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Anaesthesia for
Medical
Students

Pat Sullivan M.D.


1999 Edition
Acknowledgements: (

The author gratefully acknowledges the work of William Sullivan MA., M.D., John
c
Heng MA., Ola Rosaeg M.D., FRCPC, and medical students Susie Quackenbush and
Bing Kong for their general suggestions, proofreading and editing skills during the (
preparation of this manual. Special thanks to Robert Elliot M.D., for his assistance
in the design of the cover page. (-
(
Canadian Cataloguing in Publication Data

Sullivan, Pat

Anaesthesia for medical students

Includes bibliographical references.


ISBN 0-9699801-0-8

1. Anesthesiology. I. Ottawa Civic Hospital.


Dept. of Anaesthesia 11. Title.

Printed by DocuLink International

O Copyright 1995 by Pat Sullivan. Revised 1999. All rights reserved. No part of (
this book may be reproduced, stored in a retrieval system, or transmitted in any form (
or by any means, electronic, mechanical, photocopying, or otherwise without the writ-
ten permission of the author. (
(
Published by the Department of Anaesthesia, Ottawa Civic Hospital.
Address correspondence to: (
Patrick Sullivan MD, FRCPC (
Department of Anaesthesia
Ottawa Civic Hospital, B310
c
1053 Carling Avenue
Ottawa, Ontario, Canada, K1Y 4E9 (
T:613 - 761 - 4940
F:613 - 761 -5032 (
E: psullivan@civich.ottawa~n.ca (

a
: Contributing Authors

Dr. Gregory Allen Dr. John Kitts


- Assistant Professor Associate Professor Anesthesia
Pennsylvania State University University of Ottawa
MHAUS Hotline Consultant Vice President Medical Affairs
- Department of Anesthesia Ottawa Hospital
- Hershey, Pennsylvania '
Dr. Anne Lui
- Dr. Wayne Barry Assistant Professor
- Assistant Professor University of Ottawa
University of Ottawa Department of Anesthesia
Department of Anesthesia Ottawa Hospital - Civic Campus
- Ottawa Hospital - Civic Campus
Dr. John Penning
Dr. Greg Bryson Assistant Professor
- Assistant Professor University of Ottawa
- University of Ottawa Director of the Acute Pain Service
Department of Anesthesia Department of Anesthesia
- Director Preadmission Unit Ottawa Hospital - Civic Campus
- Ottawa Hospital - Civic Campus
Dr. Gordon Reid
Dr. Robert Cirone Assistant Prsfessor
- Staff Anesthesiologist University of Ottawa
Department of Anesthesia Director Malignant Hyperthermia
St. Joseph's Hospital Investigation Unit
Toronto Department of Anesthesia
-
Ottawa Hospital Civic Campus
Dr. Robert Elliot
Assistant Professor Dr. Linda Robinson
University of Ottawa Assistant Professor
Department of Anesthesia University of Ottawa
-
Ottawa Hospital General Campus Department of Anesthesia
Ottawa Hospital - Civic Campus
Introduction
Specialists in the fields of medicine and should know. A11 other material is
surgery may ask why medical students ~ r o v i d e dfor background reading which
should be exposed to the specialty of the student may know. The manual is
anesthesia. We believe that there are to be used as a primary reference for
basic concepts and technical skills that lectures on monitoring in anesthesia,
every physician should possess, and that and on acute and chronic pain manage-
these concepts and skills are best taught ment. The problem-based tutorial ques-
by our specialty. tion will also be on material covered in
this manual.
Medical school curricula across North
America are repeatedly criticized for The student who completes the anest-
lacking the teaching of both acute and hesia rotation should have acquired
chronic pain management. In addition, confidence in airway management skills
students who pursue a career in surgery, including mask ventilation and tracheal
emergency medicine or internal medi- intubation, as well as securing intra-
cine are expected to have the skills to venous access. Important concepts for
manage a patient's airway. However, the student to attain during their rotation
they usually have had no formal teach- include:
ing in these basic skills. Finally, medi-
cal school curricula in North America 1. Preoperative assessment.
are rapidly changing. Students are now 2. Basic principles of managing acute
asked to commit themselves to a spe- and chronic pain disorders.
cialty during the third year of their 3. The appropriate use of local anaes-
medical school training. We believe thetic agents.
that this process is unfair. We also 4. Analgesic options for women in
recognize that a student with no prior labour.
exposure to anesthesia is unlikely to 5. Basic neonatal assessment and re-
choose anesthesia as a career. suscitation.
6. Intravenous fluid and blood compo-
This manual was written with contribut- nent therapy including the potential
ing authors from the Departments of complications of a blood product
Anesthesia at the Ottawa Civic and transfusion.
General Hospitals for medical students
spending two weeks of their clinical
rotation in the specialty of anesthesia.
Six specific objectives are used to focus Patrick Sullivan MD, FRCPC
the students reading. The text is high- Assistant Professor
lighted by two asterisks (**) for University of Ottawa,
material that is essential and that the Resident Program Director
student must know, and one asterisks Department of Anesthesia
(*) for material which the student University of Ottawa
Preface
The first public demonstration of ether macology and resuscitation of acutely
was by W.T.G. Morton in the traumatized patients. The importance of
Etherdome of the Massachusetts General imparting these skills and knowledge to
Hospital in 1846. Ether anaesthesia medical students has been realized by
became widely available and would those responsible for medical school
soon be followed by chloroform and curricula. Accreditation bodies are
nitrous oxide. Surgeons were not demanding that anaesthetists teach med-
particular about who poured the ether or ical students.
chloroform so long as someone was
there to do the job. It was not until the When the new curriculum, founded on
early 1920's that physicians began to problem-based learning, was adopted in
show interest in anaesthesia as a the Faculty of Medicine at the Univer-
specialty. By the end of World War I1 sity of Ottawa, anaesthesia was given
the infant specialty was firmly estab- responsibilities in the program. Each
lished and university training programs student must spend two weeks in an
began. anaesthesia rotation and many anaesthe-
tists participate in small group sessions.
The emphasis has traditionally been on Dr. Patrick Sullivan found that an an-
postgraduate teaching. Why has aesthesia manual, which would meet the
undergraduateanaesthesia teachingbeen needs of medical students submerged in
neglected or de-emphasized? It was a new curriculum, was not available.
because the medical school curriculum The manual he and his co-authors have
was controlled by older, traditional written covers all of the important
disciplines that were unwilling to material a medical student must and
relinquish time for competing spe- should know. It is best taught by an-
cialties. This was complicated by the aesthetists because it falls almost
fact that anaesthetists originally worked exclusively in their domain. The
only in the operating room, and found it organization of the manual makes it
difficult to be freed from that responsi- essential reading for students rotating
bility to undertake teaching outside the through anaesthesia who want to
operating room. Anaesthesia has optimize their brief exposure to anaes-
expanded to include other services thesia, which has so much to offer.
which include Intensive Care, Acute and
Chronic Pain Services, Malignant
Hyperthermia Diagnostic Services, and
a Pre-admission Unit. Anaesthetists
have developed many skills which are J. Earl Wynands, M.D.
valuable to physicians, regardless of Professor and Chairman
their discipline. They have become Department of Anaesthesia
specialists in applied physiology, phar- University of Ottawa
Table of Contents

1. Rotational Objectives ...............................


2. Anaesthesia Overview ...............................
3. Preoperative Evaluation and Risk Assessment ..............
4. Premedication .....................................
5. Getting Started:
A practical approach to the OR.....................
6. Intubation and Anatomy of the Airway ...................
7. Intubation Decisions ................................
8. The Laryngeal Mask Airway ..........................
9. Rapid Sequence Induction ............................
10 .Monitoring in Anaesthesia ............................
11 .General Intravenous Anaesthetic Agents . . . . . . . . . . . . . . . . . .
12 .Muscle Relaxants ..................................
13 .Inhalational Agents .................................
14 .Narcotic Agonists and Antagonists ......................
15 .Local and Regional Anaesthetics .......................
16. Acute Pain Mechanisms and Management .................
17 .Chronic Pain ......................................
18 .Obstetrical Anaesthesia ..............................
19 .Basic Neonatal Resuscitation ..........................
20 .Intravenous Fluid and Blood Component Therapy...........
21 .Common Perioperative Problems .......................
22 .Managing the Circulation .............................
23 .Oxygen Therapy and Hypoxemia .......................
24 .Unusual Anaesthetic Complications:
Malignant Hyperthermia . . . . . . . . . . . . . . . . . . . . . . . . . .
.............................
Aspiration Syndrome
...............................
Allergic Reactions
Appendix: Intravenous Access..............................
Review Questions .......................................
Index ............................................
Notes ............................................
'
I Anaesthesia
'
) Rotational Objectives
There are six speclflc knowledge and The student will demonstrate proper
) sk111s obJect1ves4 for the two week airway and ventilatory management of
) anaesthesia rotation: the unconscious patient by:

1. To become aware of anaesthetic a. Describing and identifying basic


considerations in the preoperat- oropharyngeal and laryngotracheal
ive evaluatlon and preparation of anatomy.
the patient. b. Describing the indications, benefits
and risks of airway management by
This will be accomplished by conduct- mask and endotracheal intubation.
ing several preoperative assessments, c. Identifying and stating appropriate
including: sizes of masks, oral and nasal air-
ways, laryngoscope blades and
a. Taking and recording a pertinent endotracheal tubes.
history. d. Identifying and overcoming upper
b. Performing an appropriate physical airway obstruction with mask ven-
examination, including assessment tilation using various masks, oral
of the airway, the respiratory and and nasal airways, jaw thrust and
cardiovascular systems, and other or chin lift maneuvers.
systems as indicated. e. Successfully preparing appropriate
c. Reviewingrelevantlaboratorydata. equipment, positioning and
d. Preparing a problem list and intubating several patients with
assigning appropriate ASA phy- minimal supervisor intervention.
sical status. f. Correctly identifying within 30 sec-
e. Prescribing appropriate premedica- onds those patients in whom endo-
tion, including continuing relevant tracheal intubation was not succ-
current medications, and demon- essful.
strating knowledge of the prin- g. Recognizing and discussing the
ciples of managing specific medi- need for controlled ventilation
cations (eg. insulin,anticoagulants). using physical signs, cardiovascular
parameters, respiratory measure-
2. To learn appropriate airway and ments, and/or arterial blood gases.
ventllatory management.

Must Know ** Should Know * Page I


Anaesthesia for Medical Students

h. Discussing the various methods of - examination of the patient.


monitoring the adequacy of ventila- - pulse and blood pressure.
tion. - urine output.
i. Prescribing appropriate parameters - invasive monitoring (CVP,
for mechanical ventilation. PCWP, Arterial pressure
j. Describing and identifying criteria waveforms, cardiac output).
for extubation.
To learn local anaesthetlc phar-
3. To acqulre skllls necessary to macology approprlate to general
prescribe and conduct approprl- medlclne by:
ate fluld and blood component
therapy, lncludlng establlshlng Classifying commonly used agents
vascular access. according to amide and ester link-
age.
This will be demonstrated by: Listing commonly used local
a. Identifying common sites for anaesthetics for:
venous access. - topical use
b. Demonstrating skill at establishing - local infiltration
venous access by: - peripheral nerve blocks
-using sterile technique. - iv (Bier's) block
- Successfully inserting several - epidural anaesthesia
peripheral catheters of various - spinal anaesthesia
calibres. Listing acceptable doses of at
-Protecting the venipuncture site least two agents used for topical
and immobilizing the catheter. and local infiltration anaesthesia.
c. Describing the indications and Describing the diagnostic criteria
complications of central venous for, and management of:
access. - local anesthetic toxicity.
d. Prescribingperioperative fluid and - inadvertent intravascular injec-
electrolyte replacement, taking tion of local anaesthetic.
into account such factors as NPO - allergic reaction to a local an-
status, preoperative bowel prep, aesthetic.
NG suction, fever, blood losses,
and third space losses. To understand the management
e. Discussing perioperative indica- of pain In the peripartum period
tions for blood administration, and and the lnltlatlon of neonatal
learning rational use of blood resuscltatlon.
products, and the potential compli-
cations of blood product adminis- This will be demonstrated by:
tration. a. Discussingindications, contraindi-
f. Correctly interpreting data from cations and adverse effects of
the following monitors of volume various modes of obstetrical pain
status: relief.

Page 2
Rotational Objectives

- mask analgesia with nitrous c. Chronic low back pain.


oxide and/or volatile anaesthe- d. Post herpetic neuralgia.
tic agents. e. Cancer pain.
- narcotic analgesia (im, or iv).
- epidural anaesthesia. ANAESTHESIA CURRICULUM:
- spinal anaesthesia. KNOW LEDGEfSKILLSIATTITUDE
b. The student will develop skills in
assessment and management of
the healthy newborn by:
- administeringoxygen by mask. The following topics will be covered
- performing oropharyngeal and either in the manual, or in seminar
nasopharyngeal suction. format and problem solving sessions
- performing an initial physical during the 12-week surgical - anaes-
examination. thesia rotation.
- assigning Apgar Scores.
- recognizing newborn distress. Preoperative evaluation and preparation.
c. The student will be able to -
Anaesthetic Surgical risk assessment.
describe therapeutic steps necess- Hypoxia .
ary to begin neonatal resuscitation. Oxygen Therapy.
Intubation-indications/complications.
6. To understand the prlnclples of Principles of mechanical ventilation.
acute and chronlc paln manage- Shock.
ment. Fluid Therapy.
Blood component therapy.
This will be achieved through the pro- Acute and Chronic Pain management.
vided reading material in the anaesthesia Obstetrical anaesthesia-analgesia.
manual, a pain clinic rotation, and a Basic neonatal resuscitation.
discussion of modalities for acute pain
management including:

a. iv narcotic infusions. 1. Airway maintenance maneuvers in


b. non-narcotic analgesics. the unconscious patient.
c. iv and epidural PCA 2. Artificial airway insertion.
(patient controlled analgesia). 3. Mask ventilation.
d. peripheral nerve blocks. 4. Endotracheal intubation and ex-
tubation.
Reading material in the anaesthesia 5. Spontaneous, manual, and con-
manual and discussion of the diagnosis trolled modes of ventilation.
and management of common chronic 6. Venous cannulation.
pain syndromes will focus on: 7. Prescription, identificationand ad-
ministration of blood components,
a. Reflex sympathetic dystrophy. including equipment assembly.w
b. Fibrositis. 8. Arterial blood gas sampling.w

Should Know * Page 3


4naathaia for Medical Srudenfs

9. Spinal anaesthesia encounters do not have to be devoid of


(Lumbar puncture)." reassurance, kindness or a comforting
10. Nasogastric tube insertion." touch. We expect both positive and
negative experiences during your rota-
ti Skills number 1 to 6 must be tion to be discussed openly with us, to
achieved during the rotation. Students ensure the best possible rotation for
may acquire skills number 7 to 10 de- future students.
pending on clinical opportunity and the
students' interest level. Resources:
Attitude: Our University of Ottawa Anaesthesia
Manual will be distributed to all stud-
We hope that your two-week rotation ents, and will be used as the basic ref-
will stimulate a thirst for knowledge and erence text for the rotation. Additional
understandingof the fascinating physiol- reference material will be available in
ogy and pharmacology that occurs in each hospital's anaesthesia library.
the patient undergoing surgery. Anaes-
thesia is a somewhat unnatural if not Topics covered in this manual have
magical state. It is normal to feel tech- been classified as either must know,
nically challenged during your rotation should know, or may know material.
as you acquire vascular access and Material designated as must know will
airway management skills. Each of you be identified by two asterisks (**), and
can expect to experience (as all doctors will have a greater emphasis in content
have), a humbling but hopefully reward- and weighting in the multiple choice,
ing, technical learning curve. You short answer, and OSCE questions at
should be aware of your difficulties, the end of the surgical anaesthesia rota-
your response to them, and the response tion. Material assigned to the should
of your patient and other medical per- know portion of each chapter will be
sonnel to your difficulties. We ask that identified by one asterisk (*). All other
your eyes and senses not be clouded by topics covered in the manual provide a
technical monitors, but rather be open to general background for the student
the overall care of the patient. We during their anaesthesia rotation, and are
demand a commitment of excellence in topics which the student may know. A
your care and concern for the well- passing grade can be achieved with a
being of the patient and their family. good comprehension of the must know
We expect punctuality and honesty as a material, while an honours mark may be
basis of good medicine. awarded to students correctly answering
material covered in the should know and
While students may view anaesthesia as may know sections of the manual.
a specialty with limited patient contact,
they should ensure that opportunities for
communication with the patient and
family do not slip by. Fact-gathering

Page 4
Rotational Objectives

A computerized anaesthesia simulator


will be available as anoption during the
students rotation. (The simulator The rotation evaluation will be based on
includes models of pharmacology, four components.
pharmacokinetics, critical incidents, as
well as cardiovascular and respiratory I. Participation during problem solv-
physiology). ing sessions.
11. One or more examinations using a
The hospitals' anaesthesia library and multiple choice format, short
main libraries will be available for answer examination format, or
reference during the rotation. OSCE examination.
111. A clinical profile record.
IV. A review of the anaesthesia simu-
Notes: lator problems (optional).

M w Know ** Should Know * Page 5


Anaesthesia Overview
Modem general anaesthesia is based on iologist uses both skills in clinical
the ability to provide adequate analgesia examination and a host of technical
and amnesia during surgical procedures. monitors to provide ongoing feedback
Neuromuscular-blocking drugs may be on the patient's physiological status and
utilized to facilitatesurgical exposure by anaesthetic requirements. Table 2.1 lists
providing profound muscle relaxation. options available to the anaesthesiol-
The anaesthesiologist attempts to ogist for providing analgesia, amnesia
achieve both analgesia and amnesia, and muscle relaxation.
with or without muscle relaxation, while
maintaining the patient's normal physio- A state of general anaesthesia may be
logical functions. The challenge in induced with the injection of anaesthetic
anaesthesia is to maintain a balance drugs, or by the inhalation of a mixture
between the stress of the surgical pro- of anaesthetic vapours (figure 2.1).
cedure and the cardiorespiratory With general anaesthesia, muscle relax-
depressant effects of deepening levels of ants may be used to facilitate both tra-
anaesthesia (figure 2.1). The anaesthes- cheal intubation and muscle relaxation.

Anaesthesla Surgery
Physbbgical Stability S t w
End organ homeostasis - psychological
- cardiovascular - physiologlcal
- Blood loss - Cardiovascularstress
- respiratory
- neural - Fluid shifts - Respiratorystress
- renal - Temperature changes

Figure 2.1: The Anaesthetic - Surgical balance.

Page 6
Chapter 2 Anaesthesia Overview

Muscle relaxants are frequently used to muscles of respiration, positive pressure


facilitate surgical access, and are essen- ventilation is frequently used to main-
tial for thoracic and abdominal oper- tain normal minute ventilation when
ations. As muscle relaxants have no they are given. When muscle relaxants
effect on the state of consciousness, are not used, the patient may be allowed
additional anaesthetic medications must to spontaneously inhale anaesthetic
be given to ensure both amnesia and vapours to maintain the anaesthetic
analgesia. The use of muscle relaxants state. If efforts at spontaneous ventila-
avoids the need for excessive amounts tion are inadequate, manually assisted or
of other anaesthetic agents that would controlled mechanical ventilation may
otherwise be required to achieve the be used by the anaesthetist. Controlled
same degree of muscle relaxation. mechanical ventilation is generally used
Because muscle relaxants also affect the only when the trachea has been
intubated.
Table 2.1: Anaesthetic Options*.
Anaesthetic Options
Local Anaesthesia
Alone.
Local Anaesthesia eg. iv Propofol, midazolam, fentanyl and or music for
with intravenous sedation.
conscious sedation.
Neurolept-analgesia. Used infrequently. Achieved with high doses of drop-
eridol with a opioid (such as fentanyl) for analgesic
supplementation.
Regional Anaesthesia, eg. Spinal Anaesthesia
with or without seda- Epidural Anaesthesia
tion. Brachial Plexus Block
Intravenous 'Bier' Block
Peripheral Nerve Blocks
General Anaesthesia. May be combined with regional anaesthesia, peripheral
(see figure 2.2) nerve blocks or local anaesthesia.

Others Acupuncture
Biofeedback techniques (Lamaze)
Inhalational agents
(eg. Entonox = 5050 mixture of nitrous oxide and
oxygen).
im, po, iv sedatives, narcotics, neuroleptics, or
antiemetics

** Must Know Should Know Page 7


)
Anaesthesia for Medical Students
)

Intravenous Anaesthetics or Inhaled Anaesthetic Gases

Induction of
General Anaesthesia

Mask Endotracheal tube

No muscle Assisted Controlled


Hj
relaxants Ventilation y o n

v
Spontaneous Ventilation with
ventilation muscle relaxants

Figure 2.2: Establishment of General Anaesthesia.

Spontaneous and assisted ventilation drugs used during general anaesthesia


may be used in conjunction with a include antiemetics, neuromuscular
tracheal tube, laryngeal mask airway, or blocking agents, and neuromuscular
simple face mask (figure 2.2). antagonists.

Modem general anaesthesia uses combi-


nations of medications in an attempt to
minimize each drug's side effects, and
maximize individual benefits. Hence,
rather than using halothane alone -to
provide anaesthesia for abdominal sur-
gery, the anaesthetist often chooses a
series of medications to match the
patient's needs. These medications may
include opioids to blunt the pain
response to surgery, barbiturates to
induce the anaesthetic state, and volatile
anaesthetic agents such as nitrous oxide
and isoflurane to maintain the anaes-
thetic state. Other common anaesthetic

Page 8
/
CHAPTER 3
1

' Preoperative
I Evaluation and
: Risk Assessment
) M.D., FRCPC AND JOHNB. KITTSM.D., FRCPC
GREGBRYSON
- - -

Preoperative assessment is essential for safe and effective performance of sur-


the safety of anaesthesia. Physicians gery. The preoperative evaluation does
who have had no exposure to the spe- not replace the role of the primary care
cialty of anaesthesia are ill-equipped to provider, and should not be used to
evaluate, prepare, and institute measures address issues that are not relevant to
to minimize the patient's risk in the the performance of anaesthesia and
perioperative period. This chapter pro- surgery.
vides a framework for physicians who
need to understand their patients' risk of The preoperative visit should include
undergoing a surgical procedure, and the the following steps:
measures that can be used to optimize
their patients' condition prior to surgery. I. Problem Identification
11. Risk Assessment
Preoperative evaluation serves many 111. Preoperative Preparation
purposes. First, it offers the anaesthetist IV. Plan of Anaesthetic Technique
an opportunity to define the patient's
medical and surgical problems, and plan
the anaesthetic technique. Sewnd,
further investigation, consultation, and
treatment can be arranged for patients Identification of the problems a patient
whose condition is not optimal. Finally, brings to the operating room is one of
the anaesthetist can provide information the most vital, yet easily neglected,
and reassurance for the patient during components of the perioperative man-
this stressful time. agement of the surgical patient. A
system-oriented approach to the patient
An organized approach to the preoperat- is helpful in completing a thorough
ive evaluation will allow the anaesthetist preoperative assessment. As is the case
to perform a focused evaluation of the elsewhere in medicine, the preoperative
patient's medical and surgical condition, evaluation should progress through
and to address issues relevant to the history (including a review of the

** Must Know Should Know Page 9


Anaesthesia for Medical Students

patient's chart), physical examination, be directly sought. Valvular heart


and laboratory investigation. disease presents a special set of con-
cerns to the anaesthetist. This includes
Anaesthetic drugs and techniques have unfavourable and even dangerous alter-
profound effects on human physiology. ations in haemodynamics brought on by
Hence, a focused review of all major the anaesthesia, particularly major
organ systems should be completed regional techniques (see chapter 15:
prior to surgery. The anaesthetist pays Local and regional anaesthetics). Con- .
special attention to symptoms and dis- sider the risk of subacute bacterial ,
ease related to the cardiovascular, res- endocarditis (SBE) in these patients. I

piratory, and neuromuscular systems as I

they will directly manipulate these sys- Although less common with new anaes- ,
tems during surgery. Because one of thetic drugs, arrhythmias are frequently
'
the goals of the preoperative evaluation seen in the operating room. In the ,
is to ensure that the patient is in the preoperative visit, identify a past history ;
best (or optimal) condition, it is import- of arrhythmia or symptoms suggesting
ant not only to identify symptoms, but the need for a pacemaker. The patient /

also to document their severity and to with hypertension will require special ;
determine their stability or progress. attention to perioperative antihyper-
Patients with unstable symptoms should tensive therapy and fluid and electrolyte
be postponed for optimization prior to balance. I

elective surgery.
Respirology:
Cardlovascular: Cigarette smoke has several adverse
Patients with ischemic heart disease are effects, including alteration of mucus
at risk for myocardial ischaemia or secretion, clearance, and decrease in
infarction in the perioperative period. A small airway calibre. It also may alter
thorough history should ascertain the immune response. The chronic
whether angina is new or has recently smoker should be encouraged to abstain
changed from a previously stable pat- from smoking for at least 8 weeks prior
tern. A description of the patient's to the operation,' but stopping smoking
exercise tolerance must also be for even 24 hours may produce benefits
included. Patients with a history of a in cardiovascular physiology2 and carb-
recent myocardial infarction (< 6 oxyhemoglobin levels.
months) or unstable angina are poor
surgical candidates, with a high risk of Patients with chronic obstructive pulm-
significant morbidity or mortality. onary disease (COPD) are at increased
risk of perioperative respiratory compl-
Assessment of cardiac risk is discussed ications. Anaesthesia, surgery and
later in this chapter. As many anaes- postoperative analgesia all predispose
thetic agents are also myocardial the patient with COPD to respiratory
depressants, a history of congestive depression, atelectasis, retained secret-
heart failure or cardiomyopathy should ions, pneumonia and respiratory insuff-
Chapter 3 Preoperative Assessment

iciency or failure. The patient with papilledema. Pituitary lesions may


asthma is at particular risk as manipula- cause endocrine abnormalities. A his-
tion of the airway and cold dry anaes- tory of T M ' s or CVA's suggests signifi-
thetic gases are potent triggers of intra- cant cerebrovascular disease. The an-
operative bronchospasm. Determine the aesthetist should ask the patient about a
presence of cough and the colour and history of seizures, and determine the
amount of sputum. Ensure that there is type, frequency and time of last occur-
no acute upper respiratory infection. rence. Note any anticonvulsant medica-
tions the patient is receiving.
The patient's exercise capacity should be
evaluated by asking questions such as The patient with a history of spinal cord
how they manage around stairs at home, injury is at risk for a number of
and walking to local stores. Are they perioperative complications including
able to walk several blocks comfortably respiratory failure, arrhythmias, auto-
at a normal pace? Do they avoid stairs? nomic hyperreflexia, hyperkalemia,
If they routinely uses stairwells, how pathologic fractures and pressure sores.
many flights are they able to complete? It is important to document the date and
Do they have to rest in the stairwell? Is level of the neurological injury, as the
this the result of fatigue, shortness of incidence of many of these complica-
breath, or chest pain? tions are dependent on such variables.
Patients with lower motor neuron
Restrictive lung disease will be lesions of any kind are at risk for
worsened by upper abdominal or unusual responses to anaesthetic drugs
thoracic surgery, and place the patient at (see chapter 12: Muscle Relaxants -
increased risk for perioperative failure. Succinylcholine), and regional anaes-
Any disease process which leads to an thesia should be considered only after
altered control of breathing (obstructive careful documentation of the patient's
sleep apnea, CNS disorders, etc.) may nerve deficits.
lead to profound respiratory depression
from the drugs used in the perioperative Disorders of the neuromuscular junction
period, and may require postoperative such as myasthenia gravis, myasthenic
monitoring in a critical care setting. syndrome, etc., will cause unpredictable
Potential airway problems are of par- responses to neuromuscular-blocking
ticular concern to the anaesthetist, and drugs. Lastly, patients with muscular
must always be evaluated (see chapter dystrophies and underlying myopathies
6: Intubation and Anatomy of the Air- are known to have both an increased
way). association withmalignant hyperthermia
and an increased risk of postoperative
Neuromuscular: respiratory failure (see chapter 24:
If the patient has an intracranial lesion, Uncommon Anaesthetic Complications -
seek early signs and symptoms of raised Malignant Hyperthermia).
intracranialpressure such as headaches,
nausea, vomiting, confusion and

** Must Know Should Know P a g e 11


Anaesthesia for Medical Studenis

Endocrlne: than one week in the last six months.


Patients with diabetes mellitus require
careful management in the perioperative GI-Hepatic:
period, as the stress of surgery and peri- Patients with hepatic disease frequently
operative fasting can cause marked present problems with fluid and electro-
swings in blood glucose. Diabetics lyte imbalance, coagulopathies and
frequently have widespread end organ altered drug metabolism. Patients with
damage involving the cardiovascular, gastroesophageal reflux (GER), as well
nervous and renal systems. as those at risk for GER, are prone to
regurgitation of gastric contents and
Patients with thyroid disease may ex- aspiration pneumonitis during the perio-
perience difficulties under anaesthesia. perative period (see chapters 9 & 24:
Profound hypothyroidism is associated Rapid Sequence Induction & Unusual
with myocardial depression and exag- -
Anaesthetic Complications Aspiration
gerated responses to sedative medica- Pneumonitis). These patients should
tions. Hyperthyroid patients are at risk receive anti-reflux prophylaxis pre-
for perioperative thyroid storm. Thyroid operatively.
goitres may compress the airway and
involve the recurrent laryngeal nerve Renal:
leading to vocal cord palsy. These Disorders of fluid and electrolyte bal-
place the patient at risk for airway obst- ance are common in the perioperative
ruction. period, and management of any possible
electrolyte deficiency or excess may be
Patients with phaeochromocytoma are part of the anaesthetic management of
particularly challenging for the anaes- the patient. Generally all fluid and
thetist, surgeon, and internist involved electrolyte disorders should be corrected
in their care. These patients are at risk prior to elective surgery.
for extreme swings in blood pressure
and heart rate in the perioperative Patients with renal failure, both acute
period, and require intensive preoper- and chronic, frequent the OR. The
ative therapy with adrenergic blocking anaesthetist must be prepared to deal
drugs. Patients at risk for adrenal sup- with their fluid and electrolyte dis-
pression (history of exogenous steroid orders, dialysis requirements and altered
therapy) may not be able to increase drug metabolism. Pay careful attention
their own corticosteroid production to to the patient's dialysis schedule, as
match the imposed stress of surgery. important changes in blood volume and
The incidence of adrenal suppression is serum potassium levels occur pre- and
not predictable, and depends on the post-dialysis. If possible, plan elective
potency and frequency of steroid dose surgery so that the patient receives
and on the length of steroid therapy. dialysis either the night before surgery,
As a general rule, corticosteroid or on the morning of surgery. Patients
supplementation is provided for patients with renal insufficiency are at risk for
who have required steroids for more deterioration of their renal function, and
Chapter 3 Preoperative Assessment

careful attention must be paid to their their age alone. However, every
fluid and haemodynamic management in attempt must be made in adequately
the perioperative period. diagnosing and treating coexisting dis-
ease preoperatively. The risk of defer-
Haematologic: ring surgery must be balanced against
Anemias of a variety of causes are the potential for the patient returning on
common in the patient undergoing sur- an emergency basis.
gery. A minimum haemoglobin level of
100 gm/L was traditionally required Emergency surgery in the elderly patient
before a patient could undergo elective may lead to a four- to twenty-fold
surgery. The dogma regarding an increase in perioperative mortality.
adequate haemoglobin level has held Delay in presentation and inadequate
less sway in recent years. Now the time for optimizing coexisting disease
"transfusion trigger" must be individual- place an increased burden on a patient
ized to the patient, bearing in mind the lacking the physiological reserve to
chronicity of the anemia, the likelihood tolerate major stress and surgery.
of perioperative blood loss, and the
patient's co-existent disease (see chapter Medications and Allergies:
20). A detailed list of the patients' medica-
tions and allergies is an essential part of
Coagulopathles involving clotting fac- the preoperative assessment. Particular
tors and platelets, both congenital and attention should be paid to
acquired, require careful management. cardiovascular and respiratory medica-
Patients with a bleeding tendency are tions, narcotic analgesics, and drugs
generally poor candidates for major known to have significant side effects or
regional anaesthesia and management drug interactions.
must be individualized, depending on
the nature of the bleeding problem, the As a general rule, all cardiac and pul-
proposed surgery, and the patient's monary medications and most other
medical condition. necessary medications should be taken
with sips of water at the usual time, up
The Elderly: to and including the day of surgery.
The elderly have a higher incidence of Possible exceptions to this include
age-related coexisting disease as well as coumadin, ASA and NSAID's, insulin
both diminished organ function and (adjustment of the dose is needed on the
organ reserve. The result is that elderly day of surgery), oral hypogylcemics and
patients are generally recognized to be antidepressants. Pay special attention to
in a higher perioperative risk group. patients receiving monoamine oxidase
Perioperative morbidity and mortality (MAO) inhibitors and amiodarone.
are related to the extent of coexisting
disease rather than the patient's age Question patients with allergies to drugs
alone. Elderly patients should not be carefully on the nature of the reaction
refused elective surgery on the basis of and the circumstances under which it

** Must Know Should Know Page 13


Anaesthesia for Medical Students

occurred. Many "allergies" are simply on evaluation of the airway, the


anticipated drug side effects such as cardiovascular system, the respiratory
nausea and vomiting, or adrenaline system, and any other systems identified
absorption from local anaesthetic agents. as having symptoms or disease from the
True allergies to anaesthetics are history.
unusual, but when present, can be fatal.
General:
Prlor Anaesthetics: A general assessment of the patient's
The patient undergoing anaesthesia and physical and mental status is performed.
surgery should be carefully questioned Note whether the patient is alert, calm,
on their response to previous anaes- and cooperative, or unusually anxious
thetics and a family history of problems about their scheduled procedure. Is the
with anaesthesia. Investigate any com- patient young and physically fit, or
plication or adverse reaction to prior elderly incoherent, emaciated and con-
anaesthetics. Document the type of fined to bed? Such obvious differences
problem, as well as its management and will dictate the extent and intensity of
outcome. In the case of serious peri- the examination and the time required to
operative events, consult the old chart to listen to the patient's concerns and pro-
complete the history. Seek a family vide reassurance. The patient's mental
history of adverse anaesthetic experi- status also influences the type and
ence. Malignant hyperthermia and amount of preoperative medication
plasma cholinesterase deficiency are two required (if any), and may influence the
hereditary disorders that manifest under type of anaesthetic technique used (eg.
anaesthesia (see chapter 24: Unusual general vs. regional).
Anaesthetic Complications).
Upper airway:
Problems related to Surgery: Examination of the upper airway must
Information about the patient's general be performed on all patients. Identify
medical condition and anticipated intra- and document any loose teeth, capped
operative problems can be gained from teeth, or bridges. The patient should be
an evaluation of the proposed surgery. asked to open their mouth as widely as
Careful consideration of the surgical possible, in order to assess temporal
procedure will reveal the likelihood of mandibular joint mobility, and allow
significant blood or third space loss, visualization of the soft palate, uvula,
cardiorespiratory compromise, andlor pharyngeal arches and posterior phar-
unusual positioning requirements (prone, ynx. The thyromental distance (the
lateral, lithotomy, etc.). This informa- distance from the mentum (lower border
tion will be useful in planning venous of the chin) to the thyroid notch, the
access, monitoring, and anaesthetic mobility of the C-spine in both flexion
technique. and extension, as well as the position of
the trachea should all be assessed, as
Physlcal Examinatlon: each of these have implications with
The physical examination should focus respect to the ease of intubation.

Page 14
Assessment of the upper airway must sites for major regional anaesthetic
include evaluation of the range of techniques (eg. spinal, epidural, or
motion of the neck, as well as mouth brachial plexus blocks).
opening, dentition, and thryromental
distance. The adequacy of visualization Again, the state of health of the patient
of the hypopharyngeal structures is used will dictate the intensity of the examin-
as an indicator of potential difficulty ation required. The healthy 20-year-old
with direct laryngoscopy. A hypo- male undergoing an arthroscopy,
pharyngeal class is assigned in an requires a much more abbreviated his-
attempt to quantify the degree of diffi- tory, physical examination and chart
culty that will be encountered during review when compared to the elderly
direct l a ~ ~ n ~ o s c o (See
p y . ~Chapter
~~ 6: patient undergoing a major abdominal
Anatomy and Assessment of the Air- procedure.
way).
Laboratory Testing:
Lower airway: Obtain preoperative laboratory testing
Assess the respiratory rate. Note the only if indicated from the preoperative
shape of the thoracic cage, and whether history and physical examination. In
or not the patient is relying on their September 1993, the Public Hospital's
accessory muscles (e.g., the barrel Act in Ontario was amended so that
shaped bronchitic patient vs. the pink mandatory haemoglobin and urine an-
emphysemic puffer). Auscultate the alysis were no longer required prior to
chest for audible rhonchi on quiet and surgery. Perform these tests and all
forced expiration, and identify the pres- other preoperative tests, however, where
ence or absence of rales. Note the indicated by the medical status of the
presence or absence of cyanosis and patient, or if the patient is considered in
clubbing. a population at risk for a specific prob-
lem. "Routine or standing" re operative
Cardiovascular: tests should be discouraged.
Assess the heart rate, rhythm and blood
pressure. Identify the location of the Do a CBC for patients in whom there is
apical impulse, and whether it is significant blood loss anticipated, sus-
abnormally displaced. Assess the level pected haematological disorder (eg.
of the JVP, and identify the presence or anaemia, thalassaemia, sickle cell dis-
absence of peripheral edema. Identify ease), or recent chemotherapy. Patients
the first and second heart sounds and on antihypertensive medications, includ-
listen for the presence of heart murmurs, ing diuretics, chemotherapy, renal dis-
or a third or fourth heart sound. ease, adrenal or thyroid disorders, must
have electrolytes evaluated pre-
Anticipate any special invasive pro- operatively. Obtain an electrocardio-
cedures, and assess the anatomy for gram (ECG)for patients over 50 years
arterial line insertion, central vein of age, or those who have a history of
cannulation, intravenous access, and cardiac disease, hypertension, peripheral

** Must Know * Should Know Page 15


Anaesthesia for Medical Shtdents

vascular disease, diabetes mellitus, patient's outcome is virtually impossible,


renal, thyroid or metabolic disease. and the complexity of this issue has
Request chest X-rays prior to cardio- made research studies addressing out-
thoracic procedures and for patients come very difficult. Nevertheless, sev-
with debilitating COPD, asthma, or a eral studies attempting to determine
change in respiratory symptoms in the anaesthesia mortality and morbidity
past six months. Perform urine analysis have been c ~ m ~ l e t e dIt~is' ~difficult
for patients with diabetes mellitus, renal to separate the contributions of anaes-
disease or recent urinary tract infection. thesia and surgery to morbidity and
mortality, as patients rarely receive an
anaesthetic without undergoing a surgi-
cal procedure. Table 3.1 summarizes
There are three components that must several studies which have attempted to
be considered when evaluating peri- determine the risk of mortality due
operative risk: the patient's medical solely to anaesthesia.
condition preoperatively, the extent of
the surgical procedure, and the risk from Studies on perioperative mortality have
the anaesthetic. In general, the major yielded differing results. Differences in
contribution to increased risk is that of the definition of outcome variables,
the patient's health prior to the pro- study design, and the duration of fol-
cedure and the magnitude of the sur- low-up make these results difficult to
gery. However, patients presenting for compare. When reviewed critically,
surgery often have more fear about their these studies suggest that the often
anaesthetic than the surgery itself. quoted number for overall risk of pri-
Fortunately, anaesthesia-related morbid- mary anaesthetic mortality for all
ity and mortality is rare, but unfortu- patients undergoing all types of surgery
nately, not absent. This does, however, is approximately 1:10,000.
create its own problems. The combina-
tion of infrequent but serious events has The question to which anaesthetists and
led one author to state that "Perhaps the the patient need the answer is: "What is
most insidious hazard of anaesthesia is the risk of a particular procedure in a
its relative safety."' patient with a given medical status
receiving a specific anaesthetic tech-
Anaesthetic Mortality: nique?" Numerous investigators have
attempted to address this very complex
The wide variety of surgical procedures question. Most of the work, however,
and anaesthetic techniques, combined addresses the operative risk according to
with the diversity of a patient's coexist- the patient's preoperative medical status.
ing surgical and medical illnesses, pro-
duce a number of risk factors that con- Perloperatlve Rlsk Assessment:
tribute to overall outcome, and make
generalized statements about risk diffi- Perhaps the oldest and simplest method
cult. Specific predictions for a single for risk assessment is the American
i
Chapter 3 Preoperative Assessment

Author Country Year No. in Incidence


study of Primary
Anaesthetic
Mortality
Turnbul16 Canada 1980 195,232 15,138
~ovi-Vivander7 Finland 1980 338,934 1:5,059
Lunn & ~ u s h i n ' United Kingdom 1982 108,000 1:10,000
Keenan & ~ o ~ e United
n ~ States 1985 163,240 1:10,000
~iret" France 1986 198,103 1:13,207
Holland1' Australia 1987 550,000 1:26,000
Buck1' United Kingdom 1987 500,000 1:185,000

Table 3.1 : Estlmates of Prlmary Anaesthetic Mortality

Society of Anesthesiology (ASA) physi- patient classification. Although devel-


cal status (table 3.2). The ASA physi- oped as a tool for classifying a patient's
cal status classification system was physical condition, the ASA physical
originally proposed in 1941, and revised status has been used to stratify patient
by Dripps in 196113 to provide a uni- risk. While open to significant criticism
form assessment of a patient's preoperat- because of its vague categories and
ive physical condition. inconsistencies in its application, the
ASA physical status classification has
As this system is simple, easy to use, been shown to correlate with peri-
and requires no laboratory investiga- operative mortality.ld17
tions, it has now been widely accepted
as the standard means of preoperative

Category Description
I Healthy patient.
I1 Mild systemic disease - no functional limitation.
I11 -
Severe systemic disease definite functional limitation.
IV Severe systemic disease - a constant threat to life.
V -
Moribund patient not expected to survive with or without an
operation for 24 hours.
E A suffix E is added to denote an emergency procedure.
Table 3.2: ASA Physlcal Status Classlflcatlonhc.
1 ** Must Know Should Know Page I 7
Anaesthesia for Medical Shrdents

Operative Mortality (percent)


ASA Class Vercantit4 ~arx" &hent6 orr rest "
1970 1973 1986 1990
I .07 .06 .07 .OO
I1 24 .40 .20 .04
nr 1.43 43 1.15 59
IV 7.46 23.4 7.66 7.95
V 938 50.7 ----- -----
Table 3.3: ASA Physlcal Status vs. Operative Mortality WO).
Examples of the ASA classification: tors that predicted life-threatening car-
diac complications. A scoring system
ASA 1: Healthy patient, no medical weighted these factors in their ability to
problems. predict adverse cardiac outcome.
ASA 2: Controlled hypertension.
ASA 3: Emphysema. From these data, Goldman suggested
ASA 4: Unstable angina. that patients with a score greater than
ASA 5E: Ruptured abdominal aortic 25 be considered only for life-saving
aneurysm in shock, under- procedures. Patients scoring 13-25were
going emergency surgery. advised to have preoperative medical
consultations to lower their morbidity
Cardiac Risk: and mortality. Certainly, delaying sur-
Several perioperative risk studies have gery until the patient is more stable can
attempted to assess which perioperative significantly reduce the cardiac risk
cardiac risk factors are important. index. Waiting for 6 months after a
Ischaemic heart disease has
received the most attention
because mortality from a Risk Factor Points
perioperative myocardial in-
farction approaches 50%. Third heart sound or elevated JVP 11
MI within 6 months of surgery 10
In 1977 Goldman published Rhythm other than sinus or PAC's 7
a multifactorial risk index > 5 PVC's per minute 7
for cardiac patients undergo- Age > 70 5
ing non-cardiac procedures18 Emergency procedure 4
(table 3.4). This study, in- Abdominal, thoracic, or aortic surgery 3
volving 1001 patients, ident- Important Aortic stenosis 3
ified, by multivariate analy- Poor medical status 3
sis, nine potential risk Table 3.4: Goldman's Cardlac Rlsk Index
i
Chapter 3 Preoperative Assessment

Variable Points
MI < 6 months pre-op 10
MI > 6 months pre-op 5
CCS Class 4 angina 20
CCS Class 3 angina 10
Unstable angina < 3 months pre-op 10
Pulmonary edema < 1 week pre-op 10
Pulmonary edema ever 5
Critical aortic stenosis 20
Rhythm other than sinus 5
> 5 PVC's per minute 5
Poor medial status 5
Age > 70 years 5
Emergency procedure 10

Table 3.5: Detsky's Multltactorlal Index

myocardial infarct, delaying emergency Using likelihood ratios, Detsky was able
procedures (if feasible) and improving a to construct a nomogram relating the
patient's poor medical status all signifi- pretest probability of cardiac morbidity
cantly decrease the risk. for the surgical procedure to the
patient's risk score. This generates an
The Goldman index has high specificity overall prediction of the risk of major
but low sensitivity when predicting risk. cardiac morbidity or mortality for a
Patients with scores of 13 or greater patient of a certain medical status
should arouse suspicion. A low score undergoing a specific procedure.
correlates with a low probability of poor Although Detsky's risk index is a better
outcome. In an attempt to
improve the sensitivity of
Goldman's index, ~ e t s k y ' ~ Surgery % Cardiac
modified Goldman's criteria to Complications
include a wider range of car-
diac illness (table 3.5). Detsky Vascular 13.2
also recognized that not all sur- Orthopaedic 13.6
gery carries the same risk, and Thoracic - Abdominal 8.O
factored in the surgical pro- Head & Neck 2.6
cedures for the pretest probabil- Minor (TURP, Hernia, ...) 1.6
ity of inducing significant car-
diac complications (table 3.6).19 Table 3.6: Detsky's Pretest Probablllty
For Type of Surgery

** Must Know Should Know Page 19


Anaesthesia for Medical Students

predictor of cardiac outcome than with invasive haemodynamicmonitoring


Goldman's, it still has limitations. and aggressive therapy in an intensive
However, a review of the risk factors care unit (ICU) setting for 7 2 hours fol-
described in both these studies alerts the lowing surgery. Cumulatively, these
anaesthetist to symptoms or signs of studies suggest considerable benefit in
significant disease that may contribute delaying elective surgery for a period of
to adverse outcome. 6 months following a myocardial infarc-
tion. Before six months, invasive moni-
Both Goldman and Detsky identified toring and aggressive postoperative
recent myocardial infarction as a risk management, appear essential, for those
factor for perioperative cardiac morbid- patients in whom surgery must be per-
ity. The perioperative period is charac- formed.
terized by haemodynamic changes,
alterations inventilation, fluid and elec-
trolyte shifts, and changes in coagul-
ation, all of which place the patient with Premedicatlon: (see also chapter 4)
underlying cardiac illness at significant Anaesthetic indications: The
risk of infarction. Several important preanaesthetic visit should be designed
studies have been conducted over the to alleviate patient anxiety and appre-
past 20 years in an attempt to identify hension about the proposed surgery.
the likelihood of perioperative reinfarc- However, a benzodiazepine such as
tion in patients with a recent M L ~ " diazepam or lorazepam is also frequent-
The goal of these studies was to deter- -
ly administered orally 1 2 hours pre-
mine the safest time interval following operatively. This may provide sedation,
an MI to proceed with elective surgery, relieve anxiety, and provide a degree of
and to direct attention to appropriate amnesia for the events immediately
perioperative monitoring and care preceding the operation.
(Table 3.7).
Patients at risk for GE reflux should
In Rao's study, patients were managed receive anti-reflux prophylaxis. This is

Time from infarction Tarhan20 Steen21 Rao22


to Surgery (1972) (1978) (1983)

0 - 3 months 37% 27% 5.8%

3 - 6 months 16% 11% 23%

Greater than 6 months 5.6% 4.1% 1.5%

Table 3.7: Comparlson of Perloperatlve Relnfarctlon Rates e!).


Page 20
C h a ~ t e r 3 Preo~erativeAssessment

usually achieved with ranitidine 150 - IV: PLANNING *


TEE ANAESTHETIC*
300 mg p ~ 2. hours pre-operatively.
Other agents such as metoclopramide Having identified and evaluated our
may be added to promote gastric empty- patient's problems we now ask ourselves
ing. Sodium citrate is an effective non- five questions.
particulate antacid that may also be used
alone or in conjunction with ranitidine. I., Is the patient's condition
optimal?
Surgical indications: According to the
American Heart Association Guidelines, 2. Are there any problems whlch
appropriate antibiotic prophylaxis must requlre consultation o r speclal
be administered for patients at risk for tests?
the development of infective
endocarditis.= These include patients (For example: In a patient with poorly
for whom a bacteremia is likely to controlled angina, a cardiology consult
occur as a result of respiratory tract, would be appropriate. You may write:
genitourinary, or gastrointestinal tract -
Consult medicine cardiology. 'Please
interventions. Some patients are at high assess and advise re: optimal peri-
risk for the development of operative medical management of
postoperative deep vein thrombosis angina in this patient').
(DVT). Prophylactic measures should
be used and include low-dose heparin, 3. Is there an alternative procedure
intermittent calf compression, or which may be more approprlate?
wumadin. Patients who are currently
receiving steroids and those who have This is especially important to consider
required steroids in the previous six in the high risk patient. For example:
months may require supplemental ste- the placement of a suprapubic catheter
roids because of adrenal suppression may be more appropriate than a trans-
and a blunted response to stress. urethral prostatectomy (T'URP) in a
terminal cancer patient with a recent
Cu-existing Disease Indications: All stroke, congestive heart failure, and
important medications should be wn- obstructive uropathy. Discuss the avail-
tinued on the day of surgery. These can able options with the staff anaesthetist
be taken orally with sips of water. and the surgeon.
Some medications, including insulin,
prednisone, coumadin, and broncho- 4. What are the plans for post-
dilators, require adjustment of dosage operative management of the
and/or alternate routes of administration. pa tlent?
Oral hypoglycemics and antidepressants
should not be taken on the day of sur- Options include: Monitoring in the
gery. It is no longer mandatory to post-anaesthesia care unit (PACU) for
discontinue MA0 inhibitors two weeks an initial period of observation, then
preoperatively . either return to ward or discharge home

** Must Know Should Know Page 21


Anaesthesia for Medical Students

(e.g., daycare patients). Patients with tension for the last six years, and was
significant underlying diseases or having also found to have NIDDM at the time
major procedures may remain in a criti- his hypertension was diagnosed.
cal care setting overnight for closer
observation (eg. PACU, ICU, CCU). Our patient's problem list includes:
Consideration should be given to which 1. Elective lower abdominal surgery.
form of pain management is most 2. Controlled hypertension.
appropriate for the patient post- 3. NIDDM.
operatively. . 4. Smoking history 35 pack years.
5. Identified risk factors for CAD.
5. What premedication if any is ap-
propriate? The anaesthetic history should include:
1. A brief history of present illness.
Finally, we plan our anaesthetic tech- E.g., "Discomfort in groin for 6
nique (see chapter 2: Anaesthesia months."
Overview). This may be: 2. Current medications (including
1. Local anesthesia with 'standby' ASA, alcohol, and illicit drugs if
monitoring with or without seda- appropriate). Eg., "Enalapril 10
tion. mg and glyburide 10 mg daily."
2. Regional anesthesia with or with- 3. Allergies and type of reaction.
out intraoperative sedation. E.g., "Penicillin: hives."
3. General anesthesia with or without -
4. Significant past medical surgical
intubation. If an intubation is history. E.g., "Appendectomy".
required the anaesthetist may elect 5. Past anaesthetic history.
to control the patient's ventilation, E.g., "No known problems."
or allow them to breath spontan- 6 . Family history of any anaesthetic
eously. If controlled ventilation is problems. E.g., "No known prob-
used, the anaesthetist may or may lems." (see chapter 24).
not use muscle relaxants. 7 . Functional inquiry appropriate to
4. Combined regional anaesthesia the patient, and concentrating on
with general anaesthesia. the cardiorespiratory systems.
E.g., "Inactive lifestyle, no symp-
Discuss with your staff anaesthetist toms of chest pain or coronary
when and why we would choose each ischemia!' (See also 9 below re:
of these techniques. additional appropriate questions.
8. NPO status. E.g., "Nothing to eat
For discussion, let us work through a or drink since last night."
patient case. We recently gave an an- 9. Specific questions directed at the
aesthetic to a 50-year-old male for an identified problem list, attempting
elective repair of his inguinal hernia. to assess the severity of the prob-
He admitted to smoking one package of lem, its associated disability, and
cigarettes per day, and has done so for the patient's remaining physiologi-
the last 35 years. He has had hyper- cal reserve.
Chapter 3 Preoperative Assessment

Problem: 35 pack year smoker. Appropriate questions concerning his


cardiovascular risk factors would
Do you have a cough on most mornings include:
or a "smoker's cough"? (i.e. Chronic
bronchitis). Have you ever had a heart attack?
Do you ever wheeze? Do you ever get chest pains, or leg
Have you ever required medications for cramps with exertion? (Angina, claud-
your breathing? ication).
Does your breathing limit your physical How often? What relieves them? What
activity? are they like?
What kind of activity would make you Do you ever wake up at night short of
short of breath? (A fast walk? One breath? (PND).
flight of stairs? Two blocks? etc.). Are you able to sleep with the head of
the bed flat? (Orthopnea)
Problem: Hypertension.
Additional appropriate questions for this
When were you first aware that you had patient would include questions regard-
high blood pressure? ing gastroesophageal reflux.
How often is your blood pressure Do you ever experience acid reflux from
checked? your stomach? How often?
Has it been well controlled with your
medications? Next, a physical examination as describ-
What is your usual blood pressure when ed previously should be performed.
you see your family doctor?
Appropriate laboratory tests for this
Problem: NIDDM patient would include a CBC, electro-
lytes, glucose, and electrocardiogram.
How long have you been aware of your
diabetes? After discussion with the patient and
How has it affected you? (end organs surgeon, a spinal anaesthetic was chosen
involved include: eyes, heart, kidneys, for this patient. While a general anaes-
peripheral circulation, autonomic and thetic would also be an option, we
peripheral nerves). chose a spinal anaesthetic because we
How do you monitor your blood sugar? would be able to avoid intubation and
Have you ever had to come to the emer- its associated sympathetic stimulation
gency because of your diabetes? (increased heart rate and blood pres-
sure), as well as its potential to trigger
Identified risk factors for CAD include airway reflexes resulting in broncho-
hypertension, smoking history, male spasm.
gender, age and diabetes.

** Must Know Should Know


Anaeslhesia for Medical Students

References: of incidence and causes. JAMA


253:2372, 1985.
Wamer MA, Offord KP, Wamer Tiret L, Desmonts JM, Hatton F, et
ME et al. Role of preoperative al: Complications associated with
cessation of smoking and other -
anaesthesia a prospective study in
factors in postoperative pulmonary France. Can J Anaesth 33:336,
complications: a blinded prospec- 1986.
tive study of coronary artery Holland R. Anaesthetic mortality
bypass patients. Mayo Clin Proc in New South Wales. Br J
64:609, 1989 Anaesth 59:834, 1987.
Pierce AC, Jones RM: Smoking Buck N, Devlin HB, Lunn JL:
and anesthesia: preoperative absti- Report on the confidential enquiry
nence and perioperative mortality. into perioperative deaths. The
Anesthesiology 6 1576, 1984 Nuffield Provincial Hospitals
Mallampati SR, Gatt SP, Gugino Trust, London. The King's Fund
LD,et al: A clinical sign to pre- Publishing House, London. 1987.
dict difficult tracheal intubation: Dripps RD, Lamont A, Eckenoff
A prospective study. Can J JE: The role of anaesthesia in ,
Anaesth 32429, 1985. surgical mortality. JAMA
Samsoon GLT, Young JRB: Diffi- 178:261, 1961.
cult tracheal intubation: A retro- Vancanti CJ, VanHouten RJ, Hill ,
spective study. Anaesthesia RC: A statistical analysis of the
'
42487, 1987. relationship of physical status to
Cooper JB, Newbower RS, Kitz postoperative mortality in 68,388 ,
RJ: An analysis of major errors cases. Anesth Analg 49564,1970.
and equipment failures in anaes- Marx GF, Mateo CV, Orkin LR:
thesia management: Consider- Computer analysis of post anaes-
ations for prevention and detection. thetic deaths. Anesthesiology ,

Anesthesiology 60:34, 1984. 3954, 1973.


Tumbull KW, Fancourt-Smith PF, Cohen MM, Duncan PG, Pope '

Banting GC: Death within 48 WDB, et al: A survey of 112,000 ,

hours of Anaesthesia at the anaesthetics at one teaching hospi-


Vancouver General Hospital. Can tal (1975-83). Can J Anaesth
Anaesth Soc J 27:159, 1980. 33:22, 1986.
Hovi-Viander M: Death associated Forrest JB, et al: Multicenter
with anaesthesia in Finland. Br J study of general anesthesia. 11.
Anaesth 52:483, 1980. Results. Anesthesiology 72262,
Lunn JN,Mushin WW: Mortality 1990.
associated with anaesthesia. Goldman L, Caldera DL,
Nuffield Provincial Hospitals Nussbaum SR, et al: Multi-factori-
Trust, London. 1982. a1 index of cardiac risk in non
Keenan RL, Boyan CP. Cardiac cardiac surgical procedures. N
arrest due to anesthesia: A study Engl J Med 297:845, 1977.
Chapter 3 Preoperative Assessmenf

19. Detsky AS, Abrams HB, Forbath


N, et al: Cardiac assessment for
patients undergoing non cardiac
surgery: A multifactorial clinical
risk index. Arch Intern Med
146:2131, 1986.
20. Tarhan S, Moffitt EA,Taylor WF,
et al: Myocardial infarction after
general anesthesia. JAMA
220:1451, 1972.
21. Steen PA, Tinker JH,Tarhan S:
Myocardial re-infarction after
anesthesia and surgery. JAMA
2399566, 1978.
22. Rao TLK,Jacobs KH, El-Etr AA:
Re-infarctionfollowinganaesthesia
in patients with myocardial infarc-
tion. Anesthesiology 59:499,
1983.
23. Dajani AS, Bisno Al, Chung KJ,et
al: Prevention of bacterial endo-
carditis. Recommendations by the
American Heart Association.
J A M 264:2919,1990.

Notes:

** Must Know Should Know Page 25


)
Anaesthesia for Medical Students
)
Notes:

Page 26
i Prernedication
Most patients scheduled for surgery will part of our preoperative visit is to con-
experience some degree of apprehen- vey a reassuring, honest and caring
sion. The psychological stress a patient attitude.
experiences prior to surgery can be
more detrimental than the actual physi- The patient's desire for sedation prior to
cal insult of the surgical procedure. a planned surgical procedure is the most
Preoperative anxiety may be caused by common reason for prescribing a preop-
many factors. Some of the more com- erative medication. We also prescribe
mon causes include*: medications preoperatively to avoid
potential complications associated with
1. The fear of relinquishing control to the procedure (eg., antibiotics to pre-
someone else while under general vent the development of endocarditis in
anaesthesia. a patient with valvular heart disease), or
2. The fear of dying during the oper- to continue the patient's current medica-
ation. tions for coexisting medical conditions.
3. The fear of experiencing pain
postoperatively. Reasons* for prescribing a preoperative
4. The inability to preserve their mod- medication include:
esty and dignity during the
operation. I. Patient-related reasons:
5. The fear of separation from family, 1. Sedation
and loved ones. 2. Amnesia
6. The fear of discovering a serious 3. Analgesia
problem such as cancer. 4. Antisialogogue effect (to dry oral
7. The fear of surgical mutilation and secretions)
an altered body image. 5. Medications to decrease gastric acid-
ity and gastric volume.
It is important that time is taken to 6. To facilitate induction of anaes-
answer each patient's questions. If you thesia.
are unable to answer their questions
honestly, then reassure them that their 11. Procedure-related reasons:
questions are important to you and that,
while you may not know the answer, 1. Antibiotic prophylaxis to prevent
you will speak to the attending staff infective endocarditis in susceptible
physician and provide them with an patients.
answer. Perhaps the most important

** Must K n o w Should K n o w Page 27


Anaesthesia for Medical Students

2. Gastric prophylaxis (to minimize the Benzodiazepines are the most frequently
risk of gastric aspiration during an- used class of drugs to achieve sedation,
aesthesia). relief of anxiety, and amnesia pre-
3. Corticosteroid coverage in patients operatively. Diazepam (5 to 15 mg
who are immunosuppressed (see pa.) may be given with sips of water
chapter 3). 1% to 2 hours preoperatively. Loraze-
4. To avoid undesired reflexes arising pam (1to 3 mg) may be given either by
during a procedure (e.g., vagal reflex the sublingual or oral route. Lorazepam
during eye surgery). provides excellent amnesia and sedation,
5. Anticholinergic agents to decrease but occasionally, patients remain excess-
oral secretions and facilitate a ively drowsy after the surgery. Alterna-
planned awake intubation with a tively, lorazepam can be reserved for
fiberoptic bronchoscope. the very anxious patient who is sched-
uled for afternoon surgery. The ration-
111. Coexisting Diseases: ale of an early morning premedication
with lorazepam is to allow the patient to
1. To continue the patient's own medi- remain calm and relaxed throughout the
cations for coexisting diseases. morning without prolonging the
(e.g., beta blockers, antihypertensive postoperative recovery time. Midazo-
medications, nitrates, anti- lam (0.07 mglkg im., approximately 5
parkinsonian medications etc.) mg in a young healthy 70 kg adult)
2. To optimize the patients status prior provides excellent amnesia, sedation,
to the procedure. (e.g., bronchodil- and anxiolysis when given 112 hour
ators, nitroglycerine, beta blockers, preoperatively. Midazolam (as a
antibiotics etc.) premedication) is not available at all
hospitals. The discomfort of an intra-
Patients with significant coexisting muscular injection and midazolam's
diseases should be given a reduced associated higher costs have generally
amount of preoperativesedative medica- made it the third choice of the benzo-
tion. The obese patient does not neces- diazepine class.
sarily require more preoperative medica-
tion. It is safer to underestimate the Opioids such as morphine and
required amount of preoperative medica- meperidine provide both sedation and
tion. Additional medications can be analgesia. They are appropriate for
given intravenously as needed when the patients experiencing pain prior to their
patient arrives in the operating room. surgery, (e.g., fractured extremity await-
Patients older than 65 years of age ing surgery). Morphine has a better
should have a reduced drug dosage. sedative effect than meperidine.
Caution should be exercised in prescrib- Troublesome side effects of intramuscu-
ing sedatives to patients 75 years of age lar (im.) opioids may occur. These
or older, as they may experience excess- include nausea, vomiting, respiratory
ive depressant effects from these medi- depression, bradycardia, hypotension,
cations. and true allergic reactions. In addition,
I
Chapter 4 Premedicalion
I
) Table 4.1: Premedlcatlon
-
Drug I Dose I Route Class Comments

Diazepam* (Valium) Benzodiazepine 1% to 2 hours preop. with sips of


-
5 15 m g p o . water. Sedation, amnesia, and
anxiolysis. Anticonvulsant
(regional anaesthesia). Respiratory
depression with high doses.
Lorazepam* (Ativan) Benzodiazepine Good amnestic and sedative. Best
1 - 3 m g p o . or 6.1. given early for late case.
Occasionally excessive
postoperative sedation.
Midazolam (Versed) Benzodiazepine 112 to 1 hour preop. Excellent
0.07 mg/kg im. arnnestic, sedative, and anxiolytic.
(appmx. 5 md70 kg) Not available in all hospitals.
Morphine* Opioid 1 hour preop. Occasional side
-
5 15 mg im. effects include decreased HR,BP,
RR, nausea, biliary spasm and
allergic reactions. Better sedative
than meperidine.
Meperidine* (Demerol) Opioid 1 hour preop. Similar side effects
-
50 100 mg im. as morphine. Perhaps more
nausea, and less biliary spasm.
Atropine* Anticholinergic 1 hour preop. Fair drying agent,
-
0.4 0.6 mg im. often significant tachycardia (HR >
100). Avoid in patients with CAD.

Hyoscine (Scopolamine) Anticholinergic 1hour preop. Excellent drying


-
0.2 0.4 mg im. agent, confusion in elderly, occas.
delirium in young. Good amnestic
and antiemetic.
GIycopyrrolate Anticholinergic Good drying agent for oral secre-
(Robinal) tions, less tachycardia than atro-
0.2 - 0.4 mg im. pine, no confusion.
Promethazine Antihistamine 1 hour preop. Good sedative and
(Phenergan) antiemetic. Occasional
12.5 - 50 mg im. postoperative delirium.

** Must Know Should Know Page 29


Anacs~hesiafor Medical Students

morphine, and to a lesser extent all does not cross the blood brain barrier
other opioids, may cause biliary spasm. and causes less tachycardia than atro-
Opioids should be used with caution in pine.
patients with known cholelithiasis.
Other special premeditations include:
Drugs with both antiemetic and sedative oxygen, antibiotics, steroids,
qualities, are often used in combination antihistamines, H-2 blockers, beta
with an opioid to avoid nausea and to blockers, calcium channel blockers,
enhance the sedative effects of the nitroglycerine, bronchodilators, ant-
opioid. Promethazine is one such drug acids, desmopressin, insulin, etc. Ask
(antihistamine - phenothiazine class), your staff anaesthesiologist when and
and is given in a dose of 125 to 50 mg why they would prescribe these
im. together with the opioid. Dimen- medications.
hydrinate ( ~ r a v o l 9also possesses seda-
tive and antiemetic qualities. It is given General contraindications* to the use of
in a dose of 12.5 to SO mg im. with the a prernedication include:
opioid (e.g., 'Demerol 75 mg with
gravol 50 mg ism. in one syringe one 1. Allergy or hypersensitivity to the
hour preoperatively 9. drug.
2. Upper airway compromise, or respir-
Anticholinergics may be given with atory failure.
morphine or meperidine to avoid the 3. Hemodynamic instability or shock.
potential opioid-induced bradycardia. 4. Decreased level of consciousness or
An anticholinergic agent may also be increased intracranial pressure.
used if an awake fiberoptic intubation is 5. Severe liver, renal, or thyroid dis-
planned. The use of an anticholinergic ease.
in these patients causes decreased secre- 6. Obstetrical patients.
tions from oral salivary glands, thereby 7. Elderly or debilitated patients.
facilitating both absorption of topical
anaesthetics and visualization of the Notes:
airway by a fiberoptic scope. Both
hyoscine and atropine cross the blood
-
brain barrier. Hyoscine (0.2 0.4 mg
im.) has been associated with confusion
in the elderly and postoperative delirium
in young patients. Atropine (0.4 - 0.6
mg im.) rarely causes clinical mental
confusion. However, it is less effective
in drying secretions than hyoscine and
causes a greater tachycardia (which is
undesirable in the patient with coronary
artery disease). Glycopyrrolate (0.2 -
0.4 mg im.) is a good drying agent. It

Page 30
Getting Started
(A Practical Approach to the OR)

Medical students, beginning their rota- make sure that any information that
tion in anaesthesia, will undoubtedly was missing (eg. Hb, ECG, etc.) at
feel unsure of their role and what they the time of the preoperative visit is
ought to do to assist the anaesthes- now available and on the anaesthetic
iologist. As anaesthesiologists we record.
observe many operations, however, we 3. Monitors attached including an
recognize that passively watching a ECG, blood pressure cuff, and pulse
procedure does not give us the under- oximeter to start with. (See chapter
standing or skills required to perform it. 10: Monitoring in Anaesthesia).
Accordingly, the more active a role you 4. Establish an intravenous. Prepare
take in the anaesthetic management of your intravenous equipment before
the patient, the more you will get out of the patient arrives.
the rotation, in terms of understanding, 5. Record the patients initial vital signs
sense of accomplishment, and develop- on the anaesthesia record.
ment of technical skills. Naturally, you
should not attempt to perform tasks for The above tasks will occupy the first 5
which you have little knowledge or to 10 minutes of your time following
supervision. Of all the specialties, the patients arrival in the OR. A pre-
anaesthesia is one of the few which can anaesthetic check list can be used to
offer intensive one-on-one teaching, and ensure that YOU are ready when the
you should try to take as much advan- patient arrives to the operating room.
tage of this as possible.
There are many ways anaesthetists
What can I do when the patient arrives ensure that everything is checked and
to the operating room? ready to proceed safely with anaes-
thesia. Whatever system that is used, it
Every patient undergoing general, should be simple yet comprehensive,
regional, or monitored anaesthesia care and one that will be followed wnsist-
requires*: ently. One such method can be recalled
by using the abbreviation 'SAM'. If you
1. A safe transfer from their bed to the check with SAM before you give an
operating room table. anaesthetic, things should proceed
2. An anaesthetic record removed smoothly.
from the chart and placed on the
anaesthesia clipboard. Check to What does SAM stand for?

** Must Know Should Know Page 31


Anaeslhesia for Medical Sluden/s

SAM* (really SAMMM') stands for: B. Anaesthesla Machlne:

S Suctlon checked and functioning. 1. Oxygen and nitrous oxide pipeline


A Airway equipment checked and pressures should be at 40-60 psi.
prepared. (This includes checking 2. Check that an adequate amount of
that you have a functioning and oxygen is present in the reserve
backup laryngoscope, an appropriate cylinder on the back of the
sized endotracheal tube and stylet, machine. By turning the cylinder
oropharyngeal airways, as well as an on, the pressure can be read from
oxygen source and manual resuscita- the pressure gauge on the front of
tion bag). the machine. An oxygen reserve
M Machine checked. (see anaesthesia cylinder (E tank) has a full pressure
machine checkout procedure and of 2200 psi. The amount in the
make sure you know how to check oxygen tank varies directly with its
your machine. You can go to the pressure. Hence, a reading of 1100
operating room before or after sche- psi indicates the tank is half full. A
duled procedures to explore the full E tank contains approximately
machine. Ask your staff anaesthe- 660 liters of oxygen.
tist to go through this procedure 3. Turn the reserve cylinder on the
with you). back of the machine off after check-
M Monltors available and functioning. ing it, to prevent a possible leak
M Medications prepared and labelled. from draining the oxygen from the
You should know where the emerg- tank.
ency drugs are kept and location of 4. Test that the flowmeters for 0 2 and
the difficult intubation cart. N20 are functioning by increasing
and decreasing the oxygen and
You will notice that the last thing that nitrous oxide flows. Ensure that the
SAM has you do is check your medica- flowmeter bobbins move freely and
tions. If you follow this routine, in this do not stick. Turn the nitrous oxide
order, you will never put a patient to off.
sleep and then discover, for instance, 5. The vaporizer should be filled,
that their ECG is abnormal, or that a turned off, and the filling port
laryngoscope is unavailable. closed.
6. The oxygen bypass flush valve
Anaesthesla Machine Checkout should release a flush of oxygen
Procedure (Modified from CAS 1989; when it is activated by pressing the
36, 6 suppl. 82-7.) flush button on the front left-hand
side of the machine.
A. Gas Plpeilnes: Secure connections 7. The oxygen fail-safe device should
between terminal units (medical gas be functioning, and will produce a
outlet) and machine. shrill Ritchie whistle if the oxygen
pipeline is temporarily disconnected
from the wall or ceiling source.
Chapter 5 Getting Started

8. Check for the oxygen analyzer 5. Pressurize the circuit and check for
which will be located on the respir- leaks. (Fill the circuit with fresh
atory gas monitor or mounted on gas, occluding the outlet while pres-
the machine as a separate unit. It surizing the circuit to 30 cm H20.
should be turned on and calibrated, The circuit should maintain a pres-
if this has not been done recently. sure of 30 cm H20 with a fresh-gas.
9. The 0 2 and N20 proportioning inflow of less than one liter per
device prevents the delivery of less minute).
than 30% oxygen, and greater than 6. Ensure the high pressure relief valve
70% N20, and can be tested by is functioning. (The circuit should
varying the 0 2 and N20 flows develop a leak when the pressure is
through the flowmeter. sustained above 75 cm H20. By
10. The common fresh gas outlet occluding the end of the circuit and
located on the front left-hand side squeezing the reservoir bag, a pres-
of the machine releases anaesthetic sure of greater than 75 cm H 2 0 can
gases from the flowmeters, be created. When this is done, the
vaporizer and flush valve. high pressure release valve will
open preventing any further increase
C. Breathing Clrcult: in pressure in the circuit).
1. The two most common anaesthesia 7. Unidirectional valves are function-
circuits used for adult anaesthesia ing. (Watch the valves open and
are the circle circuit and the Bain close smoothly as you take a test
circuit. An anaesthesia circuit breath through the mask and anaes-
functions to take the anaesthetic thetic circuit)
gases from the machine to and from 8. Check that the soda lime is fresh
the patient. The circle circuit con- and that the canister is full,
tains a soda lime canister to absorb
the exhaled carbon dioxide, an D. Vacuum system:
inspiratory and expiratory valve to Suction is connected and working.
direct the flow of gases, and light
weight corrugated tubing to trans- E. Scavenging System:
port the gases. A sample port near Correctly connected to patient cir-
the patient end of the circuit is used cuit.
for analysis of the respiratory gases.
These include inspired and expired F. Ventllator functioning.
oxygen, carbon dioxide, nitrous (Test the ventilator using the 2 Litre
oxide and volatile anaesthetic gas reservoir bag as a set of test lungs.
tensions. Once the system has been filled
2. Connect the anaesthesia circuit to with fresh gas, turn the ventilator
common fresh gas outlet. on. With the fresh gas flows at < 1
3. Turn the oxygen flowmeter on. Umin, the bellows should continue
4. Check for fresh gas exiting at the to refill as the ventilator cyles. The
face mask. maximal accepted leak is 1 Umin).

** Must Know Should Know Page 33


Anaesthesia for Medical Students

" SAMMM" Preanaesthetlc Check Llst


Suction Tonsillar tip connected to suction tubing and suction J
functioning.
Airway's Laryngoscope, blades, Em,syringe, stylet, oral and 4
nasal airways, tape, mask and manual resuscitation bag.
Machine Wall-source DHSS medical gas pipelines connected, 4
N20 & 0 2 cylinder and pipeline pressures OK,
Machine tumed on, flowmeters functioning, 0 2 flush
functioning, N20 and 0 2 proportioning device function-
ing, Oxygen pipeline disconnect (Ritchie) whistle func-
tioning.
- Vaporizer Full and turned off. 4
- Circuit Assembled, valves functioning, and circuit leak less J
than 1L / min at 30 cm H20 pressure.
- Ventilator Disconnect alarm functioning, and test ventilation leak J
of less than 1 L / min.
Monitors Capnograph connected to circuit and functioning. 4
ECG,BP cuff, oximeter, peripheral nerve stimulator,
and temperature probe monitors available and working.
Meds Intravenous fluids and equipment for starting i.v. 4
prepared. Emergency medications as per staff anaes-
thesiologist where appropriate, (eg. atropine, ephedrine,
succinylcholine etc.).
Intubation and
Anatomy of the Airway
The goal of assessing a patients rotate forward freely such that the space
airways* preoperatively is to attempt to created between the tragus of the ear
identify potential problems with main- and the mandibular condyle is approxi-
taining, protecting, and providing a mately one fingerbreadth in width.
patent airway during anaesthesia. The
assessment is performed with the aid of The opening aperture of the patient's
a physical examination and a review of mouth should admit at least 2 fingers
the patients history and anaesthetic between their teeth. Note any loose,
records. capped, or missing teeth as well as any
bridge work on the teeth. If the open-
The '1-2-3' test** is used to assess ing is less than 2 fingerbreadths, it will
several factors that may affect decisions be difficult to insert the laryngoscope
concerning the patient's airway manage- blade, let alone visualize the larynx.
ment. The first component of the test is
used to identify any restricted mobility With the patient's tongue maximally
of the temporomandibular joint (TMJ). protruded, the structures visualized
Ask the patient to sit up with their head should include: the pharyngeal arches,
in the neutral position and open their uvula, soft palate, hard palate, tonsillar
mouth as wide as possible. Note the beds, and posterior pharyngeal wall.
mobility of the mandibular condyle at Technical difficulties with intubation
the TM joint. The condyle should should be anticipated when only the

Fig.6.1: 1 = TMJ mobillty. Fig. 6.2: 2 = Mouth opening.


++ Must Know + Should Know Page 35
Anaesthesia for Medical Students

Adults who have less than 3


fingerbreadths (or < 6 5 cm) between
their mentum and thyroid notch may
have either an anterior larynx or a small
mandible, which will make intubation
difficult.

Next, evaluate the mobility of the cervi-


cal spine. This is performed by asking
the patient t o flex and extend their neck.
They should be able to perform this
without discomfort. Disease of the G
spine (RA, OA, previous injury or sur-
gical fusion) may limit neck extension,
Flg.6.3: which may create difficulties during
3 = Thyromentai distance. attempts to intubate. This is certainly
true if the atlanto-occipital joint is
tongue and soft palate are visualized in involved, as restriction of this joints
a patient during this above maneuver'. mobility may impair one's ability to
The third component of this test visualize the larynx.
assesses the patient's thyromental dis-
tance. 'Ihe thyromental distance is With the patient sitting upright with
measured from the thyroid notch to the their head in the neutral position, mouth
mentum (lower border of the chin). opened as wide as possible, and the

Table 6.1: Hypopharyngeal Classlflcation used In predlctlng a difficult


Intubatlon.
)
Chapter 6 Intubalion and Anatomy of the Airway
j

Figure 6.4: Classification of the hypopharynx on the basis of the visible


anatomy. Class I - 1v2.

tongue maximally protruded, the airway conscious sedation, or the use of a


can be classified according to the stmc- laryngeal mask rather than an endo-
tures visualized in the hypopharynx2 tracheal tube.
(figure 6.4, table 6.1). In those patients
who have a class I hypopharyngeal Finally one should try to ascertain
view, adequate exposure of the glottis whether there could be any difficulty
during direct laryngoscopy should be with the lower airway (glottis, larynx,
easily achieved. A s the hypopharyngeal and trachea). This is particularly im-
class number increases, so does the portant in patients who have had a
difficulty one anticipates in performing previous airway injury, or surgery on
intubation using direct laryngoscopy. their airway such as a tracheostomy.
We can predict that a patient with a Observe the patient for hoarseness,
class IV hypopharynx, a full set of stridor, or a previous tracheostomy scar
teeth, a restricted thyromental distance suggesting a potential underlying tra-
and restricted atlanto-occipitalextension cheal stenosis.
will be difficult to intubate using direct
laryngoscopy. Patients who have a Figure 6 5 illustrates the visualization of
restricted airway may require techniques the laryngeal structures at the time of
other than direct laryngoscopy to secure laryngoscopy. Just as the visualization
an airway. Choosing regional or local of the hypopharyngeal structures has
anaesthesia, rather than general anaes- been classified, the extent to which
thesia, is one way to avoid the need for laryngeal structures may be visualized
intubation. Other airway management has also been graded from I t o IV.
options include "awake" intubation with While there is not a perfect correlation
topical anaesthesia and intravenous between the hypopharyngeal class and

** Must Know Should Know P a g e 37


I
Anaesthr~iafor Medical Students
,)

Laryngeal Grade

I
Figure 6.5: Laryngeal visualization and grading during direct laryngoscopy.
(Grades I - IV). Adapted with permission from Cormack R.S.,Lehane J.
-
Anesthesia 39:1105 11,1984.

the laryngeal grade, we anticipate that a (AO) extension. We describe this as


patient with a class one hypopharyngeal the sniffing position. This enables one
view and no other identified airway to align the axes of the patient's mouth,
abnormalities will have a grade I laryn- pharynx, and larynx permitting direct
geal view. Similarly a class IV hypo- visualization of the larynx during
pharyngeal view is a predictor of diffi- laryngoscopy (figures 6.6, 6.7, 6.8).
culty visualizing laryngeal anatomy.
Atlanto-occipital extension alone
The technique of tracheal intubation increases the angle between the axes of
involves five steps* *. the pharynx and the larynx. By con-

I. Positioning the patient. Axis of the


11.Opening the patients mouth.
Performing laryngoscopy.
111.
( Axis Mouth

IV.Insertion of the ElT through the


vocal cords and removing the
laryngoscope.
V. Confirmation of correct placement,
and securing the E?T tube.

I. Posltlonlng the patlent


When preparing to intubate a patient, Figure 6.6: Poor alignment of the
their head and neck should be pos- axes of the mouth, pharynx, and
itioned using a combination of both larynx in the neutral position.
cervical flexion and atlanto-occipital
Chapter 6 Intubation and Anatomy of the Airway

Figure 6.8: Alignment of the axes of


Figure 6.7: Alignment of the axes of the airway with cervical flexion and A 0
the pharynx and larynx produced with extension, permitting visualization of
cervical flexion. the larynx with direct laryngoscopy.

trast, the combination of cervical flexion in ensuring a successful intubation (fig-


of the neck with A 0 extension results in ures 6.9, 6.10). This is especially true
the alignment of the axes of the pharynx in obese or pregnant patients, or those
and larynx. patients in whom you anticipate a diffi-
cult intubation. It is good practice to
Optimizing the position of the patients make sure that your first attempt at
head and neck before attempting intubation is your best.
laryngoscopy is an important initial step

Flg. 6.9: Inadequate (suplne) Flg. 6.10: Optlmlzed posltlonlng


posltlonlng for Intubatlon. for lntubatlon wlth cervlcal
flexlon.
** Must Know Should Know Page 39
Anaesfhesia for Medical Shtdenfs

Flg. 6.12: Modlfled sclssors


Fig. 8.11: Scissors technlque. technique.

Repeat attempts at intubation should be 11. Opening the patlent's mouth


avoided unless there is something that The next step in performing intubation
can be done differently to improve one's is to open the mouth. Take the laryngo-
chance of success. Persistent repeat scope in your left hand as you stand
attempts at intubation traumatize the directly behind the patient's head. The
patients airway, interrupt and delay both right hand is used to open the patient's
oxygenation and ventilation, and place mouth and, later, to advance the Em.
the patient at risk of significant morbid- Mouth opening can be accomplished by
ity and mortality. using the right hand to open the
patients teeth (e.g., the scissors tech-
If you are having difficulty, retreat, nique, as illustrated in figures 6.11 and
regroup, and resume manual mask venti- 6.12), or by placing the operators right
lation and oxygenation. Call for help hand on the patient's occiput to rotate
and allow the patient to recover from the occiput backward and create A 0
-
any sedative relaxant medications that extension (see figures 6.13 and 6.14).
have been given. No more than three Using the scissors maneuver the index
attempts should be made at intubation. finger pulls the upper right incisors
Discuss with your staff anaesthetist towards the operator, and serves to open
what other options are available for the mouth, extend the atlanto-occipital
patients whom you anticipate will be (AO) joint, and protect the teeth and
difficult to intubate, or the patient in lips. At the same time, the thumb
whom attempts at intubation have depresses the lower mandible, further
failed. opening the mouth. One can modify
this technique by opening the patient's
Chapter 6 Infubafionand Anatomy of the Airway
1

Flg. 8.13 and 6.14: Rlght hand controlling atlantoscclpltal


) extenslon and facllltatlng mouth openlng prlor to laryngoscopy.

) Figure 6.15: Illustrates the position of the curved laryngoscope blade, which
) displaces the tongue to the left. Upward and forward traction brings the larynx
into view. Adapted with permission from Finucane B.T., Santora A.H. In:
iples of Airway Management. EA. Davis Co.,Philadelphia 1988.

** Musf Know Should Know Page 41


Anaesthesia for Medical Students

mouth using one's right middle finger to tongue into the back of the oropharynx,
depress the lower teeth (figure 6.12). If as this will also obscure your vision.
the clinician chooses the extraoral tech- Once the tip of the blade lies at the base
nique of mouth opening, their right of the tongue (just above the epiglottis),
hand is placed on the patient's occiput apply firm, steady upward and forward
and the patient's head is rotated into the traction to the laryngoscope. The direc-
sniffing position. With this movement, tion of force should be at 45' from the
the mandible drops and the mouth horizontal. Once the laryngoscope is
opens. This method of mouth opening properly positioned at the base of the
is more suitable for the edentulous tongue, avoid rotating it, as this action
patient than the scissors technique. might exert pressure on the upper teeth
and damage them. Damage to the im-
111: Laryngoscopy mobile upper maxillary teeth is more
The third step involves insertion of the common than to the lower mandibular
laryngoscope into the mouth (figure teeth, which are free to move forward
6.15). The tip of the laryngoscope with the jaw during laryngoscopy.
blade is advanced to the base of the Figures 6.15 and 6.17 illustrate how the
tongue -by rotating its tip around the larynx is more visible if the blade of the
tongue (figure 6.17). The laryngoscope laryngoscope moves the tongue to the
blade should follow the natural curve of left of the mouth and out of the line of
the oropharynx and tongue. The blade vision.
should be inserted to the right of the
tongue's midline, so that the tongue Students learning the technique of
moves toward the left and out of the laryngoscopy have a common tendency
line of vision. Avoid pushing the to adopt a stooped posture, which posi-

Glosso-
Eplglottlc
Ugament

Figure 6.16: The glottis and epiglottis. Adapted with permission from
Finucane B.T.,Santora A.H. Principles of airway management. FA Davis Co.
Philadelphia 1988.
Chapter 6 Intubation and Anatomy of the Airway

tions their face within inches of the the epiglottis. Try to visualize this
patient's. This posture limits the power anatomy as well as possible when you
that can be used by the arms, making perform laryngoscopy.
laryngoscopy technically more difficult
to perform. Try to maintain a good IV: Insertlon of the ETT
posture during laryngoscopy. This Intubation is performed with the iefC
allows the arms to exert traction on the hand controlling the laryngoscope blade,
laryngoscope, rather than attempting to while the right hand opens the mouth
lift the laryngoscope with the wrists. and then passes the ElT tip through the
laryngeal inlet. When a limited laryn-
The larynx is located at the level of the geal view is encountered (grade 111 IV -
4& to 6& cewical vertebrae in adults. It larynx), the epiglottis can be used as a
consists of numerous muscles, cartilages landmark for guiding the E?T through
and ligaments. The large thyroid carti- the hidden vocal cords. The tip of the
lage shields the larynx and articulates E'LT is passed underneath the epiglottis
inferiorly with the cricoid cartilage. and anterior to the esophageal inlet.
'lbo pyramidal shaped arytenoid carti- Recall that the glottis lies anterior to the
lages sit on the upper lateral borders of esophagus (or above the esophagus
the cricoid cartilage. The aryepiglottic during laryngoscopy). When the epi-
fold is a mucosal fold ruming from the glottis partially obscures the view of the
epiglottis posteriorly to the arytenoid glottis, an assistant may be used to
cartilages. The cuneiform cartilages apply cricoid pressure. This maneuver
appear as small flakes within the margin moves the larynx posteriorly and helps
of the aryepiglottic folds (fig. 6.16). to bring the vocal cords into view. A
malleable stylet, shaped so that it forms
The adult epiglottis resembles the shape a distal anterior J curve, can also be
of a leaf, and functions like a trap door helpful in guiding the E?T tip through
for the glottis. In figure 6.16, the trap the laryngeal inlet. When you have had
door' is shown in both its open and a limited view of the E m passing
closed positions. The epiglottis is through the vocal cords, the Ford
attached to the back of the thyroid carti- Maneuver can help you to visually
lage by the thyroepiglottic ligament and confirm its correct placement in the
to the base of the tongue by the glosso- glottis. One performs this maneuver by
epiglottic ligament. The covering mem- displacing the glottis posteriorly using
brane is termed the glossoepiglottic downward pressure on the ETT prior to
fold, and the valleys on either side of withdrawing the laryngoscope. This
this fold are called valleculae. The maneuver is useful in the patient with a
valleculae are a common site for the grade 111 or IV larynx for whom diffi-
impaction of sharp swallowed objects, culty was encountered visualizing the
such as fish bones. When performing glottic structures.
laryngoscopy, one should advance the
tip of the curved laryngoscope's blade to The cuff of the ETT should be observed
the base of the tongue at it's union with passing through the vocal cords and

1
** Must Know * Should Know Page 43
Anaesthesia for Medical Sludenb

a. Introduction of the larygoscope blade b. The tongue obscun the laryngeal


using left wrist rotation. view due to inadequate advancement
of the larygoscope blade .

c. The tip of larygoscope blade is


. d. Laryngeal blade inserted too deep,
. .

properly positioned at the base of pushing epiglottis over laryngeal inlet.


tongue. The blade is lifted forward

e. Laryngeal blade inserted to the left f. Laryngoscope blade inserted too far,
of midline, with tongue obscuring with visualization of the esophageal inlet.
visualization of the larynx.
Figure 6.17: Laryngoscopy. Adapted with permission from Lui PL.
inciples and Procedures in Anesthesiology. J.B. Lippincott Co. 1992
Page 44
Chapter 6 Intubation and Anatomy of the Airway

should lie just inferior (2 to 3 cm) to lung fields may reveal bronchospasm or
the cords. As soon as you withdraw the evidence of an endobronchial intubation,
laryngoscope blade from the mouth, but cannot be relied on as absolute
note the length of the ETT at the lips proof that the tube is correctly position-
using the centimetre markers on the ed in the trachea.
ElT. This may prove to be useful if
the endotracheal tube moves from its If the tube is positioned in the tracheal
original position. The usual distance lumen and the patient is breathing spon-
from the tip of the ETT to the mouth is taneously, the reservoir bag will fill and
approximately 21 to 24 cm in adult empty with respiration. If the patient is
males, and 18 to 22 cm in adult awake they will not be able to vocalize
females. The usual distance for a nasal- with an ETT positioned in the tracheal
ly intubated adult male (from the tip of lumen. On an 'A-P' CXR the tip of the
the E n to the naris) is 25 cm. The E'IT should be located between the
E l T cuff is inflated with enough air to midpoint of the thoracic inlet and the
create a seal around the ETT during carina.
positive pressure ventilation. A cuff
leak may be detected by listening at the Decreased air entry to one lung field
patient's mouth, or over their larynx. may indicate that the E l T is in a main-
stem bronchus (usually the right main-
V: Confirmation of correct stem bronchus). In this situation, the
ETT placement. patient may become increasingly
Immediate absolute proof that the E l T hypoxic, or continue to cough. You
is in the tracheal lumen may be may suspect an endobronchialintubation
obtained by observing the ETT passing when you observe one side of the chest
through the vocal cords, observing car- moving more than the other with venti-
bon dioxide (ETCOJ returning with lation. In this situation, the airway
each respiration, or by visualizing the pressures will be higher than normal
tracheal lumen through the ETT using a (greater than 25 cm H20), and an
fiberoptic scope. Indirect confirmation abnormally distant tube position at the
that the trachea is intubated with a patient's lips will be noted.
tracheal tube includes: listening over
the epigastrium for the absence of "IF IN DOUBT TAKE IT OUT:"**
breath sounds with ventilation, observ- This is prudent advice for anyone who
ing the chest to rise and fall with posi- has just intubated a patient and is
tive pressure ventilation, and listening to unsure and unable to confirm the tube's
the apex of each lung field for breath placement. It is better to be safe by
sounds with ventilation. There are, removing the ElT, resuming mask
however, numerous reports of physi- ventilation with 100%oxygen, stabiliz-
cians auscultating "distant breath ing the patient, and calling for help,
sounds" in each lung field, when the than to risk hypoxic injury and gastric
ETT was, in fact, incorrectly placed in aspiration.
the esophagus. Hence, listening to the

+* Must Know + Should Know Page 45


Anaesthesia for Medical Students
1

"IF IN DOUBT LEAVE IT IN:"**


This advice applies to the clinician who
is considering extubating a patient who
has been intubated for a period of time.
When the clinician has concerns as to
whether the patient can be safely
extubated (see chapter 7: extubation
criteria), it is generally safer to delay
extubation, continue to support ventila-
tion, ensuring hemodynamic stability,
analgesia, and oxygenation, than to
prematurely extubate the patient.
Figure 6.19: 0topharGgeal 1
Upper elrwey obstruction**: airway restoring airway patency. )
The most common cause of an upper
airway obstruction in an unconscious Excluding intubation, simple man-
' )
supine patient is from the tongue falling euvers** to overcome upper airway 1
back into the hypopharynx (figures 6.18 obstruction in the unconscious supine )
and 6.19). In the unconscious state patient, include:
there is a decrease in the tone of 1
muscles attaching the tongue to the 1. Clearing the airway of any foreign )
mandible, hyoid bone and epiglottis. material.
The respiratory efforts of the uncon- 2. Using a chin lift maneuver.
1
scious patient tend to pull the tongue 3. Using a jaw thrust maneuver. i
backward causing further airway ob- 4 Inserting an oral andlor nasal ,
struction. Finally in the unconscious airway.
patient the epiglottis tends to fall down- 5. Positioning the patient on their side
ward, also increasing upper airway in the semi-prone recovery posi- ,
obstruction. tion.

References:

1. Mallampati SR, Gatt SP, Gugino


LD, et al: A clinical sign to pre-
dict difficult tracheal intubation: A
prospective study. Can J Anaesth
32:429,1985.

2. Samsoon GLT, Young JRB: Diffi-


cult tracheal intubation: A retro-
Figure 6.18: Obstructed airway
in the unconscious supine patient. I spective study.
42:487,1987.
Anaesthesia

Page 46
~
Intubation Decisions
In chapter 6, we reviewed the technical should prepare equipment and medica-
skills required for tracheal intubation in tions for tracheal intubation.
adults. In this chapter we present four
clinical cases as an illustration of the Most open cholecystectomies today are
process used when deciding to intubate. performed under general anaesthesia
with tracheal intubation. While it may
A clinician will readily recognize that be possible to provide regional anaes-
the comatose patient with a severe head thesia (e.g., epidural anaesthesia) for
injury will need tracheal intubation for this procedure most anaesthetists today
airway protection, maintenance, and will opt to provide general anaesthesia.
hyperventilation. However, the need to The rationale for this decision includes:
intubate a dyspneic patient with chronic
obstructive lung disease and a recent 1. A high abdominal incision with the
respiratory infection is not so readily need for muscle relaxation.
apparent. Tables 7.1 and 7.2 list com- 2. Surgical retractors which may impair
mon criteria anaesthesiologists use to spontaneous ventilation.
evaluate a patient's need for intubation. 3. A moderately obese patient who will
The individual criteria are not absolute have difficulty breathing spontan-
indications. They are to be used eously when lying supine, due to the
together, in the context of the patient's surgical retractors restricting the
clinical presentation, in formulating a muscles of respiration.
decision concerning the patients need 4. Epidural anaesthesia used by itself
for intubation. would require a high level of block
to provide adequate anaesthesia.
Case Studies on intubation decisions: This could impair the patients
intercostal and abdominal muscles of
Case 1: respiration, resulting in respiratory
On the first day of your rotation, you insufficiency.
are scheduled to assist with anaesthesia
in the general surgical room. The first In the early days of anaesthesia, ether or
patient is a moderately obese forty year chloroform was administered through a
old female who is scheduled for an face mask during spontaneous respir-
open cholecystectomy. What kind of ation for this procedure. Ether produced
anaesthesia should we provide for this marked muscle relaxation when used
patient? You ponder whether you with minimal doses of muscle relaxants

** Musf Know Should Know Page 47


1
Anaesthesia for Medical Students
i )

Table 7.1 Objectlve Crlterla for Intubatlon wlth or wlthout ventllatlon*


(Oxygenatlon I Ventllatlon / Mechanlcs)
I. Oxygenatlon P a 0 2 < 70 mm Hg with Fi02 = 70% (A double
flow puritan oxygen setup with 15 Umin x 2, pro-
vides a total of 30 Umin of oxygen flow to the
patient, minimizing entrainment of room air;
see figure 233, table 23.2).
A-a DO2 gradlent > 350 mm Hg. Recall the nor-
mal A-a DO2 gradient is s 15 mm Hg, and
increases up to 37 with increasing age (Nunn
Applied Respiratory Physiology 3rd Edition p. 248)
Use an arterial blood gas sample, and alveolar gas
equation to calculate A-a DO2 gradient; where:
-
PA02 = (Pa P,)x Fi02 - PaCO2l0.8
11. Ventllatlon RR > 35 1 mln in adults
(muscles fatigue, at these rates).
PaC02 > 60 in normal adults.
PaC02 45 In status asthmatlcus, and rising
despite maximum medical management (must use
other objective and subjective criteria as well)
Respiratory acidosis with pH < 7.20 In COPD
patients.
111. Mechanics VC < 15 mL / kg (Normal vital capacity = 70 mL
per kg or approximately 5 litres; a vital capacity of
15 mL / kg is needed to cough effectively and clear
secretions).
NIF > -25 cm HZ0 (Normal negative inspiratory
force (NIF) is approximately -80 to -100 cm H20).

(e.g., curare 6 mg). Respiratory de- muscle relaxants were not available to
pression was accepted. When the ether the anaesthetist during these early years.
was discontinued the patient recovered Today, by contrast, we routinely plan
their muscle strength and increased their general anaesthesia with intubation,
ventilation to match metabolic needs. muscle relaxation, and controlled mech-
Pulse oximeten, end tidal carbon diox- anical ventilation for patients undergo-
ide monitors, nerve stimulators,mechan- ing an open cholecystectomy. This
ical ventilators, and antagonists for allows the anaesthetist to produce pro-
Chapter 7 Intubation Decisions

Table 7.2 Subjective Criteria for Intubatlon and (or) ventllatlon*


(Protect I Provide I Malntaln I T.B.T.)

I. Real or impending airway obstruction.


(e.g., epiglottitis, thermal bums, mediastinal tumours, etc.).
11. Protection of the airway.
(e.g., decreased level of consciousness, drug overdose, etc.).
111. "Tracheal bronchial toilet." For patients who are unable to clear their
secretions, the ETT provides a direct access for suctioning secretions,
(e.g., COPD patient with pneumonia.)
IV. To provide positive pressure ventllatlon during general anaesthesia.
Additional indications for intubation under general anaesthesia include:
long procedure anticipated, difficult mask ventilation, operative site
near patients airway, thoracic cavity opened, muscle relaxants required,
and if the patient is in a difficult position to maintain mask anaesthesia.
V. Clinical signs of respiratory failure and fatigue.
(e.g., diaphoresis, tachypnea, tachycardia, accessory muscle use, pulsus
paradoxus, cyanosis, etc.).
VI. Shock not immediately reversed with medical treatment (i.e. not re-
-
sponding to medical management in the first 35 45 minutes).

Normal respiratory muscles use approximately 2 - 5 % of the cardiac


output, in shock states this may increase to up to 15 - 20 %, stealing
from other organs in vital need of oxygen such as the heart and brain.
Dogs subjected to septic shock conditions, die much earlier if they are
allowed to breathe on their own, when compared to dogs who are
intubated and ventilated.

found muscle relaxation during the endotracheal tube, checking the anaes-
procedure, protect the airway from asp- thesia machine, and preparing the anaes-
iration of gastric contents, and provide thetic medications.
good ventilation and oxygenation. The
anaesthetist can also administer potent Case 2:
anaesthetic drugs, such as opioids and Having recently completed your anaes-
volatile anaesthetic agents (e.g., iso- thesia rotation, you are working in the
flurane) to minimize the stress of the emergency department, when a pale
surgical procedure. Accordingly, you diaphoretic 50 year old man stumbles
should plan to assist by preparing the through the door and collapses in front

** Must Know Should Know Page 49


Anaesthesia for Medical Students

of the receptionist. The patient is risks of aspirating gastric contents. The


quickly placed on a bed and taken to E'IT also provided a route for
the resuscitation room. Unable to find administrating epinephrine, which
a pulse, the emergency physician im- played an important role in this man's
mediately applies chest paddles, iden- resuscitation.
tifies a chaotic rhythm on the monitor,
and defibrillates at 200, then 300 and Later, a classmate asks why you didn't
finally 360 joules, in rapid succession. give any medications to intubate the
Unfortunately, the patient fails to patient. You explain that patients with
respond. You are at the head of the bed profound cardiovascularcollapse requir-
and have initiated manual ventilation ing emergent intubation, do not need
with an Ambu bag and mask. Chest any anaesthetic medications such as
compressions are initiated, while a nurse thiopental or succinylcholine to perform
attempts, unsuccessfully, to insert an tracheal intubation. In fact the adminis-
intravenous catheter. Should you pro- tration of thiopental could have a detri-
ceed to intubate the patient? mental result by further depressing his
already compromised myocardium. If
The emergency physician appreciates your colleague asks what other medica-
your help and asks you to proceed with tions can be given through the EIT,tell
tracheal intubation. After placing the him to remember the word NAVEL'.
E m , you confirm its position, secure it, This stands for the drugs: Naloxone,
and continue with controlled ventilation. Atropine, Ventolin, Epinephrine, and
At your suggestion, 10 mls of 1:10,000 Lidocaine, all of which can be given
epinephrine is injected down the E m through an E'IT.
and propelled to the lungs and central
circulation with subsequent ventilation. Case 3:
The cardiac rhythm changes to a coarser Later, another clinical clerk asks for
form of ventricular fibrillation. Repeat your opinion regarding a 68 year old
defibrillation at 360 joules converts the man with known COPD. He is evaluat-
man's rhythm to a sinus tachycardia ing this patient in the emergency room
with a systolic pressure of 110 mm Hg. because he is feeling more short of
Frequent ventricular premature beats breath than usual. Your colleague was
(VPB's) are noted, and lidocaine 100 mg ready to send him home on antibiotics
is given through the now secure intra- but hesitated after seeing his arterial
venous. An infusion of lidocaine is blood gases (ABGs). He is concerned
started and arrangements are made for that this man may need to be intubated
the patient's transfer to the CCU. because his PaCO, is so high. On room
air his ABGs were pH = 734, PaCO, =
The resuscitation of this patient could 65, PaO, = 54, HCO, = 34. How would
have proceeded with mask ventilation you assess and treat this patient.
and chest compressions. By choosing
to intubate this patient, we were able to The patients ABGs demonstrate
protected the patient's lungs from the hypoxemia and an acute on chronic

Page 50
Chapter 7 Iniubation Decisions

respiratory acidosis with metabolic When you examine him you find that
compensation. You review his old chart his breathing is laboured at 28 breaths
and note that his HCO, was 33 and his per minute with a prolonged expiratory
PaO, was 59 mrn Hg at the time of phase and a surprisingly quiet chest.
discharge 4 months previously. This, He is diaphoretic, clammy, and has
you suggest, probably represents his difficulty catching his breath to talk.
optimal blood gas values. You com- His vital signs reveal a HR of 130 bpm,
plete your evaluation by examining the BP = 1801100, with a pulsus paradoxus
patient noting a RR = 22 per minute, of 35 mm Hg, and maximal use of his
HR = 90 bpm, BP = 160185, and diffuse accessory muscles. The emergency
mild rhonchi throughout the chest with physician orders salbutamol with
no significant (i.e. < 10 mm Hg) pulsus ipratropium bromide by nebulization.
paradoxus. You also note that the An intravenous is established, ABGs are
patient is able to talk without stopping drawn, ECG, oximetry, and BP monitor-
frequently to catch his breath, and that ing is initiated, and a portable CXR is
he is not vigorously using his accessory ordered. Your classmate thinks you
muscles of respiration. Reviewing his better intubate him now. Do you agree?
other lab tests you note a Hb = 170,
WBC = 12,000, and an ECG which is As the ABGs and CXR return, the
unchanged from his former cardiogram. patient is noted to have become increas-
The CXR demonstrates hyperinflation ing drowsy, while little clinical im-
with basal bullae, but gives no evidence provement has occurred. The ABGs on
of cardiac failure or pulmonary infec- face mask oxygen at 8Umin reveal pH
tion. The patient admits to having = 7.10, PaO, = 66, PaCO, = 120, and a
stopped his bronchodilators in the last HCO, = 36. The emergency physician
week. After clinical and subjective orally intubates the patient using topical
improvement w i t h salbutamol aerosol lidocaine anaesthesia to the
(ventolinQ) and ipratropium bromide hypopharnyx and glottis, and initiates
(atrovent@), the patient is discharged hyperventilation at 20lmin in order to
home with a prescription for his inhalers 'blow off the carbon dioxide. The
and a follow-up visit with his family nurse reports that the patients systolic
practitioner. pressure is now 65 mm Hg, and his
cardiac monitor is showing sinus
Case 4 tachycardia at 120lmin with multiple
Four weeks later you are completing ventricular premature beats (VPB's).
your emergency rotation when the Your classmate reviews the CXR and
patient in the case 3 returns. You are states that he believes the patient has a
alarmed at his ill appearance. His wife pneumothorax on the left side. How are
accompanies him and relates that he you going to manage the patient?
'caught a cold' a week ago and has been
getting progressively worse. He has Before rushing to insert a needle
been unable to eat or sleep for the last thoracotomy and chest tube for a poss-
day because of his shortness of breath. ible tension pneumothorax, you review

** Must Know Should Know Page 51


Anaesthesia for Medical Students

the patient's status. Although he has respiratory acidosis, with a pH of 7.20


become unresponsive to verbal stimula- or less, indicates that the patient is no
tion, his trachea is in the midline, and longer able to compensate. His condi-
you are able to manually ventilate him tion was likely precipitated by his recent
without excessive airway pressures. chest infection superimposed on his
The emergency physician orders 100 mg former severe COPD. PaCO, levels of
lidocaine i.v., and asks you to take over greater than 95 mm Hg become increas-
ventilation while h e reviews the chest ingly anesthetic, (MAC CO, = 245, see
radiograph. A repeat CXR is ordered to chapter 14 re: MAC definition). The
verify the E l T position. A fluid bolus decreased level of consciousness may be
of 1000 mL of ringer's lactate increases accounted for by the low blood pressure
the patient's blood pressure to 100 rnm and the high arterial carbon dioxide
Hg systolic. The VPB's remain but are tension.
now unifocal and less frequent. A
mechanical ventilator is set up to pro- This case illustrates several common
vide ventilation, with an inspired 0, problems. The patient presented in an
concentration of SO%, a tidal volume of extreme condition, following an illness
850 mL, an intermittent mandatory which likely resulted in significant
ventilatory (IMV) rate of 12, and 5 cm dehydration. Upon his arrival in the
of positive end expiratory pressure emergency department, his cardiorespir-
(PEEP). atory system was being maximally
stressed. Following intubation, his
Arrangements are made to transfer the blood pressure fell precipitously.
patient to the ICU. Review of the Patients with cardiorespiratory
initial CXR shows the previous basilar decompensation who require urgent
bullae, but no evidence of a intubation will often demonstrate a fall
pneumothorax. The second CXR shows in blood pressure following intubation.
the E l T tip to be correctly positioned in This occurs irrespective of whether
the mid trachea. sedative drugs are given prior to
intubation. The fall in blood pressure
Your classmate was correct about the may be due to:
patient requiring intubation. Clinical 1. The sedative drugs given.
examination, and ABG analysis con- 2. The removal of endogenous catechol-
firmed that the patient was indeed in amines by treating the condition that
acute respiratory failure. Analysis of caused the patient to decompensate
the ABGs revealed a severe acute on (i.e., removing the work of breathing
chronic respiratory acidosis. Often we from patient).
have no background information regard- 3. Decreasing venous return to the heart
ing the patient's usual PaCO, and HCO, due to positive pressure ventilation.
levels. In patients with COPD who may 4. All of the above, plus the unmasking
retain carbon dioxide, we rely on the pH of a significant underlying hypo-
more than the CO, to guide our man- volemia or concurrent illness (e.g.,
agement (as in case 3). A primary myocardial infarction).

Page 52
Chapter 7 Intubation Decisions

The occurrence of multiple ventricular larger E n . Endotracheal tubes less


premature beats may reflect an irritable than 6 mm do not have distal inflatable
myocardium secondary to hypercapnia, cuffs. This decreases the risk of post
hypotension, and hypoxemia. Another intubation swelling and stridor, as a
explanation for the appearance of the result of trauma from the E n .
VPB's may be the result of an acutely
induced hypokalemia. Mechanical Example: A 10 year old child would
hyperventilation may result in a pre- generally use a 6.0 mm cuffed E n ,
cipitous drop in the PaCO, level. The uncuffed tubes are generally used for
sudden lowering of PaCO, will rapidly patients age 8 and less.
increase the patients pH and shift Kt 6 yr. old child = 5 5 or 6 uncuffed ETT
into the cells, creating an acute extra- Term newborn = 3 5 E l T
cellular hypokalemia. The differential -
Premature infant = 2 5 3.0 E I T
diagnosis of this patient's acute
hypotension, dysrhythmias, and abnor- P o t e n t i a l C o m p l i c a t i o n s of
mal CXR includes a tension Intubation*:
pneumothorax. In this case, the emerg- Direct injury can be caused by either
ency physician correctly interpreted the the laryngoscope, or the ETT. The lips,
lucency on the CXR as chronic basilar tongue, pharynx, larynx and trachea are
bullae, and avoided the potential disas- all susceptible to injury. Damage to the
trous consequences of a needle teeth may be caused by the laryngo-
thoracostomy and chest tube insertion in scope, or by biting on the E I T or
this patient (i.e., risk of a broncho- tonsillar suction tip. Damage to the
pleural-cutaneous fistula). teeth, though rare, is still the most fre-
quent problem resulting in litigation
In retrospect, this patient fulfilled sev- against anaesthetists. Damaged teeth
eral criteria for intubation (Tables 7.1 can fragment and may be aspirated by
and 7.2). This emergency was best met the patient.
by first supporting his ventilation. As
this patient's condition is likely to The patient who experiences a sore
require prolonged ventilatory support, throat following their operation (with
this is most easily accomplished by tracheal intubation), may obtain some
endotracheal intubation. relief with throat lozenges. This dis-
comfort rarely persists for more than 24
Typlcal Endotracheal tube slzes* hours. Beware of the patient who
Adult male 8.0, 8 5 , and 9.0 mm recalls a severely sore throat on previ-
Adult female 7.0, 7.5, and 8.0 rnrn ous operations. They may have a
restricted airway, and their larynx may
ETT slze calculation for children: have been traumatized because they
Size (mm) = age14 + 4. were difficult to intubate. Inserting the
ETT through the larynx can injure the
The presence of a soft distal cuff on the vocal cords or even dislocate the
FIT is equivalent to having a 112 size arytenoid cartilages. Patients with

** Must Know Should Know P a g e 33


Anaesthesia for Medical Students

arthropathies, such as rheumatoid arthri- impairment of chest excursion, and


tis, may have an arthritic involvement increases the chance of regurgitation
of the arytenoids, creating a 'functional and pulmonary aspiration.
laryngeal stenosis'. If symptomatic,
they may note hoarseness or pain on Criteria for extubation*:
speaking. Always consider these The criteria for extubation are generally
patients to be at an increased risk for the reverse of those for intubation. The
vocal cord and arytenoid injury, use a patient should not require an E'IT for
smaller E n ,and take extra care during airway provision, protection, mainten-
intubation. ance or tracheobronchial toilet, and
should meet criteria for adequate oxy-
If the E'IT is too short it may result in genation, ventilation, and lung mech-
accidental extubation. Excessive ad- anics. The condition that initially
vancement of the EIT into the trachea required intubation should b e corrected
may result in an endobronchial prior to extubation. The patient should
intubation. Prolonged E'IT placement be able to protect their airway, i.e., they
may lead to vocal cord granulomas or must be awake with a gag and cough
tracheal stenosis. Although a cuffed reflex. They should be hemo-
ETT will protect against gastric aspir- dynamically stable, and their RR should
ation, they do bypass the bodies natural be greater than 8/min, and less than
humidifying and warming mechanisms, 35lmin. Respiratory muscles will
and afford a potential conduit for fatigue with prolonged rates greater than
pathogens to enter the lung. 35 breaths per minute. Oxygenation
should be adequate, which means a
Upon inserting the ElT, a patient is PaO, of at least 60 mm Hg on an
subjected to a significant sympathetic inspired oxygen concentration of 50%
stress, which may precipitate or less. This should be at accompanied
tachycardia, dysrhythmias, and with evidence of adequate ventilation
myocardial ischemia. Pediatric patients with a PaCO, of less than 50 mm Hg.
have a relatively higher parasympathetic Vital capacity should be greater than 1 5
tone than adults. Hence tracheal mUkg (- 1 litre in a 70 kg patient),
intubation of infants and children may with a tidal volume of greater than 5
result in a significant bradycardia. In mUkg and the negative inspiratory
both adult and paediatric patients, medi- force (NIF) should be more negative
cations are commonly given prior to than -25 cm H,O. The vital capacity,
intubation in an attempt to minimize tidal volume, and NIF can be measured
these reflexes. at the bedside with simple spirometry
equipment.
The most serious complication of tra-
cheal intubation is an unrecognized
esophageal intubation. The resulting
gastric distension with ventilation, sub-
jects the patient to hypoxia, hypercarbia,
The Laryngeal Mask
Airway (LMA)
IV11at is the differecrtce between a LMA isoflurane because the il~ternaldiameter
and a traclteal tube*? of the L M A is relatively large compared
The laryl~gealmask airway is a special- to an ETT.
ized airway device made of wide bore
PVC tubing, which incorporates a distal Does the LMA protect the patient
inflatable non-latex laryngeal cuff against gastric aspiration*?
(figure 8.1). The LMA is inserted No. Should gastroesophageal reflux
without special equipment, in the back occur, the LMA will 1101 prevent gastric
of the patient's pharynx with the soft contel~tsfrom entering the trachea. (see
laryngeal cuff resting above the vocal chapter 24: Ul~usualAnaesthetic Com-
cords at the junction of the larynx and plications: Aspiration Pneumonitis, and
esophagus. An endotracheal tube ( E n ) chapter 9: Perioperative Aspiration
generally requires a laryl~goscopefor its Risk: The Rapid Sequence Induction).
il~sertionillto the trachea. Unlike a
LMA, the E l T passes through the vocal Wltich patients woi~ldbe si~itablefor
cords with its tip positioned in the mid general annesthesia wit11 a LMA?
trachea. Patients who have no identified risk
factors for aspiration (see chapter 9),
A foreign body in the trachea, such as and who d o not require intubation and
an endotracheal tube, evokes an inteuse col~trolledventilation, are suitable can-
reflex. This results in an increase in didates for the LMA. It may be diffi-
heart rate, blood pressure a l ~ da cough cult to obtain an adequate seal using a
reflex. The anaesthetist routinely ad- face mask in patiel~tswith no teeth or
ministers poteut anaesthetic agents such with a full beard. The LMA is particu-
as opioids a l ~ dmuscle relaxants to blunt larly useful in these patients, providing
or abolish this reflex. The tracheal a good seal and an unobstructed ainvay.
"foreign body" reflex does not result
from the il~sertiol~ of a LMA because it i"lticlt patients are not suitable for a
does not enter the trachea. Therefore, LMA?
the LMA can be positioned with mini- 1. Patients with risk factors for gastric
mal amounts of anaesthetic agents (e.g., aspiration.
propofol alone). Mailltellance of anaes- The comatose patient in the emerg-
thesia can be easily achieved by sponta- ency department with a presumed
neous respiration of a mixture of anaes- drug overdose and intermittent
thetic gases such as nitrous oxide and airway obstruction, would not be a

** Must KIIOW Should Kno\v Page 55


Anaesthesia for Medical Students

Table 8.1: Advantages and Disadvantages of a LMA and Endotracheal Tube.


I 1

LMA ETT
Provides airway protection against
1 ~ e ~ u ~ ~ ~ a e s t h hands,
when compared to a face mask
etid's gastric aspiration.
Allows for tracheal suctioning.
alone. Allows positive pressure ventilation
Provides a better airway in the without increasing the risk of gastric
unconscious patient than a face distension and aspiration.
mask alone.
Can often be positioned with
minimal anaesthetic drugs
(e.g., Propofol alone, i.e., no
"Foreign body in trachea reflex")

DISAD
LMA
Doesn't protect against gastric as-
I
ETT
Muscle relaxants are usually require
I
piration. for intubation.
Positive pressure ventilation with Technically more difficult to insert
airway pressures of > 20 cm H20 and position compared to LMA.
results in increasing gastric * Trauma and positioning complica-
insufflation and risks pulmonary tions e.g., endobronchial intubation.
aspiration of gastric contents. (see chapter 8).
Laryngospasm can occur with the "Foreign body in trachea reflex":
LMA in place. This may result in resulting in an undesired reflex sym
complete airway obstruction. pathetic stimulation (see text).
Laryngospasm can occur when the
E'IT is removed.

good candidate for the LMA, as 3. Patients with limited mouth opening.
they are at high risk for gastric asp- (e.g., wired jaw, TMJ disease)
iration. 4. Patients with a cervical vertebrae or
2. Patients with oropharyngeal or laryngeal cartilage fracture.
retropharyngeal pathology, or 5. Patients requiring positive pressure
foreign bodies in the hypopharynx. ventilation with airway pressures of
Examples include peritonsillar greater than 20 cm H20 (e.g.,
abscess, Ludwig's angina, epiglot- patients with significant restrictive
titis, and trauma to the mouth. or obstructive airway disease, trend-
elenburg position, laparoscopy).
Chapter 8 The Laryngeal Mask Airway

B. With the neck flexed and head


upwards againet the hard extended, the mask is advanced
palate as it is advanced into dong the posterior pharyngeal w

C. A wrzectly positioned LMA. The cuff D. When m e d y positioned the LMA


should be inflated without holding on cuff does not push the epiglottis
to the LMA. downward, or obstruct the glottis.

Figure 8.1: Positioning of the Laryngeal Mask Airway. Adapted with


from Brain AIJ., The lntavont Laryngeal Mask Instruction ManuaL
Second Edition 1991.

" Must Know Should Know Page 57


Anaesflresia for M e d i c a l Sfude~tts

Figure 8.2: A number 4 (top) and number 3 (bottom) laryngeal mask airway.

How do you position a LMA? be used to induce anaesthesia. Propofol


The laryngeal mask is positioned after is the preferred induction agent as it is
the induction of general anaesthesia. superior to thiopental for reducing
The laryngeal mask should be lubri- laryngeal irritability and laryngospasm
cated, and the cuff valve checked. It is during LMA insertion. If thiopental is
recommended that the cuff is fully used for LMA insertion, the use of
deflated prior to insertion. Our experi- succinylcholine will facilitate its inser-
ence, however, has been that a small tion and prevent laryngospasm.
amount of air in the cuff (6 - 10 m L in
an adult cuff) facilitates its insertion. After general anaesthesia is induced, the
The patient is placed in the supine posi- patient's mouth is opened by creating
tion with their head and neck oriented atlanto-occipital extension of the neck
in the usual 'sniffing position' used for in combination with forward displace-
intubation. ment of the jaw. The tip of the LMA i s
inserted into the mouth, and pressed u p
Anaesthesia is typically induced with against the hard palate as it is advanced
the use of propofol. Other agents such into the pharynx with the right hand.
as thiopental, ketamine or halothane can The cuff of the tube is guided along the
C k a ~ l e r 8 Tlte Larvneeal Mask Airwav

)
posterior pharyngeal wall, and inserted oxygenate or ventilate the patient, with
j as far as possible into the pharynx. secondary hypercarbia and hypoxemia.
) Stridor, a high pitched inspiratory sound
As an aid to advancing the laryngeal produced by an upper airway obstruc-
) cuff past the tongue, it is recommended tion, may be noted during laryngo-
) that the right index finger be positioned spasm. Occasionally a muscle relaxant,
at the tube-cuff interface guiding the such as a small dose of succinylcholine,
) cuff into the pharynx, while the palm of is needed to break the laryngospasm and
) the right hand pushes the proximal end permit positive pressure ventilation and
) of the LMA into the pharynx. Resis- oxygenation.
tance is felt when the cuff is positioned
at the upper esophageal sphincter. An
) assistantmay help by holding the mouth
open, or by lifting the jaw forward to
)
open the hypopharyngeal space. The
black line running longitudinally along
) the LMA tube should be facing the
upper lip. Once in this position, the
) cuff is inflated with air, causing the
) LMA to rise out of the mouth a little as
it settles into its correct position.
)
) How do you remove the LMA?
) The LMA can be left in place until the
patient is awake enough to remove it.
) Alternatively the LMA can be removed
by the anaesthetist as the patient is
emerging from anaesthesia, or while
) they are under deep anaesthesia and
) breathing spontaneous1y. The cuff may
be deflated before removing it. How- Figure 8.3: LMA Sizes and weights.
) ever, if left inflated, the cuff removes # 1: for wt. c 6.5 kg.
) any upper airway secretions as it is # 2: for wt. 6.5 - 25 kg.
) taken out. Deflating the cuff risks hav- # 3: for wt: 25 kg. up to adult females
ing secretions stimulate the vocal cords # 4: for adult males
) with the potential for laryngospasm. References:
) Deflation of the LMA cuff in the lightly 1. Brain AIJ. The laryngeal mask - a
anaesthetized patient may result in new concept in airway management.
)
laryngospasm because of stimulation of Br J Anaesth 1983; 55:801-5.
the vocal cords by secretions. Laryngo- 2. Fischer JA, Ananthanarayan C,
spasm** is an involuntary reflex closure Edelist G. Role of the laryngeal
of the glottis by adduction of the vocal mask in airway management. Can J
j cords. It may result in the inability to Anaesth 39:l-3; 1992.

i ** Must Know Sltould K I I O W Page 59


Rapid Sequence
Induction
A 'rapid sequence induction'* is used ness, and tracheal intubation with a
when a patient requires general anaes- cuffed E m .
thesia who has been identified as having
risk factors for gastric aspiration (see Without a cuffed tracheal tube, the
table 9.1). All patients are at risk of patient is at risk of pulmonary aspiration
aspirating gastric contents when general of gastric contents. Cricoid pressure is
anaesthesia is induced, because it applied by an assistant with the induc-
impedes the patient's protective airway tion of anaesthesia. It's purpose is to
reflexes. For this reason, all patients reduce the risk of passive regurgitation
requiring elective surgery are asked to and aspiration before an endotracheal
abstain from eating solid foods for at tube can be placed. Cricoid pressure is
least 8 hours, and clear liquids, for at only released when the tracheal tube
least 4 hours prior to their procedure. cuff has been inflated, and the tube
Should gastric contents reflux into the position confirmed by auscultation of
hypopharynx during the general anaes- both lung fields and measurement of
thetic, the use of a cuffed endotracheal carbon dioxide in the exhaled gases
tube prevents it from entering the lungs. (ETCOJ.

Technique for Rapid Sequence*


The predisposing factors for gastric
aspiration include a depressed level of 1. Prepare for CeneralAnesthesia. The
consciousness(4 LOC),impaired airway suction is checked, on and under the
reflexes, abnormal anatomical factors, patient's pillow. Airway equipment is
decreased gastroesophageal (GE) checked. An appropriately sized E m
sphincter competence, increased intra- with a stylet is prepared. A
gastric pressure, and delayed gastric laryngoscope and laryngoscope blade
emptying. Patients who have any of is checked. The machine is checked,
these predisposing risks for gastric the monitors applied, and the
aspiration, and who require a general medications are prepared and
anaesthetic, should have measures taken labelled.
to prevent aspiration during the peri-
operative period. The three key com- 2. If a nasogastric tube is in place, suc-
ponents of a rapid sequence induction tion and remove it, or leave it open
are: preoxygenation, the application of to drainage.
cricoid pressure with loss of conscious-

Page 60
i
Anaestlaesia for Medic&/Students
\

Table 9.1: Aspiration : Predisposing Factors and Preventative Measures**

& LOC - Drug overdose (e.g., ETOH) - Head injury


- Anaesthesia - CNS Pathology
- Trauma or shock
states
. .

Impaired Airway - Prolonged Tracheal intubation - Myopathies


Reflexes - Local anaesthesia to the airway - CVA
- & LOC
Abnormal - Zenkers Diverticulum - Esophageal stricture
Anatomy

& GE - NG tube - Hiatus Hernia


Competence - Elderly patient - Obesity
- Pregnancy - Curare

t Intragastric - Pregnancy - Large abdominal


Pressure - Obesity tumours
- Bowel Obstruction - Ascites

Delayed Gastric - Narcotics - Pregnancy


Emptying - Anticholinergics - Renal Failure
- Fear, Pain, Labour - Diabetes
- Trauma

Prevention - Preoperative Fasting - NG tube to empty


- H2 Antagonists (&acidity) stomach prior to
1 Antacids (4 acidity) induction
- Metoclorpropamide ( t motility) - Cricoid Pressure
- Antiemetics on induction of
- Regional or Local anaesthesia general anaesthesia
rather than General - Extubation awake
Anesthesia (GA) on side

about the role of ketamine or propofol relaxant for a rapid sequence induction?
as alternatives to thiopental when anaes- When would a muscle relaxant other
thesia is induced. Why is succinyl- than succinylcholine be chosen for a
choline the most commonly used muscle rapid sequence induction?

Page 62
1
Chapter 9 Rapid Sequence Induction
1

) For a discussion of the consequences of


pulmonary aspiration see chapter 24:
) Uncommon Anaesthetic Complications -
) Aspiration.

J
Notes:

** Must Know * Should Know Page 63


Monitoring in
Anaesthesia
Inspection, palpation, percussion and Monltorlng
auscultation are the cornerstones of
monitoring in anaesthesia. In addition, Current Canadian guidelines to the
numerous technical monitors are used to Practice of Anaesthesia and patient
improve our understanding of the monitoring are:
patients physiological status and
minimize the patients anaesthetic risk. 1. An anaesthetist present. "The only
indispensable monitor is the pres-
ANAESTHETIC DEPTH*: ence at all times, of an appropriate-
ly trained and experienced phys-
Patients undergoing surgery with local ician."
or regional anaesthesia are able to 2. A completed preanaesthetic
provide verbal feedback regarding their checklist. (Current history and
well being. When we induce a state of physical documented, appropriate
general anaesthesia, the onset of laboratory investigations reviewed,
anaesthesia is signalled by the lack of pre-anaesthesia evaluation com-
response to verbal commands and the pleted, ASA classification recorded,
loss of a 'blink' reflex when the eyelash and npo policy observed if it is an
is lightly touched. Inadequate anaes- elective procedure).
thesia may be signalled by facial 3. An anaesthetic record. Every
grimacing to a painful stimulus or by patient receiving general anaes-
movement of an arm or leg. In the case thesia, major regional anaesthesia,
of full paralysis with muscle relaxants, or monitored intravenous conscious
inadequate anaesthesia is suggested by sedation, should have their HR and
hypertension, tachycardia, tearing or BP measured at least every 5 min-
sweating. Excessive anaesthetic depth utes, unless impractical. The time,
may be signalled by cardiac depression dose, and route of all drugs and
manifesting as bradycardia and fluids should be charted.
hypotension. In the patient who has not 4. Oxygenation, ventilation, circula-
been given muscle relaxants and is tion, and temperature are continual-
breathing spontaneously, excessive ly evaluated both clinically and
anaesthetic depth may result in hypo- quantitatively. (Continual is
ventilation with hypercapnia (increasing defined as 'repeated regularly').
PaCOJ and hypoxemia .
Chapter 10 Monitoring in Anaesthesia

the mid trachea. The right internal jugular


vein has been cannulated and displays a
pulmonary artery catheter passing through
the right atrium (I), right ventricle (2), and
the pulmonary artery (3).

** Must Know Should Know Page 65


ST Segment 0.0 m m

158/82
Arterial
(114)
Pressure

r 4
Central
32lO
Right
27/14 (19)
Pulmonary
12
Pulmonary
J
Venous Ventricular Artery Capillary
Pressure Pressure Pressure Wedge
Pressure

Figure 10.3: Hernodynamic monitoring. Central venous pressure, right ventricular


pressure, pulmonary artery pressure, and pulmonary capillaty wedge pressure tracings
\ from positions 1 , 2 , 3 and 4 in figure 10.1.

Page 66
1
Chapter 10 Monitoring in Anaesthesia
1
I. OXYGENATION: system has electrodes positioned on the
Oxygenation is monitored clinically by right arm, left arm, and chest position.
providing adequate illumination of the Lead I1 is usually monitored with a
patient's colour and by pulse oximetry. three lead system, as the axis of this
The inspired oxygen concentration vector is similar to the P-wave axis.
(FiOJ is quantitatively monitored dur- Identification of P waves in lead I1 and
ing all general anaesthetics using an it's association with the QRS complex is
oxygen analyzer. Each analyzer is useful in distinguishing a sinus rhythm
equipped with an audible low oxygen from other rhythms. The chest elec-
concentration alarm. trode is usually placed in the left anter-
ior axillary line at the fifth interspace
11. VENTILATION: and is referred to as the V5 precordial
Ventilation is monitored clinically by lead. A five lead electrode system adds
verification of a correctly positioned a right leg and left leg electrode and
endotracheal tube as well as by observ- allows monitoring of vectors I, 11, 111,
ing chest excursions, reservoir bag dis- AVR, AVL, AVF and V5 (see figure
placement, and breath sounds over both 10.1) Today's anaesthesia monitors are
lung fields. Ventilation is quantitatively capable of analysis of the ST segment
monitored using end tidal carbon diox- as an indicator of myocardial ischemia.
ide @?'KO3 analysis as well as an Depression or elevation of the ST seg-
audible disconnection alarm on all ment may be indicative of myocardial
mechanically ventilated patients. The ischemia or infarction respectively.
measurement of expired gas volumes Over 85% of ischemic events occurring
and the ability to perform arterial blood in the left ventricle during surgery can
gas analysis are useful adjuncts in be detected by monitoring the S T seg-
assessing the adequacy of both oxygen- ments of leads I1 and V5.
ation and ventilation.
BP Measurement: The simplest
111. CIRCULATION: method of blood pressure (BP) determi-
The circulation is monitored clinically nation estimates the systolic blood pres-
by using one or more of: palpation of sure by palpating the return of the arter-
the pulse, auscultation of heart sounds, ial pulse as an occluding BP cuff is
a - a r t e r i a l pressure monitoring, deflated. Other methods include
doppler pulse monitoring, or oximetry. auscultation of the Kortokoff sounds
Quantitative evaluation of the circula- with cuff deflation. This allows both
tion includes an audible electrocardio- systolic (SBP) and diastolic (DBP)
gram (ECG) signal, and arterial blood pressure measurements. The mean
pressure measurements at least every 5 arterial pressure (MAP) can be est-
minutes. imated from this as the MAP = DBP +
1/3(SBP - DBP).
The ECG: A three or five lead elec-
trode system is used for ECG monitor-
ing in the operating room. A three lead

>
** Must Know Should Know Page 67
naesthesia for M e d i c a l Students

rable 10.1: Normal values for a healthy adult undergoing general anaesthesia*.
--- - - - - - -

Systolic Blood Pressure SBP 85 - 160 mmHg


Diastolic Blood Pressure DBP 50 - 95 mmHg
Heart Rate HR 50 - 100 bpm
Respiratory Rate RR -
8 20 rpm
Oxygen saturation by pulse oximetry Sp02 -
95 100 %
End tidal carbon dioxide tension ETCO, 33 - 45 mmHg
Skin appearance warm, dry
Colour pink
Temperature -
36 37.5 O C
Urine production 2 0.5 ml. kg-'. min"
Central Venous Pressure CVP 1 - 10 mmHg
Pulmonary Artery Pressure PAP (mean) 10 - 20 mmHg
Pulmonary Capillary Wedge Pressure PCWP 5-15 mmHg
Mixed venous oxygen saturation Sv02 75 %
Cardiac Output CO 4.5 - 6 1- mid'.

Table 10.2: Derived Cardio~ulmonarvValues:


1, Mean
Body Surface Area (BSA)
Arterial Pressure
Normal Values:
MAP = 80 - 120 mmHg
MAP = DBP + 113 Pulse pressure
Cardiac Index (CI) = COIBSA CI = 2.5 - 4.0 L. min". mq2
Systemic Vascular Resistance SVR = 1200 - 1500 dynes-cm-secSs
SVR = MAP - CVP x 79.9

Pulmonary Vascular Resistance PVR = 100 - 300 dynes-cm-sec"


PVR = PAP(mean) - PCWP x 79.9

Stroke Volume = CO x 1000 SV = 60 - 90 ml. bear1


HR

Alveolar Oxygen Tension PAO, = 110 mmHg (Fi02= 0.21)


-
PAO, = (P, P,,)Fi02- PaC0dR.Q. (where P, = 760, Pm= 47, R.Q. = 0.8)

' Alveolar-arterial oxygen gradient A-a02 gradient < 10 mmHg (FiO, = 0.21
A-a02 = P A O ~Pao, -
Arterial Oxygen Content (Ca02) CaO, = 21 mI.100ml"
= (SaOJ(Hb x 134) + PaO, x 0.0031
Chapter 10 Monitoring in Anaesthesia

Automated non-invasive BP measure-


ments are routinely performed intra-
operatively using a microprocessor- Procedures frequently requiring direct
controlled oscillotonometer such as a arterial pressure monitoring include
Dinamape. These units have replaced major cardiac, thoracic, vascular and
routine BP measurements by neurosurgical procedures. Arterial line
auscultation or palpation techniques. placement is also indicated in pro-
They automatically inflate the BP cuff cedures requiring induced hypotension
to occlude the arterial pulse at preset or induced hypothermia. Patients with
time intervals. The cuff pressure is co-existing diseases, including signifi-
sensed by a pressure transducer. cant cardiopulmonary disease, severe
Repeated step deflations provide oscilla- metabolic abnormalities, morbid obesity,
tion measurements which are digitalized and major trauma, may also require
and processed as the cuff is deflated. perioperative arterial line placement.
Rapid, accurate (+ 9 mmHg) measure-
ments of SBP, DBP, MAP and HR can A central venous pressure (CVP) cath-
be obtained several times a minute. eter provides an estimate of the right
Artifacts can occur with patient move- atrial and right ventricular pressures.
ment, arrhythmias, or blood pressure The CVP reflects the patients blood
fluctuations due to respiration. volume, venous tone, and right
ventricular performance. Serial meas-
When automated non-invasive BP urements are much more useful than a
measurements are unsuccessful, simple single value. The HR, BP, and CVP
auscultation or palpation techniques can response to a volume infusion (100 -
be used with a manual cuff. Automated 500 ml of fluid) is a very useful test of
BP measurements are routinely per- right ventricular performance. CVP
formed every 3 to 5 minutes during monitoring is useful in patients undergo-
general anaesthesia. Repeated rapid ing procedures associated with large
measurements for prolonged periods of fluid volume shifts. Shock states, mass-
time are not recommended due to a ive trauma, significant cardiopulmonary
small risk of a compressive peripheral disease or the need for vasoactive medi-
nerve injury. cations are other indications for using a
CVP catheter.
lnvasive monitoring of the circulation
may include the use of an arterial, cen- Unlike a CVP catheter that lies in the
tral venous, or pulmonary artery cathe- superior vena cava, the pulmonary
ter. An arterial line is established with artery catheter (PAC) passes through
-
a small (20 22 gauge) catheter in a the right atrium and right ventricle and
peripheral artery. The radial artery at rests in a branch of one of the pulmon-
the wrist is the most common site for an ary arteries (see figure 10.1). Inflation
arterial catheter insertion. The femoral, of a plastic cuff at the tipof the catheter
brachial, and dorsalis pedis arteries are allows occlusion of the proximal pul-
alternative sites for arterial line inset- monary artery and measurement of the

** Must Know Should Know Page 69


Anoesthesio for Medical Shtdenh

distal pressure. This distal (back) pres- peripheral nerve stimulator must be
sure is referred to as the pulmonary immediately available.
artery wedge pressure (PCWP) and
reflects the left atrial filling pressure. Cyanosb:
Thermodilution calculations of cardiac Cyanosis has been defined historically
output are performed by injecting a as the presence of 5 grn/dL of
fixed volume of cool fluid into the right deoxygenated hemoglobin (deoxy Hb).
atrial port and measuring the tempera- When the hemoglobin level is 15 gm/dL
ture change over time from a thermistor and 5 gm/dL of this Hb releases oxygen
probe at the distal tip of the PA cathe- to the tissues, the oxygenated hemo-
ter. A sample of blood taken from the globin portion (OxyHb) is 10 gm/dL.
distal tip of the PA catheter can be Hence the oxygen saturation is:
analyzed to determine the mixed venous SaO, = OxyHb 1 (OxyHb + DeoxyHb)
oxygen saturation (SvO,). Detailed SaO, = 10 1 (10 + 5) = 66%
analysis of the patient's blood and fluid
requirements, as well as the adequacy of An oxygen saturation of 66% corres-
oxygen transport can be made with the ponds to an arterial oxygen tension of
measurements obtained from a PA cath- approximately 35 mmHg (see oxygen
eter. The results of manipulating the dissociation curve figure 10.4). Should
patient's hemodynamic parameters with the patient become anemic, however,
ionotropic agents, vasopressors, vaso- the oxygen tension (PaO,) at which
dilators, diuretics, fluids or blood prod- cyanosis is detected will be even lower.
ucts, can then be followed. Assume for example that the patient's
Hb is now 10 gm/dL. The saturation at
Figures 10.2 and 1 0 3 illustrate typical which we will detect cyanosis (ie.,
cardiorespiratory variables monitored when the DeoxyHb = 5 gm/dL) will be:
during general anaesthesia. Tables 10.1 SaO, = OxyHb / (OxyHb + DeoxyHb)
lists normal cardiorespiratory values SaO, = 5 / (5 + 5) = 50%
during general anaesthesia for a healthy An oxygen saturation of 50% corre-
adult. Table 10.2 lists formulas used in sponds to an oxygen tension (PaOJ of
calculating common cardiorespiratory only 27 mmHg!
values.
We now recognize that under optimal
IV. TEMPERATURE: lighting conditions with no excessive
A temperature monitor must be readily skin pigmentation and a normal hemo-
available to continuously measure tem- globin level, the earliest that cyanosis
perature. Temperature monitoring is can be appreciated is at an oxygen
mandatory if changes in temperature are saturation of approximately 85%. This
anticipated or suspected. corresponds to a PaO, of 55 rnmHg. At
a SaO, of 70% most clinicians will be
An EKG with defibrillator, as well able to detect cyanosis (PaO, of apptox-
resuscitation and emergency drugs must imately 40 mmHg).
be immediately available. In addition a
Chapter 10 Monitoring in Anaesthesia

p
ght Shift in curve: Hb Uremia
Ci tthosis
Hypoxemia
Anemia

Hypophosphatemia
Banked blood
27 40 60 Aadosis

I Figure 10.4: The oxyhemoglobin dissociation curve. The running man


generates heat, carbon dioxide, and acid shifting the curve to the right, and
\enhancing oxygen release to his tissues.

Pulse Oximetry*: an audible tone, which varies with the


Pulse oximetry allows beat to beat ana- percent saturation, allows an auditory
lysis of the patient's oxygenation status. assessment of the patients oxygenation
Oximetry is based on the differences in status.
light absorption by hemoglobin as it
binds and releases oxygen. Red and Pulse oximetry (SpOJ includes meas-
infra-red light frequencies are trans- urements of oxyHb, deoxyHb, metHb,
mitted through a translucent portion of and carboxyHb. An over estimation of
tissue, such as the finger tip or earlobe. the true measured oxygen saturation
The signal is filtered to isolate pulsatile (SaOJ may occur in the presence of
changes in light absorption. Micropro- significant carbon monoxide poisoning
cessors are then used to analyze the (e.g., a bum victim). Oximeters may
amount of light absorbed by the two become inaccurate or unable to deter-
wave lengths of light, and this is com- mine the oxygen saturation when the
pared with an empiric table of measured tissue perfusion is poor (e.g., shock.
values to determine the concentration of states o r cold extremities), when move-
oxygenated and deoxygenated forms of ment occurs, when dysrhythmias are
hemoglobin. Once the concentrations of present, or when there is electrical inter-
oxyHb and deoxyHb have been deter- ference (e.g., electrosurgical cautery
mined, the oxygen saturation can be unit).
calculated. Current pulse oximeters
have numeric LED displays for the The oxyhemoglobin dissociation curve
heart rate and percent saturation. A describes a sigmoidal shape (see figure
pulse plethysmograph allows visual 10.4). A decrease in PaO, of less than
analysis of the pulse waveform, while 60 mrnHg (corresponding to a SpO, of

** Must Know Should Know Page 71


voestkesio for Medico1 Students

I Real time capnograpgh with


recarder speed at 12.5 mm/sec.
-
Trend speed recording at 25 mm/sec.

Expiratory phase occurs from 1 3. Inspiratory phase occurs from 3 - 1.


1 - 2: Alveolar C 0 2 increases in concentration during expiration.
2 - 3: Alveolar plateau. C 0 2 level peaks at 3 and is recorded as the ETC02.
3 - 4: Inspiratory phase begins, and C 0 2 rapidly decreases.

'Curare cleft' indicates a decreasing neuromuscular block.


This is always seen in the right 113 of the plateau.

Spontaneous patient ventilation efforts interposed between


mechanical ventilations. "Patient fighting the ventilator."

Cardiogenic oscillations. The patient's cardiac stroke


volume displaces small volumes of alveolar gas with each
heart beat. Interesting, but of no significance.

Esophageal intubation. The initial ETC02


measurement is abnormally low, and rapidly
falls to zero with subsequent ventilations.

An exponential decrease in ETC02. This may


occur with severe hyperventilation, massive
pulmonary embolism, or circulatory arrest.
Also observed when the patient is cooled to
induce profound hypothermia.

Obstructive airway disease results in an


unequal emptying of the alveoli, and a rising
alveolar plateau. The ETC02 measurement
will greatly underestimate the arterial PaC02.
A rapid fall in the ETC02 value to zero may
indicate a patient disconnection from the
ventilator. An accidental patient extubation,
kinked ETI' or blocked sample line, are other
possible causes.

Figure 10.5: Capnography. A normal capnogram, and its four components are
represented in the top figure. Examples of diagnostic capnograms are included.

P a g e 72
Chapter I 0 Monitoring in Anaeslhesia

90%) results in a rapid fall in the Measurement of ETCO, involves sampl-


oxygen saturation. The lower limit of ing the patient's respiratory gases near
acceptable oxygen saturation is 90% as the patients airway. A value is pro-
this represents an arterial oxygen duced using either an infrared gas ana-
tension just above hypoxic values. lysis, mass spectrometry, or raman scat-
tering technique (see figure 10.2 and
End-Tidal CO, Monltorlng 105). Provided the inspired CO, value
Definitions: is near zero (no rebreathing of COJ, the
Capnometry: Is the measurement of ETCO, value is a function of the CO,
the carbon dioxide (COJ concentration production, alveolar ventilation and
during inspiration and expiration. pulmonary circulation.
Capnogram: Refers to the continuous
display of the CO, concentration During general anaesthesia the PaCO, to
waveform sampled from the patient's ETCO, gradient is typically about 5
airway during ventilation. mmHg. In the absence of significant
Ca pnogra phy : Is the continuous moni- ventilation perfusion abnormalities and
toring of a patient's capnogram. gas sampling errors, an ETCO, value of
35 mmHg will correspond to a PaCO,
End-tidal C0,monitoring is standard for value of approximately 40 mmHg.
all patients undergoing general anaes- Increases or decreases in ETCO, values
thesia with mechanical ventilation. It is may be the result of either increased
an important safety monitor and a valu- CO, production or decreased C0, elim-
able monitor of the patient's physiologic ination (see table 103).
status. Examples of some of the useful
information that capnography is able to Monltorlng Neuromuscular function:
provide include*: In order to quantify the depth of
1. Confirmation of tracheal intubation. neuromuscular blockade, electo-
2. Recognition of an inadvertent esoph- myography is commonly employed
ageal intubation. during anaesthesia. This involves the
3. Recognition of an inadvertent ex- application of two electrodes over an
tubation or disconnection. easily accessed peripheral nerve. The
4. Assessment of the adequacy of venti- ulnar nerve is the most common nerve
lation and an indirect estimate of used for monitoring neuromuscular
Pa CO,. function during general anaesthesia.
5. Aids the diagnosis of a pulmonary Other nerves that may be used include
embolism (e.g., air or clot). the facial nerve and the common
6. Aids the recognition of a partial peroneal nerve. The electrodes are
airway obstruction (e.g., kinked attached to a nerve stimulator, which
Em. applies an electrical impulse to the
7. Indirect measurement of airway reac- nerve. By attaching a strain gauge to
tivity (eg., bronchospasm). the muscle being stimulated, the muscle
8. Assessment of the effect of cardio- response to stimulation may be observed
pulmonary resuscitation efforts. or measured. Ulnar nerve stimulation

** Must Know Should Know Page 73


/
Lnaesfhesia for Medical Sfudenfs
j
rable 103: Etiologies of increased or decreased ETC0,values (Modified from Gilber
HC, Vendor JS. Monitoring the Anesthetized Patient. In Clinical Anesthesia.
Second Edition 1993. JB Lippincott Co. Philadelphia).

Increased ETCO, Decreased ETCO,


I
I Hyperthermia
Changes in CO, Production
I

Hypothermia
I
Sepsis, Thyroid storm Hypometabolism
Malignant Hyperthermia
Muscular Activity
Changes in CO, Elimination
I
Hypoventilation Hyperventilation
Rebreathing Hypoperfusion
Embolism

results in the contraction of the abductor A pure depolarizing block produces a


pollicis muscle and a twitch in the uniform reduction in the height of a
thumb. Up to 70% of the single twitch, TOF stimulus, and tetanus
neuromuscular receptors may be stimulation. If excessive amounts of
blocked by a neuromuscular blocking succinylcholine are given (> 5-6
drug before a change in the twitch mgkg), the block may begin to
height can be observed. When 90% of resemble a non-depolarizing block and
the receptors are blocked, all observable is said to be a phase I1 block (see succ-
twitches are eliminated. inylcholine). Tetanus stimulation of a
nerve will demonstrate a continued
Common methods of stimulation of the weak contraction in the presence of a
nerve include a single twitch stimulus, depolarizing block, but will progressive-
four twitch stimuli, (each separated by ly fade with a non-depolarizing block.
112 second) referred to as a train-of-four
stimulus (TOF), or a continuous stimu- In the case of a non-depolarizing block-
lus referred to as a tetanus stimulation. ade, there is an increasing reduction in
The intensity of neuromuscularblockade each of the four TOF twitches. The
and type of blockade (i.e., depolarizing ratio of height of the fourth to first
versus a non-depolarizing blockade) can twitch (i.e., the TOF ratio) is less than
be characterized by the response to 0.7 in a non-depolarizing block. Also
these different type of stimuli. Clinical both the single twitch and the TOF
relaxation will occur when a single stimulus, will be increased following a
twitch or first twitch of a TOF stimulus, tetanus stimulation. This is referred to
is reduced by 75% to 95% of its orig- as post-tetanic facilitation, and only
inal height (see figure 10.6). occurs with a non depolarizing block.
I
Chapter 10 Monitoring in Anaesthesia
i
The intensity of non-depolarizing When all twitches disappear r 90% of
neuromuscular blockade can be esti- all receptors are occupied. For pro-
mated by the height and number of cedures requiring muscle relaxation
twitches that are present following a attempts are made to maintain one
TOF stimulus. When the first twitch is twitch present with a TOF stimulus.
reduced in height by 75%, the fourth Reversal of a neuromuscular block will
twitch disappears. With an 80% reduc- be easily accomplished if all four
tion in height of the first twitch both the twitches of the TOF are present, and
third and fourth twitches are lost, and will be difficult or impossible if one or
with a 90% reduction in the first twitch no twitches are observed.
the remaining three twitches disappear.

Single %itch Stimulus 11l1 Train of Four Stimulus (TOF)

( Train of Four Ratio (T4lTI) = 0.4

Tetanus Stimulation Tetanus Fade

L + I
-.
Post tetaNc facilitation

Depolarizing neummuscular block. (eg. Succinylcholine 2 mgfltg)


1 minute 1. Block established within 1 minute.
b 2. No fade with tetanus stimulation.
-
S 8 minutca 3. No post tetanic facilitation.
4. Block cannot be reversed.
5. TOF ratio > 0.4

I Non Depolarizing neummuscular block. (eg. Atncurium 0.4 mgflt)


2-25mlnutcs + -
1. Blockestablished over 2 2.5 mlnutes.
4
40minutes 2. Fades with tetanus slimulation
3. Post tetanic faciUtalion present
4. Revemes with anticholinesteraseagents,
5. TOF ratio < 0.7.

Figure 10.6 Assessing neuromuscular function. Characteristics of a


depolarizing and non-depolarizing neummuscular block.

** Must Know Should Know Page 73


)
Anaesthesia for Medical Students
j
Notes:
Intravenous
Anaesthetic Agents
For over forty years, the ultra short Classification:
acting thiobarbiturate, sodium thio- -
Intravenous anaesthetic hypnotic
pental, has been the intravenous
induction agent of choice. Thiopental's Physical Chemical Properties:
popularity is currently being challenged Thiopental is a highly lipid soluble
by a new akylphenol class of drug compound, that is supplied as a yellow
called propofol. Propofol's rapid metab- powder with a sulphuric smell and a
olism and elimination, as well as its bitter taste. When combined with
anti-emetic properties, are welcome sodium carbonate, it becomes water
features to the specialty of anaesthesia. soluble. It is bacteriostatic in water and
Ketamine is infrequently used as an has a pH of 10.6 to 10.8. When
intravenous induction agent due to its injected, sodiumcarbonate is neutralized
unpopular psychological side effects. and the thiopental is converted to its
Despite this, it continues to play an lipid soluble non ionized form (pKa =
important role in anaesthesia due to its 7.6, i.e. 40% ionized at pH = 7.4).
unique cardiorespiratory pharmaco- Thiopental is highly protein bound by
dynamics. albumen (75%), which prevents its
precipitation out of solution in vivo.
In this chapter we shall present three
commonly used intravenous anaesthetic
induction agents: thiopental, propofol,
and ketamine. For each of these drugs
we shall highlight its physical prop-
erties, pharmacokinetics, pharmaco-
dynamics, dosage, indications and
contraindications. Other adjuvant intra-
venous anaesthetic agents such as mida-
zolam and droperidol are also presented.
Opioid analgesics and neuromuscular
blocking agents are presented in the
I Figure 11.1: Sodium thiopentothd. I
following chapters.

A. Sodium Thiopental (Pentothala) Supplied: Thiopental is supplied in the


Definition: form of a yellow powder, dissolved in
Ultra short acting barbiturate water and sodium carbonate to make a

** M Y EKnow
~ Should Know Page 77
j
Lnacsthcsia for Medical Sludents
i
2 5 % solution (25 mg/ml). It is stable glands comprise the vessel rich group*.
as a solution at room temperature for a They receive 75% of the cardiac output,
period of 2 weeks. even though they constitute only 10%
of body mass. After reaching its peak
Structure Activity Relationship: serum level within these vessel rich
organs, thiopental is then distributed to
CH3 at N-1: shortens the duration the muscles, fat and the vessel poor
(eg. methohexital) group of organs (see figure 11.2). 'Ihe
S substitution at C-2: muscle group receives just less than
markedly shortens the 20% of the cardiac output (second only
duration of narcosis to the vessel rich group), and constitutes
C-5 substitution with branched chains: approximately 50% of the body mass.
increases potency and While peak serum concentrations of
toxicity thiopental are reached within seconds of
the injection, the fat group and vessel
Pharmacokinetics: (i.e., What happens poor group (e.g., bone, and cartilage)
to the drug with respect to uptake, dist- may require hours before peak levels are
ribution, metabolism, and excretion.) achieved. The longer time for
thiopental to reach peak levels in these
An intravenous dose of 3 -
5 mgkg compartments is due to the lower
results in loss of consciousness. The perfusion rates of the vessel poor
time required to render the patient un- organs.
conscious is generally 30 to 60 seconds
following administration. This time has
been referred to as the 'arm-brain' circu-
lation time. It is the time required for
the drug to pass from the site of injec-
tion to the brain as it passes through the
right heart, pulmonary circulation, and
left heart. When no other drugs are
given, the anaesthetic state persists for
5 to 10 minutes. The patient awakes
after this period of time not because the 1 1 1 4 16 64 256
drug has been metabolized ('I% -
= 5 12
16 4
Logarithmic Time Scale (minutes)
hours), but rather because the thiopental
has moved away from the brain and is Figure 11.2 Distribution of
thiopentothal in the vessel rich and
entering the more slowly perfused
vessel poor groups over time,
organs. Hence, the termination of
following a rapid intravenous
action of the drug is due to its 're-
injection. (Modified with permission
distribution' from the brain to other
from Miller RD., Anesthesia 3rd Ed.
tissues and organs.
Churchill Livingstone 1990).
\ 1
The brain, liver, kidney's, and adrenal
Chapter 11 Intravenous Anaesthetic Agents

Sulphur containing drugs, acidosis, and cardiovascular depression from high


non steroidal anti-inflammatory drugs doses of thiopental, other antiepileptic
(NSAIDS) may displace thiopental from drugs are used (e.g., a benzodiazepine
albumen. This results in an increase in class of drug).
free thiopental which increases the an-
aesthetic potency and toxicity. Liver Elevated intracranial pressure (ICP) can
and renal disease may be associated be quickly reduced by administering
with lower albumen levels, also raising thiopental. The improvement in ICP is
free serum thiopental concentrations. transitory and would require excessive
amounts of thiopental to maintain. The
Metabolism occurs primarily in the liver use of high doses of barbiturates in
with approximately 10 to 15% of the patients with persistently elevated ICP,
remaining drug level being metabolized has not been shown to improve their
per hour. A desulfuration reaction overall outcome. The reduction of ICP
occurring in the liver produces pento- from thiopental is a result of cerebral
barbital, which then undergoes oxidative vasoconstriction, reduced cerebral
metabolism yielding two compounds metabolism and oxygen requirements.
with no anaesthetic activity. Less than This is associated with a decrease in
one per cent of the administered cerebral blood volume. The overall
thiopental is excreted unchanged in the effect is an improvement in cerebral
urine. perfusion pressure (CPP), as the
decrease in ICP is generally greater than
Pharmacodynamics: (i.e., What the drug the decrease in mean arterial pressure
does in the body.) (MAP).

CNS:
Barbiturates, including thiopental, inter-
act with chloride ion channels by alter- Thiopental has an anti-analgesic effect,
ing the duration they spend in an 'open since low doses may decrease a patients
state'. This facilitates inhibitory pain threshold.
neurotransmitters such as gama amino
butyric acid (GABA), as well as block- Intraocular pressure (IOP) decreases up
ing excitatory neurotransmitter actions -
to 25% with 3 5 m a g of thiopental.
such as glutamic acid. The decrease in IOP persists for 3 to 5
minutes.
Thiopental will decrease both cerebral
) electrical and metabolic activity. CVS:
) Hence, it can be used to stop seizure Thiopental causes a dose related
activity in an emergency situation. To depression of myocardial function as
3 maintain depression of cerebral electri- measured by cardiac output (CO), stroke
) cal activity, very high doses of volume (SV), and blood pressure.
) thiopental are required. To maintain Coronary blood flow, heart rate, and
seizure control and avoid significant myocardial oxygen uptake all increase
)

Must Know Should Know Page 79


lnaesthesia for Mcdical Shtdcnts

following administration of thiopental. limited to 4 m&.


Venous tone decreases (decreased pre-
load) and contributes to the increase in Dose and Administration:
HR, and decrease in BP. Little change Thiopental must be used with caution in
in the total peripheral resistance occurs patients suffering from a shock state.
following thiopental administration. This was quickly appreciated by the
anaesthetists caring for the casualties of
RESP: pearl harbour. They presented to the
Induction of anaesthesia with thiopental operating room in shock states second-
may be associated with 2 or 3 large arily to massive blood loss. The admin-
breaths followed by apnea. The duration istration of the usual sleep dose of
of apnea following a 'sleep' dose of thiopental of 3 to 6 m a g for induction
thiopental is usually less than one min- of anaesthesia resulted in their rapid
ute. There is a dose related depression demise. For a frail elderly lady who
of the respiratory response to hyper- has fractured her hip, a dose of 25 to 50
carbia and hypoxia. Laryngospasm may -
mg (05 1 m a g ) may be all that is
occur with induction, especially at light required for the induction of anaes-
levels of anaesthesia and with airway thesia. For short procedures (eg. cardio-
manipulation. Bronchoconstriction may version) a dose of 2 mglkg is generally
be associated with thiopental, but is sufficient.
much more commonly seen following
the combination of a small dose of Indications:
thiopental with airway manipulation or 1. Sole anaesthetic agent for brief surgi-
intubation. As with any general an- cal procedures (less than 15 minutes).
aesthetic agent, the functional residual 2. For induction of anaesthesia, prior to
capacity (FRC) is reduced with the administration of other anaesthetic
induction of anaesthesia by up to 20%. agents.
3. For control of convulsive states.
GI: 4. For the supplementation of regional
Enzyme induction may occur with pro- anaesthesia, or low potency an-
longed high dose therapy, as in barbitu- aesthetic agents such as N20.
rate induced comas. Hypoalbuminemia
will result in an increase in unbound Contraindications to Thiopental*:
(free) thiopental and an increase in the I. ABSOLUTE:
potency of thiopental. 1. Lack of knowledge of the drug.
2. Lack of resuscitative equipment.
GUPregnancyIFetus: 3. Inability to maintain a patent airway.
Thiopental has little or no effect on the 4. Complete absence of suitable veins.
kidney's or gravid uterus. Although 5. Allergy or hypersensitivity to bar-
thiopental rapidly crosses the placenta to biturates.
reach the fetus, it has no significant 6. Status asthmaticus.
effect on the fetus when used for cesar- 7. Porphyria (Varigate Porphyria, or
ean section provided the dose used is Acute Intermittent Porphyria)
Chaprcr 11 Infravcnous Anaesrheric Agents

11. RELATIVE:
1. Hypotension or shock.
2. Severe cardiovascular disease.
3. Severe liver disease.
4. Myxedema.

Side Effects and Toxicity:


An extravascular injection of thiopental
will usually not cause any serious long
term sequelae, provided the concentra-
tion of the solution injected is 5 25%.
With more concentrated solutions, an
extravascular injection may cause severe
pain on injection as well as subsequent
tissue necrosis. If a solution of a 2 5 % Figure 11.3: Propofol.
thiopental is injected accidentally into
an artery, severe pain, vascular spasm,
loss of digital pulses, gangrene, and
permanent nerve damage may occur. If
an intra-arterial injection does occur, the
offending iv should be kept in place,
and 5 to 10 mL of 1% plain lidocaine
administered through it. Consideration
should be given for systemic heparin
administration (to prevent thrombosis),
and for administering some form of
sympathetic block (eg. stellate ganglion
block) to reduce the sympathetic tone of Time (minutes)
the injured area. Figure 11.4: Simulated time course
of whole-blood levels of propofol
Other side effects not mentioned above following an induction dose of 2.0
include allergic reactions, which may mglkg. (With permission from
manifest as a skin rash, pain on injec- Miller RD., Anesthesia 3rd Ed.
tion, urticaria, angioedema, broncho- Churchill Livingtone, 1990.)
spasm, laryngospasm, and cardio-
vascular collapse. 1% propofol (10mg/mL)
10% soyabean oil
B. Propofol (DiprivanB) 2.25% glycerol
Definition: 1.2% purified egg phosphatide
Intravenous anaesthetic - hypnotic
Classification: Akylphenol Propofol is a highly lipid soluble oil
Phvsical Chemical Properties: that is combined with glycerol, egg, and
soyabean oil for intravenousadministra-

** Must Know * Should Know Page 81


Lnaesthesia for Medical Shcdena

:ion. It's appearance is similar to that of blood vessels remain responsive to C 0 2


2% milk, as the solution that is used to during a propofol infusion. Cerebral
dissolve it is similar to total parenteral metabolic rate is decreased up to 36%.
nutrition (TPN) solutions. It has a pH Propofol appears to have neither epilep-
of 7 and is supplied in 20 mL ampules tic nor anticonwlsant properties.
with a concentration of 10 mg/ml.
RESP:
Pharmacokinetica: The respiratory rate is decreased with
-
TIA initial distribution = 2 8 minutes. the induction of anaesthesia, and ap-
'l?4 redistribution = 30 - 60 minutes. proximately one quarter of patients
-
'l?4 elimination = 4 7 hours. become apneic at induction. The period
of apnea depends on the dose given, the
Following a single bolus injection, peak speed of injection, and concomitant use
serum concentrations are reached rapid- of an opioid. The frequency of apnea is
ly. Propofol's high lipid solubility greater than that seen following
results in a quick transfer to the brain thiopental. Maintenance anaesthesia
and rapid onset (one 'arm-brain' circula- (100 mcg/kg/min iv) with propofol
tion time). Recovery from a single results in a decreased tidal volume and
bolus injection results from both redis- increased respiratory rate. At this same
tribution and elimination. Propofol is infusion rate the ventilatory response to
metabolized in the liver, yielding water C 0 2 is depressed similar to that caused
soluble inactive conjugated compounds by administration of 1 MAC (0.76%)
which are excreted by the kidney. Less halothane. Unlike halothane, however,
than 2% of propofol is excreted doubling the infusion rate of propofol
unchanged in the urine and feces. Pro- does not result in a marked increase in
pofol is cleared from the blood faster depression of the C02 response curve.
than hepatic blood flow, which suggests
that extrahepaticmetabolismandelimin- cvs:
ation may be occurring in the lungs. Systolic, mean and diastolic blood pres-
sure are reduced 25-40% with an induc-
Pharmacodvnamics: tion dose of 2-2.5 mg/kg. Cardiac
output, stroke volume and systemic
CNS: vascular resistance are all decreased
Unlike barbiturates, propofol is not with induction by 15-20%. The
antanalgesic. At low (subhypnotic) decrease in blood pressure is believed to
concentrations, propofol can provide be secondary to both myocardial de-
both sedation and amnesia. Patients pression and vasodilation. Heart rate
report a general sense of well being on may increase, remain the same, or
awakening from propofol anaesthesia. decrease following propofol. Concomi-
lntracranial and intraocular pressure are tant administration of an opioid tends to
both decreased by propofol. Cerebral result in a greater reduction in heart
perfusion pressure undergoes a small rate, cardiac output, and arterial pres-
decrease with propofol. The cerebral sure.

Page 82
Chapter 11 Intravenous Anaesthetic Agents

OTHERS: cardiac output (severe aortic or mitral


Propof01 neither precipitates histamine stenosis, IHSS, pericardial
release, nor triggers malignant tamponade) and those in shock states.
hyperthermia. Propofol has no effect on
muscle relaxants and is associated with C. Ketamine (KetalarB)
a low incidence of nausea and vomiting.
Pain on injection is more common than DefinitionIClassification:
with thiopental, especially if given in a Dissociative Anaesthetic Agent
small vein in the hand. The discomfort
at injection can be decreased by the Physical Chemical Properties:
administration of a small dose of lido- Ketamine is chemically related to the
caine with propofol, or by administering psychotropic drug phencyclidine (PCP),
propofol through a fast flowing more and cyclohexamine. It is water soluble
proximal intravenous catheter. and is 10 times more lipid soluble than
thiopental. It exists as two enantiomers
Intravenous Induction Dose: s (+) and r (-) ketamine, and is supplied
An induction dose of 2.5 - 3.0 mglkg is as a 50:50 mixture. It has a pH of 35 -
used for healthy unpremedicated 5 5 and is supplied as a clear colourless
patients. When an opioid, or a solution of 10 and 50 mg/mL.
premeditation has been given, the in-
duction dose is reduced to 15-2.0
mg/kg. In elderly patients the induction
dose should be reduced to s 1mgkg of
propofol.

Infusion rates of 50-150 mcg/kg/min in


combination with nitrous oxide and
opioids, can be used for maintenance of
anaesthesia.
( Figure 11.5: Ketamine. I
Intravenous conscious sedation for oper-
ative procedures with local anaesthesia
can be facilitated with propofol infu- Pharmacokinetics:
-
sions of 25 75 mcgkglmin. Ketamine may be given iv, im, po, or
pr. Extensive first pass metabolism and
Contraindications to Pro~ofol*: decreased absorption necessitates the
1. Allergy (egg allergy). administration of higher doses when
2. Lack of resuscitation equipment or given by the oral or rectal routes. Keta-
knowledge of the drug. mine undergoes biotransformationin the
3. Inability to maintain a patent airway. liver, yielding eight metabolites. The
4. Conditions in which precipitous re- most significant metabolite is nor-
ductions in blood pressure would not ketamine (also known as Metabolite I),
be tolerated; in patients with a fixed which has 113 the potency of ketamine,

** Must Know * Should Know Page 83


lnaesfheria for Medical Studenfs

and subsequently undergoes hydoxyl- due to different mechanisms, with the


ation, conjugation, and excretion in the analgesic effects resulting from an inter-
liver. action between ketamine and central or
Following administration, there is rapid spinal opiate receptors.
absorption and distribution to the vessel
rich group (see thiopental), with CNS:
recovery of consciousness probably Ketamine anaesthesia produces a cata-
secondary to its redistribution to other leptic state during which nystagmus as
tissues. Over 90% of an im. injection well as intact corneal and pupillary light
is bioavailable. Hepatic metabolism is reflexes may be observed. There is a
required for elimination, with less than generalized increase in muscle tone and
5% of the administered drug recovered purposeful movements, and vocalization
in the urine unchanged. There is a three may occur. Unpleasant dreams, hal-
phase exponential decline in ketamine lucinations, or frank delirium may occur
levels with a 'I% distribution of 24 with ketamine, especially if the patient
seconds, a l% redistribution of 4.7 is young, female, and large doses of
minutes, and 'I% elimination of 2 2 ketamine are given rapidly. The inci-
hours. dence of delirium is decreased with the
concomitant administration of a benzo-
Mechanism of Action: diazepine (eg. diazepam or midazolam),
Three current theories about ketamines and by giving small doses slowly. The
mechanism of action are: overall incidence of delirium in the 15
1. N. Methvl Aspartate receptor theory. to 35 year old population is approxi-
NMA receptors may represent a mately 20%.
subgroup of the sigma (a) opiate
receptors (the PCP site),' that block Intracranial pressure is not increased
spinal pain reflexes. with ketamine provided ventilation is
2. Opiate receptor theory. Ketamine adequate. Intraocular pressure may or
may have some affinity for opiate may not increase with ketamine.
receptors but its effects cannot be
reversed with naloxone. RESP:
3. ~iscellaneousreceptor theory. Ketamine provides general anaesthesia
Ketamine interacts with muscarinic, while preserving laryngeal and
cholinergic, and serotonergic pharyngeal airway reflexes. Despite
receptors. this, there are reports of pulmonary
aspiration of gastric contents during
Ketamine was originally thought to ketamine anaesthesia when an artificial
cause a 'functional and electrophysio- airway is not used. Ketamine is associ-
logical dissociation between the ated with mild respiratory depression in
thalamoneocortical and limbic systems'. healthy patients following 2 m a g
Ketamine is a potent analgesic at sub- intravenously. The C 0 2 response curve
anaesthetic plasma concentrations. Its is shifted to the left with its slope
analgesic and anaesthetic effects may be unchanged (similar to opiates). Func-
Chapter I 2 Intravenous Anaesthetic Agents

tional residual capacity (FRC), minute succinylcholine and curare, are


ventilation (VA,and tidal volume (V,), enhanced by ketamine.
are preserved as is hypoxic pulmonary
vasoconstriction (HPV). In dogs, keta- ENDO:
mine is as effective as halothane or Ketamine's sympathetic stimulation will
enflurane in preventing bronchospasm. result in an increase in blood glucose,
Changes in the respiratory pattern may plasma cortisol, and heart rate.
be observed with periods of prolonged
apnea, resulting in hypoxic episodes. Dosage:
Increased secretions occur with ket- -
im: 5 10 m a g
amine, and can be limited with the prior -
iv: 1 2 mgfltg (To limit the risk of
administration of an anticholinergic, delirium following ketamine, it should
such as atropine or glycopyrrolate. be injected at a rate of s 40 mdminute).

cvs: Intramuscular injections in children of 9


Ketamine produces both a central sym- - 13 m g k g produce surgical anaesthesia
pathetic stimulation and a direct nega- within 3 - 4 minutes with a duration of
tive ionotropic effect on the heart. The -
20 25 minutes. Peak plasma levels are
central sympathetic stimulation results reached approximately 15 minutes fol-
in an increase in HR, BP, SVR, pul- lowing an im injection. With iv admin-
monary artery pressures (PAP), coronary istration a dissociated state is noted in
blood flow (CBF) and myocardial oxy- 15 seconds, and intense analgesia,
gen uptake (MV02). Pulmonary vascu- amnesia and unconsciousness occur
lar resistance (PVR) is unchanged if within 45 - 60 seconds. A dose of 1 -
ventilation is controlled. If the normal 2 m g k g will produce unconsciousness
sympathetic nervous system is blocked -
for 10 15 minutes, analgesia for 40
or exhausted, ketamine may cause direct minutes, and amnesia for 1 2 hours. -
myocardial depression. Subsequent iv doses of 113 to 112 the
initial dose may be required.
GI:
Anorexia, nausea, and vomiting are Indications for ketamine*:
minimal. 1. Sole anaesthetic for diagnostic and
surgical procedures.
GU/Placenta/Fetus: 2. For induction of anaesthesia prior
Placental transfer does occur, but neona- to the use of other anaesthetic
tal depression has not been observed if agents.
the ketamine dose is limited to s 1 3. To supplement regional anaesthetic
mgfltg. or local anaesthetic techniques.
4. For anaesthetic induction in the
MSK: severe asthmatic patient or the
At the neuromuscular junction, there is patient with cardiovascular collapse
an increase in skeletal muscle tone, and requiring emergency surgery.
the effects of muscle relaxants, such as

** Must Know Should Know P a g e 85


Lnaesthesia for Medical Students

Contraindications to ketamine: muscle relaxant effects are due to an


1. Lack of knowledge of the drug. increase in the concentration of a
2. Lack of resuscitative equipment. glycine inhibitory neurotransmitter.
3. Inability to maintain a patent air- Facilitation of the effects of GABA
way. results in the sedative and anti-
4. Allergy or hypersensitivity to convulsant effects of benzodiazepines.
ketamine. Benzodiazepines are highly lipid soluble
5. History of psychosis. and highly protein bound. In patients
6. Cerebrovascular disease. with reduced albumen levels (e.g., cir-
7. Patients for whom hypertension is rhosis, renal insufficiency,malnutrition),
hazardous. the decreased plasma binding may result
(eg. severe hypertension, in an increase in free drug concentra-
aneurysms, heart failure, etc.) tion, and an increase in drug related
toxicity.
Other side effects and toxicity: Benzodiazepines are metabolized in the
Respiratory depression may occur and liver by hepatic microsomal enzymes.
should be managed with ventilatory The metabolites are conjugated with
support. Ketamine has a wide margin glucuronic acid and excreted by the
of safety, and in cases of relative over- kidneys. Elimination half times range
doses (up to 10 times the usual dose) from 1 - 4 hours for midazolam
there has been a protracted though com- -
(Versed@), to 10 20 hours for loraz-
plete recovery. -
epam (Ativana), and 21 37 hours for
diazepam (Valium@).
Other adJuvant intravenous Midazolam and diazepam are the two
anaesthetic agents: most commonly used benzodiazepines
during operative procedures.
Benzodiazepines: Features which result
in the popularity of benzodiazepines as Midazolam (Versed@):
adjuvant intravenous anaesthetic agents Midazolam's most common use intra-
include: operatively is to provide intravenous
sedation, amnesia, and to reduce
1. Ability to produce amnesia. anxiety. A dose of 0.5 to 3 mg intra-
2. Minimal cardiorespiratory venously (up to 0.1 mglkg) is effective
depressant effects. for intravenous conscious sedation.
3. Anticonvulsant activity. -
Higher doses of 0.2 0.4 m g k g may be
4. Low incidence of tolerance and used to induce anaesthesia. Midazolam
dependence. has a more rapid onset, greater amnestic
effect and less postoperative sedative
Benzodiazepines inhibit the actions of effects than diazepam. Pain on injection
glycine and facilitate the actions of the and subsequent thrombophlebitis is less
inhibitory neurotransmitter gamma am- likely with midazolam than with
inobutyric acid (GABA). Benzo- diazepam. Midazolam's duration of
diazepines antianxiety and skeletal action is less than diazepam's, but

Page 86
C h a ~ t e r 11 Intravenous Anaesthetic Aeenfs

almost 3 times that of thiopental. It is sedation recurs, infusions of 0.1 to 0.4


supplied for intravenous use as a clear mglhour may be used. Flumazenil is
liquid in concentrations of 1 to 5 generally well tolerated. The most
mglml. common side effect is nausea, and this
is seen in only 4 % of patients.
Diazepam:
Diazepam has 1/2to 1/3the potency of Droperidol:
-
midazolam. A dose of 1 10 mg is Butyrophenones such as droperidol and
effective for intravenous conscious haldol are classified as major
sedation. Higher doses of 0.15 to 15 tranquilizers. Droperidol is more com-
m a g are used to induce anaesthesia. monly used in the perioperative period
Diazepam has a high incidence of pain than is haldol, because it has a shorter
on intravenous injection, as well as a duration of action, and has less signifi-
high incidence of subsequent phlebitis. cant alpha adrenergic antagonist effects
An emulsion of diazepam (DiazemulsCO) so marked reductions in blood pressure
is available and has a lower incidence are unlikely. Droperidol acts at the
of venous irritation and phlebitis. postsynaptic receptor sites to decrease
DiazemulsB contains a diazepam the neurotransmitter function of
emulsoid of soybean oil, egg lecithin, dopamine. It is used in the operating
and a glycerol solution (similar to suite as an antiemetic and as an
propofol), however, it is more costly adjuvant to opioid analgesia
than plain diazepam. (neuroleptanalgesia). Droperidol is a
powerful antiemetic, inhibiting dop-
Benzodiazepine Antagonists: a m i n e r g i c r e c e p t o r s i n the
Flumazenil (Anexate@) is an imidazo- chemoreceptor trigger zone of the
benzodiazepine that specifically ant- medulla. The usual dose of droperidol
agonizesbenzodiazepine'scentraleffects as an antiemetic is 0.25 to 2.5 mg iv.
by competitive inhibition. The mean Adverse side effects are dose related.
elimination half life of flumazenil is
approximately one hour, considerably Extrapyramidal reactions are seen in
shorter than most benzodiazepines. approximately 1% of patients and are
Hence, repeat administration or infu- due to its antagonism of dopamine. For
sions may be required when benzodiaze- this reason, droperidol is contraindicated
pines with a longer T% elimination are in patients with known Parkinson's
being antagonized. disease. Other adverse reactions include
Flumazenil is supplied as a colourless orthostatic hypotension, and dysphoric
liquid in a concentration of 0.1 mg per reactions resulting in increased anxiety
mL. The usual initial dose is 0.2 mg iv and an agitated state. Abnormal sleep
over 15 seconds. If the desired level of patterns in the first 24 hours following
consciousness is not obtained within 60 the administrationof 1.25 mg of droper-
seconds of administration, repeated idol have been reported in healthy
doses of 0.1 mg can be given every patients undergoing minor surgical
minute up to a maximum of 2 mg. If procedures. Droperidol may be admin-

** Must Know Should Know Page 87


4naesthesia for Medical Studenk

istered in higher doses with an opioid


such as fentanyl to produce an anaes-
thetic state referred to as neurolept-
analgesia. This is characterized by a
trance like immobility and an appear-
ance of tranquility. The intense anal-
gesia produced with neuroleptanalgesia
allows a variety of minor procedures to
be performed (e.g., bronchoscopy, or
cystoscopy). The disadvantages of this
form of anaesthesia include a prolonged
central nervous system depression and
postoperative dysphoric reactions. For
these reasons, neuroleptanalgesia is only
rarely administered today.

Notes:
1
) Muscle Relaxants

Neuromuscular physiology*: muscle resulting in a muscular contrac-


The neuromuscular junction consists of: tion. Acetylcholine's action is rapidly
(< 15 milliseconds) terminated as it
1. A motor nerve ending with diffuses away from the muscles end
mitochondria and acetylcholine ves- plate, and is hydrolysed by acetyl-
icles (prejunctional). cholinesterase.
-
2. A synaptic cleft of 20 30 nm in
width containing extracellular fluid. Muscle relaxants produce skeletal
3. A highly folded skeletal muscle muscle paralysis by interfering with
membrane (postjunctional). acetylcholine at the neuromuscular
4. Nicotinic cholinergic receptors junction. Fortunately, involuntary
located on both the presynaptic muscles such as the heart are not
(nerve) and postsynaptic (muscle) affected by neuromuscular blocking
membranes. drugs.

Skeletal muscle contraction involves an


intricate series of events. As a nerve
impulse is generated, an action potential
travels down the nerve to the
neurornuscular junction (NMJ) (see
figure 12.1). The action potential
results in the release of acetylcholine
from the nerve endings into the synaptic
cleft. The acetylcholine diffuses across
to the muscles nicotinic cholinergic
receptors causing a change in the mem-
branes permeability to ions. The altered
membrane permeability results in a Figure 12.1: The neuromuscular
sodium and potassium flux across the junction. Ach = Acetylcholine;
muscle membrane. This flux of ions AChE = acetylcholinesterase; JF =
decreases the muscles transmembrane junctional folds; M = mitochondria;
electrical potential. When the resting V = Vesicle. (With permission from
transmembrane potential decreases from Drachman DB; Myasthenia gravis.
-90 mV to -45 mV, an action potential \N Engl J Med 298:136-142,1978).
spreads over the surface of the skeletal

1
** Must Know Should Know Page 89
inae$thesia for Medical Students
)
Classlflcation*: Non Depolarizing Muscle Relaxants:
Muscle relaxants may be classified Non-depolarizing neuromuscular block-
according to their duration of action ing drugs compete with acetylcholine
(short, intermediate, or long), and on the for the cholinergic nicotinic receptor.
basis of the type of neuromuscular As the concentration of muscle relaxant
block they produce. A non-competitive increases at the NMJ, the intensity of
depolarizing muscle relaxant such as muscle paralysis increases. Anticholin-
succinylcholine cannot be antagonized. esterase agents inhibit the break down
The termination of succinylcholine's of acetylcholine. This results in an
activity is dependent on hydrolysis by increase in the concentration of
plasma cholinesterase. All other cur- acetylcholine at the NMJ. Anaesthesio-
rently used muscle relaxants are com- logists exploit this pharmacological
petitive non-depolarizing agents. Their action by administering ~ t p l c h o l i n -
activity does not result in depolarization esterase
--.. . ----..
agents such as neostigmine and
of the motor end-plate or muscle fibre, edrophonium to competitively 'reverse'
and their action can be reversed by the the effects of a non-depolarizing
administration of an anticholinesterase neuromuscular blockade.
agent such as neostigmine or edro-
phonium. Mlvacurlum: Mivacurium is a new
short-acting non-depolarizing neuro-
Cholce of muscle relaxant: muscular blocking drug which, like
Considerations for choosing a muscle succinylcholine undergoes hydrolysis by
relaxant include*: plasma cholinesterase. Patients who
1. Duration of action of relaxant, and have deficiencies in the quality or quan-
duration of required muscle relax- tity of plasma cholinesterase will have a
ation. prolonged duration of action with both
2. Route of excretion. mivacurium and succinylcholine (see
3. Tendency to release histamine. succinylcholine, p.93). The effective
4. Cardiopulmonary side effects result- dose to produce a 95% reduction in the
ing from administration. Potential twitch height (ED,) is 0.08 m&g (see
adverse reactions include brady- chapter 10: Monitoring Neuromuscular
cardia, tachycardia, bronchospasrn Function). Intubation with a non-depo-
and hypotension. larizing muscle relaxant is typically
5. The ability to reverse the accomplished by the administration of 2
neuromuscular block. to 3 times the EDQ5. Intubation with
6. Cost. mivacurium can be performed approxi-
7. Contraindications to any specific -
mately 2 2.5 minutes after administer-
muscle relaxant. ing twice the EDB. With rapid injection
Table 12.1 summarizes the duration of of an intubating dose of mivacurium, a
action of some commonly used muscle transient fall in blood pressure may be
relaxants, and the extent to which they observed secondary to the release of
depend on renal excretion. histamine. Special infusion pumps are
1
Chapter 12 Muscle Relarants
)

Brand Name Block Duration % Time to Intubating


(Trade Name) (mins.) , dependent intubation Dose
Concentration on renal (90%block) (mgkg)
excietion at 2 x ED,
Succinylcholine Non Short 0 < 60 sec 1-2
(Anectine) Competitive 5 - 10
20 mg/ml (Depolarizing)
Mivacurium Competitive 25 - 30 0 2 - 3 min 0.16 .30 -
(Mivacron) Non -
2mgiml Depolarizing

Vecuronium Inter- 10 25- 2.5 - 3 min -


.07 0.10
(Norcuron) mediate '

10 mgtvial 45 60 -
Rocumnium
30 - 45
25 - 80 secs 0.6
(Zemuron)
10 mglml

Cisatracurium 20 - 60 0 3.3 min 0.1


(Nimbex)
10 mg/ml

Pancuronium Long 60 80- 3 - 8 min .06 - , l o


(Pavulon) 60 - 75
-
1 2 mg/ml

Doxacurium 50 - 130 60 - 80 3 - 10 min 0.05


(Nuromax)
1 mg/ml
)
Table 12.1: Properties of neuromuscular blocking agents.

) frequently utilized in the operating room one of 1 0 isolated isomer of it's


) to deliver opioid analgesics, sedatives, predescesor atracurium. It undergoes
or muscle relaxants. These pumps hydroiysis in the plasma by a non-
allow for both continuous infusions and enzymatic process referred to as
) bolus doses to be administered. Con- Hoffman elimination, and by an ester
-
tinuous infusions of 5 10 mcgkglmin hydrolysis reaction. Significant hista-
) of mivacurium may be used to maintain mine release resulting in hypotension,
a stable neuromuscular blockade during tachycardia, and bronchospasm, that
the procedure. may occur after rapid administration of
Cisatracurium: Cisatracurium is atracurium i s not seen with
) classified as an intermediate-acting cisatracurium. This lack of histamine
) neuromuscular blocking drug, and is release, is the main advantage of
I
** Muslfiow Should Know Page 91
\naerthesia for Medical Students

:isatracurium over it's parent compound vantage is it's ability to quickly induce
atracurium. The EDg5of cisatracurium a neuromuscular block, making it suit-
is 0.05 mglkg. A stable neuromuscular able for a rapid induction and intubation
block can be achieved using an infusion sequence. It has an ED, of approxi-
of cisatracurium' at a rate of 1 - 5 mately 0.3 m&g. The onset time (i.e.
mcg/kg/min. Cisatracurium is an ideal time to 90% depression of TI twitch
agent for patients with renal or hepatic height) for an intubating dose of ro-
insufficiency requiring muscle curonium (i.e. 2 x EDgs) is 60 80 -
relaxation. seconds. By contrast, vecuronium has a
much slower onset time of 150 200 -
Vecuronium: Vecuronium is an inter- seconds. Rocuronium's onset time is
mediate-acting neuromusc~larblocking comparable to the onset time following
agent. It is a popular agent because it 1.5 mglkg of s~ccinylcholine(50 - 70
does not' produce any undesirable seconds). Hence, rocuronium matches
cardiovascular side effects even when succinylcholine's onset time, and avoids
administered rapidly in large doses. Its its potential side effects. Nevertheless,
ED, is 0.05 mg/kg. The onset time for it must be remembered that the duration
neuromuscular relaxation following 2 x of action of this dose of succinylcholine
the ED, is 150 - 200 seconds. This can is only 8 - 12 minutes, compared to 35
be shortened by the administration of a - 45 minutes for rocuronium. Continu-
small 'priming' dose (0.01 m a g ) of ous infusions in the range of 4 - 16
-
vecuronium, followed by 2 4 times the mcglkglmin. can be used to maintain a
ED,. This can achieve conditions stable neuromuscular block. This
suitable for intubation in approximately -
should be reduced by 30 50% when
90 seconds from the time of administra- administered in the presence of 1%
tion. The duration of neuromuscular isoflurane (similar to all other
block'will be increased to more than 1 neuromuscular relaxants).
hour if a larger dose is used for
intubation. Continuous infusions of 0.5 Paneoronium: Pancuronium is a long-
- 1.5 mcglkglmin have been used to acting neuromuscular blocking drug.
maintain a stable neuromuscular block Administration of pancuronium is fre-
during the procedure. quently associated with a modest (<
15%) increase in heart rate, blood pres-
Racuronium: This new intermediate sure, and cardiac output. The increase
acting non-depolarizing neuromuscular in heart rate is due to its blockade of
relaxant may replace atracurium, vec- the cardiac muscarinic receptors, as well
uronium, and mivacurium as the relax- as an inhibition of catecholamine re-
ant of choice for short and intermediate uptake by sympathetic nerves. Pancur-
procedures. It has just recently been onium administration does not result in
released, and has a duration of action, histamine release. The ED, of pan-
route of metabolism, and lack of hemo- curonium is 0.06 m&g. Pancuronium
dynamic side-effects similar to that of is much more dependent on renal excre-
vecuronium. Rocuronium's major ad- tion than the other clinically used

Page 92
Chapter 12 Muscle Relaxants

) muscle relaxants. A prolonged neuromuscular blocking agent that is


neuromuscular block will result when clinically used. Depolarizing muscle
I pancuronium is administered to patients relaxants bind and depolarize the end-
) with renal failure or insufficiency. plate cholinergic receptors. By contrast,

'
)
d - Tebocurare: The muscle
paralyzing properties of curare were
non-depolarizing muscle relaxants com-
petitively block the action of
acetylcholine. The initial depolarization
well know to South American natives can be observed as irregular, generalized
who used this drug to immobilize and fasciculations occurring in the skeletal
) kill animals with blowgun darts. In muscles.
1942 Griffith and Johnson in Montreal
introduced the medical world to the Succinylcholine (AnectineB)
) paralyzing properties of curare. Since Classification:
) the early 1990's curare has been Non-competitive depolarizing
unavailable in Canada, and is now only neuromuscular blocking agent.
of historical interest. In the 1980's
) curare was most frequently used to _Phvsical-Chemical:
) attenuate the muscle fasciculations and Succinylcholine physically resembles
postoperative myalgias associated with two acetylcholine molecules linked end
the administration of succinylcholine. to end. It has two quaternary ammon-
) A small 'pretreatment' dose of curare (3 ium cations which interact with the
mg per 70kg) was administered approxi- anionic sites on the muscle end plate
) . mately 3 minutes prior to the adminis- receptors.
) tration of succinylcholine, and was
) appreciated f o r it's excellent Ninety percent of succinylcholine
'defasciculating' properties. Today, undergoes hydrolysis by plasma
) anesthesiologists who wish to attenuate cholinesterase (psuedocholinesterase)
1 the muscle fasculations and postop before it reaches the neuromuscular

)
' myalgia's seen with succinylcholine
administer a small (- 1/10 intubating
dose) of a non-depolarizing muscle
junction. After binding to the end plate
muscle receptors and causing skeletal
muscle relaxation, it diffuses out of the
relaxant 3 minutes prior t o NMJ. Outside the NMJ, succinyl-
succinylchole (eg., rocuronium 5 m g per choline is again exposed to plasma
70 kg). cholinesterase and the remaining 10% is
1 hydrolysed. The metabolites of suc-
Depolarizing Muscle Relaxants: cinylcholine are excreted in the urine.
1 Succinylcholine is the most frequently Peak effect is reached within 60 seconds
) used muscle relaxant that is adminis- of administration, and the neuro-muscu-
tered outside the operating room by a lar blocking effects of succinyl-choline
i
non-anaesthetist physician. Hence a typically dissipate over the next 5 to 10
detailed discussion of its properties is minutes.
, included in this chapter. Succinyl-
choline is the only depolarizing
i
1 ** M u t Know Slrould Know Page 93
naesthesia for Medical Students

'hase I and Phase I1 Blocks: 5. ~ e s ~ o nto


s ea tetanus stimulus fades
;uccinylcholine produces a 'prolonged during the stimulus
rcetylcholine (Ach) effect'. It combines 6. The neuromuscular block can be
with the Ach receptor to depolarize the reversed with anticholinesterase
:nd plate, resulting in a generalized agents
iepolarization (seen as succinylcholine
induced fasciculations). The membrane The presence of a normal amount of
remains depolarized and unresponsive active plasma cholinesterase is essential
until succinylcholine diffuses away from to terminate the effects of succinyl-

-
the endplate (due to a concentration choline. In certain conditions, the levels
gyadient). This initial neuromuscular of plasma cholinesterase may be low,
block is referred to as a phase I block. and this is referred to as a quantitative
If large amounts of succinylcholine are decrease in cholinesterase levels. The
given (eg. 4 6 mg/kg), a different consequences of a low plasma
neuro-muscular block may occur. This cholinesterase level are generally of
block is referred to as a phase I1 block. little significance. In patients with
Clinically this may occur when repeated severe liver disease with plasma
doses of succinylcholine are given, or cholinesterase levels as low as 20% of
when succinylcholine infusions are normal, the duration of a neuromuscular
used. A phase I1 block has features block resulting from the administration
which resemble a neuromuscular block of succinylcholine increases threefold
that is produced by non-depolarizing (eg. 5 to 15 minutes). Liver disease,
muscle relaxants. The actual mechan- cancer, pregnancy, and certain drugs
ism of a phase I1 block is unknown. such as cyclophosphamide, phenylzine,
and monoamine oxidase inhibitors have
p : all been associated with low
1. Similar response to a single twitch cholinesterase levels.
2. No post-tetanic facilitation
3. Train of four (TOF) ratio > 0.7 Abnormalities in plasma cholinesterase
4. Muscle fasciculations prior to paral- activity are inherited. Patients may
ysis have normal plasma levels of
5. Decreased amplitude, but sustained cholinesterase, with a severely impaired
response to tetanic stimulus enzyme activity. This is referred to as
6. The neurornuscular block is increased a qualitative decrease in plasma
,when cholinesterase inhibitors are cholinesterase. Plasma cholinesterase
administered enzyme activity is genetically deter-
mined by four alleles identified as the
Characteristics of Phase I1 Blocks: silent or absent allele (s), the usual
1. Decreased response to a single twitch allele (u), the dibucaine allele (d), and
2. Post-tetanic facilitation present the fluoride allele (f). The normal
3. Train of four (TOF) ratio < 0.7 plasma cholinesterase genotype is EuEu.
4. No fasciculations with onset of paral- Patients with abnormal cholinesterase
ysis activity are otherwise healthy and can
I
Clzapter 12 Muscle Relarants
)

) be identified only by a specific blood pressure, changes in pH, PaCO,, mean

'
)
test that identifies the genotype and
enzyme activity. The sixteen possible
genotypes are expressed as ten possible
arterial pressure, and a direct effect
from the extraocular muscles. A normal
IOP is 10 - 20 mmHg. An increase in
) phenotypes. Six of these ten IOP under anaesthesia is undesirable in
phenotypes are associated with a patients with an injury that disrupts the
) marked reduction in the hydrolysis of globe's integrity. These patients are at
) succinylcholine. Patients with the risk of vitreous extrusion and damage to
genotype EaEa have a marked reduction the eye if the IOP increases. While suc-
) in the hydrolysis of succinylcholine. cinylcholine increases IOP, crying,
) These patients will have a prolonged straining, or coughing can result in
neuromuscular block that can be much greater increases of up to 50
increased from ten minutes to several mmHg. Increases in intracranial pres-
) hours following a normal intubating sure (ICP) of up to 10 mmHg may
1 dose of 1 - 2 mg/kg of succinylcholine. occur following succinylcholine admin-
The EaEa genotype has a frequency of istration. The mechanism of the
approximately 1:3200. increase in ICP is thought to be due to
) the central mobilization of blood that

'
)
The treatment of postoperative paralysis
secondary to deficiencies in plasma .
cholinesterase activity includes con-
results from succinylcholine's general-
ized muscle contractions.

) trolled ventilation, reassurance, and REP: .


sedation. Blood samples should be A progressive paralysis from eyelids to
/ taken to confirm the diagnosis and the jaw, limbs, abdominal, intercostal
) identify the enzyme genotype. Immedi- and diaphragmatic muscles follows the
ate family members should be tested to administration of succinylcholine.
)
determine their genotypes and suscepti-
) bility. Medical alert bracelets should be cvs:
worn by any patient with a significant Succinylcholine stimulates both the
reduction in their plasma cholinesterase nicotinic and muscarinic cholinergic
activity. autonomic receptors. As a consequence
of muscarinic cholinergic stimulation,
harmacodvnamics: bradycardia, dysrhythmias, and sinus
1 b:
) Succinylcholine has no known effect on
arrest may be observed. This vagal
response is prominent among children
consciousness, pain threshold or cerebral and, after repeated doses, in adults. It
1 function. An increase in intraocular may be inhibited with anticholinergics
pressure (IOP) begins within 1 min of such as atropine.
administration of succinylcholine. A
peak rise in IOP of 6-10 mmHg occurs GI:
at 2-4 minutes, and subsides by 6 min- Succinylcholine iincreases the intra-
I utes. Factors that may increase IOP gastric in proportion to the intensity of
include: an increase in central venous the muscle fasciculations in the abdo-

** Mud Know * Should Know Page 95


i
inaesthesia for Medical Students

nen. It can be limited with prior use of patients may respond with an
on-depolarizing muscle relaxant. abnormally high tone in masseter
muscle following succinylcholine.
GZf: These patients are said to have devel-
Succinylcholine does not rely on renal oped a masseter muscle spasm, and may
excretion. It's metabolites, succinic acid represent a subgroup of patients suscep-
and choline, however, are excreted by tible to malignant hyperthermia.
the kidney. Patients with renal failure
may have pre-existing hyperkalemia, Hyperkalemia following succinyl-
and ma,y be susceptible to succinyl- choline**:
choline-induced hyperkalemia. A few cholinergic receptors are located
along skeletal muscle membranes out-
The usual serum potassium response side of the NMJ. The receptors are
following succinylcholine is a transient called extrajunctional cholinergic
and brief increase in the extracellular receptors. The numbers of these
K t concentration of -
0.5 meq/L.
Generally patients with K+ concentra-
receptors increase dramatically over a
period of 24 hours whenever nerve
tions of r 5.5 meq/L should not receive impulse activity to the muscle is inter-
succinylcholine, and all but emergency rupted. Acute disruption of nerve activ-
procedures should be delayed. Succ- ity to skeletal muscle occurs in patients
inylcholine does not cross the placenta who have sustained third degree burns
because of its low fat solubility and its or traumatic paralysis (paraplegia,
ionized state. quadriplegia). Administration of succ-
inylcholine to these patients will result
MSK: in an abnormally high flux of potassium
Succinylcholine has no direct effect on out of the muscle cells because of the
the uterus or other smooth muscles. increased number of receptors. An
Myalgias following the administration acute rise in the serum potassium to
of succinylcholine are infrequent in levels as high as 13 meq/L following
children, the geriatric population, and succinylcholine may result in sudden
pregnant patients. The incidence of cardiac arrest. Succinylcholine is abso-
succinylcholine myalgias can be lutely contraindicated in these patients.
decreased with prior administration of a The administration of a non-depolariz-
non-depolarizing muscle relaxant such ing muscle relaxant in these patients
as curare (3 mgl70kg). Fasciculations does not result in a hyperkalemic
result in the release of myoglobin into response because the receptors are sim-
the serum (myoglobinemia). The excre- ply blocked and not depolarized.
tion of myoglobin into the urine (myo-
globinuria) is more common in children,
and can be decreased with prior treat-
ment with non-depolarizing muscle
relaxants. Succinylcholine increases the
masseter muscle tone in the jaw. Some

Page 96
1
Chapter 12 Muscle Relavnnts

) Patients who are at risk of a hyper- 3. Myotonia: Patients with myotonia


kalemic response following the adminis- congenita, myotonia dystrophica, and
) tration of succinylcholine include: paramyotonia congenita may all de-
velop a severe, generalized
1. Patients with extensive third degree contracture if given succinylcholine.
) burns. Succinylcholine should be The use of a depolarizing muscle
) avoided if the injury is more than.24 relaxant such as succinylcholine in
hours old, and for 6 months follow- these patients may result in a second-
)
ing the healing of the bum injury. ary generalized contracture of the
) 2. Patients with nerve damage or skeletal muscles, and prevent airway
) neuromuscular diseases such as mus- maintenance and ventilation.
cular dystrophy are susceptible to
) hyperkalemia and cardiac standstill 4. Familial Periodic Paralysis:
) with succinylcholine. The degree of ~uccin~lcholine can precipitate a
hyperkalemia appears to be related to generalized contracture and should be
)
the degree and extent of muscle avoided in these patients.
affected.
) 3. Severe intra-abdominal infections. Dosage & Administration:
4. Severe closed head injury. Intubating dose:
) 5. Upper motor neuron lesions. With curare pretreatment:
1 1.5 - 2 mg/kg intravenously:
) Specific Diseases:
Without curare pretreatment:
) 1. Myasthenia Gravis - All muscle re- 1 - 1.5 mglkg iv.
) laxants are best avoided, if possible,
in patients with myasthenia gravis. Infusion:
) These patients behave as if partially An infusion may be used for short pro-
) curarized. They are very sensitive to cedures to maintain a stable
non-depolarizing muscle relaxants, neuromuscular block. Recommended
) rates for infusion are 50 - 150
and may be sensitive or resistant to
) depolarizing muscle relaxants. mcg/kg/min.

Myasthenic Syndrome: The Eaton- Indications:


Lambert Syndrome is a proximal 1. Skeletal muscle relaxation during
muscle myopathy associated with a endotracheal intubation
carcinoma of the bronchus. Unlike 2. Abdominal operations of short dur-
myasthenia gravis, muscle fatigue ation
decreases with exercise, and the eye- 3. Prior to electroconvulsive therapy
lids are less affected. These patients (ECT), to prevent the possibility of
are unusually sensitive to both depo- seizure induced injury (e.g., vertebral
larizing and non-depolarizing muscle fracture)
relaxants. 4. Emergency treatment for laryngo-
spasm

** Must Know Should Know Page 97


naesfhesiafor Medical Students

reversal, to block these unwanted


muscarinic effects. Common combina-
ibsolufe tions of anticholinergic and anti-
.. Inability to maintain an airway cholinesterase agents used to reverse a
!. Lack of resuscitative equipment neuromuscular block are atropine 0.01
b. Known hypersensitivity or allergy mg/kg with edrophonium (TensilonB)
I. Positive history of Malignant 0.5 - 1.0 mg/kg, or glycopyrrolate 0:01
Hyperthermia rnglkg with neostigmine (ProstigminB)
5. Myotonia (M.Congenita, M. Dystro- -
0.05 0.07 mg/kg intravenously.
phica or Paramyotonia congenita)
6. Patients identified as being at risk Timing of reversal:
of a hyperkalemic response to suc- There are numerous methods of assess-
cinylcholine (see above). ing the depth of neuromuscular block-
ade. The most common of these'
Relative: include the train of four (TOF) stimulus,
1. Known history of plasma tetanus stimulus, and the train of four
cholinesterase deficiency (TOF) ratio. The train of four stimulus
2. Myasthenia Gravis (TOF) applies four brief electrical stim-
3. Myasthenic Syndrome uli of 2 Hz each over a period of 2
4. Familial Periodic Paralysis seconds. The train of four ratio,
5. Open eye injury (T4/Tl), is the ratio of the twitch
response of the fourth stimulus (T4) to
Reversal of neuromuscular blockade: the first stimulus (TI). In most circum-
Muscle relaxation produced by non- stances, adequate muscle relaxation for
depolarizing neuromuscular agents may surgery occurs when only one of the
be "reversed" by anticholinesterase four twitches is observed. This corre-
agents such as edrophonium and neo- sponds to a r 90% blockade of the NMJ
stigmine. These agents prevent the receptors. One must consider the inten- '

.breakdown of acetylcholine in the NMJ. sity and anticipated duration of


The increased concentration of neuromuscular block before attempting
acetylcholine at the NMJ competes with to antagonize it. Reversal may be un-
the muscle relaxant allowing the successful if only one of the four
receptor once again to become respon- twitches is present. With inadequate
sive to the release of acetylcholine from reversal of muscle relaxation, the patient
the nerves. will have a weak hand grip, be unable
t o ' cough effectively, and unable to
The increased concentrations of sustain lifting their head from their
acetylcholine also stimulate the pillow for 5 seconds. Treatment of
muscarinic cholinergic receptors, result- inadequate reversal includes supportive
ing in bradycardia, salivation, and ventilation, sedation, analgesia, and
increased bowel peristalsis. Anti- adequate time for the neuromuscular
cholinergic agents such as atropine and block to dissipate.
glycopyrrolate are administered prior to

Page 98
Inhalational
Anaesthetic Agents
The intravenous anaesthetic agents inhalational anaesthetic agents such that
introduced in chapter 11 (propofol, very accurate concentrations can be
ketamine, and thiopentothal) are fre- delivered to the patient by simply set-
quently used to induce the anaesthetic ting the vaporizer dial at the desired
state. To maintain the anaesthetic state, concentration.
volatile anaesthetic agents are common-
ly vaporized and delivered to the patient The role of inhalational anaesthetic
through the anaesthetic machine and drugs in current anaesthetic practice is
anaesthetic circuit. This volatile vapour changing. The introduction of potent
is then delivered to the lungs where it intravenous agents, including muscle
diffuses across the alveolar capillary relaxants, opioids, benzodiazepines,
membrane and is dissolved in the blood. propofol, and intravenous infusion tech-
The blood then carries it to the brain niques have decreased the need for high
and other organs in the body. doses of inhalational agents. In anaes-
thesia, a number of different agents
Intravenous drugs are typically delivered representing different classes of drugs
according to a specific number of milli- are chosen to minimize the side effects
grams or micrograms per kilogram of of any one agent and capitalize on each
body tissue. Inhalational agents on the agent's benefits.
other hand are administered according
to a specific concentration. The concen-' Inhalational agents are compared to one
tration of a gas is expressed as a per- another according to their minimal
centage of the volume of anaesthetic gas alveolar concentration** or "MAC"
to the total volume of the gas mixture. values. The MAC value of an ihhalat-
For example if we deliver 2 literslmin. ional agent is the alveolar concentration
of oxygen and 4 literslmin. of nitrous in oxygen at one atmosphere of pressure
oxide (N20) to a patient, the concentra- that will prevent 50% of the subjects
tion of N20 is 4/(2 + 4) = 66%. If we from making a purposeful movement in
want to add a 1% concentration of response to a painful stimulus such as a
isoflurane to this mixture we would surgical incision. The MAC value can
have to add approximately 60 ml of a be considered the effective dose in 50%
saturated isoflurane vapour to the 6 of the subjects or the ED,. Knowledge
liters of fresh gas flow (0.01 x 6000 ml of the MAC value allows one to com-
= 60 ml). Modem anaesthetic pare the potencies of different inhalat-
vaporizers are able to vaporize liquid ional agents. The MAC values of dif-

** Must Know * Should Know Page 99


rrnesflresia for Y e d i c a l Sfuderr~s 1
Cable 13.1: Factors whlch alter anaesthetic re' ulren~ents(MAC).

Increased MAC
1
1 No change In M A C Decreased M A C
--
1
Hyperthermia Gender Increasing age
Chronic drug Duration of anaesthesia Hypothermia
abuse: Ethanol Carbon dioxide tensions: Severe hypotension
Acute use of PaC0,21 - 9 5 mmHg Other anaesthetic agents:
amphetamines Metabolic acid-base status opioids, benzodiazepines
Acute drug intoxication:
Ethanol
Pregnancy
Hypothyroidism
Other drugs:
clonidine, reserpine

ferent anaesthetic agents are additive. The rapidity with which the anaesthetic
Nitrous oxide is the only inhalational state is reached depends o n how quickly
agent that is routi~lelycombined with the anaesthetic inhalational agent
another inhalational agent such as iso- reaches the brain to exert its partial
flurane, enflurane, or halothane. It is pressure effects.
necessary to establish a n anaesthetic Factors determining how quickly the
depth equivalent t o 1.2 to 1.3 of the inhalational agent reaches the alveoli
MACvalue. The added 20 - 30% M A C include:
depth of anaesthesia will prevent move- 1. The inspired concentration of anaes-
ment in 95% of patients. The M A C thetic gas being delivered by the
value of N20is 105%, which is approx- anaesthetic machine (concentration
imately one-hundred-fold greater than effect).
the other inhalational agents. Because 2. The gas flow rate through the anaes-
the recommellded millimum concentra- thetic machine.
tion of oxygen delivered during general 3. The amount o f alveolar ventilation
anaesthesia is 30%, the maximum con- (V, = Respiratory Rate x Tidal Vol-
centration on N 2 0 is 70% (approximate- ume).
ly 0.7 MAC). Hence, nitrous oxide I~lcreasing any of these factors will
alone is unable to provide adequate result in a faster rise in the alveolar
anaesthesia. Opioid a~lalgesics,benzo- concentratio~lof the inhalational agent.
diazepines, or other inhalational agents
may be added to supplement the nitrous Factors determining how quickly the
oxide. Table 13.1 lists factors that inhalational agent reaches the brain
increase or decrease the M A C values. from the alveoli in order to establish
Table 13.2 lists differences in inhal- anaesthesia include:
ational agents a s well as their M A C 1. The rate of blood flow to the brain.
values, with and without nitrous oxide. 2. The solubility of the inhalational
agent in the brain.
Chapter 13 Inhalational Anaesthetic Agents

6 Anaesthetic Tension Cascade

alveolar concentration of
inhaled anaesthetic agent
provides a reasonable estimate
of brain anaesthetic tension
and anaesthetic depth.

h
,---c---------- Delivered Concentration

8
Nvmlar a
Brain

Fresh gas flow rate = 4 Umin.


I 1'
1 5 10 15
lime Elapsed in minutes

Figure 13.1 and 13.2: The anaesthetic tension cascade over time. Note the
difference in anaesthetic tension in the alveoli and brain compared to the set
vaporizer concentration being delivered. Increasing either the fresh gas flow
rate or anaesthetic concentration will result in a faster delivery of the
aled anaesthetic agent to the brain.

3. The difference in the arterial and The cascade of anaesthetic partial pres-
venous concentrations of the inhalat- sures starts at the vaporizer. The gas
ional agent. from the vaporizer is diluted by exhaled
Increasing any of these factors will gas to form the inspired gas. With a
hasten the onset of anaesthesia. circle system, a fresh gas flow of 4 - 5
Patients with low cardiac output states liters per minute will raise the inspired
(eg. shock states) may have a rapid rise anaesthetic tension close to the
in the alveolar partial pressure of an vaporizer's delivered concentration. As
inhalational anaesthetic agent. This will the body continues to take up the
result in a more rapid onset in anaes- inhaled anaesthetic gas, the alveolar
thesia, with possible exaggerated anaesthetic tension will remain below
cardiorespiratory depressant effects. the inspired anaesthetic tension for

** Must Know Should Know Page 101


L~~aes/lresia
for Medical Slude~lls

many hours. The brain can be co~lsider- oxide are released and flood the alveoli,
ed the final step in the anaesthetic cas- diluting the oxygen present in the
cade. The brain tension will approach alveoli. When only room air is admin-
the alveolar tension within 8 to 10 min- istered at the end of the anaesthetic, the
utes of any change. Monitoring the dilution of oxygen may be sufficient to
alveolar end-tidal concentration of the create a hypoxic mixture, and result in
inhaled anaesthetic agent provides a hypoxemia. Other factors contributing
reasonable estimate of the brain anaes- to hypoxemia at the end of anaesthesia
thetic tension (see figure 13.1 and 13.2). include respiratory depression due to
anaesthetic agents, residual neuromus-
Nitrous Oxide: cular blockade, and pain with splinted
Nitrous oxide is an inert, inorganic, col- respirations. The administration of
ourless, tasteless, and odourless gas. It 100% oxygen at the end of an anaes-
has a rapid onset and a quick recovery thetic may avoid hypoxemia resulting
of 3 to 10 minutes due to its low solu- from any of these causes.
bility in blood. Its low potency (MAC
= 105%) limits the amount that can be Finally, closed air spaces will expand in
administered, and its usefulness when the presence of nitrous oxide due to the
high concentrations of oxygen are differences in solubility of nitrogen and
required. Myocardial depression is nitrous oxide. With the administration
usually minimal in healthy patients, of 66% N20, a closed air space will
however significant cardiovascular de- expand 2 times in volume over a period
pression may occur in patients with of approximately 15 minutes. For this
coexisting myocardial dysfunction or in reason N 2 0 is contraindicated in
patients in a shock state. patients with a pneumothorax, closed
loop bowel obstruction, air embolism, or
Nitrous oxide is 34 times more soluble any other closed air space in the body.
than nitrogen. This property results in
three special anaesthetic phenomena. At Nitrous oxide undergoes very little
the begirlrling of anaesthesia, N 2 0 metabolism and is excreted uncha~lged
leaves the alveoli much faster than by the lu~lgs.
nitrogen can leave the body tissues to
fill the space left by N20. The result is The most conlrno~llyused inhalational
an increase in the concentratio~lof other agents today are nitrous oxide, iso-
gases in the alveoli (oxygen, and other flurane, enflurane, and halothane. The
inhalational agents). This increase in latter three are synthetic, colourless
concentratio~lspeeds the onset in inhala- liquids that are non flammable and
tional anaesthetic effect, and is referred administered as a vapour from a
to as the sccond gns cffcct. vaporizer on the anaesthesia machine.
A dose-related depression of cardio-
Diffusion hypoxin may result at the end respiratory function is common to each
of the anaesthetic. As nitrous oxide is of these inhalational agents. All three
discontinued, the body stores of nitrous produce smooth muscle relaxation, and
this property has been exploited to Hnlothnne:
produce bronchodilation in patients with Halothane is the agent of choice for an
status asthmaticus, and uterine relax- inhalational anaesthetic induction,and is
ation in patients with a retained pla- the most common inhalational agent
centa. Halothane, enflurane, and iso- used in paediatric anaesthesia.
flurane are all contraindicated in Halothane decreases myocardial con-
patients with malignant hyperthermia. tractility, slows the heart rate, and
decreases cardiac conduction. The
Isoflurnne: myocardium is sensitized to cate-
Isoflurane is the most common inhala- cholamines in the presence of halothane,
tional agent used for adult anaesthesia resulti~lg in severe ventricular dys-
in North America. It has a MAC value rhythmias if the body releases cate-
of 1.16%, and has the fastest uptake and cholamines (stress), or if exogenous
washout times of these three inhala- catecholamines such as epiilephrine are
tional agents. It is not as well tolerated administered. Cerebral blood flow
as halothane for an inhalational anaes- increases secondary to cerebral
thetic illduction because of its pungent vasodilation and may result in an
odour and tendency to irritate the air- undesired increase in intracra~iialpres-
ways. These irritating effects nlay sure.
result in coughing and breath-holding if
isoflurane is administered too quickly. Halothane's popularity in adult anaes-
Isofluraile is the preferred agent for thesia has declined because of its impli-
neurosurgical procedures as it causes the cation in causingpostoperative hepatitis.
least increase in cerebral blood flow and "Halothane hepatitis" is believed to
intracranial pressure. Isoflurane has the occur in approximately 1 in 10,000
least depressant effect on the halothane anaesthetics and presents as
myocardium. The reduction in blood postoperative f e v e r , jaundice,
pressure is accompanied by a similar eosinophilia, and occasionally extensive
reduction in vascular resistance such hepatic necrosis and death. Hepatitis
that there is little change in cardiac following isoflurane and enflurane expo-
output. In certain patients (especially sure is very rare, a s is hepatitis in the
young healthy patients), isoflurane may paediatric population following any
produce a significant sinus tachycardia. inhalational agent (including halothane).
111 a small percentage of patients with There is a ten fold difference in metab-
corollary artery disease, isoflurane may olism of these three inhalatioilal agents.
cause vasodilatio~l of the distal The maill route of excretioil is through
endocardia] vessels, and result in a the lungs, but approximately 20% of
'coronary steal'. A coronary steal is halothane is metabolized by the liver.
produced when blood is diverted away By contrast 2% of enflurane and only
from the collateral dependent ischemic 0.2% of isoflurane undergoe metabolism
regions of the heart to the areas of by the P, enzyme system. Both aller-
vasodilation. The significance of this gic and metabolic mechanisms may be
observation is still debated. active in producing hepatitis following

Should K I I O I V Page 103


Lt~acslhesiafor Medical S l i r d e ~ ~ ~ s

rnble 13.2: Cornpal-ison of three conlnl ~ninhnlationnl annesthetic agents.


I I I 1
I I lsofiurane
M A C in Oxygen* 1.16%
1
M A C In 70% N20 I 0.50%
I
CNS Causes the lowest Increases ICP and Increases ICP.
increase in ICP of Potential to cause
the 3 agents when CNS excitation and
ventilation is seizures at high
controlled concentrations.

Resp. Irritating to the Good for inhalational Depresses


ainvays, and more inductions, and is respiration more
difficult to use lor less irritating to the than halothane or
inhalational ainvays. Decreases isoflurane.
induction. tidal volume, and
Decreases tidal minute ventilation,
volunie and minute accompanied by an
sentilation, increase in the
( accompanied by an respiratory rate.
I increase in the
respiratoly rate.

cvs Increases heart rate. Depresses BP, HR, Depresses cardiac


Decreases BP and I CO and conduction. function more than
CO. Potential to Sensitizes the halothane or
create a 'coronary myocardium to isoflurane.
adrenaline induced
I dysrhythmias.

I Neuron~uscular Potentiates niuscle Potentiates muscle Potentiates muscle

I
relaxan ts relaxants less than relaxants.
lsoflurane or
Enflurane.

Other Most common agent Halothane Hepatitis Second choice agent


used in adult association in adulls. in adult anaesthesia
anaesthesia. Cheapest agent of the in Nonh America.
three.

exposure to halothane, Repeated Enflurane:


exposures to halothatle over a short Enflurane has a MAC of 1.68%, more
~ e r i o dof time have also beeti thought to than twice that of halothane's MAC
contribute to halothalie hepatitis in value of 0.75%. Enflurane is a potent
patients. cardiorespiratory depressant, decreasing
both respiratory drive and cardiac func-
tion to a greater extent than halothane. Desflurane and Scvoflurane:
Unlike halothane or isoflurane, Desflurane and sevoflurane are two vol-
enflurane produces abnormal electro- atile anaesthetics which have been
encephalographic (EEG) patterns recently introduced in Canada. Both
resembling seizure activity. This is have low solubilities in blood,
only observed in some patients during approaching that of nitrous oxide, s o in-
deep enflurane anaesthesia with lowered duction and emergence from anaesthesia
P a C 0 2 levels secondary to mechanical is rapid. Cardiovascular, respiratory,
hyperventilation. Occasionally tonic neurological and neuromuscular effects
clonic movements under enflurane an- of both agents are similar to those of
aesthesia have been observed. Despite isoflurane.
the lack of documented adverse
postoperative sequelae in these patients, Desflurane is unique in that i t boils at
enflurane is best avoided in patients room temperature (22.8'C). Because of
with a history of a seizure disorder. this physical property, desflurane
requires a special heated and electroni-
cally controlled vaporizer t o administer
it safely. Desflurane has a M A C value
in oxygen of 6% compared to sevo-
flurane which has a MAC value of 2%
in oxygen. Desflurane has a pungent
odour, and like isoflurane can cause
coughing and breath holding if admin-
istered too rapidly. Sevoflurane is more
pleasant smelling and is well suited for
inhalational induction of anesthesia.

Sevoflurane, like enflurane, is metab-


olized in the liver yielding inorganic
fluoride. Approximately 3% of sevo-
flurane is broken down in this fashion.
Minutes oE Administration Is is degraded by the chemicals used to
absorb the patients' C 0 2 in their
Figure 13.3. For potent anaesthetics, solubil- patient's breathing circuit. Production
ity determines the increase in the alveolar of a renal toxin called "compound A" at
(Fd) anaesthetic concentration toward the low fresh gas flows has lead t o the re-
concentration inspired (F,): the least soluble
commendation that sevoflurane be ad-
anaesthetic (desflurane) shows the most rapid
ministered with a minimum of two liters
increase; the most soluble anaesthetic
(halothane) shows the least rapid increase. of fresh gas flow. In contrast, des-
Reproduced with permission. Eger 11, flurane is the least metabolized of the
Edmond I. New Inhaled Anesthetics. volatile anesthetics (0.02%), and is
Anesthesiology 80:906-922, 1994 ideally suited for use in low flow an-
aesthetic techniques.

** Musl Know Should Know Poge I05


innestheria Tor Medical Students

jevoflurane and Desflurane have had a Our- g goals are to


n a j ~ impact
r on our anesthetic pactice. administer enough anaesthetic that the
While structurally similar to their par- patient's awareness and their pain
znts Halothane and Isoflurane, the sub- response to surgery is suppressed. Our
stitution of a couple of key chlorine goal is to provide adequate anaesthesia
atoms with fluorine atoms results in (inhibit awareness) yet at the same time
their lower observed solubilities. This avoid a relative anesthetic overdose.
translates clinically into a more rapid
induction and recovery from anesthesia. We can use the knowledge that the
MAC values of the individual inhal-
Sevoflurane, unlike isoflurane, does not ational agents are additive.
have an unpleasant smell, and is well
tolerated in adults for inhalational Let's assume our patient is under gen-
induction of anesthesia. Using high eral anaesthesia and is receiving end-
concentrations of Sevoflurane at induc- tidal concentrations of 63% nitrous
tion (5 - 8%, with or without nitrous oxide with 0.4% isoflurane. We can
oxide), the patient can be taken from an calculate the relative contributions of
awake state to an anesthetized state with these inhalational agdnts to the patients
as little as one vital capacity breath. anaesthetic.
Anesthesia sufficient for laryngeal mask
placement and intubation can be 6 3 % Nitrous oxide (MAC = 105 %)
achieved after three to five minutes of :.
631105 = 0.60 MAC
breathing a high concentration of
Sevoflurane. 0.4 % Isoflurane (MAC = 1.16 %)
:. 0.4 / 1.16 = 0.35 MAC
Desflurane is not suitable for
inhalational induction due to it's irritat-
__
0.95 MAC

ing and pungent properties. When As stated earlier we generally provide


given rapidly in high concentrations 1.2 - 1.3 times the MAC value to
(6% or more) it may result in coughing, achieve adequate anaesthesia in 95% of
breath-holding, laryngospasm, tachy- patients. In addition to the inhalational
cardia, and hypertension. Unlike agents this patient is receiving, heishe
Sevoflurane, Desflurane is essentially probably has also received a preoperat-
inert with only 0.02% undergoing ive sedative, and intraoperative intra-
metabolism. Very low fresh gas flow venous agents such as an opioid, benzo-
anesthesia can be safely practiced with diazepine, and general anaesthetic in-
Desflurane, limiting the increased cost duction agent (e.g., propofol). These
of Desflurane when compared to will also contribute to the depth of
Halothane and Isoflurane. anaesthesia for this patient. Repeated
assessments for inadequate anaesthesia
Clinical Note: or excessive depth of anaesthesia are
How do we know if the patient is re- made during the surgery, and correspon-
ceiving enough anaesthetic? ding corrective adjustments in the an-

Page 106
) Cl~npter 13 In/ralationa/ Annestlretic Agents.
1
aesthetic depth are made. These are
) based on the patients vital signs, tearing,
i or obvious movement (see chapter 10;
1 monitoring in anaesthesia).
) References:
)
1. Miller R.D.editor. Anesthesia third
) edition. Churchill Livingstone Inc.
) 1990.
) 2. Barash PG, Cullen BF, Stoelting
RK., editors. . Clinical Anesthesia
) second edition. J.B. Lippincott Co.,
) Philadelphia 1993.
3. Elliot RD. What can gas monitoring
) tell us? Winterlude symposium on
) monitoring and equipment. Univer-
sity of Ottawa 1994.
1
1
) Notes:

** Must Know * Slrould Know Page 107


inaesthesia for Medical Students
1

Narcotic Agonists
and Antagonists
Opium is derived from the dried juice mediation of the analgesic and anaes-
of the poppy plant, which contains over
twenty plant alkaloids, including mor-
phine, and codeine. An opiate refers to ' p M u ) receptor
any preparation from, or derivative of, Analgesia, respiratory depression,
opium. A narcotic refers to any sub-
euphoria, physical dependence
stance that produces both analgesia and
stupor, and includes both opium alka- K (Kappa) receptor
loid derivatives and synthetic analgesic
compounds. Analgesia, sedation, respiratory
depression, miosis
In this chapter, we shall present 5 com- . a (Sigma) receptor
monly used intraoperative anaesthetic
narcotics: morphine, meperidine, Dysphoria, hallucinations,
fentanyl, sufentanil, and alfentanil. tachypnea, tachycardia
Chapter 16 reviews other narcotic and
non narcotic analgesic agents useful in
managing acute postoperative pain. The thetic properties of narcotics. The
properties of naloxone, a pure narcotic effects of stimulation of mu (p),kappa
antagonist are presented at the end of (K), and sigma (a) receptors are sum-
this chapter. marized in the table below.
Features common to all narcotics
Site of Action: include a dose related depression of
Opioid receptors are predominately respiration, sensorium, and pain percep-
located in the brain stem, spinal cord, tion. They are rapidly distributed
and gastrointestinal tract. Narcotics through the body following intravenous
exert their analgesic action by interact- injection. Hepatic metabolism is the
ing with opioid receptors in the brain- primary route of elimination and the
stem (amygdala, corpus striatum, peri- majority of inactive metabolites are
aqueductal gray matter, and medulla), excreted unchanged in the urine. A
and in the substantia gelatinosa in the systems review of the other
spinal cord. Three classes of opioid pharmacodynamic properties of nar-
receptors are primarily involved with cotics is presented below.

Page 108
j
Chapter 14 Narcotic Agonists and Antagonisls
1
CNS: in both the blood pressure and SVR.
Opioids produce both sedation and Synthetic opioids, such as fentanyl and
interfere with the sensory perception of its related congeners, are less likely to
painful stimuli, Although large doses of release histamine. Opioids produce
opioids produce unconsciousness, they bradycardia by stimulating the vagal
are generally incapable of providing nucleus in the brainstem. Meperidine,
complete anaesthesia, and cannot guar- unlike other narcotics, does not produce
antee total amnesia. Dysphoric reac- bradycardia and may cause significant
tions rather than euphoria may occur cardiac depression due to its direct
when opioids are administered to negative ionotropic activity.
patients who are not experiencing pain.
Stimulation of the chemoreceptor trigger GIIGU:
zone by narcotics may result in nausea Narcotics slow gastrointestinal mobility
and emesis. and may result in constipatibn or
postoperative ileus. All narcotics
RESP: increase biliary tract tone and may
Narcotics result in a depression of the precipitate biliary colic in patients with
respiratory rate and minute ventilation cholelithiasis. By increasing the tone of
accompanied by an increase in the tidal the bladder sphincter, opioids may pre-
volume. The result is a slow deep cipitate postoperative urinary retention.
respiratory pattern. The extent of res- Other, less common, side effects of
piratory depression is dose related and opioids includes anaphylactic reactions,
reversible with the narcotic antagonist bronchospasm, chest wall rigidity, and
naloxone. An increase in minute venti- puritis.
lation normally corrects any increase in
arterial carbon dioxide tension. Nar- Fentanyl, sufentanil, and alfentanil are
cotics depress this response and elevated the most common narcotic agents used
levels of PaC02 may accompany the during induction and maintenance of
administration of narcotics. anaesthesia. This is due to their rapid
onset, and predictable duration of
cvs: action.
Opioids have little to no myocardial
depressant effects even when adminis- Morphine may be used in the peri-
tered in high doses. Supplementation operative period to provide long lasting
with either nitrous oxide or benzo- analgesia. It should be administered
diazepines may depress cardiac output. slowly at a rate not exceeding 5 m g per
Narcotics decrease systemic vascular minute t o avoid excessive histamine
resistance (SVR) by either decreasing release.
sympathetic outflow or, in the case of
morphine and meperidine, by direct Meperidine is less commonly used for
release of histamine. Morphine and induction and maintenance of anaes-
meperidine's tendency to release hista- thesia because of its negative ionotropic
mine produces vasodilation with a fall activity. Hallucinations and nausea are

** Must Know * S/~ouldKnow Page 109


Anaesthesia for Medical Studen&

Table 14.1: Comparison of common intraoperative narcotic agonist potencies


and doses.
The 'low dose' schedule represents typical doses administered in divided increments
intravenously for perioperative analgesia with inhalational agents when extubation is
planned at the end of the procedure.
The 'moderate dose' schedule represents opioid doses used in combination with a
nitrous oxide - relaxant technique, when extubation of the patient is planned within
the next four hours.
The 'high dose' technique is used to induce anaesthesia in patients for whom
prolonged postoperative ventilation is planned.

more common with meperidine than due to its redistribution from the CNS
with morphine. Normeperidine is an to other tissue sites in the body.
active metabolite of meperidine, which
has only half of meperidine's analgesic Sufentanil is the most potent narcotic
activity. Normeperidine may cause that is in clinical use today. It has a
CNS excitation. In patients receiving much smaller volume of distribution
large amounts of meperidine for pro- than fentanyl, and is ideally suited for
longed periods of time, or in patients intravenous infusion techniques during
with renal insufficiency, normeperidine longer procedures. Infusion rates of 0.1
levels may rise significantly and seizure to 0.5 mcg/kg/hr are appropriate for
activity may result. anaesthesia with a? inhalational anaes-
thetic agent (balanced anaesthesia).
Fentanyl is much more potent than
morphine, and because of its high lipid Alfentanil has a rapid onset and rapid
solubility, it has a rapid onset in action. recovery and is ideally suited for short
Fentanyl's short duration of action is procedures requiring intense analgesia.

Page 110
Chapter 14 Narcotic Agonists and Antagonists

) It has a small volume of distribution With the exception of using a single 1


and does not accumulate in significant ' ' mcg/kg bolus intravenous injection
) amounts in the body. An intravenous during induction of general anesthesia,
) loading dose of 15 - 30 mcglkg i.v. may intravenous bolus administration of
) be followed with an intravenous infu- remifentanil should only be used in
sion rate of 0.25 to 1.5 mcg/kg/min to intubated patients during general
maintain analgesic plasma levels. Intra- anesthesia. Remifentanil is ideally
) venous intermittent bolus doses of 5 - suited for administration with an intra-
10 mcglkg iv may be used to respond to venous infusion pump. Infusion doses
) varying intensities of surgical stimula- -
of 0.1 2 ug/kg/min with supplemental
) tion, while the infusion rate is adjusted. bolus doses of 0.5 - 1 ug/kg are recom-
Discontinuation of the infusion 15 - 20 mended during general anesthesia with
)
minutes prior to the end of the surgical 66% nitrous oxide in healthy adults.
) procedure permits rapid'patient awaken-
) ing for extubation. The rapid offset in action means that
within 5 - 10 minutes after stopping an
) Remifentanil: infusion there will be no residual anal-
) gesic activity. Patients who are antici-

'
)
Remifentanil is the newest addition to
our clinically available opioids. It is
classified as an ultra-short acting opioid
pated to have postoperative pain, must
have other measures (local anesthesia,
NSAID's, long acting opioid administra-
) agonist, and has both a rapid onset and tion, etc.), instituted to avoid sudden
peak effect. Adverse side effects such pain after discontinuing a remifentanil
) as hypotension, bradycardia, muscle infusion.
) rigidity, and respiratory depression or
arrest, may be more pronounced with Narcotic Antagonists*:
) remifentanil compared to other opioids Naloxone (Narcan@) is a pure narcotic
) because of it's rapid onset of action. antagonist, which competes with opioids
) These side effects are dose and rate of at the mu, delta, kappa and sigma
administration dependant and can be receptors. Naloxone is supplied in
) reversed with naloxone. ampules of 0.02 mg/ml, 0.4 mg/ml, and
1 1 mg/ml. The 0.4 mg/ml and 1 mg/ml
Remjfentanil should only be adminis- ampules should be diluted with saline to
) tered by persons specifically trained in provide a concentration of 0.04 to 0.05
) the use of anesthestic drugs, and in the mg/ml for ease of administration.
) recognition and management of it's
adverse effects. Immediate measures Naloxone reaches its peak effect within
) including the ability to establish and 1 - 2 minutes of intravenous administra-
) maintain a patent airway and institute tion, and has a duration of 30 to 60
controlled ventilationand cardio-respira- minutes. Perioperative surgical patients,
) tory resuscitation must be available with evidence of excessive sedation or
when administering remifentanil. respiratory depression secondary to
opioids, may be given small incremental

** Must Know Should Know Page I l l


)
Anaertltesia for Medical Students

doses of naloxone of 40 mcg Notes:


Sudden reversal of the analgesic effects
of opioids, however, may result if high
doses of naloxone are given. The sub-
sequent abrupt return of pain can result
in hypertension, tachycardia, pulmonary
edema, ventricular dysrhythmias, and
cardiac arrest. Continuous infusions of
3 to 10 mcglkg/hr of naloxone may be
required if sedation or respiratory de-
pression recur.

References:

1. Bailey PL, Stanley. Narcotic intra-


venous anesthetics. In: Anesthesia.
Third edition. Miller RD., ed.
Churchill Livingstone Inc. 1990.

2. Hickle RS. Administration of gen-


eral anesthesia. In: Clinical anaes-
thesia procedures of the
Massachusetts General Hospital.
Third edition. Firestone LL,
Lebowitz PW, Cook CE., ed. Little,
Brown and Company 1988.

3. Barash PG, Cullen BF, Stoelting RK.


Opioids. In: Clinical anesthesia.
Second edition. JB Lippincott Co.,
1993.

Notes:

Page 112
Local and Regional
Anaesthesia
Ann Lui M.D., FRCPC

INTRODUCTION ibly block impulse conduction in nerve


fibers. The molecular structure of most
Local and regional anaesthesia plays an local anaesthetics consists of an aro-
important role in modern anaesthetic matic group linked to a hydrophillic
management. This form of anaesthesia amine by either an amide link (amino
may be used as an alternative to general amides) or an ester link (amino esters).
anaesthesia, or may be used in combina- Esters are hydrolysed in the blood by
tion with general anaesthesia in the hope plasma cholinesterase with the form-
of reducing the severity of the perioper- ation of paraaminobenzoic acid, a
ative surgical stress response. While metabolite to which some patients are
numerous local anaesthetics (LA) are
available for use by the clinician, this
chapter will focus on three commonly
used LA'S; Lidocaine, bupivicaine, and
chlorprocaine. These three agents illus-
trate differences in the classification,
potency and duration of local an-
aesthetics. Understanding these agents
provides a basis for understanding other
local anaesthetic agents that you may
use in the future.

LOCAL ANAESTHETICS

Over the next two clinical years you are


likely to encounter and use local anaes-
thetics in many clinical settings. Minor
procedures in the emergency room, Figure 15.1: Hydrolysis of an ester
topical application for eye examination, local anaesthetic by plasma
and local infiltration for diagnostic and cholinesterase. Amide local
therapeutic procedures, are a few com- anaesthetics undergo metabolism in the
mon uses of local anaesthetic agents. liver. Adapted with permission from
Tucker, GT. Biotransformation and
toxicity of local anaesthetics. Acta
Local anaesthetics are drugs that revers-
\fhaesthesiol. Beig., [Supp.];123,1975J
** Musl Know Should Know Page 113
, )
Anaesthesia for Medical Students
1
allergic. Unlike ester local anaesthetics, penetrated the nerve membrane, LA'S
amides areemetabolized in the liver and that bind strongly to the membranes
are rarely associated with allergic reac- protein globules will inhibit sodium flux
tions. across the nerve membrane for a long
period of time. Clinically, we observe
Mechanism of Action* a long duration of action when the
protein binding of a LA is strong.
The mechanism of action of local anaes-
thetics is not fully understood but most The onset of action of the LA is primar-
likely involves a dynamic interaction ily influenced by its pKa. The pKa can
with the sodium channel on the axo- be thought of as the pH at which 50%
plasmic (inner surface) of the nerve of the LA is in the charged cationic
membrane. form (BHt) and 50% is in the "n-
charged (B) base form.
The nerve cell relies on concentration (BHt r. B + Ht )
gradients of ions across its membranes,
andselective permeation of ions through When a local anaesthetic is injected into
its membranes as a basis for maintaining tissues, it establishes an equilibrium
an electrical potential and generating an between its two forms (BHt, and B)
electrical impulse. The generation of which depends on the local pH. In
nerve impulses is dependent on the flow order for the LA to move through the
of specific ionic currents through chan- tissues and nerve sheath, it must be in
nels that span the nerve membrane. its uncharged base form. Hence, the
lower the pKa the higher the concentra-
The nerve membrane consists of a fluid tion of base form and the faster the
lipid bilayer interspersed with protein onset of action. In humans, the starting
globules. Local anaesthetics act by base form is almost always less than
passing through the nerve membrane to 50% since pKa's are in the range of 7.5
attach or block the sodium conducting to 8.9 and tissue pH is normally 7.4.
ion channels thereby inhibiting impulse Conversely, if you are injecting a local
generation. anaesthetic into an infected area with a
low pH, the local anaesthetic is ineffec-
We will now discuss factors that affect tive because most of the LA will be in
how fast the local anaesthetic acts the charged form and unable to pen-
(onset), how well it blocks impulse etrate the nerve membrane.
generation (potency), and how long it
will last (duration). In summary:

Agents with a high lipid solubility will Lipid solubility influences potency.
penetrate the nerve membrane easily. Protein binding influences duration.
Hence very lipid soluble agents will And Pka influences onset of action.
move in easily and will appear to be
more potent as an anaesthetic. Having Many local anaesthetics have been syn-

Page 11 4
1
Chapter 15 Local and Regional Anaesthesia
)
) thesized since the initial use of the nat- agement for labour and delivery. Such
urally.occurring cocaine for ophthalmic a block can provide excellent pain con-
) procedures. Still a search for the "ideal" trol (sensory nerve block), yet it still
) drug with the lowest toxicity and best allows the patient to move and push
clinical profile continues. The clinical during labour (minimal motor nerve
properties that are important include blockade). Hence, bupivicaine's ability
) potency, onset of action and duiation of to provide a differential nerve blockade
) action. Table 15.1 lists some of the together with its relatively long duration

'
)
commonly used local anaesthetics and
their clinical properties. Sensory nerves,
motor nerves, and autonomic nerves may
of action makes it a common choice for
epidural pain management in the obstet-
rical patient.
) all be blocked to varying degrees by
local anaesthetics. Lidocaine provides a faster onset (about
) 10 minutes) but shorter duration (about
) Bupivicaine has the ability to produce a 1 - 2 hours), as compared with bupiv-
differential nerve blockade when used icaine, which has an onset time of up to
) in dilute concentrations. This form of 30 minutes and a duration of 2 or more
) blockade is especially advantageous in hours. Memorizing the relative potencies
) obstetrical patients requiring pain man- of the drugs is generally not necessary

-
0.1 0.5 % (Epidural)
0.5 - 0.75 % (Spinal)
1
Table 15.1: Properties of three commonly used local anaesthetics wdh the manufacturer's
1 recommended marimum dose for single injection. The marimum dose may be increased by the
) addition of a vasoconstrictor such as epinephrine. The maximum recommended doses with
epinephrine are reported in brackets.
1 ** Musl Know Should Know Page 115
)
Anaesthesia for Medical Students
)
as the more potent anaesthetic agents are local anaesthetic is rapidly injected into,
commercially supplied in lower concen- or near blood vessels. To avoid these
trations (eg. 0.5% bupivicaine with a systemic side effects, inject slowly,
potency of 8, versus 2% lidocaine with aspirate to check for intravascular entry,
a relative potency of 2). consider adding a vasoconstrictor like
epinephrine, to retard vascular absorp-
Toxicity of Local Anaesthetics tion, and do not exceed the maximum
recommended dosage.
How safe are local anaestheti&? We can
distinguish the toxic effects of these Most clinicians have difficulty recalling
agents according to their local and sys- the maximum safe dose when
temic effects. administering a local anaesthetic. For-
tunately, the local anaesthetics are com-
Local toxicities of these agents include mercially prepared such that the bottle
direct injury to nervous tissue with the highest concentration of drug
(neurotoxicity), and direct injury to contains less than the maximum dosage
muscle tissue (myotoxicity). The use of for the average 70 kg adult. For
preservatives in the local anaesthetic example lidocaine's highest concentra-
solution (eg. para-aminobenzoic acid), tion for regional anaesthesia is 2% (20
and the use of a vasoconstrictor such as mg/mL). One vial's volume of 20 mL
epinephrine may increase a LA'S poten- (total 400 mg) is within the limit of the
tial neuro- and myo- toxicities. Direct maximum dosage, if epinephrine is pres-
injection of a LA into a nerve will result ent in the lidocaine. Generally, if the
in immediate severe pain and will result volume of the local anaesthetic with
in pathologic damage to the nerve. If epinephrine is restricted to a maximum
excruciating pain is experienced on of one bottle (20 mL) per adult patient,
injection of a local anaesthetic near a the clinician will remain within the safe
nerve, the injection should be immedi- limit for the total allowable dose. The
ately stopped and the needle solution can be diluted (with preserv-
repositioned. Injection of LA's into ative free saline) if a greater volume of
muscles may result in histological local anaesthetic is required.
changes in the tissues. These are, how-
ever, generally transient, reversible and The potential for systemic toxicity of
clinically insignificant. local anaesthetics increases with the
concentration of the local anaesthetic in
Systemic toxicities involve the central the blood. Absorption of LA's in the
nervous system, the cardiovascular sys- blood can be decreased by the addition
tem, and the respiratory system. Figure of a vasoconstrictor such as epinephrine
15.2 shows the positive relationship or phenylephrine. Typical concentra-
between symptoms of systemic toxicity tions of epinephrine that are used are
and increasing plasma levels of lido- 1:100,00 to 1:200:000. A 1:200,000
caine. Systemic complications are more concentration of epinephrine has 5
likely to occur when a large dose of mcg/mL of epinephrine, or 0.1 mL of

Page 116
1
Chapter 15 Local and Regional Anaesthesia

Cardiovascular collapse
-

I Unconsciousness

I
Numbness of the tongue

Figure 152: Relationshipof signs and p p t o m s of local maesthetictoxicity


to plasma concentrations of lidocaine. With permission from Covino B.O.,
Clinical pharmacology of local anaesthetics. In Neural Blockade. Cousins MJ,
\ Bridenbaugh (Eds.) 2nd edition J.B. Lippincott 1980.
) epinephrine (1 mg/mL concentration) severe cases, this may be observed as a
) added to 20 mL of LA. sudden loss of consciousness, respira-
tory arrest, or cardiovascular arrest.
) The uptake of local anaesthetics into the When the clinician administers a large
) blood will be accelerated if injected in dose of a local anaesthetic, the patient

' the proximity of 'major blood vessels


(fig. 15.3). Intercostal nerve blocks
) result in the highest peak local anaes-
should be closely monitored by main-

Intercostal Nerve Block


thetic blood concentrations, whereas
infiltrative injection achieves the lowest
4
Epidural Anaesthesia
) peak serum levels, provided direct intra-
) vascular injection is avoided.
4
Femoral/Brachial Plexus Block
) The potential for systemic toxicity is
4
Peripheral Nerve Block
) very real. High concentrations of LA in
1 the blood may result in a spectrum of 4
Local Infiltration
symptoms reflecting an initial excitation
) of the CNS followed by CNS, respira- Fig. 15.3: Regional blocks in decreasing
) tory, and cardiovascular depression. In order of systemic absorption and the poten-
tial for systemic toxic reactions.

1 ** Must Know Should Know Page 117


Anaafhesia for Medical Students .
)

Table 15.2: Treatment of Acute Local Anaesthetic Toxicity**


Ensure a clear airway. Utilize manoeuvres such as suctioning, chin lift, jaw thrust,
insertion of oral and nasal airways, and positioning the patient in
the lateral decubitus position.

Ensure adequate ventilation. Manually assist or control the patient's breathing using an Ambu
bag and mask unit. Avoid respiratory acidosis secondary to
hypoventilation, as this will increase the local anaesthetic uplake
and toxicity. If unable to control ventilation by mask, consider
intubation (may require succinylcholine 1 mg/kg iv).

Provide supplemental oxygen. Ensure the patient is receiving supplemental oxygen. Set the
ambu bag oxygen flow at 8 to 10 Vmin.

Assess the heart rate and Treat bradycardia with atropine. Initial dose of 1 mg iv., fol-
rhythm, apply monitors. lowed by 0.5 mg iv every 5 mins. to a max, of 3 mg. Use epine-
phrine as per ACLS guidelines for profound cardiovascular
collapse. Consider early electrical cardioversion for arrhythmias.

Assess the blood pressure and If the patient is hypotensive, place them in the trendelenburg
perfusion (determine respon- position. Administer an initial fluid bolus of 500 to 1000 ml of
siveness). saline or ringer's lactate. Support blood pressure with ephedrine
-
5 - 10 mg, or phenylephrine 50 mcg iv prn every 2 3 minutes.

Stop seizures. Protect the patient from physical injury during a seizure. Con-
-
sider administering 5 10 mg of diazepam iv, or 50 mg of
sodium thiopental to stop the seizure.

taining verbal contact, as well as by administration. In the case of LA toxic-


continuous ECG monitoring, pulse ity and life threatening arrhythmias,
oximetry, and blood pressure readings. bretylium is the agent of choice. Epine-
phrine can be used if indicated, accord-
Management of CNS, respiratory, and ing to the ACLS guidelines.
cardiovascular toxicity * * begins with
the ABCs (airway, breathing, and circu- REGIONAL ANAESTHESIA
lation) followed by the ACLS recom-
mendations for resuscitation. The only Many studies have examined the bene-
deviation in the algorithm is the avoid- fits of regionaI over general anaesthesia.
ance of the use of Class Ia and Ib anti- Still, there is continuing controversy
arrhythmia such as procainamide, regarding the best type of anaesthetic.
quinidine, and Iidocaine. These agents
are themselves local anaesthetics. Perhaps, what type of anaesthetic is
Hence, any local anaesthetic induced chosen may not be as important as how
arrhythmia will be exacerbated by their well the anaesthetist administers it.

Page 118
)
~ h a ~ t e15r Local and RegionalAnaesthesia .
1

Table 15.3: Reported Benefits of Regional ~naesthesia


Benefits ' Importance
Decreased perioperative nausea and , Decreased hospital stay,
emesis improved patient satisfaction

Reduced perioperative blood loss Orthopaedic surgery for total


hip arthroplasty, prostatic sur-
gery.

educed perioperative stress indicators Decreased catecholamines

Ability to monitor CNS status during Detection of myocardial


the procedure ischemia, monitoring CNS
status during prostatic surgery
(TURP syndrome) and carotid
artery surgery

Improved vascular perfusion Improved perioperative patency


of vascular grafts (eg. Femoral -
popliteal vascular graft)

Reduced deep vein thrombosis Reduced incidence of pulmon-


ary embolism

Reduced perioperative pulmonary Reduced incidence of


complications atelectasis, pneumonia

Reduced perioperative analgesic Decreased costs and side effects


requirements (pre-emptive analgesia) of other anaesthetic agents

) Table 15.3 summarizes some of the topical anaesthesia, infiltrative anaes-


) benefits of regional anaesthesia. thesia, intravenous regional anaesthesia,
peripheral neural blockade, and central
It is convenient to distinguish how local neural blockade.
I anaesthetics can be administered. The
j various routes of administration include:

** Must Know * ShouMKnow Page 119


Anaesthesia for Medical Students
i

Topical Anaesthesia may dilute the solution to give the ~ o l -


ume required to cover the area.
There are various preparations of local
anaesthetics available for topical use. Intravenous Regional Anaesthesia
They must be able to penetrate the sur- "Bier Block"
face (either mucous membrane or skin).
Cocaine 4% or 10% is often used for This technique is very useful for anaes-
anaesthetizing nasal mucosa. As this is thetizing the distal arm or leg for pro-
the only local anaesthetic that inhibits cedures of 1 hour or less. ECG, BP,
noradrenaline uptake resulting in its and oximetry monitors are applied prior
catecholamine effects it has vasocon- to performing the block. An intraven-
stricting properties that "shrink" the ous is secured in the non-operative
mucosa and effect sohe hemostasis extremity for prn drug administration
during procedures. ~idocaine2% jelly is and emergency use. A second small
Gsed for intra urethral procedures and intiavenous is inserted in the distal
catheter insertion. extremity for injection of the LA. A
tourniquet is applied to the limb and
In Canada, EMLA (a 1:l eutectic mix- tested for its ability to abolish the ex-
ture of 25 mg lidocaine and 25 mg tremities pulse by maintaining a pres-
prilocaine per gram of cream) is avail- sure of 100 mm Hg above the systolic
able in 5g or 30g tubes for application BP. The limb is elevated, wrapped with
on the skin. The cream must be applied an elastic bandage (esmarch) to ex-
under an occlusive dressing (e.g.,
tegaderm@)for more than 60 minutes to
achieve dermal analgesia to a depth of
3mm. About 5 to 10% of the drug is
absorbed systemically. EMLA is an
effective topical anaesthetic for intra-
venous catheter insertion, blood sam-
pling and minor skin surgery (e.g., laser
treatment, wart removal). This prepara-
tion'is not recommended for use on
mucous membranes.

Infiltrative Anaesthesia Figure 15.4: Intravenous regional


anaesthesia commonly referred to as
Also referred to as local infiltration, this a 'BierBlock'. Wihpermisrwn from
technique involves injection of local CovinoBG., Lambert DH. In:
anaesthetic intradermally, subcutaneously Anestheswlogyprinciples and
or in the tissue within the vicinity of the procedures. Lui PL. (ed.) JB
area of surgery. When large areas are \Lippincott Co. 199t. d

involved, avoid using more than one


bottle of local anaesthetic. Instead, one

Page 120
)
Chaprer 15 Local and Regional Anaesrh&
)
anguinate the limb, and the tourniguet is 1. Avoid intraneural injection.
j
inflated. The esmarch bandage is 2. Avoid neurotoxic agents.
) removed, loss of arterial pulse con-
) -
firmed, and a solution of 0.25 0.5% An intraneural injection can be detected
lidocaine plain (without preservative) is when patients complain of excruciating
) slowly injected in the operative limb's pain in the distribution of the affected
) iv, (max. 3 mg/kg). The local anaes- nerve at the start of the injection. Stop
thetic diffuses from the venous vascular and withdraw the needle if this occurs.
) bed into the tissues to provide operative Intraneural injection of less than 0.5 ml
) anaesthesia within 5 minutes. Care must of solution can raise intraneural pres-
) .be taken to ensure proper function of the sures to ischemic levels resulting in
tourniquet if success is to be achieved permanent damage. Use an atraumatic
) and a sudden iv infusion of lidocaine is needle; one specifically designed for
) to be avoided. A minimum of 20 min- nerve blockade, the nerve tends to "roll

'
)
utes tourniquet time'is needed to allow
adequate tissue uptake of the local an-
aesthetic to avoid toxic reactions on
off" the blunt end of these needles,
rather than being impaled.

) deflation of the tourniquet. The tech- Most preservatives contained in the


nique is illustrated in figurk 15.4. local anaesthetic solutions have the
) potential to be neurotoxic. All solutions
) Peripheral Nerve Blockade selected for peripheral nerve block (incl-
uding the normal saline used for dilut-
Local anaesthetics can be deposited ing the solutions) should, therefore, be
close to individual nerves (e.g., the ulnar free of preservatives as indicated on
nerve, median nerve, or femoral nerve), the bottle.
or to the nerve plexus (e.g., brachial
plexus and lumbosacral plexus). A thor- Central Neural Blockade
ough knowledge of the anatomy of the
peripheral nervous system is important Central neural blockade refers to either
to locate the site of injection as well as epidural or spinal anaesthesia. Epidural
to determine whether the technique will anaesthesia involves injecting drugs into
provide adequate anaesthesia for the the epidural space, which lies between
surgical site. There are many well illus- the ligamentum flavum and the dura
trated texts and workshops that describe mater, exterior to the spinal fluid. Spi-
each nerve or plexus block that can be nal anaesthesia involves passing a
used as a guide. The most devastating needle through the epidural space,
complication of peripheral nerve block- through the dura and into the CSF
ade is nerve injury which can be mini- (intrathecal) space, see figure 15.5 and
mized if two cardinal rules* are 15.6.
practiced:
In spinal anaesthesia, the local anaes-
thetic is injected into the subarachnoid

* Should Know Page 121


Anaesthesia for Medical Students

Needle In Subarachnold Space

Needle in Epidural Space

Ugamentum Flavum

Filum Terminale

Figures 15.5 and 15.6: Sagittal and


cross sections demonstrating the
relationship of the epidural space to the
subarachnoid space. Both epidural and
spinal needle placement is shown.
Adapted with permission from Raj Pl?
In: Handbook of regional anesthesia.
Churchill Livingstone inc. 1985.

Page 122
)
Chapter 15 Local and Regional ~ n a k h e s i a
) .
) space (CSF containing space), where it requires 5 - 10 times the amount of LA

' is in direct contact with the "bare" nerve


roots. By contrast, local anaesthetics
) administered in the epidural space must
that would be used for spinal anaesthe-
sia.

) pass through the myelin sheaths Continuous infusions of local anaes-


.covering the nerve roots. The dura acts thetics and .opioids into. the epidural
1 as a barrier to epidural LA'S moving into space can be used intraoperatively and
) the CSF space. Local anaesthetics that continued postoperatively. Both spinal
contact the nerves directly, as in spinal and epidural anaesthesia affect motor,
) anaesthesia, produce a very rapid and sensory and sympathetic nerves in the
) intense nerve block. By contrast, neural axis. Nerve blockade of the
epidural anaesthesia has a slower onset sympathetic nervous system results in
)
because the nerves are, in a sense insu- vasodilation, which in turn decreases
) lated, and it produces a less intensk venous'return, stroke volume and car- '

1. block. Epidural anaesthesia typically diac output. If this produces

Table 15.4: Spinal and Epidural Anaesthesia


ContraindicationsL Complications
Patient refusal Inadequate anaesthesia
Lack of resuscitative equipment Excessive anaesthesia
Lack of knowledge of procedure - 'High block' with potential
Coagulopathy respiratory insufficiency and
Previous back surgery (relative) cardiovascular collapse.
Raised intracranial pressure Sympathetic blockade (hypotension)
Fixed cardiac output: Dural puncture (headache)
- severe aortic or mitral stenosis Injury:
- IHSS -.muscles, ligaments, bone
Pre-existing neurologic disease (back pain)
- ALS, Multiple sclerosis - nerve root or spinal cord
(nerve deficit)
- epidural vien (epidural hematoma)
- anterior spinal artery
(nerve deficit)
Infection:
- bone (osteitis)
- epidural space (epidural abscess)
- CSF (meningitis)
Inadvertent intravascular injection of
local anaesthetic: see text re: local
anaesthetic toxicity.

1 ** Musl Know Should Know Page 123


. ....
Anaesthesia for Medical Students

hypotension, it is first treated with fluid Injury to the muscles, ligaments, and
boluses and, if necessary a sympatho- bone may result in transient discomfort,
mimetic drug such as ephedrine (see that can be treated with oral analgesics
chapter 22). and rest. An injury to a nerve root or
the spinal cord is very rare. The awake
Sympathetic blockade of the cardio- patient will experience severe pain if the
accelerator fibres at levels T 1 to T4 can spinal cord or a nerve root is touched,
result in unopposed vagal effects causing at which point the clinician should
bradycardia, or even asystole. Progress- reposition the needle, to avoid perma-
ive bradycardia and hypotension under nent injury. As the spinal cord termin-
spinal anaesthesia are warning signs that ates between the 1st and 2nd lumbar
suggest the block may be reaching the vertebral body in adults, insertion of an
cardioaccelerator fibres. A combination epidural or spinal needle in the low
of intravenous fluids, atropine, lumbar region (i.e., L3 - L4)reduces the
ephedrine, or phenylephrine ought to be. ' risk of direct damage to the spinal
used to treat these hemodynamic abnor- cord.
malities as soon as they are recognized.
Whenever the dura is punctured, there is
Nevertheless, misconceptions and un- a ' risk that the patient will develop a
warranted concern about complications postural headache, referred to as a
of epidural and spinal anaesthesia are. "dural pu~ictureheadache". The dura is
common in both the lay and medical intentionally punctured when per--
profession. The risks of a life threaten- forming spinal anaesthesia, it may be
ing or debilitating complication occur- inadvertent]y punctured with an epidural
ring after epidural or spinal anaesthesia needle if the needle is advanced past the
are probably less than the risks we take epidural space. The chance of a dural
when we ride in our car. Table 15.4 puncture headache varies with the size
lists the contraindications and potential and type of needle used, direction of the
complications of central neural blockade. bevel, and age of the patient. For
instance, young patients who have their
The discomfort experienced with the dura punctured with a large bore (16 ga.
performance of an epidural or spinal epidural needle) have about a 60%
block is comparable to that experienced chance of developing a headache. This
when an intravenous is inserted. If headache may be quite debilitating and
inadequate local anaesthesia is used to persist for two or more weeks. Some-
perform the block, or if musculoskeletal times another procedure called an
abnormalities are present, finding the "epidural blood patchn is required to
epidural or intrathecal space may be treat this headache.
more difficult. In this situation, pain
may be experienced from injury to the The risk of an inadvertent dural punc-
adjacent muscles, ligaments, bone, nerve ture when an epidural is performed is
roots, or spinal cord. approximately 1:100 to 1:200 patients.
Young patients having a dural puncture

Page 124
Chapter 15 Local and Regional Anaesthesia

for spinal anaesthesia with a small two greatest causes of morbidity and
needle (eg. 27 ga. needle) have a 1 - 3 mortality in pregnant patients having a
). % chance of developing a headache. general anaesthetic are aspiration of
) ~ l d e rpatients
l~ do not seem to be prone gastric contents and the failure to
to this complication. intubate, both of which are avoided by
using regional anaesthesia.
) Permanent neurologic damage following
) central neural blockade is very rare. References:
This can dccur if: direct nerve trauma
) occurs, infection is introduced into the 1. Cousins MJ, Bridenbaugh PO. (ed.)
) .spinal canal, a neurotoxic drug is Neural Blockade in Clinical
iiijected by mistake, or an epidural. Anesthesia and Management of
) hematoma develops and compresses the Pain. ' Second Edition. JB
.nerve roots. Historically there are Lippincott Co.1988.
1 reports of paraplegia following the use
of epidural or spinal anaesthetics con- 2. Miller RD. (ed) Anesthesia. Third
) taminated with neurotoxic chemicals or Edition. Churchill Livingstone Inc.
) with bacteria. Despite this, the currently 1990.

' available local anaesthetics are safe


when used in' the appropriate doses. Notes:

Although extra care should be taken


when inserting an epidural or spinal
anaesthetic in the patient with low back
pain,'this is not a contraindication to
performing the block. Moreover, the
incidence of postoperative low back pain
in patients who had regional as
compared to general anaesthesia is not
significantly different. In fact, patients
with chronic back pain problems benefit
from epidural injections of local anaes-
thetics and steroids.

Undoubtedly, some risk is associated


with any form of anaesthesia. Still the
risks of general anaesthesia are greater
than those for central neural blockade in
some cases. For example, epidural or
spinal anaesthesia are preferred to gen-
eral anaesthesia for caesarean sections.
This is because we recognize that the

Should Know Page 125


Acute Pain
Management
JOHN PENNINGM.D., FRCPC
specialists in pain management regard
intramuscular opioid administration as a
The last few decades has brought vast technique that provides inferior pain
improvements in the understanding and control when compared to other tech-
management of acute pain. Many new niques currently available.
and effective treatment modalities are
now available, including patient con- This discrepancy between recommended
trolled analgesia (PCA) and administra- and actual pain management techniques,
tion of neuraxial (epidural or spinal) spurred the American Agency for Health
opioids. Anaesthesiologists are highly Care Policy and Research Development
knowledgeable in opioid pharmacology, towards developing clinical practice
and are experts at spinal and epidural guidelines for acute pain -management.
drug delivery. In the 1980's, acute pain This extensive work involved the review
services were developed under the direc- of thousands of articles and consultation
tion of the departments of anaesthes- with hundreds of leading world experts.
iology and nursing, at leading centres The results were published in February
throughout the world. We have learned 1992 under the title: "cute Pain Man-
that acute painmanagement is attainable agement: Operative or Medical Pro-
and that the optimization of acute pain cedures and ~rauma'". This well
management leads to better patient regarded clinical practice guideline
outcome and shorter hospital stays. promises to set the standard in pain
Poorly controlled acute pain is causally management for 1990's.
related to perioperative morbidity and
mortality. The investment in acute pain We will now proceed with a review of
management has been cost effective for some basic neurophysiology of acute
both hospitals and society as a whole. pain. Following this, we shall review
the principles of analgesia therapy with
Despite remarkable progress in certain PC& neuraxial opioids and non
centres in the management of acute steroidal anti-inflammatory drugs
pain, intramuscular morphine or (NS AIDS).
meperidine on an as needed @.rn.)
basis remain the most popular form of
acute postoperative pain management at
most Canadian hospitals. Even so,

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Chapter 16 Acute Pain Management

Nociception refers to the detection,


transduction and transmission of A goal of all health care providers
noxious stimuli. Substances generated should be to provide optimal acute pain
from thermal, mechanical or chemical management. Indeed, some of the mor-
tissue damage, activate free nerve end- bidity and mortality that patients experi-
ings, which we refer to as nociceptors. ence after trauma or major surgery may
These peripheral afferent neurons have be the final result of the pathological
their cell body located in the dorsal root disturbances that are initiated by severe
ganglion and send axonal projections and poorly controlled acute pain.
into the dorsal horn and other areas of
the spinal cord (figure 16.1). Synapses Patients with large chest wall or abdo-
occur with a second order afferent minal incisions, who do not receive
neuron, as well as with regulatory adequate acute pain control, experience
interneurons. In addition, synapses significant chest, abdominal and
occur with the cell bodies of the sym- diaphragmatic muscle splinting that
pathetic nervous system and ventral limits their ability to breathe deeply and
motor nuclei, either directly or through to cough. This impairs their ability to
the internuncial neurons. These circuits clear airway secretions. The patient is
are important for understanding the rendered prone to atelectasis (collapse
reflex sympathetic and motor responses of segmental lung regions), which
that result from segmental afferent increases the risk of hypoxemia and
nociceptive input to the spinal cord. pneumonia. This muscle splinting is a
reflex response to acute pain stimuli at
The cell body of the second order the level of the spinal cord. It can be
neuron lies in the dorsal horn. Axonal prevented or alleviated by appropriate
projections of this neuron cross to the analgesic therapy.
contralateral hemisphere of the spinal
cord and ascend to the level of the The barrage of nociceptive stimuli
thalamus. Along the way, this neuron reaching the spinal cord also initiates
divides and sends axonal branches that spinally and supra-spinally mediated
synapse in the regions of the reticular reflex increases in sympathetic tone.
formation, nucleus raphe magnus, peri- This results in hypertension,
aqueductal gray, and other areas of the tachycardia, increased contractility and
brain stem. In the thalamus, the second an increase in the work demanded of
order neuron synapses with a third order the heart. If this occurs in a setting of
afferent neuron, which sends axonal decreased oxygen supply, due to blood
projections into the sensory cortex. loss and decreased lung efficiency,
myocardial ischemia, congestive heart
failure and myocardial infarction may
result.

Should Know Page 127


Anaesthesia for Medical Smdents

The increased sympathetic tone during Poorly controlled acute pain plays a
acute pain also increases intestinal se- significant role in initiating and main-
cretions, slows gut motility, and taining the stress-response associated
increases smooth muscle tone. These with the trauma of major surgery. This
changes may lead to gastric stasis with response includes the development of a
nausea, vomiting, ileus and urinary hyper-coagulable state, which can lead
retention. to deep vein thrombosis, pulmonary

I Perlaqueductal Gray

1 Reticular Formation

SplnothalamlcTract

Dorsal Horn Ganglia

Substantla Gelatlnosa

Figure 16.1 Afferent sensory pathways for detectlon and transmission of


noclceptlve Impulses. Modifled wlth permission from Lubenow TR,
McCarthy RJ, lvankovich AD: Management of acute postoperatlw pain. In
Barash PG, Cullen BF, Stoelting RK (eds): Clinical Anesthesla, 2 n d ed.
Philadelphia: JB Uppincott, 1992.

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I
Chapter 16 Acute Pain Management

embolism and myocardial infarction in capable of diffusing across the synapse,


the postoperative period. Further binding to the specific synaptic
changes associated with the stress receptors and causing depolarization of
response to trauma include decreased the secondary neuron. Substance "P" is
immunocompetence, hyper-metabolism a neuropeptide that acts as a
and mobilization of energy stores. neurotransmitter in this fashion. There
These responses explain the tendency are several neurotransmitter substances
toward hyperglycemia and large net released by modulatory neurons within
protein losses that sometimes delay the substantia gelatinosa that dampen
wound healing. transmission either by impairing the
release of the neurotransmitter (such as
substance "P") or by rendering the
neuron's post-junctionalmembrane more
Afferent neurons transmit information difficult to depolarize.
from peripheral pain receptors to the
CNS. Efferent neurons descend from Examples of such modulatory
the brainstem to the dorsal horn to neurotransmitters include: endorphins
decrease incoming nociceptive informa- and enkephalins, norepinephrine,
tion. serotonin, and gamma amino butyric
acid. Pain killers, such as the opioid
The peripheral and central components narcotics (morphine,meperidine), mimic
of the nervous system that serve to the action of the body's own pain killers
detect, transduce and transmit (endorphins, enkephalins) by dampening
nociceptive signals are subject to control the afferent pain signals being trans-
from higher centres within the CNS. mitted to the CNS.
This serves in a negative feed-back
fashion to limit the amount of afferent There are also occasions when signals
nociceptive stimulation that can be are amplified rather than dampened.
perceived as pain. Modulation can Although the mechanisms involved are
occur either in the periphery or at any complex, the important principle is that
point where synaptic transmission the system is not static. It does not
occurs. Anatomically, the most import- function like a hard wired electrical
ant site where modulation occurs is in circuit board. The system is dynamic
the outer layers of the dorsal horn, and subject to change in how the
named the substantia gelatinosa. This is nociceptive signals are handled. Inves-
where the synapse between the primary tigators have coined the term neuronal
afferent sensory neuron and the second- plasticity, to underscore this principle.
ary afferent sensory neuron occurs.

Propagation of a sensory impulse from


the primary to the secondary sensory This highly effective class of analgesics
neuron depends on the release of an operates at several levels in the nervous
adequate amount of neurotransmitter system. They directly dampen the

** Must Know * Should K n o w Page 129


Anaesthesia for Medical Students

transmission of nociception across the (im.) opioids, every three to four hours,
synapse between primary and secondary results in a cyclical pattern of peaks and
nociceptive afferent neurons in the troughs in the serum opioid levels.
dorsal horn by binding to pre-synaptic, There is a significant time delay
post-synaptic or interneuron opioid between the im. administration and the
receptors within the substantia attainment of adequate pain relief due to
gelatinosa of the dorsal horn. the slow and variable rate of drug ab-
sorption from the im. depot. Austin et
They activate descending efferent al. found that the average peak serum
modulatory pathways, resulting in the level after 100 mg of meperidine
release of inhibitory neurotransmitters (~emerol? occurred 44 minutes after
such as noradrenaline, serotonin and -
im. administration (range 15 110 min-
GABA. These efferent modulatory utes). They also noted a five fold vari-
neurons originate in the brain stem (is., ability in the maximum concentration
peri-aqueductal grey) and travel down attained and a three fold variability in
the spinal cord in the dorsolateral fasci- the minimum effective serum concentra-
culus to terminate in the dorsal horn tion for meperidine. This 3 to 4 fold
(figure 163). inter-patient variability in the minimum
effective drug concentration has also
Opioids inhibit the inflammatory been observed for other opioids. Hence
response in the periphery and decrease after im. opioid injections, the peak
hyperalgesia. Opioids also affect mood concentrations attained are often sub
and anxiety by their activity at opioid therapeutic.
receptors in the limbic regions of the
brain. This helps alleviate the affective Those patients who do have adequate
component of the perceived pain. analgesia at peak levels are still subject
to sub-therapeutic levels during the
Oral analgesics are generally limited for trough portions of the serum opioid
use in patients with mild postoperative -
cycle, which accounts for 30 50% of
pain. Moderate to severe acute the time. This is especially true in the
postoperative pain is poorly controlled early post-operative period when the
with oral analgesics alone. This is due pain is the most intense and the drug
to their prolonged time to reach peak levels fall quickly due to a rapid redis-
effect, lack of flexibility in titration, and tribution within the patient's central
dependence on a functional GI tract. compartment.

INTRAMUSCULAROPIOID Hiah incidence of side effects:


ADMINISTRATION: When opioids are administered intermit-
LIMITATIONS
DUE TO tently (every 3 to 4 hours) by im. injec-
PHARMACOLOGICPRINCIPLES tion, the therapeutic window during
which the effective concentration of the
Inadeauate analgesia: The intermit- drug is reached, may last only a fraction
tent administration of intramuscular of the time between injections. This
Chapter 16 Acute Pain Management

reflects the large variability among quence of having too little drug is pain
patients in the maximum drug level with all of its adverse sequelae. The
reached in the blood after im. injec- side effects of too much opioid in the
tions, and the large variability in the system are sedation, respiratory depress-
effective drug concentration among ion, puritis, and an increased incidence
patients (see figure 16.4). The conse- of nausea and vomiting.

PerlaquedoctalGray

Reticular Formation

) Nucleus Raphe Magnus


)
)
) Dorsolateral Fasciculus

)
Dorsal Root Ganglia

1
) i
Flgum 16.2 Efferent pathways Invoked in noclcepttve ngulatbn. Modified
)
with permission from Lubenow TR, McCarthy RJ, lvankovich AD:
Management of acute postoperative pain. in Barash PG, Culien BF,
)
Stoeitlng RK (eds): Cllnlcal Anesthesia, 2nd ed. Phlladelphla: JB
Upplncott, 1992:1548.

)
** Must Know Should Know Page 131
)
INFUSION:
OPIOIDSB Y CONTINUOUS of being simple and avoids repeated and
painful im. injections. Unfortunately,
This approach generally provides post- as with im. opioids, this modality lacks
operative analgesia that is superior to sufficient flexibility. The maximum
prn im. injections. It has the advantage rate of drug delivery allowable is often

Biofeedback, education
Tricyclic antidepressants
Relaxationtechniques
Laughter, psychotherapy
Bralndem: (opioid maptors)
Rostral spread of epidural, spinal opiolds
Oral, I.m., i.v. narcotics via biood brain ba
Antimnvulsants phenytoin, Carbarnazeplne)
(Chronic paln disorders see c h 17)

Alpha adrenergic blockers (Cionldine)


(periaqueductal g

Epldural and Spinal:


N m t i c s (spinal opiold receptors)
Local anaesthetics
Uectrlcal stimulation

Peripheral Nerve:
Peripheral Nerve 81

Local:
Anaesthetic
Infiltration
AS& NSAIDs,
Physicaltherapy:
(excercise, whirlpool,
Accupuncture
massage).
(Gate theory of Pain) t
Figure 16.3: Therapeutic Interventionsfor Pain Management According
to Anatomic Location.

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Chapter I6 Acute Pain Management

Respiratory
Depression

8 Sedation
g
8
it3 Analgesia
B
m
Pain

1 2 3 4 5 6 7 8 9
Time (hours)
Figure 16.4: Wide fluctuations in serum opioid concentrations are associated with
their intermittent intramuscular administration. This results in periods of
over-sedation alternating with periods of poor pain control. By contrast, intravenous
PCA opioid administration can be rapidly adjusted by the patient. This permits
analgesic concentrations of opioids in the serum to be maintained for prolonged
periods of time.

insufficient, especially early in the acute achieve analgesic levels. A continuous


post-operative period when the drug infusion will then maintain stable
may redistribute quickly away from the plasma levels.
therapeutic site in the CNS to the peri-
pheral compartment. However, after A continuous opioid intravenous infu-
several hours, the tissues can become sion is not able to respond to break-
saturated and the serum drug levels through pain occurring during periods
may begin to rise to dangerous levels. of ambulation, or chest physiotherapy.
This means that closer nursing supervi- Adjustment of the infusion rate may
sion must be supplied for patients that take hours to reach the effective anal-
are on continuous opioid infusions than gesic concentration, (typically 4 5 -
patients on intravenous patient con- times the drugs half life to reach a
trolled analgesia (i.v. PCA). Patients in steady state). By contrast, i.v. PCA
acute pain starting o n a continuous plasma levels can be temporarily
infusion of an opioid will require an increased when the patient requests
initial bolus loading dose to quickly additional doses, allowing the effective

** Must Know Should Know Page 133


j
Anaesthesia for Medical Students
1
concentration to be reached within min- lowing a typical PCA bolus of opioid
utes. drug.

In centres without a PCA service, an The rapid onset of analgesia allows the
alternative may be a low background i.v. PCA modality to respond quickly to
infusion of narcotic (eg. morphine 0 5 - conditions where breakthrough pain
2 mg i.v. per hour), with added p.rn. may occur (e.g., chest physiotherapy or
subcutaneous injections for periods of ambulation). An appropriate bolus dose
need (eg. morphine 5 - 7 5 mg s.q. or of i.v. opioid will be smaller than an
im. q 3 hours). This avoids over seda- im. dose, but can be given more fre-
tion with high infusion rates, which is quently. An im. injection results in
especially important in patients at lower peak serum levels of drug with a
night. It is important that infusion rates delay in the peak level when compared
are decreased as pain levels decline or with an i.v. injection. An i m . injection
sedation appears. The time required to also results in a storage depot, which
achieve analgesia with this technique continues to release drug after it has
will be slower than i.v. PCA due to been administered.
time required for:
The duration of effect after an i.v. bolus
1. The patient to signal to the nurse of opioid depends upon the rate at
that pain control is inadequate. which the drug is cleared away from the
2. The nurse to draw up and administer opioid receptor sites within the CNS.
the pain medication. This is determined by the drug's ability
3. The time it takes for the opioid to to diffuse through neural tissues, a char-
be absorbed from the s.c. or im. acteristic referred to as lipophilicity.
injection site. The duration of effect is also deter-
mined by the rate at which the drug is
I.V. PCA cleared from the plasma by redistribu-
INTRAVENOUSPATIENTCONTROLLED tion, metabolism, and excretion.
ANALGESIA
Morphine with its low lipophilicity,
Pharmacoloaical asvects: The direct i.v. diffuses slowly into and out of neural
administration of an opioid results in a tissue. This results in a slower onset
rapid peak in the serum drug level. The and a longer duration of action when
time to onset of analgesia depends upon compared with other commonly used
the rate at which the opioid is able to opioids. The level of analgesia from
diffuse from plasma to the CNS, where morphine does not closely parallel mor-
binding to specific analgesia opioid phine's serum concentration because of
receptors occurs. The major factor a time lag between the concentration at
determining the diffusion of the opioid the opioid receptor and in the serum.
from the plasma to the CNS is the By contrast, more lipophilic drugs, such
drug's lipid solubility. Table 16.1 lists as meperidine and fentanyl, diffuse into
the opioid analgesia time profiles fol- and out of the CNS quickly and their

Page 134
Chapter 16 ~ c ; t ePain Management

Table 16.1: Tlme profiles for the cIlnlcal effects of 1.v. PCA oplolds.

Drug Onset (mins.) Peak Effect (mins.) Duration (mins.)


Morphine 3-6 20 - 30 40 60 -
Meperidine 2-4 8 - 12 20 30 -
Fentanyl 1-2 4-6 6 - 10
Alfentanil < 112 1-2 3-5

plasma levels reflect the opioid receptor PCA PARAMETERS:


level concentration and their clinical
effect. There are five parameters that define
PCA therapy:
In summary, i.v. PCA has the following
advantages over im. opioid injections The Loading Dose: This is gen-
for pain control: erally reserved for patients requiring
immediate pain medication. Admin-
1. Rapid onset of analgesia. istration of small bolus doses will
2. Eliminates wide fluctuations in take too long to achieve the required
plasma opioid concentrations that plasma concentrations because of
follow i m . administration (fewer the lockout interval. A typical load-
side effects with better pain control). -
ing dose is 0.1 0 2 mg/kg for mor-
3. Accommodates patient variability in phine, administered over 10 to 20
opioid dose requirements. minutes. Most postoperative
4. Accommodates changes in opioid patients will have received narcotics
requirements during the recovery during their procedure and will not
period. require a loading dose when PCA is
5. Patients benefit psychologically started after their surgery.
when they have control over pain.
6. Avoids painful im. injections. 2. The Bolus Dose: This is the
7. Decreases the risk of accidental amount of opioid delivered to the
needle-stick injury to health care patient when the patient presses the
providers. PCA demand button requesting pain
8. Improves patient-nurse relations. medication. This should be large
(The patient regards the nurse as a enough for patients to perceive an
professional who is helping them analgesic effect, but not so large
optimize PCA use, rather than that the therapeutic window is
someone who is withholding pain exceeded (resulting in side effects).
medications). For morphine, a typical bolus dose
9. May decrease morbidity and allow -
is 1 mg (range 0 5 2 mg); for
for earlier discharge from hospital. meperidine 10 mg (range 5 20 -
mg).

** Must Know Should Know Page 135


AnaMhesia for Medical Students

3. The Lockout Interval: The Maximum 4 hour Limit: Like


PCA pump is programmed to the infusion parameter, this para-
deliver another bolus dose only after meter is also not essential, but may
a specified period of time (called the be set at the physician's discretion.
lockout interval) has elapsed since It provides an extra safeguard
the last bolus dose. If a patient against a programming error, which
presses the button before the lockout may occur while setting up the PCA
interval has elapsed, a demand delivery system.
request will be recorded, however,
no drug will be delivered. This By specifying the bolus dose, lockout
allows time to elapse for the bolus interval and infusion rate, the physician
dose to have an effect (see table has already restricted the patient in the
16.1). Typical lockout intervals are total amount of drug available each
5 to 10 minutes. hour. Example: Morphine bolus 1 mg,
lockout interval 5 minutes, and an infu-
4. Continuous Infusion: In addition to sion rate of 0.5 mg per hour, restricts
giving the patient a bolus of nar- the patient to a maximum of 12.5 mg
cotic when requested, a continuous per hour. Specifying a maximum 4 hour
iv infusion can be also be adminis- limit allows the physician to set a lower
tered (ordered as PCA + continuous limit that can be delivered to the patient
infusion). Typical infusion rates for during this period. If one contrasts this
morphine (and for meperidine,) are -
with typical im. orders of 7 5 12.5 mg
- -
0.5 1.0 mg per hour and 5 10 mg of morphine every 3 - 4 hours p.r.n., it
per hour. There is debate over the is easy to see why patients on i.m.
benefits of a continuous infusion narcotics may have inadequate pain
with PCA. Proponents of this tech- control.
nique argue that it prevents patients
from waking in the night with
severe pain because they have not
received pain medication for several After the first or second postoperative
hours. Still, studies show no clear day, the decision to add oral analgesics
benefits of a continuous infusion is based on the following consider-
over PCA alone. A continuous ations:
infusion places these patients at risk
of respiratory depression and other 1. The patient is off a continuous PCA
complications of excess opioid use. infusion.
When used in the early post- 2. The patient is requesting 2 or less
operative period, we recommend PCA boluses every 4 hours.
that the infusion be discontinued 3. The patient is having no or minimal
(PCA mode alone) as soon as the pain at rest, and
patient's bolus demands decrease to 4. The patient is able to ambulate and
to 2 per four hours. tolerate oral fluids.
Chapter I 6 Acute Pain Management

Oral analgesics such as acetaminophen brain barrier is bypassed and superior


-
with codeine (Tylenol # 3" 1 2 tablets analgesia may be obtained by contrast
-
p o . every 3 4 hours prn) should be to narcotics administered by the i.v. or
started and used as the first line anal- i.m. narcotic routes. The intrathecal
gesic, and the PCA used for any addi- administration of 0.2 mg of morphine
tional breakthrough pain requirements may provide excellent analgesia for up
(Table 163). The PCA can be discon- to 16 hours after a total hip (replace-
tinued once the patient is requiring ment) arthroplasty. A similar patient
minimal PCA bolus doses and tolerating treated with i.v. PCA morphine may
the oral analgesics. The average patient require a total of 60 mg of morphine for
having major surgery requires PCA the same initial period, and still have
therapy for 2 - 3 days. inferior pain relief as compared to the
patient who received spinal narcotics.

Subarachnoid and epidural opioids are


Within the superficial layers of the active at both the spinal cord level and
substantia gelatinosa, located in the at higher CNS levels. A portion of the
dorsal horn of the spinal cord, exists a opioids administered in the intrathecal
dense population of opioid receptors. space at the lumbar level will migrate
Their activation results in a decrease in along with the CSF circulating back to
the release of neurotransmitters, such as the brainstem. As with parentally (i.v.,
substance P, and a decrease in trans- or i .m .) administered narcotics, high
mission of painful stimuli from concentrations of narcotics at the brain-
peripheral pain fibers at the level of the stem level can result in respiratory
spinal cord. depression, sedation, nausea, vomiting
and puritis. The concentration of the
The direct administration of opioids into narcotic in the spinal fluid decreases
the CSF by a spinal needle is referred to with the distance it migrates. The
as an intrathecal opioid injection. The greater the opioid's lipid solubility, the
anaesthetist usually adds the opioid to more is taken up at the spinal cord
the spinal local anaesthetic administered level. Consequently, less drug migrates
prior to surgery. This results in a very to the brainstem. Morphine, for
high local concentration of opioid with- example, has a low lipid solubility, and
in the CSF. The opioid diffuses readily hence, has a greater tendency to migrate
to the opioid receptors located within towards the brainstem as compared with
the substantia gelatinosa, to provide meperidine or fentanyl, which have
analgesia at the spinal level (figure higher lipid solubilities.
163). Hence, this technique selectively
targets opioid receptors responsible for
regulating pain transmission at the spi-
nal level. The placement of an epidural catheter,
in the epidural space permits a continu-
By using the intrathecal route, the blood ous infusion, or repeat administrations,

Must Know Should Know Page 137


)
Anaesthesia for Medical Shrdenrs
1
of analgesics and local anaesthetics for matory drugs may also inhibit
several days. Dilute concentrations of prostaglandins that are involved at the
local anaesthetic may be combined with spinal cord level in the creating a state
epidural opioids in an attempt to exploit known as central h yper-sensitization. In
the analgesic properties of both. this case their anti-prostaglandin effect
Epidural morphine has been used clini- of NSAIDs mitigate this hypersensitivity
cally since 1980 and is now used com- state, thereby decreasing the perception
monly to control acute severe pain. of pain.

NONOPIODANALGESICS
FOR ACUTE PAIN: Table 16.3
Contraindications to NSAIDs*+
The non steroidal anti-inflammatory
b Allergy to ASA, or other
drugs (NSAIDs) are the most frequently
NSAID. Relative contraindi-
used analgesics for acute pain. They cation when there is a history
include drugs such as aspirin, ibuprofen,
of asthma, nasal polyps, or
indomethacin, naproxen, and many
angioedema.
more. One new drug in this class,
b Renal insufficiency
recently introduced in North America, is
Congestive heart failure
ketorolac (Toradol?. Extensive experi-
Peptic ulcer disease
ence with this drug in Europe and
b Active inflammatory bowel
Australia for acute postoperative pain
disease
control, has documented what appears to
b Pregnancy or lactation
be an acceptable patient safety profile.
Bleeding disorders
One of the major advantages of
ketorolac is its ability to be given both
orally, and parentally. This has an
obvious advantage in postoperative
patients who are unable to take oral When considering using NSAIDs for
medications, yet are experiencing nar- acute pain management, physicians
cotic side effects despite poor pain should review their contraindications
control. and potential side effects (see table
16.3). When indicated, NSAIDs may be
When tissues are traumatized they prescribed for short tern therapy (less
release peripheral inflammatory media- -
than 4 5 days) as an adjunct to acute
tors which sensitize and stimulate perip- pain management. For examples of
heral nociceptors. Non steroidal anti- typical regimens using NSAIDs in man-
inflammatory drugs inhibit the enzyme, aging acute and chronic pain states see
cyclooxygenase, which is involved in Table 16.2.
the production of many of these inflam-
matory mediators, through the arach- In patients for whom NSAIDs are con-
nidonic acid pathway (e.g., prosta- traindicated, acetaminophen can be an
glandin E2). Non steroidal anti-inflam- effective alternative. Since it has only

Page 138
I
Chapter 16 Acute Pain Management

'' Indomethacin (Indocid@) 25 - 75 mg po q8hrs


50 - 100 mg pr supp.
Start with 25 mg q8hrs
Max. 200 mglday
) Ibuprofen ( ~ o t r i n ) 400 - 800 mg po q 6-8 hrs
Ketorolac (Torado19 10 mg po q 4-6 hrs Max. po 40 mglday
j -
10 30 mg im q 4-6 hrs Max. im 120 mglday
)

Trlcycllc Antldepressants (TCA's)

Amitriptyline ( ~ l a v i l 9 25 - 100 mg qhs Use with caution in


Irnipramine (Tofranil? -
25 100 mg qhs patients with glaucoma or
Doxepine HCL ( ~ i n e ~ u a n ?25 - 100 mg qhs urinary retention.

Cornblna tlons

Acetaminophen t Codeinev 1 - 2 tabs po q 4-6 hrs

'+(Tylenol' # 12,and 3 contain 300 mg acetaminophen t 1 5 mg caffeine t 8,15, and


30 mg of codeine per tablet. Tylenol # 4 contains acetaminophen 300 mg, no
caffeine, and 60 mg of codeine per tablet.)

-
Narcotics Agonlst Antagonlst

Pentazocine HCL (Talwin9 -


50 100 mg po q 4hrs Useful in patients
Pentazocine Lactate (Talwin? 30 - 60 mg sc, im, iv q 4hn who cannot tolerate
codeine.

Oplolds

Morphine Sulfate 15 - 30 mg po q4hrs


Morphine 5- 15 mg im, sc q4hrs
Meperidine HCL @emerol@) 50 - 150 mg po, im, sc q 3 - 4 hrs
Codeine 30 - 60 mg po, im q 3 - 4 hrs
Table 16.2 Opioid and adjuvant medications commonly used to treat acute or chronic
) pain. Non steroidal anti-inflammatory medications are useful in patients who
J, experience side effects from opioid pain medications. The generic drugs listed are
accompanied by examples of common trade names in brackets.

** Must Know * Should Know Page 139


Anaesthesia for Medial Studen~s

weak peripheral inhibiting effects on Cognitive and behaviour interventions


prostaglandin synthesis, it lacks the side may influence a patient's pain experi-
effects and contraindications listed ence. Useful techniques in managing
above for NSAIDs. Still, acetamino- pain include:
phen strongly inhibits central prosta-
glandin synthesis, which accounts for its 1. Education and instruction.
analgesic and antipyretic effects. One 2. Relaxation exercises.
common postoperative problem is head- 3. Imagery.
aches. While a multitude of etiologies 4. Laughter.
may be responsible for postoperative 5. Music distraction.
headaches (including caffeine with- 6. Biofeedback.
drawal), acetaminophen (325 650 mg- 7. Conversation with family, friends,
-
pa. or par. every 4 6 hours) is gen- medical personnel.
erally effective, while narcotics are
often ineffective. Physical agents useful in alleviating
pain include:
NONPHARMACOLOGICAL
INTERVENTIONS 1. Applying of heat or cold.
FORACUTE PAINMANAGEMENT: 2. Massaging, exercising, and stretching.
3. Transcutaneous electrical nerve stim-
Anaesthesiologists are physicians who ulation (TENS).
specialize in applying their knowledge 4. Acupuncture.
of pharmacology and physiology to
anaesthesia and analgesia. This chapter
has focussed on pharmacological mech-
anisms and interventions in the manage-
ment of acute pain. Still, there exist References:
other alternative means of pain control
that can be employed successfully by 1. Clinical Practice Guideline. Acute
themselves or in conjunction with the pain management: Operative or
pharmacologic interventions outlined in medical procedures and trauma. U.S.
this chapter. Department of health and human
services. 1992.
Patients have unique responses to pain.
This varies according to such factors as 2. White P.F. Use of PCA for man-
their emotional and cultural back- agement of acute pain. JAMA
grounds, and previous pain experience. 259:(2) 243-7; 1988.
Clinicians should anticipate that patients
who use opioid analgesics regularly, 3. Austin K.L. et al. Multiple intra-
will have increased analgesic require- muscular injections: a major source
ments in the perioperative period (nar- of variability in analgesic response to
cotic tolerance). meperidine. Pain 8: 47; 1980.

Page 140
Chapter I 6 Acute Pain Management

4. Laurito C.E. Recent developments


in postoperative pain management.
Curr Rev Clin Anesth 12(5) 37-44,
1991.

5. Lubenow T.R. et al. Management of


acute postoperative pain. Clin
Anesth UPDATES: Vol 3; No.4,
1992.

6. Cousins N. Anatomy of an illness as


perceived by the patient. Bantam
Books New York, N.Y. 1979.

Notes:

** Must Know Should Know Page 141


\
/
Anaesthesia for Medical Students \

Notes:
)tima
te dia
:2
tients or9
sh del
Chronic Pain
agnos
age i 71d
.ute p LINDAROBINSON
M.D., FRCPC
cute F
~ssi blc
~t the: left leg amputated below the hip after a
:uralg Chronic pain induces a cascade of combat injury in Korea in 1952. On
arcoti changes in the patient involving physi- entering his room, you find a man
'f the cal, emotional and psychosocial distraught, diaphoretic and complaining
etter changes. These combine with neural of severe pain in his left lower leg and
mporr imprinting in the CNS to greatly influ- foot. Anxious to get some hands on
e ris ence the perceived severity and the experience, you proceed to examine the
lfiltra consequences of the ongoing pain. affected limb, only to find that you are
lesthe more than 40 years late! Is Mr. Ross
red s Chronic pain is defined as "an unpleas- faking his pain? How can he be having
.chnic ant sensory and emotional experience pain in a leg that he doesn't have?
:ian. associated with actual or potential tissue
damage, or described in terms of such Corporal Ross has a condition known as
I the ( damage". International Association for "phantom limb pain". Phantom limb
:quire the Study of Pain (IASP) 1979. pain, post herpetic neuralgia, and
rylenc trigeminal neuralgia are examples of
till, This chapter will focus on five common central pain states. Unlike pain which
epres: chronic pain syndromes. we have all experienced secondary to
iscuss mechanical, chemical or thermal injury,
ve. I. Post Herpetic Neuralgia this form of pain arises within the cen-
i ndro 11. Causalgia tral nervous system. In these states,
litiate 111. Reflex Sympathetic Dystrophy trauma, infection, or other conditions
IV. Myofascial Pain Syndromes have damaged nerve tissue, resulting in
i tric) V. Low Back Pain abnormal activity in the intermediate
sed a! afferent neurons in the CNS (see figure
erpeti While similar nociceptive pathways and 16.1 chapter 16). The patient perceives
lust stimuli described for acute pain in chap- real pain is occurring even though there
ffects ter 16 are also active in chronic pain, is no nociceptive stimulation.
Iderlj there are distinct differences between
used, acute and chronic pain disorders. To Altered sleep habits, inability to concen-
etenti examine these differences, let's look at trate, inability to function (work, recre-
ntichc the example of Corporal Robert Ross, ation), as well as depression, and abnor-
whom you are asked to see on your mal behavioural coping mechanisms are
medical rounds. Corporal Ross had his common sequelae of chronic pain states.

1 ** Must Kttow Should Know Page 143


inaerthesia for Medical Students )

described as the worst pain they have


ever experienced in their lives and the
l"o address the diagnostic and thera- unremitting nature of the pain is very
leutic complexity of chronic pain condi- demoralizing and can lead to suicide in
:ions, multidisciplinary clinics have extreme cases. Normally the total dur-
been established involving individuals ation of the disease is between 7 to 10
with a specific interest in these dis- days, with the skin returning to normal
orders. These units commonly staff within 2 to 4 weeks.
anaesthesiologists,psy chologists, nurses
and occupational or physical therapists. The most debilitating complication of
In addition, they have direct access to herpes zoster is the development of post
medical and surgical specialists, and herpetic neuralgia. While this complica-
various diagnostic services. tion is extremely uncommon in young
individuals, it occurs in 50% of patients
over the age of 50 with zoster. Typical-
ly the patient experiences gradual im-
Acute Herpes Zoster (shingles) is a provement over several weeks. How-
mononeuropathy caused by the reactiva- ever some patients may be left with a
tion of the Varicella-Zoster virus chronic life long neuralgic pain. After
(VZV). Varicella is commonly known about 6 - 8 weeks, the pain of herpes
as chicken pox. This extremely con- zoster is called Post Herpetic Neuralgia.
tagious infection is usually seen as a The chance of a patient developing post
benign illness in childhood. The VZV herpetic neuralgia increases steadily
may lie dormant in the dorsal root gan- with age.
glion for decades. When reactivated it
presents as pain followed by a vesicular
rash in the dermatomal distribution of
the dorsal root ganglia involved. The Various treatments may be considered
disease presents as dermatomal pain for herpes zoster, although none is en-
which precedes the rash by 2 - 3 days. tirely satisfactory. The acute Herpes
The rash is a maculopapular rash which Zoster can be treated with an antiviral
evolves into vesicular lesions. The viral agent such as Acyclovir (Zovirax@), but
reactivation causes an acute to be of any help this agent must be
hemorrhagic inflammation with demye- initiated immediately upon making the
lination and axonal degeneration. The diagnosis. Unfortunate1y, Acyclovir
damage to the nerve and root is perma- treatment is very expensive; a typical
nent and of variable severity. course can run over $1000. Even
though it may shorten the acute phase
These patients suffer with constant of H.Z. and result in lesions healing
severe burning pain. The area is ex- earlier, there is no evidence that it pre-
quisitely painful and they cannot bear vents post herpetic neuralgia.
even allowing their own clothes to
touch them. This is frequently

Page 144
Chapter I 8 Chronic Pain

Optimal treatment depends upon accu- (dilantinQ), and carbamazepine (teg-


rr~tediagnosis. Frequently, however, retolQ) have also been used with some
pi~ticntspresent with pain before the success. Capsaicin (zostrix@) cream is a
rr~shdevelops, resulting in an incorrect relatively new treatment designed spe-
dingnosis. Common diagnosis at this cifically for this problem. It contains
~lilge include myocardial infarction, c a p s a i c i n which d e p l e t e s t h e
nc.ute prolapsed disc, and kidney stones. neurotransmitter substance P in the
Ac.utc pain should be treated as soon as peripheral nerve endings and results in
1)o~sihle.Physicians often use narcotics, a decrease in nociceptive information.
lbut these are less effective for treating
1lc.urr11gicpain than other pain disorders. Some patients respond well to
Narcotics may, however, 'take the edge' transcutaneous electrical nerve stimula-
01'1'thc pain and make it more tolerable. tion (TENS), which is particularly use-
I!c.lt(.r still, nerve blocks can provide ful in elderly patients because it has few
I ~ . I I I ~ I I ) I H I Y or permanent relief without side effects. By stimulating the large
1111- risk of the narcotic dependency. diameter nerve fibres, smaller fibres
I~~l'iltrating the area with a dilute local carrying painful stimuli at the level of
1111c.sl11ctic and steroid has also been the dorsal horn are inhibited, according
I I N ~ : .~ucce~sfuIIy,
~ and requires little to the Gate theory of pain.
Ie-c'll~lic~I skill on the part of the phys-
i(~ii111. Mexilitene HCL, an oral l b anti arr-
hythmic with properties similar to lido-
III tllc chronic phase some patients still caine, has also be used to alleviate this
rrcl~~ircacetaminophen with codeine form of neuralgic pain. Despite utiliz-
('l'ylcnol No. 3 9 or a stronger narcotic. ing all these modalities, post herpetic
Still, other drugs (tricyclic anti- neuralgia sometimes remains resistant to
clrl)rcssants (TCAs) and anticonvulsants, medical treatment.
cliscusscd below) are usually moreeffec-
livt:. As with the other chronic pain
sy~~clromcs,the sooner treatment is
i~~ilistcd, the more effective it is. Causalgia is a painful disorder associ-
ated with injury of the peripheral
A tricyclic antidepressant is frequently nerves. In 1864, Wier Mitchell pres-
C ~a
~ I N HS first line drug in treating post ented a treatise entitled, "Gunshot
I~c!rpcticneuralgia. Nevertheless care wounds and other injuries of nerves".
111ust be taken to monitor for side In this paper he describes an injured
c.l'l'ccts. These patients are frequently unionist soldier as follows:
c:ldcrly, and prone to becoming con-
I't~scd, dizzy, or developing urinary In our early experience of nerve wounds, we
rc.tcntion as a result of the met with a small number of men who were
ll~~licholinergic activity of TCA's. suflering from a pain which they described
as 'burning' or as 'mustard red-hot' or as a
A~lticonwlsants such as phenytoin ....
'red hot file rasping the skin' it never
attacks the trunk, rarely the arm or

" Must Know Should Know Page 145


1naestlresia for Medical Students

'high....its favoured site is the foot or out treatment most patients progress to
....
band the part itself becomes exquisitely develop irreversible trophic changes in
hyperaesthstic, so that a touch or a tap of the affected limb. The lower incidence
the f i g e r increases the pain. Exposure to of these changes among Vietnam Vet-
the air is avoided by the patient with a care erans (1.5%) compared to WW 11 Vet-
which seems absurd, and most of the bad erans (5 - 10%) is probably due to the
cases keep the hand constantly wet, finding
more rapid treatment of injuries with
...
relief from the wet A s the pain increases
early debridement in Vietnam.
the temper changes and grows irritable, and
the face becomes anxious, and has a look of
weariness and suflering. The sleep is rest- Causalgia usually involves the median,
less....and exasperates the hyperaesthetic sciatic or brachial plexus nerves,
state so that the rattling of a newspaper, a because they carry the bulk of sensory
breath offresh air, the step across the ward, and sympathetic fibres. Nevertheless,
or the shock of the feet in walking, gives rise identical syndromes have developed in
to increase of pain. patients suffering trigeminal, occipital,
and intercostal nerve injuries.
Mitchell, provides a classical description
of the deep red, glossy, and mottled
trophic skin changes that characterize
this pain syndrome. He used the term
"causalgia" to describe these changes. Most patients develop causalgic pain
World wars I and I1 left many soldiers within a week of the injury. They ex-
with these traumatic causalgic pain perience a burning superficial pain in
disorders. Since then, centres studying the periphery of the extremity, most
these peripheral nerve injuries note that intense in the fingers and palm, or toes
victims of high velocity missile injuries and sole. The pain is so intense and
involving the brachial plexus or sciatic persistent, it overwhelms patients, pro-
nerve plexus, are at risk of developing hibiting rest, sleep, and resulting in
this chronic pain disorder. profound psychological disturbances.

The pain is aggravated by a variety of One study, using the McGill Pain Ques-
physical and emotional factors frequent- tionnaire, found a rating scale of 42 (out
ly leading to profound emotional, physi- of 50) in causalgia, as compared to 25
cal and behaviourial disturbances. In for phantom limb pain, 26 for back pain
the late stages of the disorder, and cancer pain, and 23 for Post
vasomotor (circulatory) and sudomotor Herpetic Neuralgia (see figure 17.1).
(sweat gland) changes accompany Two thirds of patients also describe a
trophic skin changes. deep, intermittent stabbing, tearing, or
crushing pain.
If the sympathetic nerves to the affected
limb can be interrupted soon after the Initially, the pain is located in the gen-
injury, prompt and complete relief of eral territory of the nerve, but as the
the pain can be obtained. Occasionally, syndrome progresses it spreads to
spontaneous remission occurs, but with-
Chapter 18 Chronic Pain

' involve areas well beyond the affected


) nerve's distribution.
Trophic changes develop and the
affected part becomes red and glossy
with denuded skin, tapering digits, and
)
Passive movement of the part, light coarse rigid nails. The small interphal-
) touch, loud noises, or emotional out- angeal joints stiffen and become fixed,
) bursts aggravate the pain. Even clothes muscles atrophy and eventually develop
or bed sheets are unbearable, and contractions. The trophic changes can
) patients go to any length to avoid mov- be avoided if treatment is instituted
) ing the part. within 1-2 months of the injury.
),
SENSORYA N D MOTOR Psychologically, the individual may
1 DISTURBANCES manifest bizarre behaviourial changes,
)
with limb guarding, and seclusion.
Allodynia (see glossary of terms at the These changes are reversible if the pain
) end of the chapter) to touch and tern- is treated adequately.
) perature develop as does hyperpathia.

' Vasodilation occurs early followed by


vasoconstriction.
Treatment options clinicians utilize for
this disorder include:

E Comparison of Pain Scores

Figure 17.1: Comparison of pain scores of common pain conditions using


the McGill Pain Questionairre. Modified with permission from Melzack R.
Psychological aspects of pain: implications for neural blockade. In Neural
blockade. Cousins MJ, Bridenbaugh PO. (eds) 2nd edit. J.B. Lippincott
Co.1988.

) ** Must Know * Should Know Page 1.47


lnacsthcsia for Medical Students

. Sympathetic blockade with local cal sympathectomy for these


anaesthetics or other agents (see l a patients, in the hope of effecting a
and l b below). This is frequently permanent cure. Unfortunately,
useful as a diagnostic tool, how- surgical sympathectomy is not
ever, patients who fail to respond always successful, and the pain
may have a condition called "Sym- may recur.
pathetic Independent Pain".
4. Others modalities that have proved
la. Local anesthetic blocks of either useful in treating this condition
the stellate ganglion (for the arm), include TENS, dorsal column
or the lumbar sympathetic plexus stimulation, physical therapy, and
(for the leg). psychotherapy.

lb. A "Bier Block" (see chapter 16,


figure 16.4) with iv guanethidine
or reserpine has also been used to
produce a localized sympath-
ectomy. Reflex sympathetic dystrophy (RSD) is
a term for a variety of conditions in-
These blocks must be repeated to cluding: minor causalgia, post traumatic
achieve lasting effect. Guanethidine pain syndrome, Sudeck's atrophy, and
displaces norepinephrine from stores in shoulder hand syndrome.
the sympathetic nerve endings and also
prevents the reuptake of norepinephrine. The precipitating factors include acci-
This results in the loss of sympathetic dental or surgical trauma, and a variety
adrenergic nerve function for days or of disease states. Pain, vasomotor
weeks. changes, autonomic disturbances,
delayed recovery of function and trophic
2. Oral alpha 1 adrenergic blockers, changes characterize RSD. Early treat-
such as phenoxybenzamine, can be ment with sympathetic interruption
used as a means of decreasing the results in pain relief and reverses the
excessive sy mpathetic barragepres- pathophysiological abnormalities.
ent in causalgic pain disorders.
Side effects are nausea and postural Compared to causalgia, a reflex sym-
hypotension. pathetic dystrophy is a more common
outcome of orthopaedic injuries and
3. Chemical sympathectomy may be industrial accidents. Hence, it must be
created by the administration of promptly recognized and treated.
local anaesthetics or other agents
(see la, lb). If a chemical The most common cause of RSD is
sy mpathectomy is effective in pro- trauma (e.g., sprains, dislocations, frac-
viding temporary relief, the tures, crush injuries, and lacerations).
clinician may recommend a surgi- There is no correlation between the

Page 148
1 Chapter 18 Chronic Pain

)
severity of original injury and the devel- TREATMENT
OF RSD *:
) opment of RSD. Even a Colles fracture
) resulting in a minor peripheral nerve Original injuries should receive proper
injury can result in RSD. and rapid treatment (including removal
) of foreign bodies, immobilization, repair
) Reflex sympathetic dystrophy is one of muscles and tendons, and pain relief)
complication of common surgical pro- in the hope of preventing the subsequent
) cedures (e.g., amputations, excision of development of RSD.

,
) ganglia, tight casts, carpal tunnel
release). It may also be due to an un-
derlying medical condition such as a
Treatment modalities include the early
use of sympathetic blocks, physiother-
) myocardial infarction (shoulder-hand apy, psychotherapy, medical therapy
) syndrome), or diabetes (diabetic (eg. phenoxybenzamine, prednisone),
neuropathy). Direct nerve compression and, when these fail, a surgical
) from a herniated disc, tumours of spine, sy mpathectomy.
) or metastases compressing the branchial
) plexus may also result in RSD. IV: MYOFASCIAL *
PAIN SYNDROME

In contrast with causalgia, where pain This chronic pain syndrome comprises
) develops rapidly, the pain of RSD de- a large group of muscle disorders char-
velops over weeks or months after the acterized by the presence of h ypersensi-
injury. tive points (called trigger points) pro-
ducing pain, muscle spasm, tenderness,
The criteria for a diagnosis of RSD are: stiffness, and weakness.
)

,
) 1. There is a history of recent or
remote accidental or iatrogenic
trauma or disease.
Various terms such as fibrositis, fibro-
myositis, and muscular rheumatism have
been used t o describe the myofascial
1 pain syndrome. The condition is most
) 2. The patient complains of a persist- commonly misdiagnosed as bursitis,

'
i
ent pain that is burning, aching or
throbbing.
arthritis, visceral disease, or a herniated
disc.

One or more of: Trauma t o the myofascial structures and


) 3.
a. vasomotor/sudomotor changes an acute overload on the affected
b. trophic changes, edema, hyper- muscles is the most common cause of
) sensitivity to cold this syndrome. Acute muscle strain
c. muscle weakness, or atrophy damages the sarcoplasmic reticulum
i releasing excessive amounts of calcium.
) 4. Relief of symptoms is obtained This initiates a complex cascade of
after regional sympathetic block- events beginning with local vasocon-
1 ade. striction,sustainedmuscularcontraction,
i decreased blood flow, increased metab-

1 " Must Know * Sltould'Know Page 149


~aesthesiafor Medical Students

ism, and culminating in the release of An acute episode of myofascial pain


:rve sensitizing substances. In the often follows overuse of unconditioned
Tfected areas, taut muscle bands may muscles (e.g., the weekend athlete),
:palpable and are referred to as trigger poor posture during prolonged activities
~ints. Pain from myofascial trigger such as computer work, or automobile
oints (TP's) is described as steady, accidents (whiplash).
eep, and aching. The pain may be
xacerbated by stretch, cold, stress, Patients present with persistent pain,
atigue, viral illnesses or direct pressure. tight or aching muscles, limited range of

'able 17.1 Comparison of Causalgia and Reflex Sympathetic Dystrophy.


I I I
1 Causalgia I RSD I
Onset Within 1 week Over weeks to months
1 I
Frequency I Rare ( More common I
Etiology Typically involves high Accidental injuries, surgical
velocity injuries of the trauma, orthopaedic injuries
brachial or sciatic nerve (e.g., sprain, fracture, tight cast,
plexus (e.g., gun shot dislocation).
wounds).
Pain Similar pain characteristics, typically described as a constant
Characteristics burning, throbbing, or aching pain. Disturbed sleep, and
profound psychological-behavioural changes are more
common with causalgia. The affected limb is guarded, and
becomes cool, pale or cyanotic, accompanied by decreased
hair growth, muscle atrophy, tendon contracture, and joint
ankylosis. Causalgia is generally recognized as the most
intense form of chronic pain, and has a McGill Pain Score
average of 42/50 (see figure 17.1).
Prevention Early treatment of the injury with debridement, repair and
immobilization of associated fractures.

Treatment Sympathetic blocks:


Stellate ganglion block (arm),
Lumbar sympathetic block (leg)
Guanethidine intravenous Bier block (see figure 15.4)
Alpha-1 adrenergic blockers (e.g., phenoxybenzamine)
Other:
Physical therapy, psychotherapy, TENS,
dorsal column stimulation, surgical sympathectomy.
Chanter 18 Chronic Pain

I
motion and generalized fatigue. They V: Low BACK PAIN*
) may experience continuous or intermit-
) tent muscular pains, aches or a burning Low back pain is one of the most com-
sensation in the overloaded muscles. mon problems our society faces. Sixty
) Applying direct pressure on these trig- to eighty percent of all adults will suffer
) ger points exacerbates the pain. Predict- with this at least once during their life-
able patterns of pain associated with time. The pain is usually self limited.
specific TP's do not follow a derma- Of those who see their doctor, more
) tomal distribution. than 90% will improve and are back to
work within 2 months. However, the
)
For effective treatment, the pain and remaining 5-10% pose a challenging
) spasm cycle must be interrupted. The problem.
) TP can be injected with local
anaesthetic, or the overlying skin Risk Factors for low back pain include:
sprayed with a vaporized coolant. Increasing age
) These treatments should be followed by Heavy labour
) stretching of the affected muscle groups. Lower education and income
Smoking
) Patients are frequently in poor physical Obesity
) condition and should slowly but meth- Whole body vibration (truck driver)
odically undertake a program of pro- Previous back pain
) gressive daily physical fitness. This
) should include aerobic exercises, such A host of clinical entities have been
as walking, exercise biking, swimming, described to explain the various types of
low impact aerobics and aqua fitness. low back pain, such as muscle strain,
) Physician's may motivate patients by degenerative disc disease, facet syn-
) reminding them that this is the most drome, and myofascial pain syndrome.
important aspect of their treatment. However, the signs, symptoms and
) radiological findings of these conditions
) These patients frequently have very overlap, making an accurate diagnosis

' poor sleep patterns. Tricyclic antide-


pressants in low doses will improve
) sleep and decrease the level of muscular
difficult. For example, a patient who,
on clinical examination, appears to have
facet joint pain and degenerative disc
) pain (possibly by increasing serotonin disease, may nevertheless have similar
levels). Cyclobenzaprine HCL radiological changes to other patients
) (Flexeril? is also commonly used as a who are entirely asymptomatic.
) 'skeletal muscle relaxant'. As this tends
to be a chronic condition, narcotics Low back pain is usually not an emer-
) should be avoided due to the risk of gency. Occasionally, conditions* * do
i opioid dependence. Plain acetamino- present as low back pain and may have
phen can be used instead. dire consequences for a patient should
the clinician fail to make the correct
diagnosis.

Sliould Know Page 151


naesfhesia for Medical Sludenfs

~ - - - - - --

Table 17.2: Causes of Low Back Paln

(Nlnety percent of all cases of back paln a r e due to "medlcal causes")


Medlcal Condltlons
Musculoskeletal: Inflammatory:
Muscle 'strain' Ankylosing spondylitis
.Ligament 'sprain' Psoriatic spondylitis
Apophyseal joint: 'facet syndrome' Reactive arthritis
Discs: 'degenerative disc disease' Inflammatory bowel disease
Bone: fractures, spondylolisthesis
Metabolic:
Neoplastic: Osteoporosis + fractures
Benign: osteoid osteoma Osteomalacia
Malignant Paget's disease of the bone
Primary: Multiple myeloma
Secondary: Metastasis Visceral:
Pelvic organs
Infectious: (endometriosis, prostatitis)
Acute: pyogenic discitis, osteomyelitis Renal disease (pyelonephritis)
Chronic tuberculosis Gastrointestinal disorder
(pancreatitis, peptic ulcer)
Aortic aneurysm

Surglcal Emergencies** (see text)


Cauda Equina Syndrome (disc herniation, tumor mass, abscess)
Aortic aneurysm (leaking, dissecting, ruptured)
Sclatlca wlth Neurologic Signs**
Ruptured intervertebral disc
Spinal stenosis

For example, the cauda equina syn- ency and rapid decompression of the
drome presents as a constellation of spinal cord is needed to avoid perma-
symptoms and signs such as a neurolog- nent nerve damage. Causes of cauda
ic deficit in the lower extremities (par- equina syndrome include central disc
alysis and loss of sensation), loss of herniation, and epidural tumours or
bowel or bladder continence, weakness, abscesses.
depressed reflexes, and loss of sensation
over the buttocks called "saddle An aortic aneurysm may present as
anaesthesia". This is a surgical emerg- back pain and may require immediate
C h a ~ l e r18 Chronic Pain

) surgical attention. Sciatica is usually Osteo-myelitis may require antibiotics


) caused by a herniated disc or by a nar- and drainage. Arthritis requires specific
row spinal canal with compression of treatment for the underlying disease.
the nerve roots (spinal stenosis). The
) patient experiences pain that radiates Mechanical low back pain is managed
) below the knee. A herniated disc tends with a several days of rest, oral anal-
to be aggravated by prolonged sitting, gesics, NSAID's, and then mobilization.
) or anything that increases intrathecal Chronic low back pain is frequently
) pressure (eg. sneezing, or coughing). difficult to treat and requires a gradual
Paresthesia and weakness may be exper- program of aerobic conditioning,
) physiotherapy, tricyclic antidepressants,
ienced in the involved nerve root dis-
tribution. psychotherapy and education about
)
proper back care.
Spinal stenosis is more common in
) patients over 6 0 years of age. Charac-
) teristically, these patients complain of
pain in the buttocks, thighs and legs, Allodynla: Pain due to a stimulus
) which develops o n standing and walk- that does not normally provide pain.
) ing, and is relieved by 15-20 minutes of
) rest. Patients find that walking with the Analgesla: Absence of pain in
trunk flexed is more comfortable. response to stimulation that would nor-
mally be painful.
) Other medical causes presenting as
sciatica include tumours, infection, and Causalgla: A syndrome of sus-
) arthritis. tained burning pain, allodynia, and
) hyperpathia after a traumatic nerve
) Conservative treatment of sciatica with lesion, often combined with vasomotor
rest, analgesics, nonsteroidal anti in- and sudomotor dysfunction and later
) flammatory medications, muscle relax- trophic changes.
) ants, or epidural steroids is usually
sufficient, (provided other more serious Dysesthesla: An unpleasant abnor-
) conditions have been excluded - see mal sensation, whether spontaneous or
) Table 17.2). Surgery is indicated if evoked.
persistent disabling pain occurs or the
)
neurologic deficit increases despite H yperalgesla: An increased response
) conservative measures. to a stimulus that is normally painful.
)
The treatment of 'medical back pain' Hyperesthesla: Increased sensitivity to
) should be specific to the medical condi- stimulation, excluding the special
) tion. A tumour with metastasis to the senses.
spine may require surgical intervention,
chemotherapy or radiotherapy. Hyperpathla: A painful syndrome,
i characterized by increased reaction to a

) ** Must Know Should Know Page 153


naesfhesia for M e d i c a l Students

timulus, especially a repetitive stimu-


us, as well as an increased threshold.

-lypoalgesia: D i m i n i s h e d p a i n
.esponse to normally painful stimulus.

Hypoesthesia: Decreased sensitivity to


stimulation, excluding the special
senses.

Neuralgia: Pain in the distribution


of a nerve or nerves.

Neuritis: Inflammation of a
nerve or nerves.

Neuropathy: A disturbance of
function or pathological change in a
nerve; in one nerve, mononeuropathy; in
several nerves, mononeuropathy mul-
tiplex; if diffuse and bilateral, poly-
neuropath y.

Nociceptor: A receptor preferential-


ly sensitive to a noxious stimulus or to
a stimulus that would become noxious
if prolonged.

Paln tolerance level: The greatest


level of pain that a subject is prepared
to tolerate.

Pain threshold: The least experience of


pain that a subject can recognize.

Paresthesia: An abnormal sensation,


whether spontaneous or evoked.

P a g e 154
Obstetrical
Anaesthesia
ROBERT ELLIOT
MD FRCPC

This chapter will focus on the following 11: Suplne Hypotenslve Syndrome**:
four topics:
The gravid uterus may compress the
1. The physiological changes of preg- inferior vena cava (IVC), and/or the
nancy and their clinical signifi- aorta when the parturient lies in the
cance. supine position. This occurs in approxi-
2. The importance of the supine mately 15% of patients as early as the
hypotensive syndrome and aorto- 20th week, and increases in frequency
caval compression. in the third trimester.
3. Available options for providing
pain relief during labour and deliv- When IVC compression results from
ery, including epidural analgesia. uterine compression, there is a decrease
4. The risks of general anaesthesia in in venous return to the heart. The
the parturient. parturient may experience signs and
symptoms of shock including
I: Physlologlcal Changes*. hypotension, pallor, sweating, nausea,
For anaesthetic interventions in the vomiting and changes in mentation.
parturient, one must consider both the Venous pressure in the lower extrem-
physiological changes that occur during ities and in the uterus increases. Blood
pregnancy, as well as the effects of flow to the uterus occurs because of a
anaesthetic drugs on the mother and difference between the uterine artery
infant. Complications during labour and and venous pressures. Hence an
delivery may threaten the life of both increase in uterine venous pressure will
the parturient and her infant. The an- decrease the uterine blood flow to the
aesthetist must be able to respond placenta and fetus.
quickly, working closely with the ob-
stetric, neonatal, and nursing teams. Compression of the aorta by itself, is
not associated with maternal hypoten-
Profound physiological changes occur sion, but, may result in arterial
during pregnancy. Changes in the nerv- hypotension in the uterus. This
ous, cardiorespiratory, and gastrointesti- decrease in uterine blood flow may
nal systems, and their implications with result in fetal distress or asphyxia.
respect to the anaesthetic management,
-
are reviewed in tables 18.1 18.3.
)
** Must Know Should Know Page 155
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Anaesthesia for Medical Students

Table 18.1 T h e physlologlcal changes of pregnancy.

Nervous System

Variable Change Cause Importance

General MAC Requirements CNS effect of General anaesthetic


Anaesthesia decrease by 25 - 40% progesterone and drug requirements are
(or) beta- decreased.
endorphin

Regional Local Anaesthef c (LA) Decrease in size Increased epidural


Anaesthesia dose requirements of epidural space spread of LA may
decrease by about 40% due to engorged occur, esp. if aorto-
epidural veins, caval compression is
and (or) hormonal not prevented.
changes.

Cardlovascular System
Blood Total BV t by 35% Hormonal effect An t of approx. 1000
Volume (BV) Plasma BV t by 45% ml compensates for
RBC's BV t by 20% the 400 - 600 ml of
blood loss with
delivery.
Cardiac t by 40% at 10 weeks Increases in CO Patients with pre-
Output (CO) gestation are in response to existing heart disease
labour t CO 45% above increased meta- may decompensate.
pre-labour values. bolic demands. (eg. Pulm. edema
After delivery CO t (Stroke volume may occur duling
60% above pre-labour increases more labour or after deliv-
values. than heart rate). ely in the patient with
significant mitral
stenosis).
Peripheral BP normal or 4 SVR decreases to Supine Hypotensive
Circulation SVR 4 by 15%. compensate for t Syndrome. (see text)
Venous return from legs in CO, leaving
decreases. BP normal or 4.
Regional Utems increases blood Blood flow in the Placental blood flow
Blood Flow now by 500 ml I min. placenta is cannot t but can 4
dependent on with maternal 4 BP
blood pressure. due to blood loss,
aortocaval
compression,
or catecholamines.

Page I56
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Chapter 18 Obstetrical Anaesthesia
1
Table 18.2 The physlologlcal changes of pregnancy (contlnued).
Resplratory System

Varlable Change Cause Importance

Upper Mucosal edema makes Capillary Trauma may occur


Airway the parturient prone to engorgement. with suctioning, and
bleeding. placing nasal or oral
airways. Choose a
smaller E n .
Ventilation Minute Ventilation Increases in O2 Normal resting
increases by 50%. consumption maternal PaCO, dmps
Tidal volume t 40%. begins in the to appmx. 30 mm Hg
Respiratory rate t 10%. Erst trimester. in the Erst trimester.
Labour may Pain from labour and
increase 0, delivery result in fur-
consumption ther hyperventilation.
more than 100%.
Lung FRC 4 20%. By Efth month Uptake of inhaled
Volumes No change in V.C. the rising uterus anaesthetics occurs
begins to force faster due to increased
the diaphragm minute ventilation with
UP. a smaller FRC.
Arterial Increased by 10 mm Hg. Due to Decreased PRC with
Oxygenation hyperventilation. increased 0, consump-
PaO, tion result in very
rapid decreases in
PaO, during apnea (eg.
induction of
general anaesthesia).
Pulse oximehy is
important

The tenn parturient should never be aorta. Lumbar regional anaesthetics


placed in the supine position. Abnor- block the sympathetic nerves and
ma1 fetal heart rate patterns indicating decrease vascular tone in the lower
insufficient uterine blood flow are fre- body. This may exaggerate the
quently observed when patients are hypotensive effects of aortocaval com-
placed in the supine position (see figure pression.
18.1). Positioning the parturient on her
-
side, or using a 10 15 cm right hip
wedge is usually sufficient to move the
weight of the uterus off the IVC and

1
** Murt Know * ShouM Know
1
Anaes~hesiafor Medical Students
j

Table 18.3 The physlologlcal changes of pregnancy (continued).

Gastrolntestlnal System

Varlable Change Cause Importance


Gastric Fluid Increased Enlarged uterus N.B. All partudents are con-
Volume displaces pylorus. sidered to have a "full stom-
Gastric emptying ach". Pain, anxiety and drugs
delayed. (esp. namotics) all retard
gastric emptying.
Mebclopramide may be
useful in reducing volume.
(see chapter 9: The rapid
sequence induction)
Gashic Fluid Increased Gastrin secreted Use of HZ-receptor
Acidity by placenta. antagonists (anitidine) and
Stimulates H+ (or) a non-particulate antacid
secretion. (Na citrate) are recommended
to increase gastric pH.
Gastro- Decreased Enlarging uterus Pulm. aspiration of gashic
esophageal competence. distorts the angle contents is the major risk of
junction. of the junction. Gen. Anaesthesia. Placement
of an E'IT is mandatory in
every patturient rendered
unconscious by anaesthesia.
(see chapter 24: Unusual
Anaesthetic Complications:
Aspiration Syndrome).

111: Analgesla optlons for transmitted from vlsceral nerve fibres


Labour and Delivery**. entering the spinal cord at TlO to L1.
During delivery somatic nociceplive
How painful is labour? impulses enter the spinal cord at S2 to
The pain of labour is generally S4, see figure 18.2. Table 18.4 lists
described as being more intense than some of the factors which influence the
any other previous pain experience (see degree and intensity of the pain experi-
chapter 17 figure 17.1: Comparison of ence during labour.
common pain conditions). In women
delivering for the first time, the pain of Psychoprophylaxls: The Lamaze
labour is described as more intense than method postulates that the parturient's
the pain of their subsequent labours. pain which arises from uterine contrac-
During labour nociceptive impulses tions and perineal distension can be
resulting from labour and delivery are replaced with conditioned "positive"

Page 158
Chapter 18 Obstetrical Anaesthesia

reflexes. This method uses a partner or have shown that two-thirds of Lamaze
friend who functions as a wach helping mothers will require some kind of anal-
the parturient concentrate on breathing gesic aid. Furthermore, it is unfair to
techniques and on releasing muscle suggest that, if the method is followed
tension. Emphasis is placed on educa- correctly, labour will be painless. This
tion about labour and delivery, to give can only lower self-esteem when "fail-
the parturient a sense of "control" over ure" occurs.
the birth process. Some proponents of
the Lamaze method advocate not using In fact, excessive pain may result in
any chemical anaesthesia for fear of more harm to the fetus than the judi-
placental transfer to the fetus. Psycho- cious use of pharmacologic analgesia.
prophylaxis reduces the need for Psychologic stress during labour may
"chemical anaesthesian,however studies cause hypoxia and acidosis in the fetus.

/ The Supine Hypotensive Syndrome

Figure 18.1: The supine hypotensive syndrome. Aortocaval compression occurs in


the supine position and is relieved by positioning the parturient in the lateral position.
(Adapted with permission from Bonica JJ: Obstetric Analgesia and Anesthesia.
World Federation of Societies of Anaesthesiologists,Amsterdam, 1980.) I

** Must Know Should Know Page 159


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Anaesthesia for Medical Students
)

Table 18.4: Factors lnfluenclng


the paln of labour and delivery*.

Parturient's psychological state


Mental preparation
Family support
Medical support
Cultural background
Primipara vs. multipara
Size and presentation of the
fetus
Size and anatomy of the pelvis
Use of medications to
augment labour (eg. oxytocin)
Duration of labour

Figure 18.2: Nociceptive pathways


in labour and delivery. opioids used in managing pain during
labour and delivery.

Meperidine is transferred very quickly


across the placenta. However, peak
levels in the fetus are not reached until
This is believed to result from decreased 2 to 3 hours after administration.
uterine blood flow secondary to elevated -
Therefore, infants born 2 3 hours after
levels of blood catecholamines and (or) maternal meperidine administration are
decreased carbon dioxide tensions at risk of opioid-induced depression.
caused by hyperventilation. With Elimination of meperidine from the
adequate pain relief, epidural anaes- neonate takes 3 - 6 days. Nor-
thesia can minimize the stress of labour, meperidine, an active metabolite, takes
and facilitate patient participationduring even longer and may be responsible for
labour and delivery. It is important to subtle behavioral changes in the new-
recognize differences in pain tolerance born infant.
and analgesic requirements in order to
promote maternal self-esteem and bond- Fentanyl is transferred to the fetus ex-
ing with the newborn. tremely rapidly and redistributes back to
the mother, much like thiopental. With
Table 18.5 lists some of the options doses of 1 mcglkg, fentanyl does not
currently available for pain management produce adverse effects on the neonate,
during labour. Table 18.6 lists some of and is eliminated from the fetus much
the pharmacokinetic properties of two quicker than meperidine.
i
Chapter 18 Obstetrical Anaesthesia
)

Table 18.5: Options available for pain management durlng labour and
delivery8*.
Nothing
Psychological support (coaches, husband, family members)
Behavioral modification (Lamaze technique)
Hypnotherapy (relaxation exercises practised in months prior to LBrD).
Education (normal expectations for labour and delivery; prenatal classes).
Massage, walking.
Sedatives.
Opioid analgesics (e.g., meperidine p.o., im., i.v., fentanyl i.v.).
-
Opioid antiemetic combinations
-
(e.g., meperidine 50 100 mg with dimenhydrinate [Gravol] 50 mg im.).
Epidural analgesia (local anaesthesia alone, or with epidural opioids
e.g., bupivacaine 0.125% with fentanyl 2 mcg/ml).
Spinal anaesthesia (see text for discussion).
General anaesthesia (see text for discussion).

Table 18.7 reviews some of the poten- 15). This results in only a minor motor
tial maternal and neonatal advantages of nerve block. As a consequence, the
epidural analgesia. The recommended patient maintains her motor strength,
doses, complications and contra- permitting her to move during labour.
indications to epidural analgesia and During the second stage of labour, the
anaesthesia were presented in chapter differential nerve block facilitates her
15: Local and regional anaesthesia. efforts to push, by minimizing the
motor block while maintaining an
Lidocaine and bupivacaine are the most adequate sensory block.
common local anaesthetic agents used
for managing epidural analgesia - Epinephrine is frequently added to the
anaesthesia. Low concentrations of LA (e.g. 1:200,000 epinephrine or 5
bupivacaine (e.g. 0.125%) can provide mcg/ml). This can increase the duration
a differential nerve block (see chapter of nerve blockade by 50%, decrease the

Opioid Agonist Dose Peak Effect Duration

Meperidine PO 50 - 150 mg. 1 - 1% hours 2 - 4 hours


(~emerol? IM 50 -150 mg. 40 - 50 mins.
IV 25 mg. -
5 10 mins.

Fentanyl -
IM 50 100 mcg. -
IM 7 8 mins. 0.5 1-
(~ublimaze? IV 25 - 50 mcg. -
IV 3 5 mins. hour

Table 18.6: Common oplold analgesics for labour and delivery.

** Must Know Should Know Page 161


Anoesthesio for Medico1 Students )

Epldural Analgesia - Anaesthesla. )


Maternal Advantages. Neonatal advantages. ,I

1. Excellent pain rellef, frequently 1. Less drug transfer to the infant, j


achieved compared to opioids due to a decrease in maternal
alone. sedatives and opioid require-
2. Normal progress of labour ments.
once established is not impeded. 2. Improved uterine blood flow
3. General anaesthesla avolded, and fetal well being may result
should a Caesarean $ection, or with the relief of the maternal
forceps manipulation be required stress response during labour and
(epidural level is increased for delivery.
C-section). 3. Reduced neonatal trauma dur-
4. Improved maternal partlclpa- ing delivery with improved con-
tlon in delivery and during ditions when the use of forceps is
bonding with the newborn. required.
4. No neonatal depresslon, when
properly managed.

Table 18.7: Epldural anaesthesla In labour and delivery.

systemic absorption by 30%, and While general anaesthesia for labour


decrease the overall amount of drug and delivery was used in the pioneer
required. Epinephrine is believed to days of anaesthesia, our understanding
cause vasoconstriction of the epidural of the risks of general anaesthesia to
blood vessels, decreasing the drug's both the mother and neonate has made
systemic uptake. Potential side effects this mode of analgesia obsolete.
of adding epinephrine include a signifi-
cant increase in motor block, accentu- IV: General Anaesthesla.
ation of hypertension in preeclamptic When regional anaesthesia is contraindi-
patients, and diminished uterine activity cated, or there is insufficient time to
due to the beta-effects of epinephrine. establish regional anaesthesia (eg.
severe sustained fetal bradycardia),
Spinal anaesthesia is generally not used general anaesthesia for operative deliv-
for labour and delivery because of the ery may be required. The anaesthetist
intense motor block it creates, making faced with providinggeneral anaesthesia
pushing during stage I1 ineffective. As for Caesarean section must consider the
spinal anaesthesia is usually provided physiological changes of pregnancy, and
by one injection, it lacks the flexibility be ready to provide care for the com-
in duration that can be achieved by promised neonate. Immediate concerns
using a continuous epidural catheter. include*:
Chapter 18 ObstetricalAnaesthesia

1. All parturients must be considered ing the nitrogen with oxygen, we pro-
to have a "full stomach" and gas- vide a reserve of oxygen for the period
tric precautions including a rapid of apnea that occurs during induction of
sequence induction with cricoid anaesthesia.
pressure are indicated for general
anaesthesia. A small dose of curare is often used in
2. Upper airway edema occurs with a 'rapid sequence induction' to prevent
pregnancy and all parturients the intense muscle fasciculations that
should be considered to have a may occur following the administration
potentially difficult airway to of succinylcholine. In the pregnant
intubate. i patient, the muscle fasciculations are
3. General anaesthesia introduces the much less intense, probably due to the
risks of a failed intubation, and the effect of progesterone. Many anaesthe-
risk of hypoxemia, andlor pulmon- tists omit curare pretreatment in the
ary aspiration of gastric acid. obstetrical patient because it prolongs
4. With general anaesthesia we must the onset time of succinylcholine paral-
consider the potential of having ysis and reduces the intensity of the
matemal drugs transferred to the neurornuscular block.
neonate. This may contribute to
neonatal depression and the need The difficult Intubatlon:
for neonatal resuscitation. On rare occasions, the anaesthetist may
be unable to intubate the patient on the
The 'rapid sequence induction' was pres- first attempt. Difficult intubations have
ented in chapter 9. In the pregnant been associated with pulmonary aspir-
patient with a potentially difficult air- ation, and carry a high mortality rate in
way, a thorough evaluation of the air- the obstetrical population. Every anaes-
way is especially important (see chapter thetist must have a plan for managing a
6). All parturients have a tendency to failed intubation in the parturient. Per-
rapid desaturation with induction of sistent attempts without alterations in
general anaesthesia. Hence 'pre-oxygen- technique will only result in airway
ation' with 100% oxygen prior to induc- edema and trauma, with subsequent
tion of general anaesthesia is critically matemal and fetal hypoxemia. Serious
important for all parturients. Pre-oxy- hypoxemia can occur after 1minute of
genation is provided with a properly apnea despite pre-oxygenation.
sealed mask applied to the patient's
face, with the patient breathing 100% Maintaining cricoid pressure at all times
oxygen. If the patient breathes 100% is imperative. In the event of a failed
oxygen for a 3 minutes, or takes four intubation, gentle ventilation with 100%
vital capacity breaths, more than 95% of oxygen using the reservoir bag and
the nitrogen in the patients FRC will be mask may be all that is necessary until
exchanged with oxygen. The normal the patient awakes. When the parturient
resting FRC is approximately 2 5 litres, has recovered from the effects of the
and contains 80% nitrogen. By replac- general anaesthetic agents, a regional

** Must Know Should Know Page 163


Anaesthesia for Medical Students

technique or alternatively an 'awake


intubation' with topical anaesthesia may Notes:
be chosen. If there is fetal distress, the
anaesthetist may decide to proceed with
the anaesthetic using a volatile agent
and ventilating the patient by bag and
mask until she begins breathing
spontaneously. If hypoxemia persists
and attempts to ventilate the parturient
are unsuccessful, a cricothyroidotomy
with a large-bore needle \and oxygen
insufflation may be life-saving. Discuss
with the staff anaesthesiologists what
other options they would consider for
managing this problem.

Induction of anaesthesia in the obstetri-


cal patient may be accomplished by
administering a reduced dose of
thiopental, propofol, or ketamine (see
induction agents, chapter 11). Muscle
relaxation for intubation is provided
using succinylcholine, while anaesthesia
is maintained with 50% nitrous oxide
and oxygen, and 0 5 MAC of a volatile
agent such as isoflurane. Once the
infant is delivered, narcotics and other
agents may be used to deepen the level
of anaesthesia.

Intermediate-acting muscle relaxants


such as atracurium or vecuronium, when
used, are reversed at the end of the
procedure with a combination of anti-
cholinesterase and anticholinergic
agents (eg. edrophonium-atropine, or
neostigrnine-glycopyrrolate). The
patient is ventilated with 100% oxygen.
Extubation is performed after suctioning
the upper airway secretions with the
patient positioned on her side, and re-
sponding to verbal commands.

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Chapter 18 Obstetrical Anaesthesia
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I
Basic Neonatal
Resuscitation
ROBERT CRONEMD, AND ROBERT ELLIOT
MD, FRCPC

Approximately six percent of newborn doppler ultrasound or phonocardiogram.


infants will require resuscitation of It may also be done internally, by
some kind in the delivery room. Health attaching an electrode to the fetal scalp
care workers providing care during when the head presents at the cervix
labour and delivery should ensure that during labour. Unlike intermittent mon-
they have the knowledge and skills to itoring, continuous monitoring facilitates
resuscitate the newborn infant. Recent- the analysis of FHR trends, and their
ly, major efforts have been made to relation to uterine contractions.
provide delivery room care-givers with
neonatal resuscitationguidelines through What are the broad principles of neo-
the Neonatal Resuscitation Program natal resuscitation that I should know*?
(NRP). 1. Clear the airway.
2. Keep the infant warm and dry.
The purpose of this chapter is to intro- 3. Provide physical Stimulation.
duce student's to the basic ABCs of 4. Assess the infants breathing and
neonatal resuscitation. We do not expect circulation.
students to develop specific skills, such 5. Consider interventions.
as intubation of the depressed neonate, (oral suctioning, airway insertion,
or to use neonatal resuscitation drugs mask ventilation, intubation, endo-
during their clerkship training. Never- tracheal ventilation, external cardiac
theless, we hope to stimulate their massage, fluid resuscitation, drug
desire to develop neonatal resuscitation administration).
skills, and encourage them to attend a
Neonatal Resuscitation Workshop and What is the APGAR score**?
become a certified NRP provider. The Apgar score is a clinical evaluation
of the status of a newborn infant. It
Fetal Heart Rate (FHR) Monltorlng: assigns a value of 0, 1, or 2 points to
Fetal heart rate monitoring is currently five variables, with the highest possible
the most accurate screening technique score being 10. It was devised by an
for assessing fetal well being in-utero. American anesthesiologist, Dr. Virginia
Fetal heart rate monitoring can be done Apgar. The score is typically recorded
intermittently with a stethoscope, or 1 and 5 minutes after birth, however,
continuously. Continuous monitoring is one may continue to assess at 5 minute
performed externally with either an intervals in depressed infants requiring
abdominal electrocardiogram (ECG), resuscitation. The most important vari-
Chapter 19 Neonatal Resuscitation

Score 0 1 2

Heart Rate Absent < 100 > 100


Respiration Absent Slow, irregular Good Crying
Colour Blue, pale Body pink, hands/feet blue Completely Pink
Reflex Irritability Absent Grimace Cough, sneeze
Muscle Tone Limp Some Flexion Active Movement
Table 19.1: The Apgar Score **

able is the heart rate. An apgar score of What is a normal FHR*?


s 6 at five minutes correlates with The normal fetal heart rate in a term
increased morbidity and mortality. infant ranges from 120 to 160 beats per
Resuscitation should never be postponed minute. It normally varies by 5 to 20
so that a "1-minute Apgar" can be done. beats per minute. A premature infant
The five variables measured can be (i.e., less than 37 weeks gestation) has
recalled using the individual letters of an average FHR of 130 to 170 beats per
Dr. Apgar's surname. minute, which is slightly higher than the
term infant.
A = Appearance (Colour)
P = Pulse (Heart rate) A fetal heart recording with a normal
G = Grimace (Reflex irritability) rate, but lacking variability, may be
A = Activity (Muscle tone) observed when the fetus is asleep, or
R = Respiration premature. It may also occur when the
infant has been exposed to drugs
What is asphyxia*? through the mother (narcotics, sedatives,
Neonatal asphyxia is the combined anaesthetics, etc.), or from chronic fetal
result of a reduced oxygen supply, and asphyxia. A completely "flat" baseline,
an accumulation of carbon dioxide in (i.e. a FHR without variability) suggests
the newborn infant. This may occur either a previous insult that has been
before, at the time of, or immediately corrected, or ongoing congenital nerv-
following delivery. The need for more ous and cardiac anomalies. The fetal
than one minute of positive pressure heart normally increases in rate when
ventilation before sustained respirations the baby is active.
are established, or an Apgar score < 6
at five minutes, is used in making a How are the fetal heart and lungs
clinical diagnosis of asphyxia. The different from the adult?
presence of perinatal asphyxia increases In the fetal circulation, blood is able to
the infants risk of morbidity and mortal- pass from the right heart to the left
ity. heart through two channels which
bypass the fetal lungs. The ductus
arteriosus acts as a conduit for blood to

** Must Know Should Know Poge 167


Anaesthesia for Medical Students

pass from the pulmonary artery directly residual capacity (FRC) volume of
to the aorta. The foramen ovale allows about 30 mlkg. During vaginal deliv-
blood from the right atrium to pass ery, most of this fluid is "squeezed" out
directly to the left atrium. The amount of the lungs, facilitating initial lung
of pulmonary arterial blood flowing expansion and oxygen exchange.
through the fetal lungs is small due to Infants born by caesarean section do not
their small volume and high vascular have this "squeeze" and may have more
resistance. Blood from the right ven- fluid in their lungs, impairing lung
tricle bypasses the lungs and eventually expansion, and oxygenation. This con-
flows through the low resistance pla- dition is frequently termed transient
centa where it picks up maternal oxygen tachypnea of the newborn, and may
and excretes waste products of metab- require supplemental oxygen therapy
olism (carbon dioxide, urea, etc.) see and observation for the first 24 hours.
figure 19.1.
Why do infants breathe when they are
?he fetal lungs contain an ultrafiltrate of born?
plasma equivalent to their functional When the umbilical cord is clamped, the
low resistance placenta is removed from
the infants circulation. The result is an
increase in the vascular resistance in the
aorta, left ventricle, and left atrium
associated with a rise in left sided pres-
sures. This creates a functional closure
of the foramen ovale and the ductus
arteriosus. As these right to left shunt
paths are closed, blood is diverted into
the lungs. A combination of mild aci-
dosis, hypoxia, touch, noise, pain, and
cold all stimulate the infant to take their
first breath. The vaginal squeeze
referred to above, facilitates lung expan-
sion. Fresh oxygen in the alveoli and
the expanded lung volume decrease the
Ductus Venosus
resistance to blood flowing into the
lungs.

Hypoxia, cold, acidosis, hypovolemia,


hypoventilation, hypercarbia, and
atelectasis will all increase pulmonary
vascular resistance, forcing blood
through the foramen ovale and ductus
arteriosus. These factors tend to cause
( Fig. 19.1 The Fetal Circulation ) a persistent fetal circulation and impede

Page 168
Chapter 19 Neonatal Resuscitation

the newborns oxygenationp'dventila- ministered. Consider changing maternal


tion. // positions for variable decelerations.
Evaluate and correct any maternal
What fetal heart rate patterns should I hypotension using an intravenous fluid
be concerned about*? bolus and/or ephedrine. Summon help.
FHR decelerations may indicate a Ensure accurate FHR monitoring, rule
change in the baby's well-being in utero out artifacts and consider more intensive
and are most significant if the rate drops fetal monitoring such as a fetal scalp
below 100 bpm. Early decelerations clip for continuous internal FHR moni-
occurring with contractions and then toring.
returning to baseline are probably a
reflex response to head compression What is meconium*?
during the contraction and are usually Meconium refers to the first discharge
benign. Late decelerations are more from the infants intestinal tract. It has
ominous, usually occurring with con- a green appearance and consists of
tractions and having a delayed return to epithelial cells, mucus, and bile. When
the baseline FNR. They often signify meconium is passed by the infant in
fetal hypoxia and acidosis. Variable utero, it colours the amniotic fluid and
decelerations are not associated with indicates that the infant has been sub-
contractions, have a quick onset and jected to a stress at some time.
recovery. They are due to transient Meconium excretion in utero is
cord compression, and are usually observed more frequently in the term or
benign. Sustained bradycardia with a post term infant. A thick "pea-soupn
FNR < 100, indicates serious fetal dis- meconium may suggest a recent episode
tress, and requires urgent intervention. of hypoxia and prompt more aggressive
Sustained tachycardia is often associated fetal monitoring or management of the
with fever or sepsis, but may be labour and delivery.
observed as a response to maternal drug
administration (e.g., atropine or Infants that inhale meconium into their
ephedrine). trachea and lungs may have difficulty
with oxygenation, ventilation and may
If serious FHR decelerations occur, develop complications such as a
what can I do*? pneumothorax or pneumonitis.
Ensure adequate left uterine displace- Meconium may collect in the pharynx
ment to prevent aortocaval compression in the infant and may be inhaled into
(see chapter 18: Obstetrical Anaes- the lungs with their first breath. It is
thesia). Provide supplemental oxygen to paramount that these infants have thor-
the mother. A common way of admin- ough suctioning of their mouth, phar-
istering oxygen is by fitting a face mask ynx, and nasopharynx at the time the
with rebreathing reservoir bag on the head is delivered and prior to their first
mother and setting the oxygen flow rate breath with delivery of the chest. The
to 2 6 litres per minute. Discontinue clinician may also decide to intubate the
the oxytocin infusion if it is being ad- infant immediately after delivery to

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Anaesthesia for Medical Students

Rlsk Factors

Anteaartum IntraDsrtum
Age > 35 Abnormal presentation.
Diabetes Operative delivery.
Pregnancy induced hypertension. Premature labour.
Chronic hypertension. Premature rupture of
No Prenatal Care. membranes.
Maternal Substance abuse. Precipitous labour.
Rh sensitization. Prolonged labour.
Drug therapy (Mg, Li, adrenergic drugs, etc.) FHR abnormalities.
Other CVS, Neuro, or Thyroid illness. Maternal narcotics
Previous stillbirth. (within 4 hrs. of delivery).
2nd or 3rd trimester bleeding General anaesthesia.
Hydramnios Meconium stained fluid.
Oligohydrarnnios Prolapsed cord.
Multiple gestation. Placental abruption.
Post-term. Placenta previa.
Small for dates. Uterine tetany.
Fetal malformation.

Table 19.2: Rlsk Factors predlctlng the need for neonatal resuscltatlon.
/

,
suction as much meconium from the vidual should be capable of perform-
trachea as possible. ing a complete resuscitation (i.e., /

includingendotracheal intubationand
Can I predict which infant may need the use of medications). In many
'
resuscitation at delivery? cases, this is the person delivering
Infants requiring resuscitation may have the infant.
associated pre-existing maternal risk 2. Even for cases when a normal infant
factors, complications arising during is expected, a second person who
labour and delivery, or underlying fetal will be primarily responsible for the /

risk factors. (Risk factors associated infant, must be present in the deliv- ,
with the need for neonatal resuscitation ery room. This person must be able
'
are presented in table 19.2 for reference to initiate a resuscitation and assist
purpose only). the fully trained person, should a full ,
resuscitation become necessary.
'
How do I make sure that I am ready to 3. When neonatal asphyxia is antici-
provide resuscitation for the newborn pated, two individuals whose sole
infant? responsibility is to the infant, should
1. At every delivery, at least one indi- be present in the delivery room and

Page 170
Chapter 19 Neonatal Resuscitation

be prepared to work as a team to preventing excessive heat loss from


perform a complete resuscitation. the neonate.
The person delivering the infant
should not be counted as one of the The Beslcs:
two resuscitators.
4. With multiple births, a team is I: Open the Alrwey**.
needed for each infant. Position the infant supine or on
5. There should be no delay in initiating their side with the neck either in a
resuscitation; waiting a few minutes neutral position or slightly
for someone "on-call" to arrive is an extended. Avoid overextension or
unacceptable practice and invites flexion, which may produce airway
disaster. obstruction. A slight trendelenburg
position is also helpful.
A 1" folded towel under the infants
Radiant heater shoulders may be useful if the
Stethoscope infant has a large occiput.
Suction and suction catheters If the infant has absent, slow, or
Oxygen source and tubing difficult respirations, apply suction
Neonatal resuscitation.bag first to the mouth and then nose.
Airway pressure manometer If the nose is cleared first, the
Face masks, Oral airways.
infant may gasp and aspirate secre-
Endotracheal tubes (2.5, 3, 3.5)
E l l Stylet tions in the pharynx. If mechanical
Laryngoscope suctioning with an 8 F or IOF cath-
Straight blades No. 0 & 1 eter is used, make sure the vacuum
Medications (see text) does not exceed -100 rnrn Hg.
Umbilical catheters (3.5 and 5 Fr.) Limit suctioning to 5 seconds at a
Umbilical catheter tray time and monitor heart rate for
Needles and syringes bradycardia, which may occur with
ECG monitor deep oropharyngeal stimulation.
If meconium is present in the
Table 19.3: Baslc Neonatal Re- amniotic fluid, special endotracheal
suscltatlon Equlpment. suctioning may be required in the
depressed infant.
Equipment: (see table 193)
(for reference only). 11: Keep the infant warm end dry**.
1. Equipment and medications should
be checked daily, and prior to an- Place the infant under an overhead
ticipated use. radiant heater. Dry the body and head
to remove amniotic fluid and prevent
2. The delivery room should be kept heat loss. The gentle stimulation will
relatively warm and the radiant also help initiate and maintain breath-
heater should be preheated. Warm ing.
blankets can also be helpful in

** Must Know Should Know Page 171


Anaesthesia for Medical Students

111: Physical Stimulation**. -


should be between 40 60 breaths per
If drying and suctioning do not minute. Initial lung inflation pressures
induce effective breathing, gently may be as high as 30 - 40 cm of 40 to
slapping or flicking the soles of the
feet or rubbing the infants back
r
may be useful.
Do not waste time continuing tac-
tile stimulation if there is no Method
-
response after 10 15 seconds.

IV: Evaluate the infant**.


Res~irations:Infants who are apneic or
gasping despite brief stimulation
attempts should receive positive pres-
sure ventilation.
Heart Rate: Monitor either by
auscultating the apical beat or by palpat-
ing the base of the umbilical cord. If
the heart rate is below 100 bpm, begin
positive-pressureventilation, even if the
infant is making some respiratory
efforts.
Colour: The presence of central
cyanosis indicates that although there is
enough oxygen passing through the
lungs to maintain the heart rate, the
infant is still not well oxygenated. A Fig. 19.2: Adapted with permission
face mask with oxygen at 5 Umin.
should be held closely to the infants
face until the infant becomes pink. ,I
987,1990.

Technique of Positive Pressure Venti-


lation (PPV): overcome the elastic forces of the lungs
Ventilatory support is required when**: if the infant has not taken their first,
Apnea or gasping respirations are breath. Subsequent ventilation should
present. be achieved with airway pressures of 1 5
The heart rate is less than 100 bpm. -20 cm H20.
Central cyanosis persists despite
100% oxygen. Adequate ventilation is assessed by**
observing chest wall motion and hearing
Most neonates can be adequately venti- breath sounds bilaterally. If chest ex-
lated with a bag and mask (see figure pansion is inadequate:
193). The assisted ventiiatory rate

Page I72
Chaplcr 19 Neonalal Rcsuscilalion

reposition the head; consider extend- accompanied by ventilation with 100%


ing the head a bit further and oxygen. Asphyxia in the neonate not
repositioning the shoulder towel. only slows the heart rate but decreases
suction any secretions. myocardial contractility, resulting in
consider an oral airway, and ventilat- diminished blood flow and oxygen
ing with the infants mouth slightly delivery to vital organs.
open.
increase ventilation pressures to 20 - When should I start chest com-
40 cm H20 pressions* *?
if unsuccessful, abandon the bag and You should begin chest compressions
mask technique, and intubate. when the heart rate remains below 80
bpm despite PPV with 100% 0,. Chest
-
After 15 30 seconds of effective venti- compressions can be discontinued when
lation, the heart rate of the neonate the heart rate is 80 bpm or greater.
should be re-evaluated. The heart rate
over a 6 second period is counted and What is the proper technique for admin-
multiplied by 10 to give an approxima- istering chest compressions to an
tion of the 1-minute heart rate. (e.g., 8 infant*"?
beats in 6 seconds = 80 bpm). There are two methods of compressing
the chest in infants. Using the thumb
Positive pressure ventilation can be method, both hands encircle the torso,
gradually withdrawn if the HR > 100 with the fingers supporting the back,
and spontaneous breathing efforts are while the thumbs are positioned side by
present. The care provider should con- side over the sternum, creating chest
tinue to provide physical stimulation compression with downward displace-
and supplemental 0,to the infant. ment of the sternum. Using the two-
finger approach, the middle and ring
If the HR is less than 100, ventilation fingers of one hand are held perpendicu-
should continue. Chest compressions lar to the chest as the finger tips apply
are initiated if the HR is less than 80 pressure to the sternum. The other hand
and decreasing. When the heart rate is is used to support the infants back from
less than 60, immediate ventilation with below (see figure 19.2).
100% oxygen is instituted with simulta- The amount of pressure applied with
neous chest compressions. compressions is adjusted to achieve 1.5
cm of displacement. A full "cycle
Chest Compressions: consists of both a compression and
Compression of the sternum results in release phase. This rate is adjusted to
compression of the heart and increases achieve 2 cycles per second or I20
intrathoracic pressure. During compres- compressions per minute.
sion, blood is pumped into the arterial
circulation. Release of the sternum Once the fingers (thumbs) have been
results in an increase in venous return to correctly positioned over the sternum,
the heart. Chest compressions must be care should be taken to ensure that the

** Must Know Should Know Page 173


Anaesthesia for Medical Students

hands are not moved from this position. Prolonged PPV is required (to mini-
Valuable time may be wasted attempt- mize gastric distention).
ing to relocate the correct hand position. Ventilation with a bag and mask is
Complications of incorrect hand place- ineffective (poor chest expansion,
ment and chest compression include persistent low HR).
fractured ribs, lacerated spleen, and Tracheal suctioning required (thick or
pneumothorax. particulate meconium).
Diaphragmatic hernia suspected (to
When the infant is intubated and re- prevent bowel distension in the
ceiving simultaneous ventilation and chest).
chest compressions, ventilation at a rate
-
of 40 60 per minute with independent, While endotracheal intubation may play
concurrent chest compressions at a rate an essential part of an infants resuscita-
of 120 per minute is recommended. tion, it is neither the purpose, nor in the
scope of this chapter to discuss the
Air may be forced into the infants stom- technique, confirmation, or complica-
ach if they are receiving simultaneous tions of this intervention. We hope that
PPV (with a bag and mask) and chest this chapter will provide you with a
compressions. Hence when the infant is stepping stone for your future courses in
being ventilated with a bag and mask, neonatal resuscitation.
ventilation should be interposed between
compressions. Every three chest com- Which four common drugs used in re-
pressions are followed by a pause to suscitation of the depressed neonate
interpose an effective breath. The re- should I be familiar with?**
sulting 90 compressions with 30 ventil-
ations yield a combined rate of com- 1. Oxygen.
pressions and ventilation of 120 per 2. Intravenous Fluids.
minute. The variation in recommended 3. Epinephrine.
rates of ventilation and chest compres- 4. Naloxone.
sions between the intubated and non
intubated infant is an attempt to mini- Oxygen:
mize the risk of gastric distention and
(or) aspiration. For the majority of infants who require
resuscitation, the only medication
Compressions are interrupted after the needed will be 100%oxygen delivered
first 30 seconds, to make a six second with effective ventilation. Some will
heart rate count. Compressions are require chest compressions, and a small
stopped once the heart rate is above 80, minority of resuscitated infants will
and ventilation is stopped when the require other medications, such as epin-
heart rate is above 100. ephrine, intravenous fluid resuscitation,
or other special drugs.
Endotracheal intubation is indicated
when*:

Page 174
Chapter 19 Neonafal Resuscitation

Intravenous flulds: What is the normal blood pressure and


How will I know whether or not the blood volume in a term infant?
infant is hypovolemic?
On average, the blood pressure in a
Conditions which result in acute term infant is 70144. Hypotension in
maternal hypovolemia prior to delivery the neonate has been defined as a sys-
of the infant, should make the clinician tolic blood pressure of less than 50 mm
suspicious that the infant may also be Hg in a term infant (see table 19.4).
suffering from the effects of hypo- The normal blood volume in a term
volemia. Maternal hemorrhage prior to -
neonate is 80 100 mllkg. Hence in a
delivery is one such condition. A few 3 kg infant with a blood volume of 250
of the causes of maternal hemorrhage ml, a loss of only 50 ml represents 20%
prior to delivery include placental ab- of their blood volume.
ruption, placenta previa, transection of
the placenta during caesarean section,
and maternal trauma. Other conditions Weight SBP DBP MAP
that may result in neonatal hypovolemia
(grams)
include multiple gestation pregnancies,
umbilical cord tear during delivery, and 1000- 49 26 35
a strangulating umbilical cord requiring 2000
umbilical cord transection for delivery.
2000- 59 32 43
3000
Hypovolemia occurs more frequently in >3000 70 44 53
the newborn than is commonly recog-
nized. Blood loss is often not obvious Table 19.4: Average blood pres-
and initial tests of hemoglobin and sures at blrth.
hematocrit are usually misleading. The
increase in vascular volume secondary
to a volume expander should improve What conditions, other than hypovol-
tissue perfusion and reduce the develop- emia, may result in hypotension in the
ment of metabolic acidosis. neonate ?
Other conditions include:
Clinical signs of hypovolemia resulting Hypoglycaemia (diabetic mother)
from an acute loss of greater than 20% Hypocalcemia (Intrauterine asphyxia)
of the blood volume include: Hypermagnesemia ( ~ g - therapy for
Pallor persisting after oxygenation. the pre-eclamptic mother)
A weak pulse despite a good heart Sepsis (chorioamnionitis or prolonged
rate. rupture of membranes)
A poor response to resuscitative Pneumothorax (meconium aspiration)
efforts. Cardiac pathology
A decreased blood pressure (< 55/30). Diaphragmatic hernia

** Must Know Should Know Page 175


Anaesthesia for Medical Students

Assuming we've made a correct diag- ml or 0.1 mg per ml). The intravenous
nosis of hypovolemia, how can we cor- dose is 0.01 to 0.03 mg per kg. In a 3
rect it? kg infant, a 114 ml to 314 ml of epin-
The most commonly used volume ephrine would be an appropriate starting
expanders are normal saline and ringer's dose, as this would be equivalent to 25
lactate. Other volume expanders to 75 mcg (approximately 0.01 to 0.03
include 5% albumen, and 0-negative m a g ) . If an intravenous route is un-
blood cross matched with the mother's available, epinephrine can be given
blood. The volume of fluid adminis- through the endotracheal tube. Epin-
tered should be equivalent to 10 mlkg, ephrine given by endotracheal route
and this should be given as an infusion should be diluted with 1-2ml of saline.
-
over 5 10 minutes. In a 3 kg infant When given by the E n , plasma con-
this would be equivalent to 30 ml. centrations may be lower compared to
the intravenous route. If the infant does
Eplnephrlne: not respond to the initial E'JT epin-
ephrine dose, the endotracheal epin-
When should I consider giving epin- ephrine dose is increased by a factor of
ephrine*? ten (0.1 - 0 2 mgkg).
Epinephrine is indicated if no heart rate
can be detected or if the heart rate per- Naloxone*:
sists below 80 bpm despite adequate What is naloxone and when should I
ventilation with 100% oxygen and chest consider giving it?
compressions for at least 30 seconds. Naloxone is a pure opioid antagonist
without intrinsic respiratory depression
Why is epinephrine such an important activity. Naloxone is indicated for the
drug in neonatal resuscitation? reversal of respiratory depression when
Epinephrine has both a (alpha) and the mother has received opioids within
(beta) adrenergic stimulating properties. 4 hours of delivery and the infant is
The alpha effect causes vasoconstriction observed to have depressed respirations.
which raises the perfusion pressure While naloxone works very rapidly,
during chest compressions, augmenting adequate ventilatory assistance should
oxygen delivery to both the heart and always be provided first. The duration
brain. The beta effect enhances cardiac of naloxone is shorter than that of some
contractility, stimulates spontaneous opioids, making respiratory monitoring
contractions and increases the heart rate. mandatory for a further 4 to 6 hours.

How can I give epinephrine? Naloxone can be given either intra-


Epinephrine can be given either intra- venously or by an endotracheal tube.
venously or by the endotracheal tube Subcutaneous or intramuscular routes
every 3 to 5 minutes as required. The can also be used if the infants perfusion
epinephrine concentration used in neo- is adequate, however, the onset of
natal resuscitation is supplied as a action may be slower with these routes.
1:10,000 dilution (i.e. 1 gram in 10,000 If maternal opioid addiction is suspect-

Page 176
3
/ Place under radiant heater
-
(Suction trachea if meconium stained fluid)
Dry thoroughly
Remove wet linen
Position
Suction mouth then nose
Provide tactile stimulation

Chest Compressions

HR c 80 after 30 secsdespite Figure 19.3: An overview of Resuscitation in the Delivery Room.


PPVwitt~1000b02and Reproduced with permission. Textbook of Neonatal Resuscitation.
chest Compressions @ 1994 American Heart Association.
Anaesthesia for Medical Students

ed, it is probably prudent not to give References:


naloxone. Rather, simply support 1. Bloom RS, Cropley C. Textbook
ventilation until respiratory drive is of Neonatal Resuscitation. ed.
adequate. Administrating naloxone to Chameides L and the AHAIAHP
infants of opioid dependent mothers Neonatal Resuscitation Steering
may result is a withdrawal reaction and Committee. American Heart Asso-
severe seizures in the infant. Naloxone ciation, 1990.
is supplied in a 0.4 mg/ml concentration
for neonatal resuscitation. The dose is 2. Emergency CardiacCare Committee
0.1 mg/kg for infant resuscitation, and and Subcommittees, American
hence a typical 3 kg infant would Heart Association. Guidelines for
require 314 of a m l (iv, Em, im, or sc) cardiopulmonary resuscitation and
of naloxone (0.4 mg/ml) as an initial emergency cardiac care, VII: neona-
dose. tal resuscitation. JAMA 1992;
268:2276-2281.
Notes:
3. Christenson JM, Solimano AJ,
Williams J, et al. The new
American Heart Association
guidelines for cardiopulmonary
resuscitation and emergency care:
presented by the Emergency
Cardiac Care Subcommittee of the
Heart and Stoke Foundation of
Canada. Can Med Assoc J
1993;149:585-590.

Page 178
i
Chapter 19 Neonatal Resuscitation
1

" Must Know Should Know Page I79


Intravenous Fluid and
Blood Component
Therapy
WAYNEBARRYMD., FRCPC

Optimal perioperative fluid therapy Body Fluid Compartments:


requires an understanding of the Total body water (TBW) constitutes
changes that occur in the volume and 60% of the body weight, or approxi-
composition of the body fluid compart- mately 42 liters in a 70 kg adult. Two
ments. Intravenous fluids are used to thirds of the TBW is contained within
replenish fluid losses while maintaining cells as intracellular fluid (ICF). The
the blood volume, coagulation status, ICF represents 40% of the body weight,
and oxygen delivery. Inadequate fluid which is approximately 28 liters in a 70
therapy risks organ hypoperfusion, kg adult. The remaining 113 of the
coagulopathy, and electrolyte imbal- TBW exists outside the cells as extra-
ances. Excessive fluid therapy risks cellular fluid (ECF). It represents 20%
circulatory overload as well as organ of the body weight or 14 liters of water
and tissue edema. To avoid inadequate in a 70 kg adult (see table 20.1).
or excessive fluid therapy, the clinician
must makes serial evaluations of the Sodium (140 meqA) and potassium (150
patients fluid requirements in terms of meqA) are the principle cations in the
their maintenance fluids, fluid deficit, ECF and ICF respectively. Albumen
third space losses, and ongoing blood (40 g d ) is the primary molecule res-
losses. ponsible for the oncotic pressure gener-
ated by the ECF. Aldosterone and
With this in mind, this chapter shall antidiuretichormone (ADH) increase the
enable the reader to calculate: extracellular fluid volume by increasing
salt (aldosterone) and water (ADH)
1. Maintenance fluid requirements reabsorption. Atrial natriuretic protein
2. Fluid deficit estimation decreases the ECF volume by promoting
3. Ongoing fluid 3rd space losses, and salt and water excretion.
4. Fluids required to replace blood lost.
I. MalntenanceFluidRequirements*:
We shall also review the indications and Intravenous fluid requirements for
complications of transfusing blood prod- periods of less than one week can be
ucts. provided for with water, sodium, and

Page 180
Chopfer 20 Infrovenous Fluid ond Blood Component Theropy

Compartment % Body Welght Volume In llters 1 70 kg

Total
Male (70 kg) 60 42
Female (70 kg) 50 35

ECF' 20 14
Plasma 4 2.8
Interstitial Fluid 16 11.2
I CF 40 28

Table 20.1: Distribution of body water. *Ihe ECF represents approximately 113
-
(range 27 45%) of the total body mass, while the ICF occupies approximately 213
of the total body mass.

potassium; Chloride, magnesium, cal- of 112 normal saline with 15 - 20 meq


cium, and other trace mineral of potassium per liter. At maintenance
supplementation is required for patients infusion rates, this will meet the patients
needing chronic intravenous mainten- daily water, sodium and potassium
ance therapy. As hyperglycemia is a requirements.
notmal response to surgery, dextrose is
recommended only for those patients at Intravenous fluids for surgery scheduled
risk of hypoglycemia (e.g., infants and to be performed within 24 hours:
diabetic patients). N o m l saline, or ringer's lactate are the
preoperative intravenous fluids of choice
A normal 70 kg adult requires approxi- for surgery scheduled within 24 hours.
mately 2 5 liters of water a day with 75 The rationale for this recommendation
meq of sodium, and 40 meq of potas- includes:
sium. Water and salt administration in 1. Potassium replacement is not
excess of this, will result in their excre- required for brief periods of time.
tion in the urine (provided cardiac and 2. Intravenous fluids containing potas-
renal function are normal). sium pose a potential hazard should
the patient receive an inadvertent
Intravenous fluids for a period of > 24 fluid bolus (e.g., rapid i.v. adminis-
hours and < 1 week: Preoperative fluid tration for hypotension associated
requirements during this period of time with the induction of anaesthesia).
can usually be met with a solution of 3. Normal saline and ringer's lactate are
213 of 5% dextrose with 113 normal the most common fluids administered
saline (referred to as 2/3rds, 1/3rd) with intraoperatively, as they are used to
-
15 20 meq of potassium per liter. replenish the sodium rich plasma and
Alternatively, we could use a solution interstitial fluid compartments.

" Must Know Should Know Page 181


Anaesthesia for Medical Students

Table 20.2: Maintenance water requirements


Per hour* * Per Dav * *
1st to 10th kg 4 mlkg 100 mlkg
11th to 20th kg 2 mlkg 50 mlkg
21st to nth kg 1mlkg 20 mlkg

Exercise caution when administering ments by the number of hours fasted.


crystalloids such as NS or RL to (Fluid Deficit = Maintenance require-
patients with congestive heart failure, ments per hour x number of hours
renal failure, or advanced age. In these fasted). A fluid deficit resulting from a
patients, a preoperative intravenous pathological process is much more
solution of 2L3rds and 1/3rd may be difficult to quantify accurately. Table
more appropriate. 20.3 lists clinical conditions frequently
associated with fluid deficits, with asso-
Maintenance fluid requirements for any ciated physical and laboratory findings.
body weight can be calculated using the For example, a patient with a fractured
" 4 - 2 - 1 h l e for hourly fluid require- -
hip may have 1 2 liters of blood se-
ments or the "100-50-20"mle for daily questered in their thigh tissues. When
fluid requirements (see table 20.2). For such significant fluid deficits are not
example, a 75 kg adult will require: appreciated and corrected prior to anaes-
thesia, profound cardiovascular collapse
Per hour: may occur with induction of anaes-
10 kg x 4 mlhr = 40 mlhr thesia.
10 kg x 2 mlhr = 20 mlhr
55 x 1mlhr = 55 mlhr 111. Third Space Losses*:
Total: 75 kg 115 mlhr A reduction in ECF volume during
surgery results from evaporative losses,
Per day: exudative losses, tissue edema second-
10 kg x 100 mllday = 1000 ml ary to surgical manipulation, and fluid
10 kg x 50 mllday = 500 ml sequestration in organs, such as the
55 x 20 mllday = 1100 ml bowel and lung. These fluid losses can
Total: 75 kg 2600 mllday be surprisingly extensive. The simplest
guideline for replacing third space fluid
losses is a 4 - 6 - 8 mllkglhr rule. Four
11: Fluld Deficit Estimation*: for minor, 6 for moderate, and 8
A fluid deficit may develop as a result mlkg/hr for major surgical trauma. For
of a period of fasting or a pathologic example, we can anticipate that a bowel
process. The fluid deficit from fasting resection will have 6 mlkg/hr of 3rd
can be calculated by multiplying the space fluid losses during the operation.
patient's hourly maintenance require- This fluid is usually administered as

Page 182
Chapter 20 Intravenous Fluid and Blood Component Therapy

Table 203: Common conditions associated with preoperative fluid deficits.

Fractured hip, femur, pelvis Protracted vomiting and diarrhea


Bowel obstruction Bums
Preoperative bowel preparation Sepsis
Trauma Pancreatitis

Common physical findings supporting a preoperative fluid deficit.


Tachycardia Tachypnea
Orthostatic hypotension Decreased jugular venous pressure (JVP)
Supine hypotension Dry mucous membranes
Oliguria (c 0 5 ml/kg/hr) Decreased tissue turgor
Common laboratory findings associated with a fluid deficit.
Elevated urea Elevated urine osmolarity
Elevated creatinine Elevated hematocrit
Low urinary sodium
concentration (U, c 20 mM)

either normal saline or ringer's lactate, solutions may be synthetic (e.g., penta-
and must be given in addition to the span, hetaspan, dextran), or collected
patient's maintenance requirements, from the donor blood pool (eg. albu-
calculated fluid deficit, and ongoing men, plasma, whole blood).
blood losses. Mobilization of third
space fluid occurs approximately 72 If 1000 ml of NS is infused intra-
hours after surgery, and may result in venously, only 113 (approx. 300 ml) will
circulatory overload in the patient with remain in the intravascular compart-
compromised cardiac or renal function. ment. The remaining 213 (- 700 ml)
will move into the interstitial and intra-
IV. Blood Loss Replacement*: cellular compartments. As a conseq-
Intravenous crystalloid or colloid sol- uence, 3 to 5 times the volume of
utions may be administered to replenish blood lost must be infused when crys-
the intravascular volume. Crystalloid talloids such as NS or R L are used to
solutions are salt containing solutions maintain the intravascular volume.
that are semipermeable to cellular mem- With colloid solutions, however, blood
branes. Examples of crystalloid sol- losses can be replaced on a 1:l volume
utions include NS, RL, and 213, 113 basis.
intravenous solutions. By contrast,
colloid intravenous solutions contain D5W:
aggregates of molecules that resist diffu- Similarly,the intravenous administration
sion across cellular membranes. Colloid of 1000 ml of D5W (5% dextrose in

** Must Know Should Know Page 183


Anaeslhesia for Medical Students
)

Table 20.4: Common intravenous solutions and their cornponenls.


SoluCon Dextrose Na CI K pH Osm Other
&dl meqA
Plasma 140 103 4 7.4 290 Ca 5 meqA
D5W 5 5.0 253
u3 D5W,l/3 NS 3.3 51 51 4.8 270
2/3,1/3 + 20 meq KCL 3.3 51 51 20 4.8 290
0.9% Saline (NS) 154 154 5.7 308
Ringer's lactate 130 109 4 6.7 273 Ca l.SmeqA,
lactate 20
meqA
0.45% Saline (SNS) 77 77 5.3 154
Pentaspan 154 154 5.0 326 10gmIdl
pentastach

water), results in minimal intravascular Sallne:


volume expansion, because most of the The infusion of large amounts of intra-
fluid moves into the interstitial and venous NS (e.g., trauma resuscitation)
intracellular compartments. Hyponat- may be accompanied with a hyper-
remia, hyperglycemia and a decrease in chloremic, hypematremic non anion gap
serum osmolarity will result when large metabolic acidosis. In trauma patients,
volumes of D5W are infused. For these this source of acidosis is commonly
reasons, D5W is a poor choice for cor- overlooked by clinicians. An increase in
recting a blood volume deficit. More- minute ventilation, produces a respira-
over, large amounts of D5W should be tory alkalosis, which is the normal com-
avoided in patients receiving oxytocin, pensation for an acute metabolic acido-
because oxytocin's inherent ADH effect sis. This additional respiratory work, in
may result in hyponatremia and water a spontaneously breathing patient, may
intoxication. be detrimental in a patient with other
coexisting disease.
The severity of an ischemic cerebral
event may be increased if iatrogenic Chronic gastric losses may produce a
hyperglycemia is induced with the ad- hypochloremic metabolic alkalosis. The
ministration of dextrose containing administration of NS can be used to
fluids. This has special relevance for correct this abnormality.
neurosurgical procedures, and patients
with cerebrovascular pathology.

Page 184
.avenous Fluid and Blood Component Therapy

Ringer's lactate: dilution of platelets and coagulation


Ringer's lactate solution contains 4 factors4. A maximum volume of 2000
meqfl of potassium, and should be used ml per 24 hours is recommended.
with caution in patients with pre-exist-
ing hyperkalemia or renal failure. Side effects of pentaspan include circu-
Patients with chronic diarrhea may latory overload (pulmonary edema,
develop a h yperchloremic metabolic congestive heart failure), altered coagu-
acidosis. This will respond to treatment lation (prolonged clotting times, pro-
with a bicarbonate (lactate) containing longed INR and P'fi), and hypersensi-
solution, such as ringer's lactate. tivity reactions such as wheezing and
urticaria. It is contraindicated in
The administration of hypotonic sol- patients with bleeding disorders, renal
utions to patients with brain injury may disease, and circulatory overload. It is
contribute to brain cell swelling. As supplied in 100, 250, and 500 ml infu-
saline is relatively more hypertonic than sion bags. Hetaspan and dextran are
RL, it is generally the preferred two other synthetic intravenous colloids.
crystalloid for these patients (see table We use them less frequently at our
20.4). centre because there is an increased
incidence of anaphylactoid reactions
Pentaspan: associated with them.
Pentaspan has the same sodium and
chloride concentration as NS. Each 100 Albumen:
ml contains an additional 10 grams of Albumen is available as a 5% and 25%
pentastarch, of which 70% is eliminated solution. It is heat treated at 60°C for
by the kidneys within 24 hours. The 10 hours to eliminate bacterial and viral
plasma volume expansion achieved is contamination. Administration of the
equal to the volume of pentaspan ad- 5% solution will produce an equal
ministered (1:l ratio). Pentaspan is increase in intravascular volume expan-
more expensive than crystalloid so- sion. Administration of the 25% sol-
lutions, but less expensive than other ution will draw interstitial fluid into the
blood substitutes such as albumen. intravascular space and increase the
intravascular volume by a factor of 4
Note, however, that pentaspan is not a times the albumen volume. Albumen
RBC substitute and has no oxygen can be used as a plasma volume
carrying capacity. The hemodynamic expander in patients with adequate
effects of pentaspan are equal or oxygen carrying capacity, however it is
superior to those of albumen. Both not recommended as a method of cor-
result in expansion of the plasma vol- recting nutritional deficiencies.
ume, with increases in preload, cardiac
output, and oxygen delivery. Increases Autologous blood:
in bleeding and clotting times resulting Autologous blood involves the preoper-
from an infusion of albumen or penta- ative collection of blood from a patient
starch are believed to be secondary to a who is scheduled to have surgery, and

** Must Know Should Know Page 185


Anaest/tesia for Medical Students

for whom one anticipates the need for a 3 0 to 5 0 gm1L. Such an acute decrease
perioperative blood transfusion. Con- in hemoglobin is only tolerated when
trary to popular belief, autologous blood normovolemia is maintained, and mech-
is discarded if it is not administered to anisms to increase oxygen transport by
the donor. As it is not placed in the increasing cardiac output and 2,3 DPG
general donor homologous blood pool, levels are intact. Patients with cardiac
patients should not be encouraged to disease or atherosclerotic lesions that
donate autologous blood on the basis restrict blood flow to vital organs are
that it could benefit someone else. limited in their ability to adapt to acute
Patients with bacterial or viral infections anemia. A balance between the risk of
are not suitable donors, as there is a risk transmitting an infectious disease, and
of exposing other patients to the con- the need for administering blood prod-
taminated blood (e.g., clerical error). ucts for their oxygen carrying capacity
Suitable candidates are able to donate a and coagulation properties, must be
maximum of 1 unit of blood every 4 to reached in each patient undergoing
7 days, and should stop donating three surgery.
or more days prior to the planned pro-
cedure. Unsuitable candidates include Postoperative hemoglobins in the range
patients with a hemoglobin level less of 60 to 8 0 gm/L are now considered
than 110 gmL, and patients with acceptable in patients who do not have
unstable angina or critical aortic cardiovascular disease. Transfusion
stenosis. As the maximum shelf life of should be used only to replace losses
stored blood is 3 5 days, a donor could beyond this level. Nevertheless, even a
donate up to 4 units prior to surgery. modest anemia with hemoglobin levels
Oral iron andlor recombinant erythro- of 8 0 to 100 g& requires an increase
poietin therapy may be used to increase in heart rate and stroke volume to meet
the number of units that can be coll- the body's oxygen requirements. This
ected preoperative1 y. Autologous blood introduces an additional cardiac stress.
is not separated into components like Physicians must consider the con-
homologous blood, but rather is stored sequences of this imposed cardiac stress
as whole blood. when deciding to transfuse patients with
moderate anemia and coexisting
Acceptable blood loss*: atherosclerosisorcardiovasculardisease.
We do not have a universal answer to In the end, each patient must be evalu-
the question "What is the minimal ac- ated individually.
ceptable hemoglobin?" Evidence sug-
gests that a r~ormalcirculating blood Questions that may be helpful in formu-
volume can be reduced by as much as lating a decision to administer blood
25% with little stress being placed on products to a particular patient include:
the patient, provided that the intra-
vascular blood volume is maintained. 1. Does the patient accept the possibil-
Animals are able to tolerate acute reduc- ity of receiving blood products?
tions in hemoglobin to levels between 2. If anemic, is this an acute anemia or
Chopfer 20 I ~ ~ f r a v e ~ r oFluid
us artd Blood C o m p o ~ i e ~ tTl~erapy
r

a chronic anemia to which the fusing blood products, we can calculate


patient has adapted? the acceptable blood loss (ABL).
3. Is the patient likely to lose more
blood in the immediate future? ABL = Hb(i) - Hb(Q x EBV
4. Does the patient have risk factors for Hb(i .)
atherosclerosis, coronary artery dis- Hb(i) = Initial hernoglobill
ease, or cerebrovascular disease? = 150 gm/L
(e.g., Smoking history, hypertension, Hb(Q = Final hemoglobin
diabetes, hypercholesterolemia, per- = 90 gm/L
sonal or family history of heart
disease). Therefore:
, 5. Is their evidence of a coagulopathy
in which additional blood loss is 150
-
ABL = 150 90 x 4900 = 1960 ml

1 anticipated (prolonged INR, PIT, or


decreased platelets)? The most common blood products ad-
6. Does the blood loss exceed what was ministered are whole blood (autologous
calculated as the acceptable blood blood donors), packed red blood cells
1 loss for this patient? (see text below). (RBCs), platelets, and fresh frozen
7. Is the patient hemodynamically plasma. One unit of whole blood has a
) volume of 500 ml, while a unit of
unstable despite other fluid resuscita-
tion? packed RBCs has a volume of epproxi-
mately 300 ml (including their
i - - - - - -
anticoagulant volume). One unit of
i Table 20.5 Blood Volume packed RBCs will raise the hemoglobin
rnllkg by 10 gm/L in the average adult. Alter-
natively, 3 m l k g of RBCs will raise the
) Premature infant 90
hemoglobin by 10 gm/L. This later
Term infant 80 formula is useful for calculating the
Slim male 75 volume of blood required for transfusion
Obese male 70 in neonates and infants. Packed RBCs
Slim female 65 are indicated when there is a deficiency
Obese female 60 in the patients oxygen carryingcapacity.

Fresh Frozen Plasma:


Calculation of tire acceptable blood Fresh frozen plasma contains all coagu-
loss: lation factors at levels close to normal
Since, an adult male has a blood vol- plasma levels. It is indicated to replace
ume of 70 ml/kg (see table 20.5), the deficiencies of factors 11, V, VII, IX, X,
estimated blood volume (EBV) is 70 kg XI and antithrombin 111. All coagu-
x 70 ml/kg = 4900 ml. If the initial lation factors, with the exception of
hemoglobin is 150 gm/dl and we have factors V and VIII, are stable in whole
decided that we will allow the hemo- blood. Factors V and VIII decrease to
globin to drop to 90 gm/L before trans- 15 and 50% respectively by 21 days of

** Must Know SItould K I ~ O I V Page 187


i
Pnaesthesia for Medical Shtdents

\
/ Potential Cornplicatlons of Blood Tramfuslonsn

5. WBC's -
3. Cold ---+ Hypothennia
4. RBC1s +MajorIMinor reactions
Febrile reaction

Dilutional coagulopathy

9. Microaggreg+Dyspnea

Figure 20.1: The components of whole blood all have potential side
effects. By recalling the components of whole blood, one can readily
recall their potential complications with their administration.

storage. However, only 20 percent of A dilutional coagulopathy may result


factor V, and 30% of factor VIII are when coagulation factor levels decrease.
needed for adequate hemostasis. This occurs with a RBC transfusion
equivalent to one blood volume ( z 10
Packed RBCs, however, do not have units of PRBCs in adults). When the
adequate amounts of coagulationfactors, blood loss approaches one blood vol-
and fresh frozen plasma is frequently ume, in a patient with a previously
useful in correcting deficiencies in normal coagulation status, fresh frozen
factors V and VIII when transfusing plasma should be considered. Once
multiple unitsts of packed RBCs. Fresh fresh frozen plasma is required, one unit
frozen plasma is also indicated in will be required for every two units of
patients with liver disease who are PRBCs.
bleeding and have multiple coagulation
defects. Patients taking coumadin re- Platelets:
quiring emergency surgery may benefit Platelet transfusions are indicated after
from vitamin K, and FFP to correct massive transfusion (> 1blood volume
their coagulation defect. transfused), associated with abnormal

Page 188
Chapter 20 Intravenous Fluid and Blood Component Therapy

bleeding and dilutional thrombo- step becomes especially important when


cytopenia. Acute thrombocytopenia administering multiple units of blood.
(platelet count 50,000 - 100,000 x 109/1) Figures 20.2 and 2 0 3 illustrate a simple
accompanied by microvascular bleeding method of checking the ABO com-
is an indication for platelet transfusion. patability when type specific blood is
Platelets may be indicated prophylactic- not available and another ABO group
ally in the severely thrombocytopenic must be used for blood product adminis-
patient (e.g., thrombocytopenia second- tration.
ary to chemotherapy). Patients with
disorden resulting inplatelet destruction 1. A i c During operative procedures
or sequestration (e.g., hypersplenism)do when blood loss is brisk, the blood
not usually require platelet transfusions. products may be pressurized to
The administration of one unit of facilitate rapid administration.
platelets to an adult will raise the Whenever blood is administered
platelet count by approximately 5,000 - under pressure, the risk of air em-
10,000 x lo9A. Once platelet products bolism exists. Blood units that are
-
are required, 1 2 units of platelets for now used to warm blood during
every two units of PRBCs, are needed rapid administration incorporate an
to maintain hemostasis. air trap to minimize this risk.

Potentlal Compllcatlons of blood 2. Volume: Excessive administration


transfusions**: of blood products may result in
The most common cause of an ABO circulatory overload with pulmon-
incompatible transfusion results from a ary edema, and congestive heart
clerical error in patient and blood identi- failure.
fication. Each unit must be checked
prior to transfusion, preferably by two 3. Cold: The rapid administration of
individuals. The patient's name and cold blood (massive transfusion)
identification number must be identical can result in a precipitous drop in
to that on the unit of blood. The ABO the core body temperature.
and Rh type, blood product number, Ventricular dysrhythmias are more
requisition number, expiry date, and any likely if the temperature drops
special precautions should also be below 30°C. 7he risk of
checked. ventricular fibrillation peaks at
28OC.
Figure 20.1 lists the potential complica-
tions of blood transfusions. As ABO 4 . RBCs: Immediate hemolytic
errors are the most common and serious transfusion reactions are caused by
errors made in the administration of the recipient's red cell antibodies
blood products, it is prudent to know (e.g., anti-A or anti-B) binding
the patients ABO blood group and compliment and lysing the
ensure this is correct before checking transfused RBCs. They are usually
and administering blood. This simple the result of an ABO incom-

1
** Must Know Should Know Page 189
/
4naesrhesia for Medical Shtdenrs
)
patibility. The destruction occurs lets, FIT, or cyroprecipitate as indi-
immediately, and as little as 20 ml cated.
may initiate a reaction. The
reaction is characterized by severe RBCs: Delayed hemolytic transfu-
signs and symptoms which may -
sion reactions occur 2 21 days
include: chills, fever, dyspnea, after the transfusion. Unlike the
nausea, and chest or flank pain. immediate ABO transfusion reac-
Under anaesthesia, other signs such tion, these reactions are often not
as hypotension, wheezing, hypox- preventable. They are usually due
emia, abnormal bleeding, and to trace antibodies formed after a
hemoglobinuria may be noted. previous transfusion or pregnancy.
Free hemoglobin is released from The concentration of these antibod-
the lysed RBCs and is present in ies is so low they go undetected at
the urine and plasma (red urine and the time of compatibility testing.
plasma). The most serious compli- The antibodies in the recipient's
cations are acute renal failure (from blood coat the transfused blood
the hemoglobin obstructing the cells but do not result in immediate
.
tubules), and coagulopathy Treat- lysis. Later, the reticulo-endothelial
ment includes: system (RES) removes the cells
from the circulation. The usual
A. Stop the blood immediately. course is benign and often only
B. Notify the blood bank of the prob- detected because of the drop in
lem. hemoglobin and rise in bilirubin.
C. Send the remaining blood, as well
as blood samples from the patient 5. WBCs: White blood cells cause
to the lab. febrile reactions. These reactions
D. Send a urine sample for analysis may be accompanied by nausea,
(hemoglobinuria). chills, headaches and myalgias.
E. Administer oxygen. Less commonly, chest pain,
F. Support the circulation (ephedrine, hypotension, and vomiting may
epinephrine, dopamine). occur. Other causes of a fever
G. Promote a diuresis and renal excre- during a transfusion includes major
tion of hemoglobin by administer- transfusion reactions (see above),
ing fluids, mannitol, furosemide, reactions to platelets, and fever
and/or dopamine. Consider alkalin- arisingfrom bacterial contamination
izing the urine with intravenous of the blood. Acetaminophen may
sodium bicarbonate administration. be helpful in minor reactions.
Maintain a minimal urine output of Occasionally, WBC filters, or WBC
-
1 2 ml/kg/hr. reduced blood products may be
H. Monitor for disseminated intravas- required if repeated febrile reactions
cular coagulopathy (DIC). Follow occur.
the platelet count, fibrinogen level,
INR,and P'IT, and treat with plate-

Page 190
Chapter 20 Intravenous Fluid and Blood Component Therapy

' Packed RBC donation Plasma donation

Figure 20.2: Donors with ABO Figure 20.3: Donors with ABO
blood p u p 0 may donate packed blood group 0 may receive plasma
RBC's to patients with blood group from donors with blood group 0, A,
0,A, B, or AB, and are referred to B, or AB. However, patients with 0
as universal donors. Donors with blood, can only donate their plasma
the ABO blood p u p AB are only to patients with 0 type blood.
able to donate packed RBCs to AB
\ recipients.

6 . Plasma: A dilutions1coagulopathy cytopenia with a platelet count of


may result when coagulation factor less than 100,000 x 109/1occurs in
levels decrease (see text above). over 90% of patients receiving 10
Allergic reactions are due to foreign or more units of packed RBCs.
proteins in the blood. The most This is the most common cause of
common manifestation of an aller- a coagulopathy in a massively
gic reaction is urticaria, which transfused patient.
usually responds to antihistamines
such a s d i p h e n h y d r a m i n e 8. Biochemical abnormalities:
(benadryl@). More severe reactions Rapid administration of packed
may result in an anaphylactic trans- RBCs (> 100 mllminute) may result
fusion reaction with hypotension, in citrate toxicity. Citrate is used
and require the administration of as an anticoagulant in packed
corticosteroids, epinephrine, and RBCs. Citrate binds calcium, pro-
fluids (see chapter 24: Unusual ducing hypocalcemia, decreased
Anaesthetic Complications; myocardial contractility, hypo-
Anaphylaxis). These patients may tension, and a widened QRS
be found to be deficient in IgA and complex with a prolonged QT
to have formed anti-IgA antibodies. interval. Administration of calcium
Subsequent transfusions may chloride 10 - 15 mg/kg, infused in
require specific RBCs that are -
slowly iv over 2 3 minutes, is
washed free of IgA. indicated with documented hypo-
calcemia, or ECG changes accom-
7 . Platelets: Dilutional thrombo- panying hypotension.

** Must Know * Should Know Page 291


dnaesthesia for Medical Shtdents

Potassium concentrations of > 25 screened for hepatitis B and syph- )


meqA, with pH values of < 6.7 are ilis. Testing the blood for malaria,
normal values in stored packed cytomegalovirus, Epstein-Bar virus 1
RBCs. As the blood is transfused (infectious mononucleosis) and 1
and the pH normalizes, the potas- many other potentially transmissible
sium rapidly shifts back into the diseases, is not done unless
i
RBC. Hence either hyperkalemia, specifically requested. j
or occasionally hypokalemia may
be observed after a blood transfu- Immune: There is a non-specific
sion. suppression of the immune system
that occurs after transfusing blood
9. Microaggregates: Standard blood products. This property has been
administration sets are equipped exploited to improve renal allograft
with 170 pm filters. They prevent survival. Adverse effects of the
small clots present in the donor immuno-suppression may be associ-
units from being transfused and ated with an increased risk of
lodging in the pulmonary circula- postoperative infections and recur-
tion. These filters should be used rence of cancer.
on RBC products, platelets, FFP,
and cyroprecipitate. Micro- References:
aggregates consist of platelets,
WBCs, and fibrin which aggregate 1. Transfusion Practices. Second edi-
to form clumps in RBC products. tion 1992. American Society of
Standard 170 pm blood filters, Anesthesiologists Committee on
however, do not filter out micro- Transfusion Medicine.
aggregates. Microaggregate filters
-
(20 40 pm) are not recommended 2. McIntyre, BG. Blood conservation
as their use has never been shown and transfusion practices. Contemp
to reduce the incidence of respira- Anaesth 1994; 4: 4-7.
tory distress syndrome following
multiple transfusions. 3. Barash PG, Cullen BF, Stoelting
RK. (ed.) In: Clinical anesthesia.
10. Infections: The most common type Second edition. JB Lippincott Co.
of infection following a transfusion 1993.
is viral. Screening tests for
hepatitis C, HIV and HTLV-I 4. Doyle DJ. Complications of blood
depend upon detection of the transfusion. Contemp Anaesth
antibody to the virus, which may 1994; 3:18 - 19.
not have formed, despite the
presence of a viremia. Antibodies 5. Waxrnan K.,et al. Hemodynamic '

can take up to 1 year to reach de- and oxygen transport effects of


tectable levels in the case of an pentastarch in bum resuscitation.
HIV infection. Blood is also Annals of surgery 1989; 29: 3.

Page 192
Chapter 20 Intravenous Fluid and Blood Component Therapy

Notes:

** Must Know Should Know Page 193


Common
Perioperative Problems
This chapter provides a general For any resuscitation problem, a
approach to common perioperative stepped XBC' (airway, breathing,
problems. Abnormalities in heart rate circulation) approach is used.
and blood pressure are common prob-
lems for which an organized approach
in their initial management is essential. 1. Evaluate and ensure the patient
-
Tables 21.1 21.5present the classifica- has an adequate and unobstructed
tion and differential diagnosis (Ddx.) of airway.
common hemodynamic problems.
These tables may be used for reference, Maneuvers to resolve a partial or com-
and are not to be memorized. plete airway obstructiontake precedence
over any other interventions. The
I A common approach to clinician must be able both to recognize
emergency problems an airway obstruction and utilize man-
I1 Ddx. of Bradycardia euvers to resolve it.
I11 Ddx. of Tachycardia
IV Ddx. of Hypertension If the patient is not intubated:
V Ddx. of Hypotension and
shock states. Quickly assess whether the patient has
M Nausea, emesis an airway obstruction preventing them
MI Confusion, agitation from breathing. In the unconscious
and delirium patient maneuvets such as a chin lift,
jaw thrust, removal of foreign bodies,
I. A Common Approach to and insertion of oral or nasal airways
Emergency Problems. may be used to overcome an airway
obstruction. Signs of an obstructed
Over the next few years of your medical airway include lack of air movement
training, you will undoubtedly be faced despite respiratory efforts, noisy or
with emergency situations requiring stridorous respirations, intercostal in-
your intervention. The following dis- drawing, tracheal tugging, accessory
cussion of common problems aims to muscle use, and lack of air entry on
prepare you for this situation. This may auscultation of the chest.
occur on the ward, in the emergency
department, or in a critical care setting
such as the operating room.
Chapter 21 Common Perioperarive Problems

If the patient is intubated: ministered with this device when the


patient is not breathing (see figure
If the patient is intubated it is important 23.4).
quickly to ensure that the endotracheal
tube is in fact in the trachea. Indirect Examine the patient. Is there evidence
confirmation includes listening for equal of cyanosis? Quickly scan any monitors
air entry to both lung fields and observ- attached to the patient. Ask for assist-
ing chest excursion during positive ance in applying monitors such as a
pressure ventilation. You should be blood pressure cuff, ECG monitor, and
able to pass a suction catheter through pulse oximeter. Ensure that oxygen is
the tracheal tube without meeting any being delivered from the source to the
obstruction. Final1y, epigastric patient.
auscultation should be negative for air
entry to the stomach during positive 3. Evaluate and ensure the patients
pressure ventilation. A portable chest ventllation Is adequate.
X-ray can be used to confirm that the
tip of the tube is in the mid-trachea. There are many conditions that can
result in respiratory insufficiency. Ven-
Direct confirmation that the tracheal tilation must be provided when a patient
tube is in the trachea can be immediate- is not breathing. Auscultation, palpa-
ly obtained by visualizing the tube tion, and percussion of the chest, in
passing through the glottis during direct combination with the vital signs and
laryngoscopy. When doubt exists con- pulse oximetry, are used in the immedi-
cerning the positioning of the tracheal ate evaluation of the patient. Arterial
tube or its patency, a fiberoptic blood gas analysis, chest X-ray, and
bronchoscope can be passed through the pulmonary function tests may also be
tube into the trachea. Observing carbon required to formulate a working diag-
dioxide returning with each exhaled nosis of the etiology of the respiratory
breath (end-tidal C02 monitoring) pro- insufficiency.
vides immediate confirmation of tra-
cheal intubation. 4. Assess the heart rate and rhythm.

2. Evaluate and ensure that the Quickly confirm or rule out an arrest
patient Is receiving adequate oxy- situation.
gen. Severe bradycardia must be assumed to
be secondary to hypoxemia until proven
In any emergency situation, it is always otherwise**.
wise to apply oxygen. The Arnbu bag
and mask provide a rapid method of 5. Assess the blood pressure and
providing 100% oxygen. It allows the perfusion.
patient to breathe 100%oxygen with the
option of assisting their spontaneous Hypotension may result in decreased
efforts. Manual ventilation can be ad- organ perfusion. Clinical findings that

** Must Know Should Know Page 195


Anaesthesia for Medical Students

are associated with decreased organ temperature losses. Temperature losses


perfusion include: result from evaporative, conductive,
radiant and convective loss of body
CNS: anxiety heat. Patients undergoing surgery are
confusion exposed to a cold operating room with
unconsciousness cold instruments, intravenous fluids and
CVS: dysrhythmias or ECG an open wound through which heat loss
evidence of ischemia occurs. The resulting hypothermia may
Renal: decreased urine output. result in postoperative shivering, with a
rise in heart rate, blood pressure and 5
The blood pressure should be confirmed to 6-fold increase in oxygen consump-
by a manual cuff if there is any ques- tion. Increases in temperature peri-
tion concerning its validity. Arterial operatively may result from drugs such
lines, automated blood pressure cuffs, as atropine, or from the administration
and human error can all be responsible of blood products. Other causes of an
for factitious blood pressures. increased temperature include fever,
sepsis, active intraoperative warming
6. Assess the patients volume status. efforts, and underlying disease states
such as thyrotoxicosis or malignant
Important changes in a patient's blood hyperthermia.
volume status may be clinically subtle.
Significant alterations in vital signs and 8. Scan for obvious causes of the
mental status may result. Assess the abnormality.
jugular venous pressure and the patients
recent urine output. In the operating Correct any obvious underlying abnor-
room, it would be appropriate to review mality. Hypotension and tachycardia
the patient's duration of fasting, examine with inadequate fluid replacement, and
the surgical wound, sponges, suction hypertension and tachycardia with inad-
apparatus, and nasogastic drainage. An equate analgesia are common examples.
overall assessment of the blood losses, Scan any monitors that are attached to
and third space losses as well as the the patient, and consider establishing a
adequacy of fluid replacement should be large bore intravenous.
made (see chapter 20: Intravenous and
Blood Component Therapy). 9. Establish addltional monitors
where appropriate.
7. Check the patients temperature.
Examples of additional monitors that
Alterations in temperature associated may be appropriate include an ECG
with anaesthesia and surgery may result monitor, blood pressure cuff, pulse
in important cardiorespintory abnor- oximeter, and temperature probe. Invas-
malities. Both hypothermia and ive monitors may include a foley cath-
hyperthermia may occur. Hypothermia eter, arterial line, central venous pres-
is frequently the result of intraoperative sure line or pulmonary artery catheter.
Chapter 21 Common Perioperotive Problems

cardiac output is determined by the


heart rate, preload, contractility and
Common investigations that may aid in afterload (SVR).
confirming the diagnosis include a
CBC, INR, PlT, ABG, CXR, ECG, In a normal adult, hypotension is gen-
glucose, electrolytes, and creatinine. erally defined as a systolic blood pres-
sure of less than 90 mm Hg, or a mean
11. Formulate a plan, and recruit arterial pressure of less than 60 mm Hg.
additional help if necessary. The most common cause of a
hypotensive state is a decrease in intra-
In an emergency situation, you may not vascular volume. This may result from
have the luxury of having an extensive an acute hemorrhage or from a loss of
history before you are required to act. fluids and electrolytes (see table 203:
Nevertheless, you can proceed with Common conditions associated with
assessing the status of the patient's fluid deficits). Acute hypovolemia
airway, oxygenation, ventilation, heart reduces the venous return to the heart
rate, rhythm, and blood pressure. Once (preload) resulting in a decrease in
the patient is hemodynamically stable cardiac output and systemic blood pres-
and receiving adequate oxygen and sure. Carotid and aortic baroreceptors
ventilation, review the patient's history, sense the decrease in arterial pressure,
recent lab data, perioperative course (in and initiate a series of events resulting
the case of recent surgery), and formu- in an increase in sympathetic output
late a provisional diagnosis so that you from the central nervous system and
may initiate treatment. Remember to adrenal gland. The resulting release of
recruit help in any emergency. norepinephrine and epinephrine increase
the heart rate, contractility and SVR in
-
I1 IV: Tables 21.1 to 213 list the an effort to redirect and maintain blood
causes of alterations in heart rate and flow to vital organs.
increases in blood pressure peri-
operatively. Hypovolemic shock is the most com-
mon type of shock. A low central
V: Hypotenslon venous pressure and low pulmonary
The purpose of the cardiopulmonary capillary wedge pressure (PCWP) is
circulation is to deliver oxygen and diagnostic of hypovolemia. Other forms
nutrients to body tissues. When tissue of circulatory shock include distributive
needs are not met, a state of shock is shock, obstructive shock and cardio-
said to exist. The blood pressure is genic shock. Table 21.4 characterizes
used as a gross indirect measurement of the hemodynamic features of the differ-
organ perfusion and assessment of the ent forms of shock.
adequacy of the circulation. It repre-
sents a complex interaction between
cardiac output, blood volume and sys-
temic vascular resistance (SVR). The

** Must Know Should Know


)
4naesthcsia for Medical Students

Table 21.1: Differential Diagnosis of a Decreased Heart Rate


RESP Hypoxemia Hypercarbia Acidosis
CVS Congenital Heart Block Decreased Sympathetlc
Increased Parasympathetic tone: Tone:
- Vagal reflexes (see CNS) -
Beta Blockers
- Drugs -
High spinal or epidural
- Paediatric patients anaesthesia (> T1 T4) -
-
Neurogenic shock

Decreased Conductlon: - Atrial Fibrillation with a


-Sinus bradycardia slow ventricular response
-Junctional bradycardia - Type I1 Second degree AV
-Idioventricular escape rhythm block
- Sick Sinus Syndrome - Complete Heart Block
-
- Ventricular Asy stole
CNS Baroreceptor reflex
secondary to increased blood pressure or increased ICP
Vagal Reflexes: Drugs:
- Vasovagal reflex -Anaesthetic overdose
-
oculocardiac reflex -Succinylcholine
-
carotid sinus reflex - Opioids
-
airway manipulation (especially -Edrophonium, neostigmine
important in paediatric patients) - Halothane
-Digoxin
-Beta blockers
Other Hypothermia Hypothyroidism Athlete

8 Treatment options might include: - atropine


- oxygen - ephedrine
- fluids - isuprel
- Trendelenburg position - epinephrine
- remove offending cause - transcutaneous or
- treat underlying drug toxicity transvenous pacemaker
(eg. Digibind for digoxin toxicity) - cardiopulmonary
resuscitation

Distributive shock is characterized by tributive shock is septic shock.


systemic vasodilation, relative hypo- Arteriovenous shunting at the tissue
volemia and an increase in cardiac out- level results in an accumulationof lactic
put. The most common form of dis- acid and tissue anoxia. Table 21.4 lists

Page 198
Chapter 21 Common Ptrioperative Problems

Table 21.2: Dlfferentlal Dlagnosls of a n Increased Heart Rate


RESP Hypoxia Hypercarbia Acidosis
CVS Slnus Tachycardla: A reflex sinus tachycardia may occur in
shock states (see Table 21.5: Classification of Shock States).
Sinus tachycardia may arise due to decreases in preload, afterload
or contractility. Increased sympathetic stimulation arising from
anxiety, pain, drugs and surgical stress is a common cause of
sinus tachycardia.
Other rhythms:
-paroxysmal atrial tachycardia (PAT)
- accelerated junctional rhythm
-multifocal atrial tachycardia (eg. COPD patient)
-atrial flutter with or without heart block
-atrial fibrillation
-pre-excitation syndromes with accessory pathways
-ventricular tachycardia
CNS Awareness under anaesthesia Anxiety Pain
GU Full bladder
HEME Anemia Transfusion reaction
END0 Hypermetabollc states: Other:
-fever - Addisonian crisis
-sepsis - porphyria
- pheochromocytoma - hypoglycemia
-thyrotoxicosis - hypercalcemia
-malignant hyperthermia
-malignant neuroleptic syndrome
IMMUNE Anaphylaxis
DRUGS Atropine Ephedrine
Cocaine (used for local anaesthesia) Isoflurane
Dopamine Isoproterenol
Epinephrine Pancuronium
Treatment is directed at the underlying cause of the increased heart rate.

examples of the four classes of shock. heart fails to perform its pumping func-
tion. This occurs as a result of a
Cardiogenic shock results when the myocardial, valvular, or electrical

" Must Know Should Know Page 199


.i
Anaesthesia for Medical Students
j

Table 21.3: Differential Diagnosis of a n


Increased Blood Pressure Perloperatlvely
RESP Hypoxia Hypercarbia
CVS Essential hypertension
Coarctation
Post-carotid endarterectomy
(acute denervation of carotid baroreceptors)
CNS Pain Full bladder Autonomic mass reflex
Shivering Light Anaesthetic level (quadraparetic or
Hypothermia Emergence delirium paraplegic patients)
Anxiety Increased ICP
GU Renal artery stenosis
Parenchymal Disease
Pregnancy induced hypertension
Toxemia
END0 Hyperthyroidism Carcinoid
Cushings disease or syndrome Hyperparathyroidism
Pheochromocytoma - hypercalcemia
Conn's syndrome (hyperaldosteronism)
MSK Malignant hyperthemia
Malignant neuroleptic syndrome
DRUGS Ephedrine Rebound from stopping
Epinephrine antihypertensive drugs:
Cocaine - clonidine
Phenylephrine - beta blockers
Ketamine
Acute narcotic reversal with naloxone
Drug interactions:
-Monoamine oxidase inhibitors (MAOI's) with meperidine
-MAOI's with indirect acting vasopressors (eg. ephedrine)
Treatment is directed at the underlying cause of the increased blood pressure.

problem. Amyocardial infarctionis the with a cardiac index of less than 1.8
most common cause of cardiogenic Umin/m2 and a systolic BP less than 80
shock. Characteristic findings include mm Hg (see table 10.1 and 10.2 for
an increase in CVP, PCWP, and SVR, derivations and normal values).
Chapter 21 Common Perioperalive Problems

Obstructive shock occurs when there is maintained, but digital capillary refill is
an obstruction preventing cardiac filling slightly retarded. Urinary output is only
or emptying. Two immediately treat- mildly depressed. Postural hypotension
able causes of obstructive shock include may be associated with class I1
a tension pneumothorax and cardiac hemorrhage, as may subtle central nerv-
tamponade. ous system changes such as fright and
hostility.
Hemorrhagic Shock Classification:
The normal response to increasing Class 111 hemorrhage:
hemorrhage produces characteristic -
Defined as a 30 40% loss of blood
physiological signs. These signs have volume. Patients with class I11
been used to classify hemorrhagic shock hemorrhage present with tachycardia,
according to the quantity of blood loss. systolic and diastolic hypotension,
Table 21.6 defines 4 classes of hemor- delayed capillary refill (>2 seconds),
rhagic shock based on the patient's vital reduced urinary output, and an appre-
signs, and predicts the percent blood hensive, slightly clouded sensorium.
loss and appropriate initial therapy.
Class I V hemorrhage:
Class I hemorrhage: Defined as a blood loss of 40% or more
Defined as the loss of as much as 15% of the blood volume. The patient mani-
of blood volume. It is associated with fests signs of frank shock with cool,
minimal physiologic changes. diaphoretic, ashen skin, tachycardia,
hypotension or unobtainable blood pres-
Class I1 hemorrhage: sure, anuria, and a reduced level of
Defined as a 15 - 30% loss of blood consciousness.
volume. Class 11 hemorrhage is associ-
ated with modest elevations in heart rate Patients with class Ill and IV
and decreases in pulse pressure as dia- hemorrhages will require immediate
stolic pressures rise with smaller stroke intravenous fluid administration to sur-
volumes. Systolic pressures tend to be vive. Patients with class IV hemorrhage

** Musf Know Should Know Page 201


Anaes~hesiafor Medical Students
)

Table 21.5: Classification and Etlology of Shock States

Hypovolemic Shock
- most common cause of shock - occult blood or fluid losses
Cardlogenic Shock
Myocardial: Myocardial (continued):
-relative drug overdose -arrhythmias
(anaesthetic drugs) -cardiomyopathy (congestive,
-other drug effects hypertrophic, restrictive, or
(p-blocker, ca2+channel blocker) obliterative)
-ischemia Valvular Disease:
-infarction (esp. NB when stress is
-rupture superimposed)
(papillary muscle, ventricular Aortic regurgitation
septum, chordae tendonae) Mitral regurgitation
Distributive Shock

Anaphylaxis, Anaphylactoid reaction Addisonian crisis


Sepsis Transfusion reaction
Drugs (Vasodilators) Severe liver disease
Neurogenic shock A - V fistulas
High regional sympathectomy Thyrotoxicosis
(eg. high spinal anaesthesia) Hypothyroidism
Obstructive Shock
Tension pneumothorax Aortic dissection
Pericardial tamponade Aortic cross-clamping
Pulmonary embolism Atrial myxoma
(blood clot, fat, air, tumor, etc) IHSS
Supine hypotension during Valvular heart disease with stress
pregnancy (aortocaval compression (eg. Aortic or mitral stenosis with
gravid uterus) pregnancy or trauma).
IVC, or heart compression by surgical
instruments

will require blood transfusion to sur- Hematocrits as low as 20 to 25% may


vive, but class 111 hemorrhage patients be well tolerated if total blood volume
may tolerate post-resuscitationanemia if is adequate. The use of clinical signs to
fluid resuscitation is accompanied with estimate traumatic blood loss is very
immediate control of the hemorrhage. important because soft tissues and body
Chapter 21 Common Perioperative Problems

Table 21.6: Classlflcatlon of Hemorrhagic Shock

Hemorrhage 46 Blood Physlologlcal changes. Treatment


Volume
loss

Class I s 15 HR < 1001min. Rapidly infuse 1 - 2


SBP normal liters of balanced salt
PP:normal or increased solution (BSS), then
CR: normal maintenance fluids.
-
RR: 14 201min.
CNS: Anxious

Class 11 -
15 30 HR > 1001min. Rapidly infuse 2 liters
SBP normal of BSS, re-evalua te
DBP increased continued needs
Postural hypotension
PP: decreased
CR: delayed
RR: 20 - 30Imin.
CNS: more anxious

Class 111 -
30 40 HR > 120lmin. Rapidly infuse 2 liters
SBP decreased of BSS; re-evaluate;
PP: decreased replace blood losses
CR: delayed or absent with 1:3 BSS or 1:l
-
RR: 30 401min. with blood (PRBC's,
CNS: Confused colloid, other blood
products). Maintain
Class IV r 40 HR > 140jmin. urine output > 0.5
SBP decreased ml/kg/hr.
PP: decreased
CR: absent
RR > 35lmin.
CNS: Lethargic
i
'
j
HR = heart rate (bpm); SBP = systolic blood pressure; DBP = diastolic blood
pressure; PP = pulse pressure; CR = capillary refill; RR = respiratory rate;
CNS = central nervous system
)
cavities frequently conceal large quan- VI: Nausea and vomltlng.
) tities of blood with minimal external
) body changes. Nausea and vomiting, have a profound
effect on the patients perception of their
)
i
** Must Know Should Know Page 203
Anaesthesia for Medical Students

perioperative care. It has been shown to Nausea and vomiting perioperatively


significantly increase the time the must be assumed to be secondary to
patient spends in the post anaesthetic bradycardia and hypotension until
care unit (PACU), and places the patient proven otherwise**.
who is recovering from anaesthesia at
risk of gastric aspiration. When assessing a patient with peri-
operative nausea and vomiting, quickly
Preoperativepatient risk factors include: evaluate the patients vital signs. Vagal
reflexes, with a decrease in blood pres-
1. Previous history of anaesthetic asso- sure and heart rate, may present as
ciated nausea and vomiting (review nausea and vomiting.
old chart if possible).
2. Young age. A differential diagnosis for nausea and
3.. Female gender. (The probability of vomiting includes:
postoperative nausea and vomiting Hypotension
has been linked to a woman's men- Bradycardia
strual cycle.) Drug induced nausea
4. Operative procedure. (Increased - opioids
incidence with eye, middle ear, and - anaesthetic agents
female pelvic surgery). Surgical manipulation
5. Obesity. Pain
- surgical
Many anaesthetic agents have been - biliary or renal colic
associated with nausea and vomiting. - migraine
The mechanisms are multiple and com- Drug toxicity:
plex. Opioids are perhaps the most - digoxin
potent emetics. They have been shown - theophylline
to directly stimulate the chemoreceptor - ASA
trigger zone of the fourth ventricle, - alcohol
stimulate the vestibular apparatus, delay Hyponatremia
gastric emptying, and increase gastric - postoperative TCIRP patients
secretions. Hypercalcemia
- cancer patients
Nitrous oxide may have a direct action Diabetic ketoacidosis
on the chemoreceptor trigger zone, as Pregnancy
well as acting on the middle ear, and Coexisting gastroenteritis
cause both gastric and bowel distension. Acute hepatitis
Other common agents associated with Other:
perioperative nausea include sodium - renal failure
thiopental, inhalational agents, and - hepatic failure
cholinesterase inhibitors. - adrenal failure
- hypothyroidism
- raised ICP

Page 204
Chapter 21 Common Perioperative Problems

There is no one treatment for this prob- tered- one hour prior to anaesthesia in
lem. Frequently a number of factors patients with a ,history of resistant
contribute to the patient's nausea. nausea and vomiting associated with
Switching the opioid used for, anaesthesia. This is followed by 2
postoperative analgesia, or adding a non additional doses of 8 mg each at 8 hour
steroidal anti-inflammatory agent may intervals. Alternatively, established
resolve the problem. nausea and vomiting may respond to a
single injection of 4 mg intravenously.
Common agents used to treat peri-
operative nausea and vomiting include: A combination of antiemetic drugs may
be more effective in preventing
roperi idol^ postoperative nausea and vomitting.
-
0.25 0.5 mg iv pm The combination of ondansetron and
~imenh~drinate (Gravel@) dexamethasone has been shown to be
-
10 50 mg iv/im/po effective in reducing the incidence of
-
(maximum 50 mg q 3 4 hours). nausea and vomitting in cisplatin
Metochlorpropamidet chemotherapy. Ondasetron (4mg) and
10 - 20 mg iv every 6 hours pm. dexamethasone (8 mg) has recently
(contraindicated in bowel obstruction) shown promising results in preventing
Prochlorperazine (Stemetil@)t nausea and vomitting postoperatively4.
10 mg im every 6 hours prn.
VII: Postoperative Agitation and
Dopamine re~e~tor'antagonists.The delirium.
potential for extrapyramidal reactions
increases as dosage and number of The agitated, delirious, or aggressive
agents used increase. Dysphoric patient is rarely seen in the PACU
reactions and disturbed sleep patterns today. This is due perhaps to a combi-
have been reported with moderate nation of our improved understanding of
doses of droperidol (2.5 mg iv). pain management, the availability of
shorter-acting anaesthetic agents, and
Less common agents used include: improvements in our monitoring equip-
Propofol 10 mg iv. ment (oximetry, peripheral nerve
One mglkgfhr infusions have been used stimulator, and end-tidal carbon dioxide
successfully to prevent nausea and monitoring).
vomiting in patients receiving chemo-
therapy, who have a past history of An initial ABC approach is used, with
nausea and vomiting. the use of physical restraints if needed
to protect both the patient and the medi-
Ondansetron is a new selective cal team. The physical restraints are
serotonin antagonist. It is more com- removed as soon as the offending cause
monly used to treat radiation or chemo- is removed or chemical restraints substi-
therapy-related nausea and vomiting. tuted.
An oral dose of 8 mg may be adminis-

** Must Know Should Know Page 205


Anaesthesia for Medical Studen& .

Upper airway obstruction, residualpar- Following clinical evaluation, appropri-


alysis, hypercarbia, and hypoxemia are .ate investigations may include a
all potent stimulants which can produce measurement of the patient's glucose,
an agitated state**. electrolytes, calcium, arterial blood gas,
and tests of neuromuscular strength.
A gross neurological examination
should be performed quickly (e.g., If a thorough search fails to identify any
pupillary assessment,movement of arms of the above causes of postoperative
and legs, Glascow coma scale (GCS) agitation, small doses of a benzo-
score), while communicating reassur- diazepine such as midazolam (0.5 - 1.0
ingly with the patient. mg iv), or an antipsychotic such as
haldol (2.5 - 5.0 mg ivlim) may be
Elderly patients are particularly prone to warranted.
postoperative confusion and agitation.
Common causes of agitation include Consider small doses of:
pain and bladder or bowel distension. Naloxone (0.04 - 0.08 mg increments)
Patients recovering from anaesthesia Flumazenil '(0.2 - 0.6 mg iv), or
may appear able to communicate Physostigmine (0.5 - 2 mg iv)
verbally, but unable to recognize that respectively, if excessive sedation is felt
the cause of their distress is pain or a to be secondary to opioids, benzo-
full bladder. diazepines, or anticholinergic agents.

Less common causes of an agitated References:


postoperative state include:
Drug effect 1. Review Article: Anaesthesia and
- ketamine emesis. I, 11. Palazzo MGA,
-anticholinergics: Strunin L. Can Anaesth. Soc. J.
-
atropine 1984; 31: 178-87, 407-15.
-
scopolamine
-
tricyclic antidepressants 2. Review Article: Postoperative
TURP syndrome nausea and vomiting: Its etiology,
- hyponatremia treatment and prevention. Watcha
-glycine toxicity MF, White PF. Anesthesiology
Hypercalcemia 1992; 77: 162-84.
- cancer patients
Hypoglycemia 3. Larijani GE, GratzI, Afsar M,
Acute Stroke Minassian S. Anesth Analg 1991;
Raised ICP 73; 246-9.
Anxiety
Fear 4. Rajeeva V, Bhardwaj N, Batra YK,
Separation from caregivers Dhaliwal LK. Can J Anesth 1999;
Acute drug withdrawal -
46: 40 44.
Acute drug intoxication
Chapter 21 Common Perioperative Problems

Notes:

j
** Must Know * Should Know
Managing the
Circulation
Hemodynamic abnormalities of the a factor of 10 during extreme exercise
circulation may necessitate interventions in normal adults. The three determi-
to maintain normal oxygen transport and nants of the stroke volume are the pre-
organ perfusion. This may occur in the 10~4afterload, and contractility.
perioperative period as a result of pain,
anxiety, hypoxia, hypercarbia, and The preload is defined as the end-dia-
abnormalities of temperature or intra- stolic stretch of the left ventricle. As
vascular volume (see chapter 21). preload increases so does the left
Correcting these abnormalities should ventricular work, cardiac output, blood
precede the administration of any pressure, and stroke volume (recall the
vasoactive agents. Frank-Starling curves). Excessive
increases in end-diastole stretch results
Pharmacologicmanipulation of both the in a decline in cardiac performance
parasympathetic and sympathetic when the left ventricle becomes over-
nervous systems may be required to distended. The left ventricular end-dia-
correct hypotensive, ischemic or stolic volume (LVEDV) is our best
hypertensive emergencies. Table 22.1 measurement of preload. Since the
lists the different classes of medications LVEDV is difficult to measure clinical-
that may be used to restore circulatory ly, the filling pressures of the left ven-
homeostasis. tricle at end-diastole (LVEDP) may be
estimated by the measuring the pulmon-
Central to our understanding of the ary capillary wedge pressure (PCWP)
circulation and oxygen transport is the with a pulmonary artery catheter. Gen-
concept of cardiac output. The cardiac erally, an increase in the LVEDP corre-
output (CO) is defined as the amount of sponds with an increase in LVEDV. In
blood pumped to the peripheral circula- patients with normal a right and left
tion per minute. It is expressed as the ventricle, mitral valve, pulmonary
product of the heart rate multiplied by vasculature, and airway pressures, the
the stroke volume. assessment of the central venous
pressure (CVP)may be used to estimate
the LVEDV and preload.

A normal CO value for an adult is 25 Afterload is defined as the myocardial


to 35 Umin/m2, or 4 5 to 6.0 Umin in wall stress of the left ventricle during
a 70 kg adult. The CO can increase by ejection. It is a measure of the work

Page 208
Chapter 22 Managing the Circulation

the left ventricle performs with each Patients presenting to, or leaving the
contraction. In the absence of aortic operating room with vasoactive medica-
stenosis, afterload depends on the elas- tions infusing, must be considered to be
ticity of the large arteries and on the serious1y ill. All vasoactive agents have
systemic vascular resistance (SVR). serious potential side effects that must
The SVR can be estimated using a be considered whenever they are used.
calculation incorporatingthe mean arter- Indiscriminate infusions of vasopressors
ial blood pressure, cardiac output, and may produce the desired increase in
CVP (see table 10.1 and 10.2). blood pressure, but may also severely
restrict blood flow to vital organs such
Contractility is the myocardium's intrin- as the bowel, liver and kidney. Marked
sic ability to perform work at any given increases in peripheral vascular resis-
level of end-diastolic fiber length tance produced by vasopressors may
(preload). It is primarily determined by precipitate cardiac failure.
the availability of intracellular calcium.
All agents that increase myocardial The principle goal of circulatory support
contractility produce an increase in is to optimize tissue perfusion with
intracellular calcium. Contractility oxygenated blood. To achieve this, one
increases with sympathetic stimulation must assess and optimize the preload,
and inotropic drugs, such as digoxin. afterload, heart rate, contractility, oxy-
Hypoxia, acidosis, beta blockers, cal- gen transport and organ perfusion (see
cium channel blockers, and myocardial table below).
ischemia or infarction are common
conditions that depress contractility.
Increases in preload, heart rate, contrac- Optimize Assessed by:
tility or decreases in afterload, all pro-
Preload PCWP: 10 - 15 mmHg
mote forward flow and an increase in
cardiac output.
-
CW: 8 12 mmHg
Aftedoad SVR = 900 1500-
Vasoactive drugs may be classified as dynes.sec.cm4
acting by either a catecholamine or a
ContracClity CI > 2.5 L./inin/mz
non-catecholamine mechanism. Drugs
acting through a catecholamine mechan- Heart Rate -
60 90 bpm
ism may have either agonist or antagon-
ist receptor activity. Most Oxygen Arterial blood gas
catecholamine vasoactive drugs have a Transport Mixed venous oxygen
saturnlion (MvOJ
combination of alpha and beta
Hemoglobin
adrenergic receptor activity (see tables
223 - 22.5). When choosing to use a Organ MvO, saturation
vasoactive medication, one ought to Pefision Serum lactate
consider the risks of using the drug, the ABG
hemodynamic goals one seeks, and the Urine output
pharmacologic properties of the drug. CNS sensorium

** Must Know Should Know Page 209


j
Anaesfhesia for Medical Students

Table 22.1: Cardiorespiratory effects of receptor stimulation. 1


)
Receptors Agonlst Antagonlst 1
Adrenergic: )
Alpha-1 Vasoconstriction of the skin, Peripheral vasodilation, )
gut, kidney, liver, and heart reflex tachycardia,
(e.g., phenylephrine). hypotension (e.g., prazosin) j

Alpha-2 Reduces sympathetic outflow CNS stimulation, increased )


from the CNS inhibiting sympathetic outflow. J
norepinephrine release increased HR,contractility,
j
(e.g., clonidine, and cardiac output.
dexametomidine).
Beta-1 Increased heart rate, myocardial Decreased HR, contractility, J
conduction, and contractility and conduction, )
(e.g., isoproterenol) (e.g., esmolol).
Beta3 Bronchodilation, peripheral Bronchospasm, peripheral )
vascular smooth muscle vasoconstricton.
relaxation, (e.g., salbutamol). 1
1
Dopamine-1 Peripheral vasodilation of the
renal and splanchnic
vasculature, (e.g., dopamine). 1
Cholinergic Decreases heart rate, conduct- Anticholinergics increase
(Muscarinic) ion, and cardiac output. heart rate, conduction, and
Increases bronchial secretions, contractility. They also
(e.g., edrophonium). decrease bronchial se-
cretions, (e.g., atropine).
Calcium Increases contractility, vaso- Decreases contractility,
channel constriction (e.g., calcium). increases vasodilation,
(e.g., nifedipine).
Other Phosphodiesterase inhibitors:
Produce a concentration dependant increase in
contractility with arterial and venous dilation
(e.g ., amrinone).

Cardiac glycosides:
(e.g., digoxin)

Page 210
Chauter 22 Mananina the Circulation

Table 22.2: Manipulating the determinants of cardiac output to correct hemodynamic


disturbances in the circulation. Tables 21.1 - 21.6 are presented for reference only.

Determlnants Hemodynamlc Disturbance


of Cardiac (accompanied by lists of vasoactlve agents and
Output lnterventlons used to treat the disturbance)

Preload Increased Preload Decreased Preload


Venous vasodilators Crystalloid, colloid infusion
-nitroglycerine (see chapter 20)
-nitroprusside
Diuretics
-furosemide
Phlebotomy
Heart Rate Increased Heart Rate Decreased Heart Rate
Beta blockers Anticholinergics
- propranolol - atropine
-metoprolol Beta Agonists
- esmolol - isoproterenol
Calcium channel blockers -ephedrine
- verapamil Pacemaker

Contractlllty Increased contractlllty Decreased Contractlllty


General anaesthetics Digoxin Norepinephrine
-halothane Amrinone Epinephrine
Beta blockers Dopamine Surgery
Calcium channel blockers Ephedrine Intra-aortic
Dobutamine balloon pump

Afterload Increased afterload Decreased afterload


Arterial vasodilators Alpha agonists
-sodium nitroprusside - phenylephrine
- hydralazine - norepinephrine
Labetalol
Amrinone Crystalloid or colloid fluid
ACE inhibitors therapy
- captopril
-enalapril
-lisinopril
Dobutamine

** Must Know * Should Know Page211


Anacslhesia for Medical Students
i
In October 1992, the National Confer- 3. Merin RG. Autonomic nervous
ence on Cardiopulmonary Resuscitation system pharmacology, Anesthesia
(CPR) published the current recommen- third ed. Edited by Miller RD.
dations for adult cardiac life support Churchill Livingstone 1990, pp 471
(ACLS). A summary of the algorithms - 504.
are presented (for reference) in figures
22.1 to 225. 4. American heart association: Text-
book of advanced cardiac life sup-
The Guidelines for Cardiopulmonary port. 1992.
Resuscitation published in JAMA in
1992classified therapeutic interventions 5. Emergency Cardiac Care Committee
as: and Subcommittees, American Heart
Association. Guidelines for
Class I: Recommendation is cardiopulmonary resuscitation and
definitely helpful. emergency cardiac care, 111: Adult
Class IIa: Recommendation Advanced Cardiac Life Support.
acceptable, and probably JAMA 1992; 268: 2199-241.
helpful.
Class Ilb: Recommendation
acceptable and possibly
helpful.
Class 111: Recommendation is not Footnotes for figure 22.1, page 213:
indicated, and may be
harmful. a. Unstable condition must be related to
the tachycardia. Signs and symptoms
The properties of vasoactive medica- may include chest pain, shortness of
tions used in manipulating circulatory breath, decreased level of conscious-
abnormalities are presented (for refer- ness, low blood pressure (BP), shock,
ence) in tables 2 2 3 to 22.7. pulmonary congestion, congestive
heart failure, acute myocardial
References: infarction.
I
1. Hug CC, Kaplan JA: Pharmacology b. Carotid sinus pressure is contraindi-
-
cardiac drugs, Cardiac Anesthesia, cated in patients with carotid bruits; '
Edited by Kaplan JA. Grune and avoid ice water immersion inpatients ;
Straton, 1979, pp 39 69. - with ischemic heart disease.

2. Thys DM, Kaplan JA. Cardiovas- c. If the wide-complex tachycardia is ;


cular physiology, Anesthesia, third known with certainty to be PSVT and
ed. Edited by Miller RD. Churchill
Livingstone 1990, pp 551 583. -
BP is normallelevated, sequence can
include verapamil.
I

Page 212
Chapter 22 Managing the Circulation

/ Egure22.1,Tachycardia Algorithm
> 150 bpm, prepare
for immediate
Assess vital signs
Review history cardioversion

I
Administer oxygen May give trial of
Perform physical exam.
I Attach Monltor, pulse oxtmeter, medications based on
Order 12 lead EGG
and automatic blood pressure arrhythmia.
Order portable CXR
Immediate
cardioverslon Is

I -
Unstable, wlh serlous signs or ~ ~ m ~ t o m s ? ~ l
I
seldom needed for
yes*~HR<150bpmm JI
~ t r i flutter
a~ b supraventrlcular tachycardia of

3 3
p G G G q I Lldocaine 1 - 1.5 1 ( tidocaine 1 - 1.5 1
Oiltiazem
Beta blockers 3 Imgkgevew
lv push ) ( mgkg iv push ]
6 - 10 mlns every 6 - 10 mlm
Verapamil
Digoxin

Qulnldine
Anticoagulants
rapid iv push

(~denosine12 rng;)
mgkg Iv push,
maxjmum 3 mgkg
5.
I
'

\
~docal&0.5475
mgkg iv push,
maximum 3 mglkg
J
I
rapid iv push ( Adenosine 6 mg , \
-
over 1 3 secs rapid iv push
(may repeat once

(may repeat once

Procalnarnide
-
20 30 mglmin
Normal maximum total 17 mgkg
or elevated or unstable

** Must Know Should Know Page 21 3


Anaesthesia for Medical Students

R1uw22.2: Bradycardia algorithm


(Patient is not in cardiac arrest)

Assess ABCs Assess vital signs


Secure airway Review history
Administer oxygen Perform physical examination
Start iv Order 12 lead ECG

I
Attach monitor, pulse Order portable CXR
oximeter, and automatic
blood pressure
Too slow (< 60 beatslmln)
1

( Serious signs or symptoms? I


NO I Yes

I
C
I
C
' ~ 11 second-degree'
~ ~ e 'intervention sequence:
AV heart block? Atropine 0.5 - 1.O mg" (I & Ila)
or TCP, if available (I)
Third-degree Dopamine 5 - 20 ug/kg/min (Ilb)
\ AV heart block? , Epinephrine 2 - 10 ug/min
NO I yes Isoproterenol
.1
d

[observe I Prepare for transvenous pacer


Use TCP as a bridge device

Footnotes for bmdycardia algorithm:


a. Serious slgns or symptoms must be related to the slow rate. Cllnlcal manlfestatkms Include chest
pain, shortness of h t h , decreased level of consciousness, b w BP, shock, pulmonary congestion,
CHF; acute myocardial Infarcfion.
b. Do not delay TCP u3rlle awaiting lvaccess or for atropine to take effect If patient Is symptomeb.
c Denervated fmsplanted hearts wfll not respond to atmpine. Qo at once to pacing, catechohine
Infusion, or both.
-
d. Airoplne should be given In repeat doses In 3 5 mln krtervels up to 0.04 m g . Gmdder shorter
daslng Intervals In severe conditions.
e. Never treat thid-degreeheart block plus ventricular escape beats wlth Ildocalne.
f. lsopmterenol should be used, if at all, with extreme cautlon. At low doses It Is Class Ilb (possibly

\ helpfuu; at hlgher doses it kr Class 111 (hamfull.


g. VenW patient toleranceand mechanical capture. Use analgesia and sedation as needed.

Page 214
Chapter 22 Managing the Circulation

/ ngureP.3: Asystoe treatment algorithm


(* Continue CPR 1
I lntubate at once
Obtaine iv access
Confirm asystole in
1
more than one lead

1 Class I: definitely helpful


f~onsiderpossible Class Ila: acceptable, probably helpful
Class Ilb: acceptable, possibly helpful
Hypoxia
Hyperkalemia
Hypokalemia
Preexisting acidosis
Drug overdose
\. Hypothermia I
I

Consider immediate

Atropine 1 mg iv
-
repeat every 3 5 mlns up to 0.04 mghg.

+
[ Consider termination of effortsf 1
Foolnotes lbr asyslde algoijttun:
a TCP Is a class Ilb Intervenlion. Lack of success may be due to delays In pacing. To be effectl~,TCP
must be p d m n d ear& eimuhaneously wkh drugs. Eddencs does not support rwtlne use of T W
for asystole.
b. The rewmmendeddose of eplnephifne Is 1 mg Ivpush every 3 - 5 mlns. If thls approach MIS, s e w d
-
Class IIb dosing regimens can be considered: lntermedlateeplnephme 2 5 mg Ivpush, evew 3 5 -
-
mln; Escalating epinephifne 1 mg 3 mg - 5 mg Ivpush, 3 d n aper;, Hlgh ephephifne 0.1 n@g Iv
-
push, every 3 5 mln.
c. Sodium bicarbonate 1mE& Is Cless 1Ifthe patient has known perexldlng hyperkalmla.
d. Shorter atropine b l n g Intervals are Class Ilb In asystollc errest.
e. Sodium bicarbonate 1 mE&:
Class Ila: if known preexlstlng bkatbonate-responsive addosls; if overdose wkh tifcydlc
entldepresaants;to alkalinlze the urine In drug overdoses.
Class Ilb: if lnhrbated end oonlbued long arrest Interval; upon return of spontaneous clrculetion seer
bng arrest Interval. Class 111: hypoxk lactic acMosls
f. If patlenl remalns In asyetole or other agonal rhythms after successful lntubetbn and InillaI medkations
and no reversible causes en,Identified, oonslder tennlnetion of resuscitative efforts bye physlclen.
Conslder time interval shce arrest.

" Must Know Should Know Page 225


Anaesthesia for Medical Students

Ventricular Fibrillation
rng~r.221: -
Pulseless Ventricular Tachycardia
Algorithm (VF I VT)
ABCs
Perform CPR until defibrillator attached a

Provide medications
appropriate for BP,

'continue CPR
lntubate at once for
FOOE~~IBS M/ ~7dgotithm:
Obtain IVaccess a. PrecordLl thump is a Class Ilb action In witnessed
arrest, no pulse. and no defibrillator Immediately
4 avalble.
Epinephrine 1 mg iv pushG b. ~ypolhermiccardlac arrest lo treated diiferently
repeat every 3 - 5 mins. aner lhls point. SeeACLS sedlon on hypothemla.
4 c. The recommended dose of epinephrine Is 1mg iv
Defibrillate 360 J within -
push every 3 5 mlns. If fhlsapproad fells,

-
.30 60 s e a
sewel Class Ilb d d n g reghens can be
consMered (see footnotes figure 22.3 b).
# d. Sodlum bhrbonate (I mErykgI Is Class I Ifpatlent
Administer medications of probable' h a known~reexlsti& h~p&!+mla.
benefit (Class Ila) in persistent or a M U I I ~S~BI ~Q U W ~ ~ S (~ O2 J. ~~ -
rn 300 J,
360 4 are acceptable hen, ( a s s I), eespeclal&
Lrecurrent VF / VT g / when medlcatbns are delayed.
4 f. Medicatbns:
-
'~efibrillate360 J, 30 60 secs after- Udmlne l.5mMgivpush. R e ~ m l l 3
to total loading dose of 3 mglkg; lhen use
n - 5 mins
each dose of medication Eretyllum 5 mgkg ivpush. Repeat In 5 mlns at 10
Pattern should be mag
,drug-shock, drug-shock , -
Magnesium sulfete I 2gm iv dn tomade de
polnfes or suspected hypomagnesemlcstate or
severe retkachvy M
PmcahmMe 30 m&mln h rehadory VF
( m l m u m total 17m&g).
g. Sodium blaubonate (I mEWg iv):
(see footnotes figure 22.3 e)
C
$ Table 223: Properties of cardiovascular drugs. (n invasive pressure monitoring manditory)
?i
s

Drug Receptor Activity Single Bolus Infusion Rate and Comments


a-1 a-2 p-1 8 2 Dose Preparation
Epinephrinen 2+ 3+ 1+ 2+ Anaphylaxis: 0.01 - 0.2 -
Inotropic beta effects at 0.02 0.09 mcgkghnin,
(Adrenalin) -
3 5 mcgkg mcgkgbin; pressor alpha effects at > 0.09 mcg/kg/min. Used
Arrest 1 mg 4 mg in 500 ml for hypotension with myocardial depression.
(8 mcghnl)
Amri none Phosphodiesterase 0.75 mgkg 2 - 10 mcgkghnin CO increased, HR unchanged, BP may decrease.
(Inocor) inhibitor with positive over 2 3- PAP, PCWP, SVR all decrease. Used as an
inotropic action mins. inotrope in patients with end stage heart disease.
independent of Produces arterial and venous vasodilation and may
adrenergic receptors. decrease BP.
Dopamine 1-4+ 0 1+ 2-4+ -
1 10 mcg/kg/min Renal effects via dopaminergic DA-1 receptor at 1
(Inotropin) plus 400 mg in 500 ml - -
4 mcgkghnin. At 5 10 mcgkghnin beta effects
Dopamine receptor (800 mcghnl) predominate with an increase in HR,and CO.
agonist Above 10 mcgkghnin alpha effects predominate
and renal blood flow may decrease. Commonly
used in lower doses to increase CO while
preserving renal perfusion.

Dobutaminen 0-1+ 0 1+ 3+ -
1 20 mcgkg/min CO increases, SVR and PCWP decrease. At lower
(Dobutrex) 500 mg in 500 rnl doses CO increases without severe tachycardia or
(1 mg/ml) -
hypotension. At 10 15 mcg/kg/min, HR and
vasodilation become more prominent BP may not
change. Used to increase CO.
L \ . - % - L L , L b L L L b L L L L b b b b L b L L L b - - - -

Table 22.4: Properties of cardiovascular drugs. (%vasive pressure monitoring manditory)

DNg Receptor Activity Single Bolus Infusion Rate Comments


a-1 a-2 fk1 8 2 Dose and Preparation
Norepinephrine 4+ 4+ 2+ 0 0.05 - 0.5 Direct alpha and beta receptor agonist Decreases in
(Levophed) mcg/lr&infi renal blood flow occur with even low doses. At
4 mg in 500 ml low doses the alpha effects increase blood pressure,
(8 mcghnl) causing vasoconstriction, and reflex bradycardia. At
higher doses, beta receptor stimulation increases
contractility.
-
Phenylephrine 4+ 0 1+ 0 SO - 100 0.1 0.5- Phenylephrine represents an almost pure alpha-1
(Neosynephriae) mcg mcg,kghninfi agonist Beta stimulation only occurs at very high
10 mg in 500 doses. Phenylephrine may be used temporarily to
ml provide profound vasoconstriction while the
(20 mcgEml) underlying cause of hypotension is corrected.
Reflex bradycardia may occur. May be useful in
patients with hypotension associated with a
decreased SVR and tachycardia.

Ephedrine 3+ 0 2+ 1+ -
5 10 mg iv Onset within 1 Ephedrine is an indirect acting alpha and beta
-
25 50 mg minute with a agonist It causes vasoconstriction and an increase
im duration of in heart rate, blood pressure and cardiac output It
-
5 10 minutes. is useful in patients with hypotension without
Genetally not tachycardia. It is the drug of choice for hypotension
used as an due to regional anaesthesia during labour and
i b s i o n due to delivery as its combined adrenergic effects result in
tachyphylaxis. an increase in blood pressure without uterine
(50 mghnl amp) vasoconstriction.
Anaesthesia for Medical Students
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Table 22.6: Properties of cardiovasc Iar drugs.

Single Bolus Dose 1 Comments


1

Action
- - - -

Calcium No beta adrenergic Used to treat hypocalcemia, ECG changes of


Chloride activity. Rapid hypocalcemia in the presence of hypotension, and
direct acting calcium channel blocker overdose. May also be useful
inotrope with a in the treatment of hypermagnesemia, and to protect
-
duration of 5 10 the myocardium from the effects of hyperkalemia.
minutes.
- -

Metoprolol Selective beta-1 - -


1 5 mg iv every 2 5 mins pm., Useful in controlling hypertension, tachycardia, and
(Betabloc) antagonist may require up to 15 mg for full reducing myocardial ischemia. Potential side effects
beta blockade. include bradycardia, heart block, pulmonary edema,
bronchospasm, and impaired insulin release resulting in
hypoglycemia.

Esmolol Selective beta-1 Single bolus: 0.5 mgkg iv Rapid onset of less than 2 minutes with a duration of
(Brevibloc) antagonist less than 30 minutes. Lndicated in the treabnent of
Iafusion: 1 m g h l solution hypertension and tachycardia in patients at risk of
50 - 300 mcgkghnin hernodynamically induced myocardial ischemia. Also
indicated in the control of the ventricular rate in acute
atrial fibrillation and atrial flutter.
- - - - - - -

verapamil Calcium channel -


Single bolus: 2.5 5 mg iv Useful in terminating a supraventricular dysrhythmia.
(Isoptin) antagonist maximum 10 mg iv. Also used in controlling the ventricular rate in patients
with atrial fibrillation and atrial flutter.
Contraindicated in preexcitation syndromes (e.&,
Wolff-Parkinson-White syndrome) as it may increase
conduction in the accessory pathway.
3 Table 22.7: Properties of cardiovascular drugs.
2
h
h

D N ~ Mechanism of Single Bolus Dose Comments


Action

Atropine Anticholinergic 0.3 - 0.6 mg iv increments Most commonly used to treat bradycardia (heart rate c
max. 3 mg 45 bpm). Also useful as an antisialogogue to dry oral
secretions and aid oropharyngeal topical anaesthesia for
an awake fiberoptic intubation.
Adenosine Antidysrhythmic 6 mg iv Useful in p a m y m a 1 supraventricular tachycardia's.
(Adenocard) May be associated with significant hypotension, facial
flushing, and shortness of breath. Does not convert
atrial fibrillation, atrial flutter, or ventricular
tachycardia to a sinus rhythm, but may be useful in
distinquishing an SVT h m other tachydysrhythmias.

Enalapril Angiotensin 1.25 mg iv Useful in treating hypertension and h e a Failure. Onset


(Vasotec) converting enzyme within 15 minutes, with maximum effect between 1 - 4
inhibitor maintenance 1.25 mg iv q6hrs. hours. Use with caution in patients with renal
insufficiency. Decrease in BP is exagerated in patients
on diuretics. Hypotension responds to volume
expansion.

Nifedipine Calcium c h a ~ e l 10 mg sublingual Used in treating hypertension, coronary vasospasm, and


(Adala t) blocker angina. Especially useful in treating hypertension in
-
Usual dose is 10 20 mg po tid the npo patient Vasodilation is accompanied with a
Maximum dose is 120 mg per day. decrease in BP, SVR and an increase in HR. Negative
inotropic action of nifedipine with beta blockers may
precipitate heart failure. Nifedipine displaces digoxin
and increases it's plasma level.
Oxygen Therapy
and Hypoxia
Oxygen is an essential and vital feet, the barometric pressure is only 270
substrate used for many metabolic func- mm Hg. Hence the partial pressure of
tions. Over 200 oxidase enzyme sys- oxygen is only 47 mm Hg (270 mm Hg
tems participate in our body's metabolic x 21% = 47 mm Hg).
processes. The cytochrome c oxidase
enzyme system in the mitochondria is The oxygen cascade refers to the pro-
responsible for over 90 percent of the gressive decrease in the partial pressure
bodies oxygen consumption. This of oxygen from the ambient air to the
enzyme system provides energy as tissue level (see figure 23.1). At sea
adenosine triphosphate (ATP) for bodily level, the inspired partial pressure of
functions through the oxidative
phosphorylation of food products.

Under normal resting conditions, circu-


latory arrest with anoxia will result in
brain cell injury within 1 minute and
irreparable damage by 5 minutes. The
heart, liver, kidney, and skeletal muscle
have decreasing sensitivities to the
effects of anoxia. Skeletal muscle is
able to tolerate anoxic periods of up to
two hours without suffering irreversible
damage.

The Oxygen Cascade:

The partial pressure of oxygen is the


concentration of oxygen multiplied by
the barometric pressure. At one atmos- 1 Tssue Level --+

I
phere of pressure, the partial pressure of Figure 23.1: The oxygen cascade,
oxygen is 160 mm Hg (760 mm Hg x illustrating the decreasing levels of
21% = 160 mm Hg). While the oxygen PO2 from the ambient air to the
concentration on top of Mount Everest mitochondria.
remains at 21% at an altitude of 26,000

1
** Must Know Should K n o w Page 223
Anaesthesia for Medical Students

Table 23.1: Factors influencing oxygenation at various levels in the oxygen cascade.

Partial Pressure Affected by:


I: Inspired Oxygen Barometric Pressure Oxygen Concentration
PiO, pa FiO,
11: Alveolar Gas Oxygen Consumption Alveolar Ventilation
PAO, vo2 VA
111: Arterial Blood Dead Space Ventilation Shunt
Pa 0, t V/Q 4 VIQ
IV: Cellular Cardiac Output Hemoglobin
PO, CO Hb

oxygen is 160 mm Hg. At the tissue 111: Arterial hypoxemia may occur as a
level, the partial pressure of oxygen in result of ventilation perfusion ab-
the mitochondria varies from 4 to 23 normalities. These mismatches
mm Hg. Hence, there is a progressive occur with an increase in either
decrease in the partial pressure of oxy- dead space ventilation or shunted
gen from the alveolar and arterial level, blood.
to the cellular level. Table 23.1 lists
various factors that influence theoxygen IV: Tissue hypoxia will result when-
partial pressures at each level of the ever any of the above factors cause
cascade. a decrease in the PiO,, PAO,, or
PaO,. In addition, tissue hypoxia
I: A decrease in either the inspired results from either inadequate car-
oxygen concentration or the baro- diac output (with poor tissue
metric pressure (e.g., in a high alti- perfusion), or from an insufficient
tude environment) will lower the amount of hemoglobin to carry
inspired oxygen partial pressure oxygen to the tissues.
(FiOJ.
Hypoxia is defined as a low level of
11: An increase in either oxygen con- oxygen in the air, blood, or tissues.
sumption (e.g., as a consequence of Hypoxemia is a low level of oxygen in
sepsis or shivering) or a decrease in the blood. Cyanosis is a descriptive
alveolar ventilation will decrease the term used to describe the dark bluish or
alveolar oxygen partial pressure purplish coloration of the skin and
(PAOJ. mucous membranes accompanying
hypoxemia. Cyanosis becomes evident
when the reduced hemoglobin (deoxy-

Page 224
Chapter 23 Oxygen Therapy and Hypoxia

Table 23.2: Oxygen delivery systems for spontaneously breathing patients.

0, Dellvery Devlce Flow Rate Percent Oxygen


(Limln.)
Nasal prongs 1-6 24 44% -
FiO, increases by approximately 4%
for every 1Vmin. increase in 0, flow.
Simple face mask 5-6 40%
(Hudson mask) 6-7 50%
7-8 60%
Venturi mask 4 - 12 24,28,31, 35,40%
Non-rebreathing 6 60%
mask with reservoir 7 70%
bag. 8 80%
9 - 10 80% +
Puritan mask with:
Single bottle setup > 10 Umin. -
35 50%
Double bottle setup -
50 80% +

hemoglobin) exceeds 5 grams per 100 postoperative atelectasis are common


ml of blood. It may be detected at an candidates for supplemental oxygen
oxygen saturation as high as 85%. pro- therapy. These patients do not necessar-
vided there is a normal hemoglobin ily require mechanical ventilatory sup-
level, good lighting conditions, and no port (see criteria for ventilation; table
excessive pigmentation. At an oxygen 7.1). A general goal of oxygen therapy
saturation of 75%, which corresponds to is to achieve an oxygen saturation of at
a PaO, of approximately 40 mm Hg, least 90%. At our institution, the mini-
cyanosis is generally easily detected mal acceptable saturation for post-surgi-
(see figure 10.4 oxygen dissociation cal patients who are cared for in a non
curve). Anemia, poor lighting condi- critical care setting, such as a hospital
tions, and dark pigmentation may mask ward, is 92%.
cyanosis and the presence of
hypoxemia. There are a number of oxygen delivery
systems available for providing supple-
Oxygen Therapy: mental oxygen to patients who are
Postoperative surgical patients, patients breathing spontaneously (table 23.2).
with pneumonia, and patients with Oxygen delivered by nasal prongs is

** Must Know Should Know Page 225


Nasal prongs Simple face mask oxygen
(Hudson face mask)

Venturi face mask Non-rebreathingface mask


with reservoir bag.

Figure 23.2: Oxygen delivery systems for spontaneously breathing


patients.
Figure. 23.3: The puritan face mask provides a high level humidity and
predicatable concentrations of oxygen. Shown here with a single bottle set
up for delivering inspired concentrations of up to 50%.

Figure 23.4: The Ambu manual resuscitation bag and mask unit. Used for
providing primary airway management in patients requiring positive pressure
ventilation and oxygenation. Note the hand and finger positioning on the
mask. The fingers are used to displace the mandible forward and create a seal
( between the mask and the patient's face.
Anoesfhesio for Medical Sfudenfs

generally well tolerated, provided the The puritan mask delivers the highest
flow rate is limited to less than 5 or 6 level of humidified oxygen of all these
liters per minute. Flow rates above systems. When two outlet sources are
these levels cause an uncomfortable connected to the puritan mask, oxygen
drying of the nasal mucosa. Common flow rates of greater than 30 liters per
masks used to provide supplemental minute can be achieved, ensuring a
oxygen include the simple (Hudson) consistent inspired oxyen concentration
face mask, the venturi mask, and the by minimizing room air entrainment.
non-rebreathing mask with reservoir One ought to use a double flow setup or
bag. The type of mask utilized depends a non-rebreathing face mask with reser-
on the patient's tolerance, the desired voir bag, when greater than 50%
inspired concentration of oxygen, the inspired oxygen concentration is
desired level of humidification, and required.
economic considerations.
A manual resuscitation unit, such as the
Entrainment of room air will result in a Ambu bag and mask is used to provide
decrease in the inspired oxygen concen- positive pressure ventilation and oxy-
tration. In general, the higher the genation (figure 23.4). This can be
patient's minute ventilation the greater used as the primary system for airway
will be the reduction in the inspired management in the patient requiring
oxygen concentration. A simple face ventilatory support. Adequate oxygen-
mask and nasal prongs are two ation and ventilation can be maintained
examples of low flow oxygen delivery for prolonged periods of time while
systems. These devices have a limited other supportive therapy is initiated. If
reservoir to store oxygen and are unable tracheal intubation is required, mask
to deliver consistent inspired oxygen ventilation should be maintained until
concentrations in the setting of varying all the equipment is available and
respiratory rates and tidal volumes. properly checked. The mask should fit
over ihe bridge of the nose, producing
The venturi, non-rebreathing, and puri- an air tight seal around the nose,
tan face masks are high flow oxygen cheeks, and chin. Change the size of
delivery systems. They are suitable for mask, or insert an oral or nasal airway
delivering consistent and predictable if you encounter difficulty maintaining
concentrations of oxygen (see figures airway patency or positive pressure
23.2 and 233). The venturi mask is ventilation.
designed to deliver specific percentages
of oxygen by varying the size of the air Note the hand and finger positions used
entrainment port and the oxygen flow when providing positive pressure venti-
rate. A non-rebreathing mask with a lation with an Ambu bag and mask unit
reservoir bag allows high concentrations (figure 23.4). The thumb is positioned
of oxygen to be delivered to a sponta- over the nasal bridge of the mask. The
neously breathing patient. index finger exerts downward pressure
on the base of the mask over the chin.

Poge 228
Chapter 23 Oxygen Therapy and Hypoxia

The middle finger lifts the mandible Causes of Hypoxemla:


forward into the base of the mask. The
little finger is hooked around the angle Hypoxemia may result from a decrease
of the mandible and displaces the man- in the inspired oxygen concentration, a
dible forward to create an open airway. decrease in the minute ventilation, an
increase in shunted blood, or a decrease

Table 23.3: Causes of Hypoxemla


Decreased Fi 0, Decreased inspired oxygen concentration
Decreased barometric pressure (high altitude)
Decreased alveolar Hypoventilation
ventilation -
hypoventilation secondary to sedative drugs
or pain are common causes.
Increased dead space venti- Unlike hypoxemia from shunted blood,
lation hypoxemia from V/Q inequalities responds to
-
(ventilation perfusion supplemental oxygen therapy.
inequality) - conditions which increase zone I in the lung

4
will result in an increase in dead space
ventilation. Examples include hypovolemia,
and high airway pressures with positive
pressure ventilation. Other examples of
dead space ventilation include pulmonary
embolism, emphysema, and bronchitis.
Increased shunt Perfusion of alveoli without ventilation results
in an intrapulmonary shunting of blood.

&
Examples include atelectasis, aspiration, con-
gestive heart failure, pneumonia, and endo-
bronchial intubation with lobar collapse.
Shunting of blood may also occur outside the
lung as a result of intracardiac shunts, or peri-
+ pheral arteriovenous shunts.
Decreased diffusion Problems with oxygen diffusing across the
alveolar capillary membrane are rare, but may
occur with high altitude, anemia, or severe
exercise in normal individuals. Pulmonary
fibrosis, emphysema, and interstitial pulmonary
pathology such as sarcoidosis, may also result
in a decrease in diffusion of oxygen and
hypoxemia.

** Must Know Should Know Page 229


Anaesthesia for Medical Students

Table 23.4: Causes of Tlssue Hypoxla


Decreased functional hemoglobin Anemia, hemoglobinopathies
Decreased PaO, Hypoxemia (see table 233)

Decreased tissue perfusion Shock states (see table 215)


- hypovolemic
- cardiogenic
- distributive
- obstructive
Cellular hypoxia Histotoxic hypoxia
- cyanide poisoning

in the diffusion of oxygen across the 4. Nunn JF. Oxygen. Applied respira-
alveolar capillary membrane (see Table tory physiology. Third edit.
233). Butterworth and Co. 1987;pp. 235 -
383.
Tissue hypoxia will result from a
decrease in circulating hemoglobin, a
decrease in the arterial oxygen tension
(PaOz), a decrease in tissue perfusion, or
from a cellular toxin such as cyanide
(see Table 23.4).

References:

1. Shapiro BA., et.al: Oxygen therapy.


Clinical application of respiratory
care, 4th ed. Mosby year book.
1991;pp. 123 - 150.

2. Finucane BT, Santora AH. Airway


management equipment. Principles
of airway management. FA Davis
Co. Philadelphia. 1988;pp. 34 68. -
3. Barash PG, Cullen BF, Stoelting RK.
Monitoring the anesthetized patient.
Clinical anesthesia. Second edit. JB
Lippincott Co. Philadelphia, 1993.

Page 230
Chapter 23 Oxygen Therapy and Hypoxh

Notes:

)
** Must Know Should Know Page 231
Unusual Anaesthetic
Complications
ALLENM.D., FRCPC AND GORDON
GREGORY REIDM.D., FRCPC

In this chapter we shall present three increases in oxygen consumption, carbon


life threatening anaesthetic related com- dioxide production and heat result in
plications. desaturation or cyanosis, elevated end-
tidal C 0 2 values and rapid increases in
I. Malignant Hyperthermia (MH) temperature (up to 1°C / 5 min), as well
as a host of other abnormalities (see
What is MH*? table 24.1).
Malignant hyperthermia is a rare clinical
syndrome that has been observed during How serious is it?
general anaesthesia. Patients may ex- The mortality of MH has decreased from
perience an acute fulminant form, which over 80% in the 1960's to less than 10%.
can be triggered by certain anaesthetic Only about 10% of MH episodes are
drugs, and result in a hypermetabolic fulminant, with a rapid onset and severe
state because of acute uncontrolled physiological derangements and compli-
skeletal muscle metabolism. Rapid cations.
,,
Table 24.1: Cllnlcal features of mallgnant hyperthermia.

Hypermetabolism: Muscle Rigidity:


Increased oxygen consumption Masseter muscle spasm
Dark blood in surgical wound (unable to open mouth)
Cyanosis Chest wall rigidity
Increased C 0 2 production (difficulty ventilating)
Increased end-tidal C 0 2 Abdominal rigidity
Respiratory acidosis Limb rigidity
Elevated temperature
Sweating Rhabdomyolysis:
Metabolic acidosis Hyperkalemia
Increased lactate levels Painful, tender, swollen muscles
Tachycardia Elevated creatinine kinase (CPK)
Tachypnea Myoglobinemia, myoglobinuria
Arrhythmias
Unstable BP

Page 232
Chapter 24 Unusual Anaesthetic Complications

Can you predict who is susceptible? What anaesthetic agents trigger MH*?
MH is an inherited disorder of skeletal The triggers of MH include the depolar-
muscle. History and physical examin- izing muscle relaxant succinylcholine,
ation are usually not helpful in the pre- and any of the volatile anaesthetic agents
operative diagnosis of MH-susceptibil- (isoflurane, halothane, enflurane, and
ity. A history of uneventful anaesth- sevoflurane).
etics in the past is no guarantee that the
patient does not have the disorder. A What anaesthetic agents are safe?
history of intraoperative cardiac arrest, Intravenous agents including any barbitu-
muscle rigidity or stiffness under anaes- rate (eg. pentothal), benzodiazepine (eg.
thesia, high fever under anaesthesia, midazolam, diazepam), as well as pro-
dark urine after anaesthesia, or family pofol or ketamine may be used safely to
member who died unexpectedly under induce andlor maintain anaesthesia.
anaesthesia warrant further investiga- Nitrous oxide and any narcotic may be
tions and a review of any available used. Muscle relaxants such as pan-
medical records. Patients with muscular curonium, vecuronium or atracurium can
dystrophy or myopathy have been all be used, and their action reversed
observed to have an increased associ- with a combination of an anticholin-
ation with MH. esterase and anticholinergic agents such
as neostigmine and glycopyrrolate, or
The pattern of inheritance is autosomal edropl~oniumand atropine. Local anaes-
dominant. Molecular geneticists have thetic agents including the amide class
identified an abnormal locus on chromo- (e.g., bupivicaine, lidocaine), and ester
some 19q in the area of the skeletal class (e.g., tetracaine, chlorprocaine),
muscle ryanodine receptor (RYR 1). with or without epinephrine, have been
The ryanodine receptor is associated used safely in MH patients.
with the calcium influx channel in the
skeletal muscle sarcoplasmic reticulum, How do you treat an MH crisis?
and is thought to be the site of the MH Early diagnosis and administration of
defect. Unfortunately a simple screen- dantrolene are the primary focus of
ing blood test is not likely to be avail- treatingand reversing the hypermetabolic
able in the near future because of the abnormalities of MH. Measures such as
complicated genetics. The only test cooling, treating hyperkalemia,
currently used to make the diagnosis arrhythmias, etc., focus on dealing with
reliably and accurately involves taking the consequences of the MH reaction.
a muscle biopsy from the patient's Dantrolene is classified as a skeletal
quadriceps muscle. Muscle from a muscle relaxant, and is used occasionally
patient with MH is noted to develop an in patients with disorders of skeletal
abnormally strong response when muscle spasticity. It may result in
exposed to caffeine or halothane. The skeletal muscle weakness, but typically
test is only done at certain special test- does not result in muscle paralysis. It is
ing centres, and is not used for screen- supplied as a yellow powder in vials
ing patients. containing 20 mg of dantrolene and 3

** Must Know Should Know Page 233


Anaesthesia for Medical Students

grams of mannitol. Each vial of dan- anaesthetic services is required to keep a


trolene is mixed with 60 mL of water, current stock (minimum 36 vials) of dan-
which can be a time consuming task trolene available in their pharmacy
because dantrolene is so insoluble. department.
Every hospital that provides general

Table 24.2: Treatment of a suspected MH crlsls.


Malignant Hyperthermla Assoclatlon guldellnes (Revlsed 1993).

1. Immediately discontinue volatile anaesthetic agent and succinylcholine.


Hyperventilate with 100% oxygen at high flow rates (> 10 Umin).
-
2. Administer dantrolene sodium 2 3 m g k g initial bolus, up to 10 mgikg.
3. Administer bicarbonate to correct metabolic acidosis as guided by blood gas
-
analysis. In the absence of blood gas analysis, 1 2 mgflcg should be
administered.
4. At the same time institute cooling measures for the hyperthermic patient,
(goal = 38'C). Administer iced saline 15 mUkg iv q 15 minutes x 3.
a. Lavage stomach, bladder, rectum and open cavities with iced saline as
appropriate.
b. Surface cool with ice and hypothermia blanket.
c. Monitor closely since over-vigorous treatment may lead to hypothermia.
5. Dysrhythmias will usually respond to treatment of acidosis and hyperkalemia.
Persistent dysrhythmias may be treated as per ACLS protocol, with the
exception of calcium channel blockers (calcium channel blockers in these
patients may result in hyperkalemia and cardiovascular collapse).
6. Determine and monitor end-tidal C02, arterial, central or femoral venous
blood gases, serum potassium, calcium, clotting studies and urine output.
7. Hyperkalemia is common and should be treated with hyperventilation,
bicarbonate, intravenous glucose and insulin (10 units regular insulin in 50 mL
50% glucose titrated to potassium level). Life-threatening hyperkalemia may
-
also be treated with calcium administration (eg. 2 5 mglkg of CaClJ.
8. Ensure urine output of greater than 2 mUkg/hr. Consider central venous or
PA monitoring because of fluid shifts and hemodynamic instability that may
occur.
9. Boys less than 9 years of age who experience sudden cardiac arrest after
succinylcholine in the absence of hypoxemia should be treated for acute
hyperkalemia first. In this situation, calcium chloride should be administered
along with other means to reduce serum potassium. They should be presumed
to have subclinical muscular dystrophy.

Source: Malignant Hyperthermia Association of the United States, Westport, CT, USA
Chapter 24 Unusual Anaesthetic Complications

Potential complications of MH include: MH related issues:

Acute hyperkalemia (from cell lysis) Postoperative fever:


Acute renal failure (myoglobinuria) An increase in body temperature above
Arrhythmias 38S°C in the perioperative period is the
Pulmonary edema result of either (1) an increase in body
ARDS heat production, (2) a decrease in body
Severe muscle pains, weakness heat elimination, or (3) the result of
Hepatic dysfunction active warming measures. Postoperative
Hemolysis fevers are very rarely due to MH. More
Disseminatedintravascularcoagulation common causes of an elevated tempera-
-
Cerebral injury seizures, coma ture in the perioperative period include:

Following the initial treatment of an coexisting infections


MH suspected crisis: anticholinergic medications
(e.g., atropine resulting in decreased
A. The patient should be observed in sweating)
an ICU setting for at least 24 hours, transfusion reaction
since recrudescence of MH may dehydration
occur, particularly following a excessive coverings on the patient
fulminant case. elevated room temperature
active warming measures
B. Administer dantrolene 1 mglkg iv (blankets, fluids)
-
every 6 hours for 24 48 hours after thyrotoxicosis
the episode.
Heat stroke:
C. Follow ABG, CPK, potassium, cal- MH patients may be more susceptible to
cium, urine and serum myoglobin, heat stroke compared to the normal
clotting studies and core body tem- population. However, most patients
perature until such time as they suffering from heat stroke are not MH
return to normal values (eg. 6 susceptible. Patients who have suffered
hours). Central temperature (eg. from heat stroke and also have an abnor-
rectal, esophageal) should be con- mal family history of anaesthesia prob-
tinuously monitored until stable. lems suggestive of MH, should be in-
vestigated for MH.
D. Counsel the patient and family re-
garding MH and further precautions.
Refer the patient to the MH North
American registry, and biopsy
centre.

i
** Must Know + Should Know Page 235
Anaesthesia for Medical Students

11: Asplratlon Syndrome. any antacid if aspirated. Gastric


emptying by nasogastric tube is im-
Chapter nine introduced the concept of portant in patients with a bowel ob-
a rapid sequence induction and ident- struction.
ified factors that placed a patient at risk
for gastric aspiration. The severity of 3. In patients with an anticipated diffi-
gastric aspiration is related to the vol- cult intubation, topicalization and
ume and acidity of the aspirate, the local anaesthetic blocks of the upper
presence of contaminated particulate airway will permit the trachea to be
matter (e.g., bowel contents) and the intubated with the patient awake.
former health of the patient. This reduces the chance of a failed
intubation, difficult mask ventila-
Strategies useful in reducing the peri- tion, and subsequent gastric aspir-
operative risk of gastric aspiration ation.
include*:
4. Patients with identified risk factors
1. Avoid impairing airway reflexes. for gastric aspiration who require
The risk of gastric aspiration is general anaesthesia (see Table 9.1),
reduced in the awake patient. Sur- must have a rapid sequence induc-
gery that can be accomplished with tion. This involves a period of pre-
local or regional anaesthesia should oxygenation, the application of
be considered in the patient at risk cricoid pressure, and tracheal
of aspiration. intubation with a cuffed E'lT (see
chapter 9; Rapid Sequence Induc-
2. Reduce gastric volume and acidity. tion). Extubation should only be
A period of fasting (minimal 8 performed when the following cri-
hours for solid foods and 4 hours teria are met:
for clear liquids) is mandatory in a
patient undergoing non-emergency a. the patient is responding to verbal
surgery. A planned regional or local commands
anaesthetic does not negate the need b. the patient has regained an
to fast as unforseen events may arise oropharyngeal gag reflex
necessitating a general anaesthetic. c. the patient is positioned on their
Metochlorpropamide and domper- side, and
idone have been used to stimulate d. the need for tracheal intubation is no
gastric motility and promote gastric longer present.
emptying. H-2 antagonists and
antacids are useful when given pre- The consequences of gastrlc
operatively to reduce both gastric asplratlon:
secretion and acidity. Sodium
citrate is the antacid of choice in an- Apiration of a liquid causes a vigorous
aesthesia as it is non-particulate cough, accompanied by a transient
and produces the least damage of period of hypoxemia in the normal

Page 236
t
Chapter 24 Unusual Anaesthetic Complications
)

awake adult. Significant cellular dam- be the only indication of aspiration.


age occurs in a dog model when the pH Gastric contents in the upper airway and
is less than 2.5 and the volume is mouth, may or may not, accompany
greater than 0.4 mlkg. If the liquid has gastric aspiration.
a pH of 2.5 or more, it will generally
not cause cellular damage. When gas- Treatment of asplratlon:
tric acid is aspirated, surfactant is
destroyed, the alveoli collapse, and The first few minutes following an aspir-
hemorrhage and exudation into the ation are critical, and attempts must be
alveoli and interstitium occurs. Severe made to remove as much material as
bronchospasm usually accompanies a possible from the mouth, pharynx and
significant aspiration. Lung compliance trachea. As the most common site for
decreases as alveoli collapse, and areas aspiration is the apical posterior segment
of shunt occur, resulting in severe of the right lung, the patient should be
hypoxemia. positioned head down in the right lateral
position to limit spread to the left lung,
Aspiration of particulate (food or fecal) and aid drainage by gravity. Immediate
matter may result in blockage of distal bronchoscopy is used to remove any
bronchi, resulting in large areas of col- particulate matter that has been aspirated.
lapse, edema formation and shunting.
Within the first few days a mononuclear With a significant aspiration, severe
foreign body response occurs. The lung hypoxemia with decreased lung compli-
distal to the obstructed bronchi collapses ance and difficulty providing positive
and fills with secretions. Without resol- pressure ventilation are expected to
ution, lung infection or abscess forma- occur within the first 30 to 60 minutes.
tion are inevitable. Positive pressure ventilation with con-
tinuous positive airway pressure (CPAP)
Dlagnosls of asplratlon: or positive end expiratory pressure
(PEEP) are used to prevent alveolar
Early diagnosis and treatment may collapse, limit the reduction in residual
reduce the severity of the aspiration volume, and prevent further atelectasis
syndrome. During mask anaesthesia and shunting. Crystalloid solutions are
with either a face or laryngeal mask, the preferable to colloid solutions (see chap-
detection of aspiration may be difficult. ter 20), because the pulmonary capillary
Sudden laryngospasm, coughing or membrane is injured, and may allow
stridor may be the first indication that colloid solutions to cross into the alveoli,
aspiration has occurred. Bronchospasm increasing the degree of pulmonary
may also occur, and the compliance of edema.
the chest may decrease resulting in
increased airway pressures during mech- Steroids are not generally indicated, and
anical ventilation. Alternatively, de- may promote granuloma formation in
saturation with hypoxemia and the need cases of aspirated food particles. Anti-
for higher concentrations of oxygen may biotics are also not indicated, unless

** MUSI Know Should Know Page 237


Anaesthesia for Medical Students

there is evidence of gross aspiration exposure to the drug. This form of


from bowel contents. Bronchodilators reaction can be diagnosed with skin tests
are used in treating bronchospasm. and specific antibody assays.
Prolonged positive pressure ventilation
and critical management of intravascular An anaphylactoid reaction occurs when
volume status, oxygenation, and ventila- the allergen causes direct release of
tion are the principles of treating a histamine. This reaction is not immune
significant aspiration. Invasivemonitor- mediated and IgE antibodies are not
ing and frequent blood gas analysis may involved.
be required. Mortality and morbidity
usually results from the initial severe
hypoxemia that occurs at the time of Table 243: Clinical Features*
aspiration. This emphasizes the need
Anxiety, headache, nausea
for initial aggressive treatment.
Impending sense of doom
Dyspnea, tachypnea
111: Allergic reactions
Tachycardia
Flushing, hives, urticaria (70%)
Muscle relaxants and exposure to latex
Facial, orbital, mucous
materials are the two most common
membrane edema, sneezing
causes of an allergic reaction occurring
Hoarseness, laryngeal edema
during anaesthesia. The frequency of
Hypotension (85%)
anaphylactic shock is 1 in 3500 anaes-
Bronchospasm (35%)
thetics. The allergic response manifests
Hypoxemia
within minutes of an intravenous injec-
Desaturation
tion of the offending agent. By con-
Increased airway pressures
trast, signs of an allergic response re-
sulting from latex are delayed.

Definitions: Table 243 lists the clinical manifesta-


tions of an allergic reaction. Exposure '
Anaphylactoid is a general term used to to the allergen results in the release of ,
describe the clinical features of an aller- histamine, tryptase, leukotrienes and ,
gic reaction. The term anaphylactoid cytokines from mast cells and basophils.
shock is used to designate an allergic These act on both histamine (HI and
reaction in which the mechanism may H2) receptors throughout the body pro- ;
be either the result of a direct release of ducing the clinical features. An immedi-
histamine, or from an immune mediated ate brief surge in plasma histamine '
mechanism. levels occurs followed by a gradual rise
in tryptase levels which are specific to ,
Anaphylactic or anaphylaxis is used anaphylactic reactions and can be
when an allergic reaction is immune measured in the serum (see figure 24.1).
mediated, and implicates IgE antibodies Analysis of the urine can be used to ,
and prior sensitization from previous detect a metabolite of histamine, urinary

Page 238
Chapter 24 Unusual Anaeslhe~icComplications

the antigenic site. As this is common to


many muscle relaxants, cross reactivity

I Histamine
between different relaxants is common.
Prior exposure to a muscle relaxant is
not required, as previous sensitization
may have occurred following exposure
to household products containing sub-
stances with ammonium structures (e.g.,
disinfectants, cosmetics). Latex allergy
accounts for approximately 12% of
allergic reactions. Patients with repeat
exposure to latex products have an
increased risk of a latex allergy. These
include patients requiring repeat urinary
catheterization (paraplegia, spina bifida),
Figure 24.1: Schematic time profile and health care workers who frequently
of the release of histamine, tryptase, work with latex gloves. Less than 15%
and urinary methylhistamine of allergic reactions are the result of
exposure to blood products, opioids,
benzodiazepines, and antibiotics.

methylhistamine, and aid in the diag- Treatment of anaphylaxis:++


nosis. Elevated levels of urinary
methylhistamine and serum tryptase A useful memory tool in recalling the
support the diagnosis of an anaphylactic emergency treatment steps for
reaction, but do not identify the anaphylaxis is to recall the "Anaphylaxis
allergen. Serum IgE antibodies can be ABCsW:
used to perform radioimmunoassays
(RIAs) to identify the responsible A Airway, and adrenaline
allergen. Specific antibodies to B Breathing and benadryl
thiopental, propofol, muscle relaxants C Crystalloids and cimetidine
and latex are now available. Blood and s steroids
urine samples should be taken at 1 to 3
hours, and 24 hours after the reaction to Tachycardia with an allergic reaction
measure these mediators. The patient results from the chronotropic effects of
should be referred for skin testing with H2 receptor stimulation. Epinephrine is
cutaneous skin prick tests within two the principle initial drug treatment. In
months of the reaction. cases of severe hypotension or laryngo-
spasm, 0.1 ml of 1:1000 epinephrine
Muscle relaxants account for 70% of the may be given intravenously, and
cases of anaphylaxis during anaesthesia. repeated as needed. A single bolus dose
The tertiary or quaternary ammonium of epinephrine should generally not
group on muscle relaxants is frequently exceed 0 5 ml (05 mg). Excessive

** Must Know * Should Know Pogc 239


Anaesthesia for Medical Students

epinephrine administration risks References:


malignant arrhythmias (ventricular
tachycardia, and ventricular fibrillation) 1. Allen GC. Malignant Hyperthermia.
severe hypertension, pulmonary edema, -
Aether 1994; 1: 3 6.
myocardial infarction and stroke.
Nevertheless, patients taking beta- 2. Gibbs CP, Model1 JH. Management
blockers may be resistant to the effects of Aspiration Pneumonitis,
of epinephrine, and may require higher Anesthesia 3rd edition. Edited by
doses of epinephrine. The Miller RD. Churchill Livingstone
administration of beta- blockers, to Inc. 1990. pp. 1293 - 1319.
control the heart rate response, is
contraindicated in patients experiencing 3. Laxenaire MC, Moneret-Vautrin DA.
an anaphylactoid reaction. Allergy and Anaesthesia. Aether
1994: 2: 14 - 17.
Table 24.4: Management of Notes:
Anaphylaxis during Anaesthesia
Stop drug or allergen
administration
Provide 100% oxygen
Discontinue surgery and
anaesthesia as soon as feasible.
Give epinephrine 50 100 mcg -
iv with hypotension, 0 5 1.0 -
mg iv with cardiovascular
collapse.
Epinephrine infusion 0.05 0.2 -
mcglkglmin (see chapter 22).
Crystalloids (e.g., NS, RL) iv,
-
may require 2 4 liters for a
-
70 kg adult, i.e., 25 50 ml/kg.

-
Diphenhydramine 50 mg iv
(~enadryl" 1 m a g )
Cimetidine 300 mg iv, or
ranitidine 50 mg iv

-
Hydrocortisone 100 mg iv
(Solucorte~ 1.5 mgtkg), or
methy lprednisolone
(Solumedrol@) 1m a g iv q6hn
x 24 hours.
Inhaled salbutamol (ventolin?
for bronchospasm.
Avoid beta blockers.
) Appendix:
)
)

J Intravenous Access
/
Intravenous (iv) cannulation provides The Hagen-Poiseuille equation explains
direct access to the venous circulation. why a 5 inch long 16 gauge central
) This discussion will focus on practical venous catheter will achieve less than
aspects of securing venous access to the half the maximum flow rate of a 2 inch
) peripheral circulation. Students are not long 16 gauge peripheral catheter.
) expected to acquire skills for insertion Alternatively, by halving the radius of
of catheters into the central circulation, the catheter, the maximum flow rate
or for performing a venous cutdown will decrease to 1/16. Warming the
during this rotation. Intravenous intravenous fluids will cause
) catheterization is most commonly venodilation, decrease fluid viscosity,

'
)
indicated for administering medications
or fluids, or to sample blood for analy-
sis.
and increase the maximum flow rate.
Similarly, pressurizing the fluid in the
intravenous bag will increase the
pressure differential between the fluid
A plastic catheter, which is inserted and venous system and permit more
) over a hollow needle, is the most rapid fluid administration.
) common intravenous catheter system
used for peripheral venous cannulation. Venous Anatomy:
) The length of the catheter, and it's
) internal diameter, the viscosity of the The upper extremities venous anatomy
intravenous fluid, and the pressure dif- is relatively consistent. Digital veins
ferential between the vein and the fluid run proximally from the digits to the
) being administered all determine the dorsal arch of veins on the dorsal sur-
) maximum flow rate, as specified by the face of the hands. A vein can usually
Hagen-Poiseuille equation: be located just above the head of the
1 3rd and 4th metacarpals. The dorsal
) Hagen-Poiseuille equation: arch turns radially to the anatomical
snuff box, where a large superficial vein
can be located at the level of the distal
radial tubercle. This vein continues
along the lateral forearm to the anti-
cubital fossa where it joins other veins
) P = pressure across the catheter to form the cephalic vein. The cephalic
) r = radius of the callteter vein can sometimes be followed up the

' n = viscosity of the fluid


1 = length of the cadeter
arm over the biceps muscle, crossing the
deltoid muscle anteriorly, and disappear-

) ** M u s t Know * Sl~ouldKnow Page 241


Anaesthesia for Medical Studertts

ing between the heads of the deltoid and the knee, passing behind the femoral
pectoralis muscles to enter the axillary condyle. It continues proximally along
vein. Other superficial veins travel up the medial thigh entering the thigh
the forearm to form the basilic vein muscles approximately 1.5" below the
located just medial to the insertion of inguinal ligament, where it joins the
the biceps muscle in the anticubital femoral vein. The anatomy of the
fossa. The basilic vein continues prox- femoral vessels (lateral to medial) can
imally (becoming obscured in the lower be recalled using the pneumonic
113 of the arm as it enters the muscles NAVEL* where:
of the ann) to join the axillary vein in
the axilla. Identification of superficial N = Nerve
veins may be difficult in obese patients. A = Artery
Fortunately, the volar aspect of the wrist V = Vein
generally lacks adipose tissue. Examin- E = Empty space
ation of this area may reveal small veins L = Lymphatics
that can be used for access when
attempts at other sites have failed. (*recall that the NAVELpneumonic was
also used for drugs which can be given
The upper extremity is used for venous through a tracheal tube. See pg. 50).
cannulation in the vast majority of
patients. Patient anxiety (increased The femoral artery is located at the
catecholamines), a cold environment midpoint between the anterior superior
(venoconstriction), adipose tissue, or a iliac spine and the pubic symphysis.
pre-existing fluid deficit, may make the The femoral vein lies approximately 1
identification of suitable veins for cm medial to the artery. Cannulationof
venous cannulation difficult. To the femoral vein is less popular than
improve the chance of successful other veins because of the restriction in
cannulation, keep the extremity below patient mobility, and the risks of infec-
the level of the heart, use a tourniquet tion or thrombosis. Peripheral intra-
around the biceps muscle to distend the venous catheters are generally too short
vein, avoid cooling the patient, and to be used for the femoral vein, and a
consider using warm blankets or heating longer central venous catheter (approxi-
pads on the extremity to dilate the mately 5 inches in length) is more suit-
veins. When venous cannulation of the able.
upper extremity fails, one can use the
lower extremity. The foot has a dorsal Cholce of site for intravenous
venous arch that can be used for venous cannulatlon:
access. The saphenous vein is the equi-
valent to the superficial radial vein in The most common sites used for iv
the forearm. It continues from the cannulation are the dorsum of the hand,
dorsal arch of the foot to pass over the medial aspect of the forearm, and the
anterior aspect of the medial malleolus. anticubital fossa. Of these, the dorsum
It then travels up to the medial aspect of of the hand is perhaps the most com-
Appendix: I n t r t ' v e ~ ~ o uAccess
s

Figure 1: Peripheral venous anatomy.

** Must Know Should Know Page 243


Anaestl~esiafor Medical Students

mon choice. It allows one easy.access 24, and 26 gauge catheters. The 24 and
to the vein, and, should the intravenous 26 gauge catheters are generally only
fail, one may still use a more proximal used in the neonatal or paediatric popu-
site. For patients who will require their lation. Sixteen to 20 gauge catheters
intravenous for a period of time greater are the most common sizes used in
than 24 hours, the forearm may be a adults. Catheter lengths for peripheral
better choice. It restricts their activities veins vary from 1" to 2".
less, and remains relatively inimobile'
when they move their arms. They are Patients who may require blood prod-
also less likely to catch their intra- ucts and large amounts of intravenous
venous on other objects. fluids should have several large boie
intravenous catheters (i.e., 14 or 16
The anticubital fossa is a good choice gauge). We routinely manage patients
when a large vein is required, and the undergoing minor ~rocedures,in which
anticipated period in which the catheter the need for rapid fluid administration is
will be used is a short one. As a gen- remote, with a single 18 or 20 gauge
eral rule, however, it is best to chose a intravenous catheter.
site for the intravenous that does not lie
over a joint. When a patient flexes and Intravenous catheters of 18 gauge or
extends their joint, the intravenous site larger may cause moderate discomfort
will be uncomfortable, and this motion when inserted in the awake patient. By
may dislodge the catheter from the vein using local anaesthesia, you may be
making it interstitial. One also risks able to decrease this discomfort. A 25
injuring the median nerve or or 27 gauge needle can be used to
catheterizing the brachial artery when administer approximately 114 ml of 2%
attempting anticubital vein cannulation. lidocaine into the dermis either directly
over the vein or immediately lateral to
The lower extremity and femoral veins the vein. Aspiration before injection is
. are less commonly chosen for iv access not necessary. Insert the intravenous
because they restrict patient's mobility cannula through the local anaesthetic
and increase the risk of complications wheal.
including infection, phlebitis, and
thromboembolism.
Technique of Intravenous
Choice of Intraveno~~s
Size: Cannalation:

Intravenous catheters are supplied in Assemble your required equipment in-


various sizes and lengths. The size of cluding: iv bag and tubing, iv cathe-
catheter increases as the gauge number ters, tourniquet, alcohol swab, gloves,
of the catheter decreases. In adult an- tape, (+/- povidone-iodine swab, 114 ml
aesthesia, we consider a 20 gauge cathe- 2% lidocaine local anaesthetic in a 3
ter to be small. The catheters come in ml syringe with a 25 or 27 gauge
even numbers i.e., 14, 16, 18, 20, 22, needle, and gauze to clean spilt blood).

Page 244
Appendix: InIravenous Access

3 cc syringe, 2%lidocaine,
27 gauge needle, intravenous
catheter, tape, tourniquet, and
gauze.

Intravenous bag, tubing and tape.

Intravenous catheter and needle. Common intravenous cannulas.


1 Note that the needle is longer Small bore = 22 and 20 gauge,
1 than the catheter. Large bore = 16 and 14 gauge.

Figure 2: Equipment for peripheral intravenous access.


I
)
) ** Must Know Should Know Page 245
1. Apply a tourniquet to the extremity. 11. Advance the catheter and needle
2. Identify a suitable vein. Gently tap (maintaining skin traction and vein
over the vein to facilitate veno- immobilization) visualizing where
dilation. the tip of the needle is in relation to
3. Cleanse the area with an alcohol the vein, watching for a flash of
swab (or povidone-iodine swab blood in the hub of the catheter.
followed by an alcohol swab). 12. When blood comes back into the
4. Wear disposable gloves hub, advance the needle and cathe-
(recommended). ter another 2 mm to ensure the
5 . Optional: Inject local anaesthesia catheter is in the vein (and not still
with a 25 or 27 gauge needle into outside the wall of the vein).
the dermis either directly over the 13. Without moving the catheter, with-
vein or 2 - 3 mm lateral to it using draw the needle approximately 1
114 ml of 2%lidocaine. cm. (Alternatively, without moving
6. Optional: Break the seal between the needle, the catheter can be
the catheter and the needle (this advanced over the tip of the needle
may make it easier to advance the by approximately 1 cm).
catheter off the needle once you 14. With the needle back from the tip
enter the vein). of the catheter, advance both the
7. Immobilize the vein by applying needle and catheter together until
traction to the skin distal to the you feel resistance or the catheter is
insertion site with the hand that is fully inserted.
not holding the intravenous catheter. 15. Release the tourniquet.
Maintain immobilization of the vein 16. Using the hand that was maintaining
during iv insertion. Avoid putting skin traction, occlude the vein by
your hand immediately below the pressing with your finger proximal
vein as this will prevent you from to the tip of the catheter (lying in
lowering the intravenous catheter the vein). This prevents blood from
into the same plane as the vein. coming back out of the catheter
8. Hold the hub of the needle between when the needle is removed.
your thumb and forefinger with the 17. Remove the needle, leaving the
bevel facing up. Watch for the catheter in the vein.
blood to flash back into the plastic 18. Secure the intravenous tubing to the
hub when you enter the vein. catheter (a luer lock connecting end
9. Puncture the skin through the an- accompanies certain iv tubing sys-
aesthetic skin wheal holding the tems).
needle at a 30 - 45 degree angle to 19. Open the intravenous roller clamp,
the vein. Advance the needle until and adjust the flow to the desired
the catheter is beneath the skin. rate.
10. Lower the angle of the intravenous 20. Secure the intravenous to the patient
catheter to approximate that of the with tape.
vein you are attempting to enter.

Page 246
Appendix: Intravenous Access

Figure 3: Venous anatomy, immobilization and cannulation.

j I Superficial radial vein. Basilic vein. - I

Immobilization of the dorsal Immobilization of the


veins of the hand. superficial radial vein.

)
I Local anaesthetic skin wheal. using the catheter hub.

Forearm vein cannulation: Angulating the catheter prior to insertion


I
permits insertion of the cannula in the same plane as the vein.
)

) ** Must Know Should Know Page 247


Anaesthesia /or Medical Students

Fig. 4: Note that vein immobilization is maintained throughout iv insertion.

I Puncture skin at 30 45' - Decrease angle of insertion. I

Blood flashes back into cannula -


Advance another 2 3 mm to
hub as the vein is entered. ensure catheter is in the vein.

Catheter is left in the vein while


the needle is withdrawn 1 cm.
With the needle back 1 cm, the
catheter is advanced to the hub.
I

Once the vein is occluded (to prevent back-bleeding), the needle is


removed and the iv tubing is connected. The iv is then secured with tape.

Page 248
) Appendix: Inrravenous Access

i
1
)
1 Puncture the skin holding the
needle at a 30 - 45 degree
) angle and advance the needle
) until the catheter tip is beneath
the skin.
)
)
1 Decrease the angle of the
) intravenous catheter in
1 relation to the vein. Watch for
blood in the iv hub as the vein
1 is entered.
)

i
Advance the needle and
) catheter another 2 mm to
1 ensure the catheter is in the
vein.
1

) Without moving the catheter,


withdraw the needle
approximately 1cm back from
1 the tip of the catheter. Now
i advance both the catheter and
needle into the vein.
i
i Release the tourniquet.
i Occlude the vein proximal to
) the catheter tip. Remove the
needle, and secure the
intravenous tubing to the
1 catheter.
i
Figure 5: Establishing peripheral intravenous access.

/I

) ** Must Know Should Know Page 249


Anaestl~esiafor Medical Students

Problems with Intravenous 3 . You advance the catheter easily into


cannulatlon: the vein but then encounter resis-
tance before it is completely
1. Resistance is felt when attempts are inserted.
made to advance the catheter over
the needle. The catheter tip is likely lying next to a
valve or junction in the vein. Do not
The most likely problem is the catheter force the catheter, you may be able to
is outside or only partially through the connect the catheter to the intravenous
wall of the vein. Make sure that the tubing and advance the catheter once
needle and catheter are advanced ap- fluid is flowing through the tubing. If
proximately 2 mm into the vein after not, you may still be able to achieve
the flash back occurs so that the cathe- adequate administration of fluids and
ter will be in the vein before attempts medications without having the catheter
are made to advance the catheter over advanced all the way into the vein.
the needle. If the catheter is at a sharp
angle to the vein you will only have a 4 . The patient experiences excessive
short distance before the tip of the pain when inserting the intravenous.
needle is through the vein when it is
advanced. T o avoid this, try t o lower The intravenous needle and catheter
the angle of the catheter to keep it in may be dissecting along the vein wall.
the same plane as the vein. The vessel walls have sensory fibres
and if the needle scrapes along the wall
2. A large hematoma develops when rather than entering it cleanly, the
attempting to insert the intravenous. patient may experience significant pain
with even a small intravenous. Other
A hematoma may develop whenever the possibilities include nerve injury with
vein is entered. This may occur when needle insertion (e.g., median nerve in
injecting local anaesthetic if the local is the anticubital fossa, radial nerve in the
injected beneath the skin and into the anatomical snuff box). Remove the
vein. By injecting local anaesthetic intravenous and use an alternative site
immediately lateral to the vein, the with local anaesthesia.
chance of causing a hematoma is less.
If a hematoma results while you are 5. Unable to enter the vein with the
attempting to insert the intravenous, and intravenous catheter.
your ability to visualize the vein is lost,
you should remove the catheter and Inadequate stabilization of the vein is
apply pressure with a gauze to prevent the most common mistake made when
further bleeding. Release the tourni- learning to insert an intravenous.
quet, and hold the site for a couple of Immobilize the vein by applying skin
minutes before trying again at another traction distal to the vein. Try to
site. visualize where the tip of the needle is
in relation to the vein. Lift the tip of

Page 2J0
Appendix: Intravenous Access

the needle up so that you can see its


\
relation to the vein. Line up the needle / The iv catheter is
direction and plane with that of the angulated prior to
vein. If you have advanced the needle
and cannot enter the vein, withdraw the
needle and catheter such that the cathe-
ter tip is just below the skin, and start
again, adjusting to a different angle and
depth. With time, the needle may
become obstructed by clotted blood IV catheter
preventing a flash back from occuring
when the needle is in the vein. Con-
sider changing the intravenous needle during cannulation.
and catheter after attempting
catheterization for several minutes.
I
) Other helpful hints:
Figure 6:
) To approximate the plane of the intra- Cannulation of forearm veins:
) venous catheter with the plane of the Angulating the iv catheter prior to

' vein being cannulated, it is often useful


to create a slight (10 - 15 degree)
angulation in the iv catheter before
insertion may decrease the chance
of passing through the back wall
of the vein during cannulation.
) inserting it. This is particularly useful
in cannulation of veins of the forearm,
) where it is difficult to hold the catheter
at a low enough angle to approximate
the plane of the iv catheter with the
vein (figure 6).

The plastic iv housing unit which is


supplied with the iv catheter can be
used to create this angle just distal to
) the catheter hub. Angulate the catheter

' such that the bevel is facing up. The


angulation allows the catheter hub to be
) held at a comfortable angle, and
matches the plane of the iv catheter
with the vein.
)

** Must Know Should Know Page 2111


Review Questions
Chapter 3: Chapter 6:
Preoperative assessment. Intubation and anatomy of the airway.

1. Define the ASA physical status 1. What is the "1-2-3" test?


classification. 2. What does a class I hypopharyngeal
2. How long should elective surgery view mean? What structures are
be postponed following a visualized in a class I hypo-
myocardial infarction? What is the pharyngeal view?
basis of this recommendation? 3. What structures are visualized in a
3. What information should be grade 111 laryngeal view?
obtained in the anaesthetic history? 4. What is the optimal position of the
4. What common anaesthetic tech- head and neck for intubation using
niques can be used to provide an- direct laryngoscopy?
aesthesia for lower abdominal sur- 5. How is tracheal intubation con-
gery? firmed?
5. What anaesthetic risks might be 6. Name 4 simple maneuvers that can
associated in a patient who smokes be used t o overcome an upper air-
regularly? What information way obstruction.
obtained from history, physical, or
laboratory examination might be Chapter 7:
useful in assessing this risk? Are Intubation decisions.
there any means of decreasing the
risks of perioperative complications 1. What laboratory criteria should you
related to smoking? use to assess the objective need for
intubation and ventilation?
Chapter 4: 2. What are some important historical
Premedication. and clinical factors that suggest the
need t o intubate and ventilate a
1. Why are patients premedicated prior patient?
to surgery?
2. What are the general contra- Chapter 8:
indications t o the use of Laryngeal mask airway.
benzodiazepine or opioid pre-
medications? 1. What is the difference between a
LMA and an endotracheal tube?

Page 252
Review Questions

2. Why would a laryngeal mask air- 2. Why would one choose propofol
way be used rather than a endo- over thiopental as an intravenous
tracheal tube? induction agent?
3. When would one choose ketamine
Chapter 9: over either thiopental or propofol as
Rapid sequence induction. the intravenous induction drug?
4. What are the concentrations and
1. What is the purpose of a rapid induction doses of thiopental and
sequence induction? propofol?
2. Describe the sequence of maneuvers
used in a rapid sequence induction. Chapter 12:
3. What is the purpose of pre- Muscle relaxants.
oxygenation?
4. Which patients should be regarded 1. What is the difference between a
as being at risk of pulmonary aspir- depolarizing and non-depolarizing
ation of gastric contents? muscle relaxant? Give examples of
5. What measures can be taken to each.
decrease the risk of aspiration? 2. What are the absolute contra-
indications to the use of succinyl-
Chapter 10: choline?
Monitoring in anaesthesia. 3. Which patients are susceptible to
hyperkalemia following succinyl-
1. What information does the anaes- choline?
thetist use to assess the depth of 4. What is the concentration that succ-
anaesthesia? inylcholine is supplied? What is the
2. What information can be obtained dose for intubation?
by monitoring the capnograph? 5. Which drugs can be used to
3. What relationship does the ETCO2 antagonize a neuromuscular block?
value have to the PaC02? What
conditions might result in a ETCO2 Chapter 13:
measurement of 20 mm Hg with a Inhalational anaesthetic agents.
PaC02 measurement of 40 mm Hg?
1. What is MAC?
Chapter 11: 2. What is the relationship between the
Intravenous anaesthetic agents. anaesthetic concentration that is set
on the anaesthetic vaporizer and the
1. Why do patients awaken from a anaesthetic concentration in the
sleep dose of thiopental within 5 to patient's brain?
10 minutes of its administration 3. What is diffusion hypoxia?
when the elimination half life is of 4. What are the MAC values of iso-
the order of 5 - 12 hours? flurane, enflurane, and halothane in
oxygen?

Page 253
Anaesthesia for Medical Students

Chapter 14: 10.What is the difference between a


Narcotic agonists and antagonists. spinal and an epidural anaesthetic?
11. How many milligrams of lidocaine
1. What undesirable effects do opioids are in 20 mls of a 2% solution?
have?
2. Name an opioid antagonist. What Chapter 16:
dose of this drug would be appropri- Acute pain management.
ate to reverse opioid induced
respiratory depression. What, if any, 1. List the physiological effects of
are there any potential problems of acute pain.
giving too much of this antagonist? 2. Contrast intramuscular and PCA
opioid administration.
3. What are the adverse effects result-
Chapter 15: ing from the administration of ex-
Local and regional anaesthesia. cessive opioid analgesics?
4. What non-opioid analgesic agents
1. Name two classes of local anaes- are available for the control of
thetic agents, and give examples of acute pain?
each. 5. What are the contraindications to
2. What is PABA, and what role does administering a non-steroidal anti-
it have in local anaesthesia? inflammatory drug?
3. Name 4 techniques of administering 6. List an appropriate dose and sched-
a local anaesthetic drug. ule for two common NSAID's used
4. Why is a vasoconstrictor often used to control of acute pain.
with a local anaesthetic? Give an
example of a LA vasoconstrictor and Chapter 17:
its concentration. When would the Chronic pain.
use of a vasoconstrictor be contrain-
dicated? 1. What is the difference between
5. Which regional block results in the acute and chronic pain?
highest concentration of local an- 2. What is RSD? What conditions
aesthetic in the blood? may lead to the development of
6 What is the maximum recommended RSD?
dose of plain lidocaine, and of lido- 3. What modalities are commonly
caine with a vasoconstrictor? used to treat RSD?
7. Why might a regional anaesthetic be 4. How is a diagnosis of RSD made?
given as well as a general anaesthe- 5. What are trigger points?
tic? 6. Name two surgical conditions that
8. Describe some of the signs and may present with back pain and
symptoms of local anaesthetic toxic- require emergency surgical inter-
ity. vention ?
9. Describe the steps in treating an
acute local anaesthetic toxicity.

Page 254
Review Questions

Chapter 18: 2. List conditions that may b e associ-


Obstetrical anaesthesia. ated with a significant preoperative
fluid deficit.
1. What is the supine hypotensive 3. What is the difference between a
) syndrome? How can it be pre- crystalloid and a colloid? Give
) vented? examples of each.
2. What factors may influence a 4. Which patients should consider
) patient's experience of pain during autologous blood donation? For
) labour and delivery? which patients is this not suitable?
What options are available for deal- 5. Calculate the acceptable amount of
) 3.
ing with the pain of labour and blood that can be lost in a 70 kg
) delivery? male if his initial hemoglobin is
) 4. What are the major risks of general 140 gmldl, and the accepted

'
)
anaesthesia in the parturient under-
going a cesarian section?
minimal hemoglobin after surgery is
80 gmldl.
6. What is the most common cause of
) Chapter 19: an ABO incompatible blood trans-
Basic neonatal resuscitation. fusion?
7. Name three different blood compo-
What is the Apgar score of a baby nents that may be transfused.
that is limp, blue, has no response
to oropharyngeal suctioning, a heart Chapter 21:
rate of 60 bpm, and irregular gasp- Common perioperative problems.
ing respiratory efforts?
Describe the basic steps in neonatal 1. Define shock? Classify the differ-
resuscitation. ent types of shock and give
When is positive pressure ventila- examples of each.
tion (PPV)indicated in the newborn 2. What are some treatable causes of
infant? Describe the technique of an agitated postoperative state?
PPV.
Assuming a newborn infant weighs Chapter 22:
3 kg, what is the concentration and Managing the circulation.
dose of epinephrine, and how ought
it be administered? 1. What are the broad goals in control-
ling the circulation?
Chapter 20: 2. What are the differences between an
) Intravenous fluid and blood component alpha-1 and beta-1 adrenergic
therapy. agonist? Give examples of each.
) 3. What are the factors which deter-
) 1. How are the hourly and daily main- mine cardiac output?
) tenance fluid requirements calcu-
lated?
I

Page 255
~aestltesiafor Medical Students

hapter 23:
Xygen therapy and hypoxia.

. List some devices that are common-


ly used to deliver oxygen to spon-
taneously breathing patients.
. When should a puritan face mask
be used? When should one use a
manual resuscitation device, such as
a n Arnbu bag and mask unit?
i. List the five categories of condi-
tions causing hypoxemia.
I. List the four categories of condi-
tions causing hypoxia.

Bapter 24:
Unusual anaesthetic complications.

1. What is MH?
2. List two anaesthetic agents that may
trigger an MH reaction.
3. Which drug is used specifically to
treat an MH reaction?
4. What strategies are useful in reduc-
ing the perioperative risk of pul-
monary aspiration of gastric con-
tents?
5. Describe the steps used to treat an
anaphylactic reaction.

Page 256
j Index

J
) Acceptable blood loss, 187 Anemia, 13
Acetaminophen with codeine, 137,139, Angina, 10
140,145 Anoxia, 223
) Acupuncture, 7, 140 Anti-cholinesterase agent, 164
) Acute pain pathophysiology, 127 Aorto caval compression, 155
Acyclovir, 144 Apgar score, 166
) Adenosine, 222 Arm-brain circulation time, 78
) Adrenal suppression, 12, 28 Arrhythmias, 10
Adrenergic receptors, 209 - 210, Arterial oxygen content, 68
I 218 - 222 Arterial oxygen partial pressure (PaOJ,
) Afterload, 207, 211 157, 223, 224
Airway assessment, 35 ASA classification, 17
) Airway obstruction, 45, 204 Asphyxia, 167
Albumen, 184, 185 Aspiration syndrome, 158, 236 - 238
Alfentanil, 107 - 109, 135 Asthma, 10
Allergies, 13, 14 Atelectasis, 10
) Alveolar arterial oxygen gradient, 68 Atlanto-occipital extension, 36, 40
) Alveolar oxygen partial pressure Atracurium, 94, 164
(PAOJ, 223,224 Atropine, 29, 98, 164, 222
Alveolar oxygen tension, 68 Autologous blood, 185
) Ambu resuscitation bag, 228 Bier block, 7, 119, 148
) h i d e local anaesthetic, 112 Biofeedback techniques, 7, 140, 158,
Amitriptyline, 139 161
) Amrinone, 223 Blood pressure, 67
Anaesthesia machine check, 32 Blood replacement fluids, 180, 182
Anaesthesia monitors, 64 - 75 Blood transfusion complications,
) Anaesthetic depth, 6, 64 -
188 193
) Anaesthetic family history, 14 Body fluid compartments, 180
Anaesthetic morbidity, 16 Brachial plexus block, 7
) Anaesthetic mortality, 16,17,18 Bradycardia, 194, 198
) Anaesthetic record, 31, 35, 64 Breathing circuit, 32
) Anaesthetic tension cascade, 102 Bupivicaine, 112, 114, 161
Anaphylactic shock, 238 - 240 Calcium chloride, 221
-
Anaphylaxis, 238 240 Capnogram, 73

Page 257
Anaesthesia for Medical Students

Capnography, 73 Diabetes mellitus, 11,23 1


Capnometry, 73' Diazepam, 20,28,29, 87
Capsaicin, 145 Differential nerve blockade, 114
. )
Carbamazepine, 145 Diffusion hypoxia, 103
Cardiac index, 68, 209 Dimenhydrinate, 205 )
Cardiac output, 68, 156, 208 Diphenhyramine, 191 )
Cardiac risk, 10, 18 Distributive shock, 198, 201, 202
Cardioaccelerator fibers, 122 Dobutamine, 218 1
Cardiogenic shock, 199, 200, 202 Dopamine, 199, 218 )
Cardiopulmonary values, 68 Dopamine-1 receptor, 210, 218
Cauda equina syndrome, 151
1
Doxacurium, 91
Causalgia, 143, 145 - 148 Doxepine, 139 )
Cellular oxygen partial pressure (POJ, Droperidol, 87, .205 )
223, 224 Dural puncture headache, 122, 123
Central disc herniation, 151 Edrophonium, 98, 164 1
Central neural blockade, 120 Effective dose in 50% (ED,& 100 1
Central venous catheter, 69 Electrocardiogram, 67
Central venous pressure, 68, 208, 209 Emergency surgery, 18, 19 I
Cerebrovascular disease, 11 Enalapril, 222 )
Chest compressions, 173 End-tidal concentration, 102, 103
Chlorprocaine, 112 Endotracheal tube sizes, 52
Cholinergic muscarinic receptor, 210 Enflurane, 103, 105 )
Chronic obstructive resp. disease, 10,16 Entonox, 7 )
Chronic pain clinics, 144 Ephedrine, 219
Chronic pain definition, 143 Epidural anaesthesia, 7 )
Cisatracurium, 91 Epidural anaesthesia complications, 122 )
Closed air spaces, 103 Epidural anaesthesia contraindications,
Coagulopathy, 13 )
122
Codeine, 107 Epidural blood patch, 123 I

Colloids, 182 Epidural opioids, 126, 137, 138 I


Congestive heart failure, 10 Epinephrine, 161, 176, 218, 240
Contractility, 208, 209 Esmolol, 221
Coronary Steal, 104 Ester local anaesthetic, 112
Cricoid pressure, 6 1 Estimated blood volume, 187
Crystalloids, 182 Extubation criteria, 54
Cyanosis, 224 Familial periodic paralysis, 97
d-tubocurare, 92 Fentanyl, 107 - 109, 135, 137,160, 161
Dantrolene, 233, 234 Fetal circulation, 167, 168
Depolarizing neuromuscular block, 74, Fetal heart rate monitoring, 166
90, 92 Fiberoptic intubation, 28
Desflurane, 106 Fluid deficit estimation, 180, 183
Detsky's multifactorial risk index, 19 Flumazenil, 87, 206
Dextrose 5% in water (DSW), 183 Fresh frozen plasma, 188

Page 258
Index

Gastric aspiration, 60, 163 Local anaesthetic duration, 113


Gastroesophageal reflux, 12,20, 23,56 Local anaesthetic lipid solubility, 113
.General anaesthesia, 7
Geriatric, 13 Local anaesthetic maximum dose, 114,
Glycopyrrolate, 29, 98, 164 115
Goldman risk index, 18 Local anaesthetic onset, 113
Halothane, 103, 104 Local anaesthetic pKa, 113
Halothane hepatitis, 104 Local anaesthetic potency, 113
Hemorrhagic shock'classification, 201 Local anaesthetic protein binding, 113
Hyoscine, 29 Local anaesthetictoxicity, 115,116,117
Hypertension, 10, 23, 100, 127, 194, Local anaesthetic vasoconstrictor, 114,
200 115,161
Hyperthyroidism, 12, 74, 100 Lorazepam, 20,28, 29
Hypopharyngeal classification, 15, 36 Low back pain, 143, 151 - 153
Hypotension, 100, 195 - 197 Maintenance fluid requirements, 180
Hypothyroidism, 12, 100 Malignant hyperthermia (MH), 11, 14,
Hypovolemic shock, 197 74, 232 - 2350
Hypoxemia, 127, 163,195,205,224, Masseter muscle spasm , 232
229,230, 238 McGill Pain Questionnaire, 146, 147
Hypoxia, 224 Mean arterial pressure, 68
Ibuprofen, 139 Meconium, 169
Imipramine, 139 Meperidine, 28,29, 107 - 109, 126,
Indomethacin, 139 129, 135, 137, 160, 161
Infiltrative anaesthesia, 119 Metochlorpropamide, 20,158,205,236
Inhibitory neurotransmitters, 130 Metoprolol, 211, 221
Intramuscular opioids, 130, 137 Mexilitine, 145
Intrathecal, 137 Midazolam, 28, 86
Intubation criteria, 48, 49 Minimal alveolar concentration (MAC),
Intubation, complications of, 53 100, 156, 164
Intubation, difficult, 163 Mivacurium, 90,91
Ischemic heart disease, 10 Mixed venous oxygen saturation,
Isoflurane, 103, 104 68, 209
Ketamine, 77, 83, 100 Monitoring neuromuscular function,
Ketamine contraindications, 86 73, 74
Ketorolac, 139, 168 Monitoring oxygenation, 67
Labetalol, 211, 220 Monitoring the circulation, 67
Lamaze technique, 7, 158 Monitoring the temperature, 70, 196
Laryngeal classification, 37, 38 Monitoring ventilation, 67
Laryngeal mask airway, 55 - 59 -
Morphine, 28, 29, 107 109, 126, 129,
Laryngoscopy, 38, 42, 43 135, 137
Larynx, 43 Muscular dystrophy's, 11, 233 .
Lidocaine, 112, 114, 161 Myasthenia gravis, 11, 96
Local anaesthesia, 7, 112 Myasthenic syndrome, 11, 96

Page 259
4naesthesia for Medical Students

Myocardial infarction, 10 134


Myocardial ischemia, 128 PCA bolus dose, 135
PCA continuous infusion, 135
Myofascial pain syndromes, 143, 150, PCA loading dose, 135
151 PCA lockout interval, 135
Myotonia, 97 PCA maximum limit, 135
Naloxone, 107, 110, 176, 206 Pentaspan, 184, 185
Narcotic tolerance, 140 Pentazocine, 139
Nausea and emesis, 193,203 - 205 Perioperativemyocardialreinfarction,20
Neonatal depression, 163, 164 Peripheral nerve blockade, 120
Neonatal resuscitation equipment, 171 Phaeochromocytoma, 12
Neonatal resuscitation overview, 177 Phase I and I1 block, 93
Neonatal resuscitation program, 166 Phenylephrine, 211, 219
Neonatal resuscitation risk factors, 170' Phenytoin, 145
Neostigmine, 98, 164 Physostigrnine, 206
Neuroleptanalgesia, 7, 87 Plasma cholinesterase, 112
Neuromuscular antagonists, 98 Plasma cholinesterase deficiency, 14,94
Neuromuscular junction, 89 Platelets, 187
Neuromuscular physiology, 89 Positive pressure ventilation, 172
Nifedipine, 222 Post herpetic neuralgia, 143 - 145
Nitroglycerine, 220 Post traumatic pain syndrome, 148
'Nitroprusside, 220 Postoperative agitation and delirium,
Nitrous oxide (N20), 100, 101, 103 205 - 206
Nociception, 127 Pregnancy, physiologic changes of, 155
Non Depolarizing neuromuscular block, Pregnancy, risks of general anaesthesia,
74, 75, 90 155, 162, 163
Non steroidal anti-inflammatory drugs Preload, 208, 209
(NSAID'S), 138 - 140, 153 Premedication, 20
Norepinephrine, 219 Preoperative anxiety, 27
Normal saline, 184 Preoperative testing, 15
Obstructive shock, 201, 202 Prochlorperazine, 205
Ondansetron, 205 Propofol, 77, 81, 100, 164, 205
Opioid infusions, 133 Propofol contraindications, 83
Opioid receptors, 107 Propranolol, 220
Osteomyelitis, 153 Psychologic stress, 6, 27, 159
Oxygen cascade, 223 Pulmonary artery catheter, 69
Oxygen concentration, 223 Pulmonary artery pressure, 68
Oxygen delivery systems, 225 Pulmonary capillary wedge pressure, 68,
Oxygen partial pressure, 223 208, 209
Packed red blood cells, 188 Pulmonary vascular resistance, 68
Pancuronium, 92 Pulse oximetry, 71
Paraaminobenzoic acid, 112 Raised intracranial pressure, 11
Patient controlled analgesia (PCA), 126, Ranitidine, 20, 158

Page 260
Index

Rapid sequence induction, 60 - 62, 158, Systemic vascular resistance, 68


163, 236 Tachycardia, 127, 194, 199
Temporomandibular joint, 35
Reflex sympathetic dystrophy, Tetanus stimulus, 74, 98
143, 148,150
Regional anaesthesia, 7, 107, 116, 117 Thiopental, sodium, 77, 100, 164
Remifentanil, 111 contraindications, 80
Renal failure, 12 Third space fluid losses, 180, 182
Respiratory failure, 10 Thyromental distance, 14, 36
Rha bdomyolysis, 232 Tissue hypoxia, 230
Ringer's lactate, 184 Topical anaesthesia, 119
Risk assessment, 16 Train of four ratio, 98
Sciatica, 152 Train of four stimulus, 75, 98
Second gas effect, 103 Transcutaneous electrical nerve
Sevoflurane, 106 stimulation (TENS),140, 145, 148
Shock states, 194, 201 Tricyclic antidepressants (TCA's), 139,
Shoulder hand syndrome, 148 145, 153
Shunted blood, 229 Trigger points, 150
Smoking, 10, 22 Valvular heart disease, 10
Sniffing position, 38 Vecuronium, 92, 164
Sodium channel, 113 Ventilation perfusion inequalities, 229
Sodium citrate, 21, 158, 236 Verapamil, 221
Spinal anaesthesia, 7 Vessel rich group, 78
Spinal anaesthesia complications, 122 Whole blood, 188
Spinal anaesthesia contraindications,
122
Spinal cord injury, 11
Spinal opioids, 126, 137
Spinal stenosis, 152, 153
ST segment, 67
Stroke volume, 68
Subacute bacterial endocarditis, 10, 21,
27
Substance P, 129, 137
Substantia gelatinosa, 129, 130
Succinylcholine, 93
Succinylcholine contraindications, 97
Succinylcholine hyperkalemia, 95
Sudeck's atrophy, 148
Sufentanil, 107 - 109
Supine hypotensive syndrome, 155
Surgical stress response, 6, 129
Sympathetic blockade, 122, 148

Page 261