
Outdoor environments, oxygen transport and, 16
Outpatient care; see Home-based care, Facility-based care
Oxygen
Pain
management of, 623
cascade, 12, 12
consumption,4,6,
262
Oxyhemoglobin,cardiopulmonary physiology and. 67-68,68
oxygen transport
II, 13
IABP and, 244, 244-245
threats <Lilli, 255
respiratory failure and,579, 5801, 581
Palpation, patient asscssments and, 222-225
supply-dependent, 13, 14
chest wall, 224, 224
vs. delivery , 14, 14, 19
edema, 223
Index
tactile fremitus, 225, 225, 226
intcrdisciplinary care and, 46J
tenderness, 223
learning needs asse.SSlllcnts, 457. 459

areas, 457, 45 7, 459
tracheal d viation, 225, 226

Pancreatic disorders, cardiopulmonary ef fe ct s of, 107, 109
findings, 45 9
Pancreatic dornase (Dornavac),pharmacology of, 786
goals, 459
Pancreatic function. laboratory tests in, 193, 193t
tools, 457
Paradoxical breathing patterns, poliomyelitis and, exercise training

for, 438--439
Parasympathctic neurotransmission
methods in, 459--461, 460t, 461

needs-based,456
patient adherence and, 462
defined,779-783
secretion mobilization, 371-372,372
fight
teacher-learner relationship and, 462
or
fl ig ht system and,776
Parkinson" disease
cardiopulmonary <:Ffeets of, 104

treatment of, 783
Paroxysmal nocturnal dyspnca . patient hi s tory and, 134-135
for transpl a nt patients, 706

Patient history, 127-142
c h es t pain , 137-138
cardiac, 138-139
c hest wall, 139
esop hageal , 139
pericardial, 139
Partial thromboplastin (PTT), laboratory tests of, 190, 191t
pleuritic, 138
Particulate matter, in ambient air, 16
pulmonary hyper tension, 139
Passy - Muir valves, 766,767, 768, 768
cough, 135,136(,137
Pa tau ' s sy nd ro me , card iology of. 639t
dyspnea,128-130,129
Patient assessments,209-228
acute, 130
anatomic features in,210-211, 211, 212, 213
in cardiac pa l ients, 134
auscultation and, 217, 217-221, 218,219
exercise limiting,131t
breath sounds, 218-220,219
on exerlion, 130--131, 131.
chest sou n ds,217-218
functional, 135
heart sounds, 221-222
orth opnea, 134
techniques in, 217, 218

for barrel chest, 214-216, 216
breathing patterns and, 216
case studies and, 225-228
paroxysmal nocturnal, 134-135

platypnea, 135
trepopnea, J 35
exerc ise testing/training in, secondary dy sfullction , 428, 428,
429,430
chart review/interview in, 209-210

chest wall cunfi gura lion in. 214-216, 216
family, 142
differential diagnosis in,227t
fatigue/weakness, 140
general appearance in, 212-213
heart discasc classification, 133
jugular venous distension and, 214, 215
hemoptysis, 140
medi a te percussion in, 222, 222

diaphragmatic movement, 222, 223
techniques in, 222, 222
hoarseness, 141
interview, 127-128
occupational, 141
neck and, 214, 215
pedal edema, 140--141
palpation
prior treatment,142
chest wall, 224, 224
questionnaires, 128
edema. 223
smoking,141-142
tactile fremitus, 2 5. 22<;, 2:!6

tcnde rn e s s,
22]
tracheal de v i ation, 225, 226

palpation and, 222-225
wheezing, 135
Patient management
exercise testing/training in, secondary dysfunction, 432--433,435
in leUs, 565-577
physical cxams in, 210
assessments, 572
skin in, 214,214
death,576-577,577
vi " ual inspl!ction in,211-214, 214
discharge,574
Patient education, 453--463
1-23
environment, 576, 576y
defined,454--456
function optimization, 570,571
effectivenl!SS in, 461--462
goals, 568-572, 570
fundamentals of, 454--456
immobility/recumbency, 568
1-24
Index
Perfusion
infection, 574
cardiopulmonary physiology of, 61-65,62,63,64
monitoring,572, 572
ventilation matching,61-65,62. 63. 64
patient information, 571-572, 572
personal recognition, 574-575
myocardial,199-200,201t
pharmacological agents,572-573
preventive care, 571-572
Pericardial chest pain, patient history and. 139
team work, 574,575
Perioperative management,primary dysfunction/acute surgical
conditions and, 496, 496-500, 498
therapist expertise,568, 569
Peri phera I chemoreceptors
treatment in,569-571,570,572-574
arterial blood gases and,response to hypoxemia,155
upright to supine position, 570
cardiopulmonary physiolugy of,54-55
transplant,703-718
PD; see Postural drainage (PD)
anatomy 01',48-49
Pectoralis facilitation,ventilation and, 401-402,402
Pectoralis major, anatomy of, 29. 30
in dying patients, 577,577
Pectoralis minor, anatomy of, 30
laboratory tests in, 192,192t
Pectus carinatum,patient assessments and. 214-216, 216
Pectus excavatum,patient assessments and,214-216,216
Pedal edema,patient history and,140--141
Peripheral nervous system, systemic disease effects on, 106
Pediatrics
Peripheral vascular disease, chronic primary
asthma in,642
management of,530--531
43, 660--661
bronchopulmonary dysplasia in,64 I
cardiac development in, 636-638
Peritoneal cavity,oxygen transport and,17-18
cerebral palsy in,644,644-646, 645t
PET imaging; see Positron emission tOl1lography (PET)
chest physical therapy in
for children,657
PFT; see Pulmonary function tests (I'I'T)
Pharmacologic stn.:ss testing,cardiovascular,199
60,658
positional rotation,658-659, 659,660
Pharmacological agents; see Dl1Jgs
pre/postoperative,659-660
Pharynx,anatomy of, 33,34-35
Phenoxybenzamine (Dibenzyline), pharmacology of, 778
for infants,649,649,650--651, 652
Phentolamine (Regitine)
airway suctioning,653,657
chest percussion/vibration,652
for epinephrine reversal, 778
53,657
pharmacology of,778
positional rotation,649,649,650--651
postural drainage,652,653r,654
common diagnoses in, 638t,638
cardiac,639t, 639
pulmonary,64
cystic fibrosis in,643
Phenylephrine (lsophrin,Neo-Synephrine), pharmacology of,
56
777-778
48
Pheochromocytoma, phentolamine and,778
40
Phonation, musculoskeletal/neuromuscular disorders and,699-700
48
44, 661
Physical exams,patient assessments and,210
Down syndrome in,645t,646-647, 647
Physical therapist requirements, in ICUs,568, 569
endocardial cushion/artrioventricular defects in,640
Physical therapy
hyaline membrane discase in, 64
41
body positioning,299-318
intubation tracheostomy in, 644
motor therapy in, 661
considerations in,316-317
gravity/physiology and, 300-301,30 I
63,662
muscular dystrophy in,647
head down,312
mechanical, 316
myelomeningocele in,646,646
patent ductus arteriosus in, 639
monitoring of,317-318
pneumonia in,642
physiological effects of,301-313, 302
pulmonary development in,637,638,638t
frequent changes,313,315
prescription for,313-316.314
rehabilitation in, 660--661
vs. routine,301
tetralogy of fallot in, 640
prone,312-313
transient tachypnea in, 641
Pelvis mobilization, secondary dysfunction and,436
side-lying positions, 311,311-312
Pentolinium (Ansolysen),pharmacology of,783
supine,308-309,309, 310
PEP; see Positive expiratory pressure (PEP)
Percussion
upright, 302-308, 303, 304,305, 306,307, 308
exercise/mobility,265-296
in airway clearance,323-324
acute responses to, 270--271,271,272,273,274, 274t
clinical applications of,344-346,345
assessment of, 295-296
1-25
Index
bed rest and, 291, 291-295
Pneumotaxic centers, cardiopul monary physiology of. 54
cellular responses to 269 -270
Pneumothorax
de fined 265-266
different ial diagnosis of, 227t
long term responses of, 278-280,279
radiography of. 164. 165
monitoring and. 275, 285-286,288, 289,290, 291-292

multi syst em effects of. 278-280,279
secondary dysfunctiun/ICU and. 605

Point of maximum impulse (PM!), defined, 220
oxyge.n transport/metabolic d em and and, 267-268,268,270
Poisons, respiratory failure and, 579, 580t,581
pathophysiological c on d iti ons. 270--271,271
Poland's syndrome, pediatric management of, 648
prescription for. 266-267. 268. 270--276. 273, 274t,276,278t
Polio, respiratory failure and,579,580t,581
preventivc crfc(,ts or. 291 292 . 295
Poliomyelitis
stimulus in, 277-27R. 278
impact of sy temic diseases on, 99-100
oxygen ll'llnsport and, 3-20
pediatric, 648--663
with s econdary kyphoscoliosis, exercise training for 437-440,
cardiac,648 - 649
438,439
positional release therapies,secondary dysfunction and 437
Pontine respiratory center, c ardiopulmonary physiology of, 54
shock,627-628
Positional release therapies. secondary dys function and. 437
Positioning, 299-318
Physiology
cardiopulmonary, 53-69
b ody mechanics. 737-747
blood transport of oxygen,67--68,68
lifting, 741-743. 742, 743, 744
breathing control, 53-55. 54
moving, 744, 744-745. 745, 746. 747, 747
carbon diuxide transport. 68--69
uptimal ventilation, 737-738. 740-741
cardiac. 65,65--67,66. 67t
side lying. 740
diffusion, 60,60--61
supine, 738. 739, 740
mechanical, 56-59, 57,58,59
upright, 740,740--741,741
perfusion,61--65. 62. 63, 64
considerations in, 316--317
reflexes, 55, 55-56
cough/suction,367-382
ventilation, 59--60
in tra n splant patients,707
anterior chest compression, 375,375
Physostigmine (Eserine), pharmacology of, 781
costophrenic, 373,373-374
Pilocarpine,pharmacology of, 781
counter rotation, 375, 376, 377
Planar imaging. defincd, 198-199, 201t
hands knees rocking,381-382
Plasma, in oxygen transport, 11-12,15
long sitting self, 379, 379-380, 3S0
Plasma volume. albumin for,234
Platelet count. laboratory tests of, 190, 191 t
self, 377-382
Platelet inhibitors, pulmonary hemorrhage and, 108
gravity/physiology and, 300--30 I, 30 I
Platypnea, patient history and, 135
head down, 312
Pleural effusions
mechanical 316
cardiopulmonary effects uf, f02-I03, 103, 109
moni toring of,317-318
congestive heart failure and, 101
obstructive lung disease, primary/ICU, 585-586
physiological effects of, 301-313,302
patient a"",,ments and,2 27- 228

radiography of, 164, 165, 166
Pleural tluids, imbalance dkcts of, 101
Pleuritic chest pain, paticnt history and. 138
frequent changes, 3 I 3,315
prescripti on for, 313-316,314

vs. routine, 30 I
prone, 312-313
PMI; sec Point uf maximum impulse (PMI)
rotation for infants,649,649, 650--651
Pneumonias
side-lying positions, 311, 311-312
di f ferential diagno sis of, 227t
supine, 308-309,309,310
management of, 472476
upright,302-308,303,304,305,306,307,308
ventilation facilitation and, 383-415
patient assessments and 227
asymmetrical dysfunction and,405-406
pediatric, 642
butterfly techniques and, 408,409, 410
radiograph s of, 162,162,163, 164, 164,167
chest/shoulders and, 392
counter rota tion 407-408, 409
1-26
Index
Preoperative management
diaphragm inhibition and, 402-405,404,405

diaphragmatic breathing and,389,3'10,391,392,394
pediatric chest physical thelapy,659-660

primary dysfunction/acute .surgical conditions anu, 502
395,396
Pressure gradients (P)
dressing techniques and, 389
in blood now, 15
dynamic activities and,388-389

eccentric resistance techniques and,414
Pressure support ventilation (PSY),ucfJllcd, 7. X
expiration and,388
Pressure/volume, cardiopulmonary physiology and,57-58, 58,66
glossopharyngeal breathing and, 410-4 I 2,4 I 2
Preterm infants
associated cardiology of, 639t
inspiration and,387-388
lateral costal breathing and,396, 397,399
bronchopulmonary dysplasia and,641
manual. 413-414
chest therapy for
mobilizing the thorax in,399-401,400
airway suctioning,653, 657
muscles and,401-405,402,404,405
postural drainage, 652, 653t,654-656

dysfunction factors in, 638t
normal timing and,399

postural inhibition, 406
hyaline membrane disease in,640-641
primary vs. secondary dysfunction and, 390,391
patent ductus arteriosus in,63lJ-MO

respiration in,637-638, 638t
pursed-lip breathing,410
repatterning, 393
Preventive care, ICUs and, 571-572
rolling,388
Primary cardiovascu.lar disease. chronic primmy dysfunction and

sitting, 388
snifli ng, 392
Primary dysfunction
standing,389
chronic
strategies for,387-389
symmetrical,405-406
angina, 525-526
verbal,414-415
asthma, 519-520
bronchiectasis, 520-521
vocalization enhancement, 412-41.5
chronic airnow limitation, 514
Positive expiratory pressure (PEP)

in airway clearance,327-328
chronic bronchitis,514-516
clinical applications and,354--358,355
cystic fibrosis,521-522
Positron emission tomography (PET), defined,199,20 I t
diabetes mellitus,533-535
Posteroanterior (PA) radiographs,interpretation of, 159-160
emphysema,516-518
Postoperative complications,621,621--624, 622
hypertension,531-533
interstitial lung disease,522-523
in artificial airways,763-764
lung cancer, 523- 524
mcchanical, 764
hypoxemia and, 621

management of, 621, 621-624
obstructive patterns in,514-522
pain and, 623
peripheral vascular disease,529-531
pulmonary embolism and,623-624
primary cardiovascular disea,,:, 525-535

restrictive patterns in, 522-523
Postoperative manngcment
pediatric,659--660
valvular diseasc, 528-529
primary/acute surgical conditions and,502, 502-505,506,507

exercise testingitraining in, 417-423

intensive calC of,579-596
asthma,589-591
clinical applications and,343-344,345

contraindications for,330-331
caruiopulll1onary failule,579,580l, 581
for infants. 652, 653t,654-656
congestive heart failure, 594, 594,596

coronary artery disease,592-596
Postural inhibition, ventilation facilitation and,406

Potassium iodide, pharmacology of,786
myocardial workload redLtction,592, 593-594, 596
Powder u inhalers, spacers for,786
obstructive lung disease, 581--589,589
Prazosin (Miniprcss),pharmacology of, 778
open heart surgery, 595,596

restrictive lung uiseasc, 590-592
Precapillary arteriole function,in oxygen transport,18

Prednisone
for organ transplants,717
primary vs . secondary,390,39 I
secondary to acute medical conditions,469-492
side effects,7 I 8
alveolar proleinosis,478
pharmacology of, 785
alveolitis,477-478
Preload, cardiopulmonary physiology of,65
angina,488-490
Preload function, in oxygen transport, 13
asthma, 481-483
Index
atelectasis, 470-472, 471
Pulmonary deVelopment
bronchiolitis, 477
in rmr cllloskclctal/neuromuscul"r disorders, 695-696
chronic airl10w limitation, 478-41:1 I
pediatric, 637--638, 63 t
cardiac, 636-637
cy stic fibrosis, 483-486

em phy se ma , 478-481
Pulmonary disorders
respiratory failure and, 618-619, 619
hypL'rlellsion, 488
sy:;temie, cardiac diseases and, 10 I-I 02
intL'rstitial pulmonary fibrosi" 486
Pulmonary edema, noncardiogenic, defined. 625, 625
myocardial inrarction, 490-491
Pulmonary embolism
pn ulllonias, 472-47/i
differential d i agnosis of, 227t
tuherculosis, 4 7-4gS
sectlillidry to a utc surgical conditions, 495-508
respiratory failure and, 579, 580t, 581
c'ardiovascu idr surcry. 501-502
Pulmonary eosinophilia, palhorhysiology of, 85
extrinsic' ractors. SOO
Pulmonary functio n tests (PFf), 145-151
intnnsiL' ract,llS. SOli
air flow measurements, 147, J 48, 149
11\(,bility!rclulllhency. SOO
flow volume cu rve , 147, 148, 149
pathophysiology, SOli
forced expira tion . 147
c lo sing volume/airway closure, 149, 149-150
peri<>pcrativc course, 4l)(,. 4Sl6-501l, 4t)K

postoperative manageillent, 502, 5()2-, ()5. 5116,507
maximal voluntary ventilation, 149, 149-1 SO
prL()p r;Jliyc 1ll00Ilagl:IllL'llt, 50'2
ckad space. 145-140
surgical errects ..'iOO
clel'ineel, 145
surgical prcp, 499
diagnosis and
obstructive lung disease. 150, 150-ISI
thoracic, 500-502
Progressive systemic s clerosis (sclerodcrma), pathophysiology oL 89
restrictive lung disease. 150, 15(),-151

lung capacities, 14 6. 147
Pronc positioning, 312-31
lung volumes. 146, 1 46 - 1 47
on elbows assist techniqucs, 371:\, 378-379

infant positional rotation. 64Sl, 649, 650-651
Puirllonary hemorrhages
anticoagulant.s and. 108
Propranolol (Inderal), pharmacology of. 778-779

Proteins, laboratory tests or, 190, 19 1 t, 194, 194t
hematologic conditions and, lOS

'
Pulmonary hemosiderosis, idiopathic, p athophy si 'log y 01.
Pseudomonas acruginosa
Pulmonary hypertension
in bacterial pneumonias, 474-475
exercise testing/training for, primary dysfunction, 41 X
pediatric cystic fibrosis and, 643-644
patient history and, 139
PSV: see Pressurc support vcntilation (PSV)
Pulmonary scans, defined. 20 I t, 205-207
Psychological considerations, exercise testing/training and,
Pulmonary thrombocmboli, hematologic conditions and, lOS
secondary elysfunction, 425-426, 426
Pulmonary Lransplants
Psychosocial considerations
oxygen transrorr thrcats and, 255
assessments in, 708
transplant paticnts "nel, 705-706
considerations in
PTT: see Panial thromboplastin (PIT)
availability, 704
Pulleys, for oxygen transport treatment. 259-260, 260
ethical,704-705
Pulmonary aging c hanges
organ donation. 704
exercise and, 675-677, 677, 677t
organ preservation, 704-706

patieot education, 706
structural/functional, 674-677,675, 675t

Pulmonary alveolar proteinosis. pathophysiology of, 86, 86--87
psychosocial implications, 705-706
Pulmonary aneritis, cardiopulmonary ef fects of, 102-103, 103
rejection, 704
Pulmonary ,u1cry balloon Ilotation catheters: see Swan Ganz catheters
trends, 706
Pulmonary artery occlusion prcssure (PAOP). intensive care units
wai ting list criteria, 705, 705
w a it ing time, 70S
measurement of, 241-243

Pulmomuy artery pressure (PAP), intensive care units measurement
of. 241-241
equipment/monitoring in, 708-709, 715
Pulmonary artcry wedge pressure (PA WP), intensive c<lre units

measurement of, 241-243
Pulmonar'Y circulation
when to, 704

facility vs. horne based rehabilitation in, 716-718
goals in, 709, 7J2, 713t, 7J5
h istor y of, 704
anatomy of. 4Sl-50
interventions in, 709, 712-713,713t, 715-716, 716
oxygen transport threats and, treatment, 261
medication in, 717-718
1-27
1-28
Index
other transplants and, 709-710
metabolic demand and, 267
RBC; see Red blood count (RBC)
post-transplant care in, 708. 712-713, 713t
Recording, electrocardiograms and, 172, 172-174. 173
pre-transplant care in. 708-709. 710
Recumbency
rejection signs in, 715
intensive care units and, 568
surgery and. 706
respiratory failure and. 579, 580t, 581
Red blood count (RBC), laboratory tests of, 190-192, 191t
therapy in
assessments. 707-708
Ret1exes, cardiopulmonary physiology of, 55, 55-56
defined. 708-709. 710, 710-713
Rejection
medical management, 707, 707t
cardiac signs of. 714. 715, 716
musculoskeletal considerations. 707, 709-710
of organ transplants. 704
physiology, 707
pulmonary signs of, 715
Renal disorders
therapist requirements, 706
Pumps, cough, 368
acid base imbalances and, 154
Pursed-lip breathing
for primary dysfunction, 420-421
chronic secondary dysfunction and, 560-561
management of. 560-561
ventilation facilitation and. 410
Push-ups. serratus, 405
effects of, 108, 108
organ damage and, 108
Quadriplegic patients, chronic secondary dysfunction and.
Questionnaires. for patient histOlY, 128
respiratory failure and. 620
systemic, J08, 108
Repatteming techniques, ventilation facilitation and, 393
Reserpine, pharmacology of. 779
RA; see Rheumatoid arthritis (RA)
Respiratory centers, cardiopulmonary physiology of, 54-55
Radiography
Respiratory distress syndrome (RDS); see also Adult respiratory
distress syndrome (ARDS)
abscesses. 164, 164
alveolar disease, 162, 162
atelectasis, 164-165, 165, 166
basic structures/shapes, 160
preterm infants and. 637-638, 638t
Respiratory fai lure, 617-630
bronchi, 162, 162
acid-based abnormalities and, 6 I 9
bronchiectasis, 162, 163, 164
arterial blood gases and. 156
bronchograms in, 162. 162
cardiac dysrhythmias and. 619--Q20
congestive heart failure,164. 165, 166, 167
complications of, 618--Q19, 619
description of, 159-161,160
fluid/electrolyte abnormalities and, 6 I 9
edema, 165,166
gastrointestinal dysfunction and, 620
emphysema, 162, 163
metabolic dysfunction and, 617--Q I 8
fixed position, 159-160
myocardial dysfunction and, 620
interstitial pulmonary disease, 162, 163
neurological dysfunction and. 62O--Q2 I
kyphoscoliosis, 167, 167
primary dysfunction and. 579, 580t, 58 I
lateral chest, 159-160
pulmonary dysfunction and, 618--Q19, 619
malignancies. 163, 165, 166
renal dysfunction and, 620
motion, 159-160
pleural effusions. 164, 165, 166
thromboembolism. 620
Respiratory muscles
pneumonias. 162, 162, 163. 164,167
defined, 26--40
pneumothorax. 164, 165
exercise training for fatigue, 443-451
assessments in, 447
posteroanterior (PA), 159-160
requirements for. 159-160. 161-162
etiology of, 444-447
routine exams, 160-161
inspiration. 444-448, 448-450. 450
suspended motion, 159-160
isocapnic hyperpnea, 450-451
uremia. 165, 166
isocapnic hyperventilation, 449-450
Radiopharmaceuticals, nuclear imaging and. 197-207
Rales, defined, 219-220
treatment for, 447-448
Range of motion (ROM) exercises
dying patients and, 577, 577
oxygen transport thn;ats and, 254
secondary dysfunction and, 427-428, 432-433, 435
Index
secondary dysfunctionllCU,training for, 610-- 612, 61 I, 612

Rest, bed
1-29
Sclerosis (scleroderma)
alternatives to,293-294
progressive systemic,pathophysiology of,89
hazards of, 293
SCM; see Sternocleidomastoid (SCM)
indications for, 294
Scoliosis, respiratory failure and, 579, 580t,581
as therapy, 291-292
Secondary dysfunction
chronic
Restrictive lung diseases
ankylosing spondylitis and, 557-558

diffuse interstitial pulmonary fibrosis, 83-85
cerebral palsy and,546--547
eosinophilic granuloma, 85-86
chronic renal insufficiency and,560--561
idiopathic pulmonary hemosiderosis,87
collagen vascular/connective tissue diseases and, 555-556
progressive systemic sclerosis (scleroderma),89
hemiplegia and, 541-543
pulmonary alveolar proteinosis, 86,86--87
late sequelae of poliomyelitis and, 550--552
pulmonary eosinophilia,85
multiple sclerosis and, 544-546
pulmonary infiltrates, 85
muscular dystrophy and,538-539
rheumatoid arthritis,88
osteoporosis and, 553-555
sarcoidosis, 87-88, 88
Parkinson's disease and, 543-544
systemic lupus erythematosus (SLE), 88-89
rheumatoid arthritis and,558-560

scleroderma and. 556--557
primary/ICU,590--592
spinal cord injury and,548-550
pathophysiology of, 590--591
systemic lupus erythematosus and, 555-556

thoracic deformities and,552-553
pulmonary function tests and, diagnosis, 150,150-151
ICUs, 599-615
Rheumatoid arthritis (RA)
burns, 612-615
fractures,605-606
head injuries, 606--609, 607, 608

hemothorax, 605
Rhonchi, defined, 219-220
musculoskeletal trauma, 603-604, 694
Rhythms, electrocardiograms and, 176--177, 177
neuromuscular disease, 600--602
Ribs
obesity,602-603
anatomy of,24-25, 25y
pneumothorax, 605
secondary dysfunction and. cage mobilization,436
respiratory muscle training, 610-- 612,611, 612
secondary dysfunctionfICU,fractures,604-605
rib fractures, 604-605

spinal cord injuries, 609-612
Right ventricular ejection fraction (RVEF'), nuclear imaging of, 200
trauma, 605
Right ventricular pressure (RVP),intensive care units measurement

of,241-243
vs. primary, 390, 391
Rocking assist techniques, knees-hands, 381-382
Secretions
Rolling techniques, ventilation facilitation and,388
obstructive lung disease and,primary dysfunctionfICU,587-588

treatment of, 782,783, 786
ROM exercises, metabolic demand and, 267

Rowing machines, for oxygen transport treatment, 259-260,260
Rural environments,oxygen transport and, 16
RVEF; see Right ventricular ejection fraction (RVEF)
Sedatives
for ICUs, 572-573
respiratory failure and, 579, 580t,581
Self assist techniques, 377-382
Sepsis, management of, 628t,628-629
SA; see Sinoatrial node (SA)
Serratus
Sacrum mobilization,secondary dysfunction and, 436
anterior anatomy of, 29-30
Salmeterol (Servant), pharmacology of,778
push-ups for, 405
Sarcoidosis, pathophysiology of,87-88,88

Scalenes
anatomy of,29, 29
ventilation and, 402
Shaking
in airway clearance, 325
clinical applications of,346--349, 347, 348
Shock
Scintillation detectors,defined, 198
cardiogenicfICU and, 245
Scleroderma
management of, 627-628,777,778
chronic secondary dysfunction and,556--557
Shoulders
progressi ve systemic, 89
mobilization, 436
respiratory failure and, 579,580t, 581
ventilation facilitation and,392
130
Index
Sickle
SIMV;
of, 108
anemia, cardiopulmonary
Side-lying body positioning, 311, 31

,ce
Stretch reflex, cardiopulmonary physiology of,
12
Synchronized intermittent mandatory ventilation (SIMV)
Single crystal cameras, for nuclear imaging, 198
Suctioning, of artificial airways, 768, 769-77 I, 77!, 772, 773, 773t
Supine positioning. 308-309, 309, 310
Single photon emission tomography (SPECT), defined, 198-199,
201 t, 202-203
ICUs and, 570
Supraventricular arrhythmias,
In
electrocardiograms, 177,
I
179,179,180,181
Sinoatrial node (SA)
Surfactants, for
oxygen transpOl1 and, 18
Surgery
Sitting techniques, 379,379-380, 380
transport treatment, 259-260, 260
open heal1, primary dysfunction/ICU, 595, 596
for primary dysfunction, 421
organ transplant, 706
primary dysfunction secondary to, 495-508
Skin, patient assessments and, 214, 214
SLE; see Systemic lupus erythematosus (SLE)
extrinsic factors, 500
Sleep apnea
mobilnylrecumbency, 500
respiratory failure and, 579, 580t. 581
Sleep di:;turbance, oxygen transport threats and, 255
perioperative course, 496, 496-500, 498
SI\1I;
postoperative management,
Sustained maximum inspiration (SMI)
502-505,506, 507
Smoking
oxygen transport
16
;,urgical effects, 500
patient history and, .141-142
surgical prep, 499
Sniffing techniques, ventilation facilitation and, 392
thoracic, 50( 502
Sodium iodide, pharmacology of, 786
Suspended motion nldiographs, interpretation of. 159-160
Soft tissue therapies, secondary dysfunction and,
Sustained maximum im:piration (SMI), defined,
Spacers, for metered-dose inhalers (MDI), 786
Swan Ganz catheters, in ICUs, 233, 241-243, 243
SPECT imaging;
Single photon emission tomography (SPECT)
Spinal cord injuries
Symmetrical positioning, ventilation facilitation and, 405-406
Sympathomimetic drugs, pharmacology of. 784-785
Synchronized intermittent mandatory ventilation (SI\1V), defined,
pathophysiology of,
Systemic circulation, anatomy of, 48-49
secondary dysfunction/ICU, 609-612
Systemic diseases. cardiopulmonary effects of. 99-112
cardiac, 100-10 I
connective tissue, !O3,103
Spirometers, f1uner, for oxygen transport treatment, 259-260. 260
endocrine. J 09110. I 10
Spondylitis, respiratory failure and, 579, 580t, 581
gastrointestinal, 107, 107
Standing techniques, ventilation facilitation and, 389
hematologic, 108-109, 109
Glireus,
755
Sympatholytic drugs, pharmacology of, 779
S/aph)loCliccus
55-56
Stroke, cardiopulmonary effects of, 104
pediatric cystic fibrosis and, 643
Starling effect
immunological, J 10
liver, 107-108, 108
cardiac effects on, 101
musculoskeletal, 102,102-1 m
cardiopulmonary physiology of, 65
neurological, 103-107, 104
nutritional, 110- I I I, I J I
plasma protein disorders and, 109
Sternocleidomastoid faciliwtion, ve-lltilalion and, 402
phy:;ical
Sternocleidomastoid (SCM), anatomy of, 28-29, 29
pulmonary, 101-102
Sternum, anatomy of, 24
impact, 99-100
rellal, 108, 108
Stethoscopes, auscultation and, 217, 217
Systemic lupus erythematosus (SLE)
Sirepiococcus B, pneumonia in neonates, 642
StreplOcoccUS pyogenes, in bacterial pneumonias, 474-475
chronic semndary dysfunction and
Stress
emotional, 3
Stress testing, nuclear/cardiovascular
exercise, 199
Systemic sclerosis (sclerode!ma), progressive, pathophysiology of, 89
Systole, ventricular. cardiopulmonary physiology of, 66
pharmacologic, 199
Index
Thorax
anatomy of, 23-25, 24. 25
T3; sec Triiodothyronine (T3)

T4;
1-31
mobilization of, 399-401,400
Thyroxine (T4)
ec
secondary dysfullcl"ion and. 436
Tachycardia, trc.<ltmem of, 777-778, 779
Thromboembolism
Tachyuysrhythmias. intensive care of, 239, 240t-241t
cardiopulmonary
Tachypnea. patient assessments and, 216

Tactile fremitlls. patient assessments and, 225, 225,226
Thrombosis, deep vein, management of, 623--624
Tc-99M-macroaggregated albumin; see Technetium-99M-
Thyroid function, laboratory tests of,193t,194
Illacroaggregatcc\ albumin
Thyroid stimulating hormone (TSH), laboratory tests of. 194
Tc-99M-Pyp; scc Technctiulll-99M-pyrophosphate (TcPyp)
Thyroxine (T4), laboratory tests of, 194
Tc-99M-sl)stamibi; sec Ted1l1etium-99M-sestamibi
TI A; see Transient ischemic attack (TI A)
Tc-99M-teboroximc, Technctium-99M-tcboroxime
Tc-99mDTPA; see Technetium-99M-diethylene triamine penta-
acetic (DTPA) aerosol
home-based care communication in, 728-729
Tissue assessments, in oxygen transport treatment, 262
in ICUs, 574, 575
Tissue extraction, oxygen transport and, 18-19
Tec hnct ium-99M-die t hy l ene triamine pe nta-ac etic (DTPA)
Tissue perfusion
aerosol,for ventilation-perfusion scans,20 It, 206
in oxygen transport,S
Technetium-99M-mncroaggregated albumin, for ventilation-
oxygen transpOIt threat.s
perfusion scans, 20 It, 206
TLC; see Total lung capacity (TLC)
Technetiull1-99M-pyrophosphate (TcPyp),defined, 20 I t,203
TLSO; see Total contact thoracic lumbar sacral orthosis (TLSOs)
Technetium-99M-sestamibi, defined,20 I t, 202
TOF;
Technetium-99M-teboroxime, defined,20 I t, 202
see Tetralogy of fallot (TOF)
Total contact thoracic lumbar sacral orthosis (TLSOs), defined,
TEE; see Transesophagcal echocardiography (TEE)
384-385
Tenderness. patient assessments and, 223
Total lung capacity (TLC)
Tcrazosin (Hytrin), pharmacology of,778
sickle cell anemia and, 109
Terbutaline (Brethine, Bricanyl), pharmacology of,778
systemic disease effects on, 106
Testing
Toxic-inhaled materials,oxygen transport and, 16
arterial blood gases and, 153-157
Tracheas
documentation and, 123-126
anatomy of, 36-40, 37, 39t
electrocardiograms, 169-187
deviation assessments and,225, 226
exercise
pre scriptions and,274, 274, 276-277, 280--285, 281, 282t,
283t, 284-286,290, 290--291
TracheomaJacia, respiratory failure and,579, 580t, 581

Tracheostomy tubes, artificial airways, 764-766, 765,767-771,
768,771-774,773t
training and, secondary dysfunction, 426-432
cuff inhalation, 765-766
ICU unit monitoring systems,229-246
metal,764
measurements and, 117-123
plastic, 764-765, 765
multisystem laboratory assessments and, 189-195
Training,exercise and, 274,274, 276-277, 280--285, 281,282t,
nuclear imaging/radiopharmaceuticals, 197-207
283t,284, 285, 286. 290, 290-291
Tranquilizers, for I CUs, 572-573
pulmonary function, 145-15 I
Transesophageal echocardiography (TEE), defined, 197, 20 It,
routine radiographs, 16(}-161
204, 205
x-ray interpretation, 159-167
Transient ischemic attack (TI A), transesophogeal
Tetanus, respiratory failure and, 579, 580t, 581
echocardiography (TEE) for, 205
Tetralogy of fallot (TOF), pediatric management of,640
Transient l<lchypnea of the new horn (TINB), pediatric
ThAIRapy (TM), clinical applications and, 358, 358-359
management of, 641
Thallium 20 I, for cardiovascular testing, 200-202, 20 It
Transplant patients, 703-718
The Flutter (TM), for airway clearance, 328
cardiac, 708
Theophylline,phannacology of, 785
acute phase care, 710--711,714
Thempist requirements
assessment, 708
in I CUs, 568, 569
equipment/monitoring, 708-709
for transplant patients, 706

see
Tidal volume (TV),systemic disease effects on, 106

Timing
asymmetrical dysfunction and, 406
Teams
Therapy, physical;
effects of, 108
exercise guidelines, 712
Physical therapy
Thoracic disorders, primary dysfunction secondary to, 500--502
facility vs. home based rehabilitation, 716-718

goals, 7 J 2
1-32
Index
interventions, 710-711,714
Tumors,respiratory failure and,579, 580t, 581
medication, 716-718
Turner's syndrome, associated cardiology of,639t
outpatient care, 713-714, 714
TV; see Tidal volume (TV)
post-transplant,708
Two-lumen catheters, in ICUs, 241-242
pre-transplant, 708
rejection signs, 714, 715,716
considerations for
Upper airways, anatomy of,32-36,33, 34, 35
Upper/lower extremity exercise,testing/training and,primary
availability,704
ethical, 704-705
dysfunction,419-420
Upright body positioning,302-308,303,304,305,306, 307,308
organ donation,704
organ preservation, 704-706
to supine positions, lCUs and, 570
Urban environments, oxygen transport and, 16
psychosocial implications, 705-706
Uremia, radiography of, 165,166
rejection,704
Urinary retention, treatment of,780-781
trends, 706
waiting list criteria,705, 705
Valves
waiting time,705
when to,704
flutter,259-260,260
history of, 704
in heart anatomy, 45,45-47, 46
Valvular disease
other transplants and,709-7.10

pulmonary
assessments in, 708
equipment/monitoring in, 708-709,715
facility vs. home based rehabilitation in,716-718
goals in,709, 712, 713t, 715
interventions in,709, 712-713,713t,715-716,716
medication in, 717-718
VAPS; see Volume-assured pressure support (VAPS)
outpatient in,714-716, 716
Vascular resistance
post-t.ransplant in,708,712-713,713t
Vascular systems
(R), in blood flow,15
pre-transplant in,708-709, 710
aging changes in,673,673-675, 674t
rejection signs in, 715
peripheral laboratory tests and,192, 192t
surgery and,706
Vasodilators, treatment with, 777, 778
therapy in
Vasopressor agents, for lCUs,572-573
Ventilation facilitation,3 3-415
assessments, 707-708
defined, 708-709, 710, 710-7!3
asymmetrical dysfunction and,405-406
medical management,707,707t
buttertly techniques and,408, 409,410
musculoskeletal considerations, 707, 709-710
cardiopulmonary physiology of,59-60
physiology, 707
chest/shoulders and, 392
diaphragm inhibition and,402-405, 404, 405
therapist requirements,706
diaphragmatic breathing and,389,390,391, 392,394,394,
Trapezius
anatomy of, 30,30
395,396,396
ventilation and, 402
dressing techniques and,389
Trauma, secondary dysfunctionllCU and, 605
dynamic activities and, 388-389
Treadmill, for oxygen transport treatment, 259-260, 260
eccentric resistance techniques and,414
Trepopnea, patient history and,135
expiration and,388
Trihexyphenidyl HCL (Artane), pharmacology of, 783
glossophMyngeal breathing and,410-412,412
Triiodothyronine (T3),laboratory tests of, 194
inspiration and,387-388
Trisomy 13, associated cardiology of, 639t
intrapulmonary percussive, 363, 364
Trisomy 18, associated cardiology of,639t
lateral costal breathing and, 396, 397, 399,399
Trisomy 21, associated cardiology of,639t
manual, 413-414
Trypsin (Tryptar), pharmacology of, 786
mobilizing the thorax in,399-40 1,400
TSH,Thyroide stimulating hormone (TSH)
muscles and,401-4D5, 402, 404, 405
TINB; see Transient tachypnea of the new born (TINB)
musculoskeletal/neuromuscular disorders and, 680
Tuberculosis
normal timing and, 399
management of,488
oxygen rransport and,5,16
to perfusion ratio, 17
Glossary
Vital capacity (VC), Duchenne's muscular dystrophy and, MH
positioning in, 383-385,385, 386, 392,413
primary vs. secondary dysfunction and, 390,39 J
G-33
Vitamin-K deficiency, pulmonary hem orrh age and, lOR
pursed-lip breathing and,410
Vo,: see Oxygen, consumption
repalterning and, 393
Vocalization enhancement, ventilation facilitation and, 412-415
rolling,388
Voice breath sounds,patient
sitting, 388
Volume-assured pressure support (YAPS), defined, 758
assessments and, 220
sniffing, 392
Volume/pressure, cardiopulmonary physiology and 57-58, 58,

,
standing, 389
strategies for, 387-389
Waiting lists,for transplant patients, 705, 705
verbal, 414-415
time of,705
voc liz tion enhancement,412-415
Ventilation-perfusion lung scans, defined,201t, 206
Walking,primary dysfunction and, 421
V.:ntilator withdrawal, obstructive lung discas.: and, primary
Wall motion,nuclear imaging of,200
dysfunction/ICU, 588,5RH-589,589
WBC; see White blood count (WBC)
Weights, for oxygen transport treatment, 259-260, 260
Ventricular function
Wheezing
al'tcrload in, 13
defined,219-220
cardiopulmonary physiology of, 65, 65--67, 66,67t
patient history and,135
diastol.: physiology of,66
electrocardiograms and, 180-184, 182, 183,184
White blood count (WBC),laboratory tests of, 190-192,1911
alThythmias, 177, 178, 179-184,179-184
Williams syndrome, associated cardiology of, 639t
conduction, 170--172, 171
Work environments
facility-based
blocks, 184-186,185,186
myocardial infarction, 186-187, 187
ratc,174, 174-176, 175, 176
recording, 172, 172-174, 173
177
use of,169-170
care and,724-725
evaluation of,174, 174-177, 175, 176, 177
rhythms,176-177,
X-ray testing
abscesses. 164,164
alveolar disease, 162, 162
atelectasis, 164-165, 165,166
left
assist devices/ICU,245
basic structures/shapes, 160
ejection fraction,200
bronchi, 162, 162
end diastolic volume, 13
bronchiectasis, 162,163, 164
output,636
bronchograms in,162, 162
pressurenCU, 241-243,245
left atrial pressure, 241-243
output and,
II,
66
12, 14,17,636
patient assessments and,220--221
congestive heart failure,164, 165,166,167
description of, 159-161, 160
edema, 165,166
emphysema, 162,163
preload, 13
fixed position, 159-160
right
interstitial pulmonary disease, 162, 163
ejection fraction, 200
kyphoscoliosis, 167,167
prcssurenCU,241-243
lateral chest, 159-160
septal defects/ICU and,245
Venue function, oxygen transport and, 18
malignancies,163, 165,166
motion,159-160
Verbal techniques, ventilation facilitation and, 414-415
pleural effusions, 164,165, 166
Vesicular breath sounds, patient assessments and,218-219
pneumonias, 162, 162, 163, 164, 164, 167
Vibration th.:rapy
pneumothorax, 164,165
posteroanterior (PA), 159-160
clinical applications and, 346-349,347, 348
requirements for, 159-160, 161-162
for infants, 652--653,657
routine exams, 160-- 16 J
Viral p ncumo nias

management of, 474
in secondary
dysfunction, 426-427
suspended motion, 159-160
uremia, 165,166
Viscosity,of blood, 14
Xanthines, pharmacology of,785
Visual inspection, pntient assessments and,211-214,214
133Xe gas, for perfusion testing,20 It, 206

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PRINCIPLES AND PRACTICE OF

PRINCIPLES AND PRACTICE OF

Programs in Physical Therapy

Elizabeth Dean, PhD, PT

University of British Columbia

School of Rehabilition Sciences

Vancouver, British Columbia

With 22 contributors and 40] illustrations

Tokyo Toronto Wiesbaden

Dedicated to Publishing Excellence

Vice President and Publisher: Don Ladig

Anne Mejia Downs, PT, CCS

Michael Wade Baskin, PT, RRT

Department of Physical and Occupational Therapy

GT Physical Therapy and Rehabilitation

Instructor, Division of Physical Therapy

West Point, Mississippi

Jean K. Berry, PhD, RN

University of North Carolina

Senior Research Specialist

Chapel Hill, North Carolina

Willy E. Hammon, BSe, PT

Chief of Rehabilitative Services

Gary Brooks, MS, PT, CCS

Special Instructor in Physical Therapy

Health and Rehabilitation Sciences

Clinical Instructor, College of Nursing

The University Hospitals

The Sage Colleges

University of Oklahoma Health Sciences Center

Troy, New York

Oklahoma City, Oklahoma

Susan M. Butl er, MMSe, PT, CCS

Scott M. Hasson, EdD, PT

Division of Physical Therapy

Department of Rehabilitation Medicine

Maine Medical Center

School of Physical Therapy

Texas Woman's University

Margaret K. Covey, MS, RN

Lyn Hobson, PT, RRT

Rush-Presbyterian-St. Luke's Medical Center

University of Illinois at Chicago

Gail M. Huber, MHPE, PT

Programs in Physical Therapy

Division of Physical Therapy

University of Miami School of Medicine

Claire Peel, PhD, PT

Associate Professor in Radiological Scienccs

Department of Physical Therapy

University of Oklahoma Health Sciences Center

Oklahoma Citv. Oklahoma

Rehabilitation T herapy Services

Henry Ford Hospital

Elizabeth J. Protas,PhD, PT, FACSM

Mary lnaSS l"

Texas Woman's University

Assistant Professor of Medicine

Mary Mathews, BS, RN, CCRN,RRT

Neonatal and Pediatrics Chest

Luke's Medical Center