Ventilator Management Asthma, COPD, and Pulmonary Edema

Ventilator Management: Maximizing
Outcomes In Caring For Asthma,

COPD, And Pulmonary Edema
August 2008
Volume 10, Number 8

Authors
Andrea DeGiorgi, BS, RRT
Respiratory Care Practitioner, Carolinas Medical Center, NC
You realize that its been just a little too quite tonight when the radio
suddenly cackles to life: Teenage girl... asthma cant breathe
diaphoretic giving nebs No IV 2-minute ETA. Within minutes,
two medics rush in with a diaphoretic cyanotic girl perched forward on her
hands. Her pleading glance catches yours as you watch her take her last
voluntary breath; intubation is obviously required ventilator management
is your concern since you realize her life depends on it .
As you resuscitate the crashing asthmatic, your 60-year-old male patient
on the other side of the curtain, who has been sleeping comfortably, begins
to complain that his breathing is getting worse. He is a frequent flyer with
a known history of bad emphysema and a worse attitude. He adamantly
refuses the mask ventilation. You think back about his chest x-ray, which
showed extensive bilateral pulmonary infiltrates, and wonder how long
your luck can hold up before you need to intervene with him. His voice
and attitude sound oddly weak, but you remember that the last time he was
intubated he developed a pneumothorax .
Just as you ponder these thoughts, a seasoned pair of medics burst
into the ED. The hiss of nebs can be heard under the rushing sound of
high pressure CPAP. Sorry Doc, tried to raise you on the radio but no
one answered. This lady is sick and not moving much air. We got her on
CPAP at 20, 100%, but were not making much progress; heart rate of 170
and cant get her sats higher than 60%. Shes got CHF. Had no time to
intubate. Just then their short, morbidly obese, pale, diaphoretic patient
Editor-in-Chief
Michael A. Gibbs, MD, FACEP

Chief, Department of EM, Maine
Andy Jagoda, MD, FACEP
Medical Center, Portland, ME
Professor and Vice-Chair of
Academic Affairs, Department
Steven A. Godwin, MD, FACEP
of EM, Mount Sinai School of
Assistant Professor and EM
Medicine; Medical Director, Mount Residency Director, University of
Sinai Hospital, New York, NY
Florida HSC, Jacksonville, FL
Editorial Board
William J. Brady, MD
Professor of EM and Medicine Vice
Chair of EM, University of Virginia,
Charlottesville, VA
Peter DeBlieux, MD
Professor of Clinical Medicine,
LSU Health Science Center;
Director of EM Services, University
Hospital, New Orleans, LA
Wyatt W. Decker, MD
Chair and Associate Professor
of EM, Mayo Clinic College of
Medicine, Rochester, MN
Francis M. Fesmire, MD, FACEP
Director, Heart-Stroke Center,
Erlanger Medical Center; Assistant
Professor, UT College of Medicine,
Chattanooga, TN
Charles V. Pollack, Jr, MA, MD,

FACEP
Chairman, Department of EM,
Pennsylvania Hospital, University
of Pennsylvania Health System,
Philadelphia, PA
Michael White, MD
Director, Department of Emergency Medicine, Shands Lake
Shore Hospital, Lake City, FL
Peer Reviewers
Peter DeBlieux, MD
Professor of Clinical Medicine, LSU Health Science Center;
Director of EM Services, University Hospital,
New Orleans, LA
Michael F. Murphy, MD
Professor and Chair, Department of Anesthesia; Professor
Emergency Medicine, Dalhousie University,
Halifax, Nova Scotia, Canada
Scott D. Weingart, MD
Assistant Professor, Director, Division of Emergency
Department Critical Care, Department of Emergency
Medicine, Mount Sinai School of Medicine, New York, NY
CME Objectives
Upon completion of this article, you should be able to:
1. Describe the management of mechanical ventilation as
it applies to asthma, emphysema, and acute pulmonary
edema.
2. Summarize basic lung mechanics and how they provide
insights into the pathophysiology of the lungs.
3. Describe the role of ventilator graphics and waveforms
as tools for detecting adverse effects of mechanical
ventilation.
4. Identify common pitfalls associated with mechanical
ventilation.
Date of original release: August 1, 2008
Date of most recent review: June 11, 2008
Termination date: August 1, 2011
Time to complete activity: 4 hours
Medium: Print & online
Method of participation: Print or online answer form
and evaluation
Prior to beginning this activity, see Physician CME
Information on the back page.
Corey M. Slovis, MD, FACP,

FACEP
Professor and Chair, Department
of EM, Vanderbilt University
Medical Center, Nashville, TN
International Editors
Valerio Gai, MD
Senior Editor, Professor and Chair,
Department of EM, University of
Turin, Turin, Italy
Jenny Walker, MD, MPH, MSW

Peter Cameron, MD
Assistant Professor; Division Chief, Chair, EM, Monash University;
Family Medicine, Department
Alfred Hospital,
Gregory L. Henry, MD, FACEP
of Community and Preventive
Melbourne, Australia
CEO, Medical Practice Risk
Medicine, Mount Sinai Medical
Assessment, Inc; Clinical Professor Robert L. Rogers, MD, FAAEM
Amin Antoine Kazzi, MD, FAAEM
Center, New York, NY
Assistant Professor and Residency
of EM, University of Michigan,
Associate Professor and Vice
Director, Combined EM/IM
Ron M. Walls, MD
Ann Arbor, MI
Chair, Department of EM,
Program, University of Maryland,
Chairman, Department of EM,
University of California, Irvine;
John M. Howell, MD, FACEP
Baltimore, MD
Brigham & Womens Hospital;
American University, Beirut,
Clinical Professor of EM,
Associate Professor of Medicine
Lebanon
Alfred Sacchetti, MD, FACEP
George Washington University,
(Emergency),
Harvard
Medical
Washington, DC; Director of
Assistant Clinical Professor,
Hugo Peralta, MD
School,
Boston,
MA
Academic Affairs, Best Practices,
Department of EM, Thomas
Chair of Emergency Services,
Inc, Inova Fairfax Hospital,
Jefferson University,
Hospital Italiano, Buenos Aires,
Research Editors
Falls Church, VA
Philadelphia, PA
Argentina
Nicholas Genes, MD, PhD
Keith A. Marill, MD
Scott Silvers, MD, FACEP
Maarten Simons, MD, PhD
Academic Chief Resident,
Assistant Professor, Department
Medical Director, Department of
EM Residency Director, OLVG
Program in EM, Mount Sinai
of EM, Massachusetts General
EM, Mayo Clinic, Jacksonville, FL
School of Medicine, New York, NY Hospital, Amsterdam,
Hospital, Harvard Medical School,
The Netherlands
Lisa Jacobson, MD
Boston, MA
Mount Sinai School of Medicine,
EM Residency, New York, NY
Michael S. Radeos, MD, MPH
Assistant Professor of EM, Lincoln
Health Center, Bronx, NY
Accreditation: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing
Medical Education (ACCME) through the joint sponsorship of Mount Sinai School of Medicine and Emergency Medicine Practice. The Mount Sinai School of
Medicine is accredited by the ACCME to provide continuing medical education for physicians. Faculty Disclosure: Dr. White, Dr. DeGiorgi, Dr. DeBlieux, and
Dr. Weingart report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation.
Dr. Murphy is a shareholder in The Airway Site. Commercial Support: Emergency Medicine Practice does not accept any commercial support.
rips her CPAP mask aside and screams, I cant

breathe. Her eyes then roll back, and she begins to have a
hypoxic seizure.
overcome the frictional forces of respiration is primarily

directed at overcoming airway flow resistance. This
resistance can be quantified using Poiseuilles law which
relates resistance directly to viscosity and inversely to
the fourth power of the radius of the airway.
Approximately 20 million Americans have asthma.1
Asthma is the third leading cause of preventable
hospitalization in the United States.2 It accounts for
approximately 2 million visits to the ED each year.3,4
Direct health care costs in the United States were greater
than $14.5 billion in the year 2000.5 This represents
more than a 100% increase from the previous decade.
About 10% of patients admitted to the hospital for
asthma go to the intensive care unit; 2% of those are
intubated.6 However, lower complication rates and
fewer in-hospital deaths show that overall outcomes for
severe asthma are improving.7
BC or Airway, Breathing, Circulation is a mantra

of emergency medicine. There are numerous
courses on airway management, most of which
focus on assessment and intubation. However, postintubation care (i.e., ventilator management) is often
overlooked despite the critical importance of this
component to patient outcome.
Understanding ventilators and their use is an
essential competency in emergency medicine. First,
appropriate ventilator management improves patient
care while a mishandled ventilator is a dangerous
tool. Indeed, misguided ventilator management can
be a patients worst enemy and significantly worsen
their prognosis. Second, emergency physicians are
responsible for both the immediate and short-term care
of intubated patients. In the current age of hospital
overcrowding, intubated patients are spending an
increasingly longer period of time in the ED; at times,
they are even weaned and extubated in the ED before a
bed becomes available upstairs.
The goal of this Emergency Medicine Practice issue
is to provide an overview of mechanical ventilation
in the acute care setting. Basic ventilator technology
will be discussed and placed in the context of various
disease pathophysiologies with a focus on asthma,
emphysema, and acute pulmonary edema.
Emphysema
Emphysema is a disease characterized by the
destruction of elastic fibers in lung tissue and the
alveolar septal wall. These changes lead to decreased
lung compliance secondary to reduced elastic
recoil. For this reason, the lungs do not return to an
appropriate resting volume at the end of exhalation.
Air that is not dynamically moved during ventilation
acts as functional dead space. The narrowing of the
smaller airways in conjunction with diminished elastic
recoil leads to atelectasis and can further increase
residual lung volumes.
Emphysema, and chronic obstructive pulmonary
disease (COPD) in general, continues to be a leading
cause of morbidity and mortality in the United States.8
The numbers related to this disease are staggering:
12.1 million people age 25 and older were diagnosed
with COPD in 2001,9 there were 1.5 million ED visits
in 2000,10 and there were 119,000 deaths in that year
alone.11 COPD is the fourth leading cause of death in
the United States and is projected to be the third leading
cause of death for both males and females by the year
2020.11 The total estimated cost of COPD in 2002 was
$32.1 billion.12 Medicare expenses for COPD patients
were nearly 2.5 times that of the expenditures for all
other patients.12
Critical Appraisal Of The Literature

A broad-based search was employed using the
Cochrane database of systematic reviews and PubMed.
Key terms for the search included ventilators,
ventilator management, mechanical ventilation,
positive pressure ventilation, invasive positive
pressure ventilation, noninvasive positive pressure
ventilation, PEEP, auto-PEEP, emergency department,
emergency room, respiratory failure, asthma, COPD,
emphysema, CHF, congestive heart failure, and
pulmonary edema. Articles were then categorized
into type of study (e.g., prospective, randomized),
consensus opinion, or review article. Priority was
given to prospective, randomized, controlled studies.
The references from these articles were also reviewed
for additional sources of studies and reviews.
Acute Pulmonary Edema

The Starling relationship determines the fluid balance
between the alveolar and vascular beds. In acute
pulmonary edema, pulmonary capillaries enlarge and
hydrostatic pressures overcome oncotic pressures.
Fluid is pushed into the interstitial spaces and, in
some cases, directly into the alveoli. This increased
pulmonary fluid can be seen on chest x-ray with
findings of Kerley B lines and a batwing perihilar
radiographic picture. Gross effusions can develop as
well. The fluid that enters the alveoli blocks ventilation
of alveoli and disrupts the alveolar surfactant layer
leading to alveolar collapse. Intrapulmonary shunting
Epidemiology
Asthma
Asthma is an obstructive process associated
with significant airway resistance secondary to
bronchospasm, increased mucous production, edema,
inflammation of the mucosal lining, and plugging of
the bronchi and bronchioles. The energy required to
Emergency Medicine Practice 2008
EBMedicine.net August 2008
results following the alveolar consolidation (alveolar

flooding) and alveolar collapse (atelectasis) (Figure
1). This will cause loss of functional alveoli and,
consequently, reduced surface area for gas exchange.
As interventional cardiac care improves, more
people are living with weaker hearts. Nearly 2% of
the U.S. population has congestive heart failure. This
percentage increases dramatically with age to include
5% in ages 6069 and 10% over 70.13 Congestive heart
failure (CHF) accounts for about 260,000 deaths per
year.14 The number of ED visits for congestive heart
failure in 2004 was 3.4 million.15 The annual cost for
2007 in the U.S. alone was $33.2 billion.16
management of acute respiratory distress. There are

numerous randomized trials that demonstrate that
NPPV lowers intubation rate, mortality, and hospital
stay.1724 Most recent studies suggest NPPV should
be considered first-line therapy for patients with
acute hypercapnic and hypoxemic insufficiency.2529 A
randomized controlled trial performed by Brochard
et al compared 85 COPD patients and found the
endotracheal intubation rate was 74% for controls
receiving standard medical treatment compared
to only 26% in the NPPV group.18 Despite the
demonstrated advantages of NPPV, there are scenarios
where the inappropriate application of NPPV may
be harmful,30 and intubation is the only appropriate
approach to managing the patients respiratory failure.
There are both good and poor candidates
for NPPV (Table 1). Merlani et al published a
retrospective study of 104 patients which found
that NPPV failures had the following shared
characteristics:31
A Glasgow Coma Scale score < 13 at ED admission
A pH 7.35 after 1 hour on NPPV
A respiratory rate 20 bpm after 1 hour on NPPV
Basics Of Breathing
When a person inspires, the diaphragm contracts and
pulls the lungs downward. This produces negative
pressure within the alveoli that is transmitted to
the airway; air is then drawn in. During expiration,
passive relaxation of the chest wall musculature allows
the chest cavity to naturally recoil to elastic neutrality.
Between each regular inhalation and exhalation,
there is a brief expiratory pause when intrathoracic
pressures match atmospheric pressures. This process
is referred to as spontaneous negative pressure
breathing. Ventilator breathing is markedly different
in that ventilated lungs have air pushed rather than
drawn into them. This is referred to as positive
pressure ventilation. Positive pressure ventilation can
be provided invasively (as when a patient is intubated
and on full ventilatory support) or non-invasively
(continuous positive airway pressure [CPAP] or bilevel positive airway pressure [BiPAP]).
Confalonieri et al analyzed prospective data

collected from 1033 patients with COPD exacerbation
and found the following variables to predict the risk of
failure > 70% on admission:32
A Glasgow Coma Score < 11
A pH < 7.25
A respiratory rate 30 bpm
The risk increased to > 90% failure rate if a pH <
7.25 persisted after 2 hours on NPPV.
Evidence from prospective studies of over 500
patients demonstrates that early failed response
to NPPV is highly predictive for invasive airway
management and mechanical intervention.3137
Ultimately, the decision to intubate is a clinical
one. While data is important in directing decision
making, clinical acumen or gut instinct is probably
the best guide in making this decision. There is
no clinical study or evidence that suggests any
single value for arterial pCO2, pH, or PaO2 by itself
signifies an indication for mechanical ventilation.
Clinical assessment of patient muscle fatigue, mental
status, and stability relative to their entire emergent
presentation should direct care.
Non-Invasive Positive Pressure

Non-invasive positive pressure ventilation (NPPV) is
the application of mechanical breaths without airway
invasion and is delivered by a nasal or face mask.
BiPAP delivers continuous positive airway pressure
with different levels of inspiratory and expiratory
support. NPPV has been a major advance in the
Figure 1. Intrapulmonary Shunting
Mechanical Ventilation
Intrapulmonary Shunt
Alveolar Collapse
Decreased V/Q ratio
The primary use of mechanical ventilation is to assist

patients in generating sufficient alveolar ventilation
Table 1. Predictive Factors Of Failure For NPPV

Blood
Blood is shunted from the right to the left side of the heart
as it passes lung tissue without gas exchange.
August 2008 EBMedicine.net
Uncontrolled arrhythmias
Altered level of consciousness
Poor patient cooperation
APACHE II score > 29
Glasgow Coma Score < 11
Respiratory distress persists after 2 hours of NPPV
Hemodynamic impairment requiring vasoactive drugs38
and oxygenation. Key to the successful management

of the intubated patient is adequate sedation and
analgesia; this is generally best accomplished through
standing nursing protocols. Paralytics should be used
sparingly, and other means should be employed to
make the patient comfortable on the ventilator.
Table 2. Abbreviations Associated With Mechanical Ventilation

AC
Volume
control
Mode that delivers each breath with

constant volume and flow.
AutoPEEP
Intrinsic PEEP
Positive end-expiratory pressure

caused by inadequate expiratory
time on a ventilator. Equals Total
PEEP Set PEEP.
CPAP
Continuous
positive
airway
pressure
Constant pressure maintained at

the airway opening throughout
the breathing cycle. CPAP refers
to PEEP during spontaneous
breathing.
E-Time
Expiratory
flow
The period from the start of

expiratory flow to the start of
inspiratory flow. Controlled by
patient. Remains constant only if
patient is sedated or synchronous
with ventilator.
FIO2
Fraction of
inspired
oxygen
The percentage of oxygen delivered

(21%100%).
I:E Ratio
Inspiration to
expiration
ratio
Time constant determined by total

respiratory rate and inspiratory
time.
While this mnemonic may be simplistic, attention

to each of its components will help ensure quality and
comprehensive care is offered.
I-Time
Inspiratory
time
The period from the start of

inspiratory flow to the start of
expiratory flow. This is a required
setting on the ventilator.
Mode
The mode in mechanical ventilation describes how
the ventilator controls pressure, volume, and flow
for each breath, along with a description of how the
breaths are sequenced.39 No evidence conclusively
proves one mode of ventilation provides a better
outcome than another for initial management of acute
respiratory failure. The principles of ventilation are
more important than the mode used to practice them.
The most commonly used mode is assist/control.
Assist/control covers both aspects of volume control
(AC) and pressure control ventilation (PC/AC).
During AC, the ventilator will deliver a set
number of breaths at a preset tidal volume (in volume
control mode) or pressure control level (in pressure
control mode, adjustments in pressure are necessary
until the desired expired volume is achieved). In the
absence of a patients spontaneous effort, the ventilator
will deliver the controlled breaths. This approach
ensures a minimum level of minute ventilation. A
set respiratory rate is compulsory for an adequately
sedated and possibly paralyzed patient since the
ventilator does all the work.
PBW
Predicted
body weight
Males: 50 kg + 0.91 (Height in cm

152.4)
Females: 45.5 kg + 0.91 (Height in
cm 152.4)
PC/AC
Pressure
control
Mode that delivers each breath with

a constant pressure.
PEEP
Positive endexpiratory
pressure
Positive pressure is held in the lungs

during the exhalation phase of a
mechanical breath.
PIP
Peak
inspiratory
pressure
Pressure recorded at end

inspiration. Dependent on volume
or pressure delivered and airway
resistance.
Pplat
Plateau
pressure
The static transalveolar pressure

at end inspiration during an
inspiratory hold for an assisted
breath.
RR
Respiratory
rate
Number of preset mechanical

breaths the patient will receive per
minute.
VE
Minute
ventilation
The average volume of gas entering

or leaving the lungs per minute (L/
min). Calculated by tidal volume x
respiratory rate (VE = VT x RR).
Volume Control (AC) (Figure 2)

Volume-controlled breaths deliver a constant volume
with constant flow.
VILI
Ventilatorinduced lung
injury
Lung injury resulting from

barotrauma, volutrauma,
atelectrauma, biotrauma, and
oxygen toxicity in ventilated
patients.
VT
Tidal volume
The volume of gas inhaled or

exhaled during a breath.
Terminology
The most common abbreviations, acronyms, and
terminology associated with mechanical ventilation are
listed in Table 2.
General Approach
A framework for remembering the basics of ventilator
management is provided by the mnemonic: MOVE
AIR.
M = Mode
O = Oxygen
V = Volume (VT) or Pressure (PC)
E = Expiratory PEEP
A = Adequate Sedation

I = Inspiratory Time
R = Rate
Flow = Tidal Volume/Inspiratory Time

Since flow is constant, inspiratory flow can be
set and adjusted by manipulating the inspiratory
time (I-time), flow knob, or % I-time knob based on
the total respiratory rate. When using a volume

mode, a constant volume will be delivered, but pay
close attention to the peak pressure alarm to prevent
barotrauma. While the volume delivered remains
constant, airway pressure will vary dynamically
based on lung compliance and airway resistance. If
set correctly, the peak pressure alarm will indicate
changes in any of these variables. Peak pressure alarm
should be set < 10 cm H2O above the PIP to deliver an
acceptable tidal volume.
breathe spontaneously between mandatory breaths

from the ventilator. In this mode, patients retain some
of the work of breathing as they add pressure support
breaths between the set ventilator rate.
Oxygen
Oxygen saturation should be maintained > 90%. The
concentration of oxygen delivered is adjusted by
changing the FIO2 (fractional percentage of oxygen)
from 21% (room air) to 100%. An arterial blood gas
(ABG) will calculate the initial partial pressure of
Pressure Control/Assist Control (PC/AC) (Figures 3 and 4)
oxygen (PaO2) and the arterial partial pressure of
A pressure-controlled breath provides a constant
carbon dioxide (PaCO2). These values can be correlated
preset pressure. In this mode, the tidal volume (VT),
to noninvasive end tidal CO2 and pulse oximetry to
rather than the airway pressure, is variable. Flow is
allow for a noninvasive means of guiding ventilator
variable as well, as the ventilator delivers as much as is adjustment. It is reasonable to adjust FIO2 according
needed to achieve the preset pressure limit. Therefore, to the pulse oximeter as long as a good waveform is
volume and flow will change based on the patients
available and corresponding correctly with the rhythm
lung compliance and airway resistance. Pressure
strip and ABG. A reasonable goal is to reduce the
is set with a target volume in mind. The volume is
delivered oxygen concentration to < 50%.40
only a target because, unlike volume control, the
VT may be higher or lower than intended. On the
Volume/Pressure (Figure 5)
alarm settings, the tidal volume parameters are set
Volume or, more specifically, tidal volume (VT) is
above and below this target volume so the alarm
the amount of gas the ventilator delivers during each
will sound if the patients volumes are outside of the
Figure 4. Overview Of Settings: MOVE AIR
desired range. As opposed to volume control mode,
where the ventilator is set to alarm for high pressures,
in pressure control mode, setting a low and high VT
MODE
ASSIST CONTROL
limit will serve as an alert to inappropriate changes in
volume delivered as a result of dynamic alteration in
the patients lung mechanics.
Volume
Pressure
As an aside, synchronized intermittent mandatory
Control
Control
RATE
ventilation (SIMV) is a form of assist control where
the ventilator is programmed to deliver a set number
of breaths at either a predetermined tidal volume or
pressure control level. SIMV allows the patient to
Figure 2. Flow In Volume Control Mode
I-time
% I-time
Flow
FLOW IS CONSTANT
Flow
(L)
SET
ACTUAL
TIDAL
VOLUME
SET PC
FOR
TARGET
VT
I-time
% I-time
FIO2
21%100%
PEEP
Time
Volume Control Mode
Figure 3. Flow In Pressure Control Mode
INCREASE SEDATION IF SPONTANEOUS BREATHS PRESENT
FLOW VARIES
Figure 5. Factors For Increasing Peak Inspiratory Pressure
With in Volume or in Resistance
Pressure
PIP
Flow
(L)
Causes
Decreased Compliance
Increased Resistance
Increased Flow
Increased Volume
Time
PEEP
Time
Pressure Control Mode
VOLUME CONTROL MODE
machine breathing cycle. A couple of caveats must

be kept in mind. First, volume is certainly dependent
on the mode used. A volume mode delivers a preset
volume whereas a pressure mode delivers a variable
volume based on the preset pressure and the flow
resistance of the airway. Additionally, a set volume
does not always equal the delivered tidal volume as
air is lost along leaks and in mechanical dead space.
Mechanical dead space, or compressible volume,
represents volume lost in distention of the ventilatory
circuit. Adjusting the tidal volume setting on the
ventilator will help resolve volume loss.
Adequate sedation is also necessary to determine

appropriate settings for mechanical ventilation based
on lung mechanics such as airway resistance, autoPEEP (air trapping) and plateau pressures (alveolar
overdistention). Measurement of these values is only
accurate when the patient is properly sedated.41 For
the first 1224 hours of mechanical ventilation, sedation
is normally required to optimize ventilator settings,
to detect adverse effects from mechanical ventilation,
and to minimize complications due to mechanical
ventilation.
Inspiratory Time
Inspiratory time is the period between inspiration and
the start of expiratory flow. I-time is a mandatory
setting and will remain constant from breath to breath.
In volume control mode, the I-time can be adjusted
by 3 different settings: desired I-time, % I-time (%
based on set respiratory rate), or the flow rate knob.
In contrast, for pressure control, I-time can only be
adjusted by 2 settings: desired I-time or % I-time knob.
The patients expiratory time is calculated based on
the set inspiratory time and respiratory rate (Table 4).
The expiratory time represents the time during which
a patient passively exhales. Since I-time is constant,
E-time will vary if the patient is adding breaths to the
set rate. Therefore, in order to control the I:E ratio, the
patient must be adequately sedated.
Positive End-Expiratory Pressure (PEEP)

PEEP (also known as extrinsic PEEP) is the airway
pressure maintained by the ventilator during the
expiratory phase. Ventilator-added PEEP helps to
augment the baseline expiratory pressure, to splint
open the airways during expiration, and to decrease
physiologic alveolar shunting. This maximizes gas
exchange while minimizing overdistention of the
lungs. PEEP helps maintain functional residual
capacity and works at the alveolar level.
Adequate Sedation
Passive ventilation occurs when the patient is sedated
and, if necessary, paralyzed. In this scenario, all
respirations are machine triggered and the patient
does not initiate any spontaneous breaths. This allows
for control over a patients alveolar ventilation through
manipulation of minute ventilation, respiratory rate,
and I:E ratio. This approach not only rests the patient
but also helps to avoid dynamic hyperinflation and
ventilator-induced lung injury (VILI) often associated
with obstructed expiratory flows, collapsed airways,
and/or patient-ventilator dyssynchrony.
Respiratory Rate
During the initial management of a fully sedated
ventilated patient, the respiratory rate is determined by
Figure 6: Lung Compliance
Compliance (C)
C = Tidal Volume
PplatPEEP
Table 3. Key Features Of Ventilator Settings And Mechanics

Volume (AC)
Pressure (PC/AC)
Minute ventilation VT x RR
VT delivered x RR
Flow
Variable with changes

in compliance and
resistance
Constant
I-time
Constant
Constant
Decreased
Compliance
Volume constant
PIP increases
Pressure constant
VT decreases
Increased
Resistance
Volume constant
PIP increases
Pressure constant
VT decreases
Strengths
Known tidal
volume
Known minute
ventilation
Control of peak airway

pressures
Decelerating inspiratory
flow pattern
Weaknesses
Uncontrolled PIP
may increase
risk for VILI
No guarantee of tidal
volume
Controlling pH
and pCO2
Adjust minute
ventilation by
either VT or RR
Adjust minute ventilation

by either PC setting for
target VT or RR
Controlling PaO2
Adjust FIO2 and

PEEP
Adjust FIO2 and PEEP
DECREASES WITH:
Pulmonary edema Dynamic hyperinflation
Consolidation
Tension pneumothorax
Atelectasis

Mainstem intubation
Overdistention
ARDS
Pulmonary fibrosis
Normal compliance for a normal subject on mechanical ventilation

is 50100 mL/cm H2O.
Figure 7: Inspiratory Resistance

RESISTANCE (Raw)
Raw = PIP Pplat
Flow
INCREASES WITH:
Bronchospasm
Obstruction
Secretions

Artificial airway
Inflammation

Increased Flow
Poiseuilles Law:
Resistance = (8 x viscosity x length) / Pi r4
R = resistance
n = viscosity
l = length
r = resistance
Because of the fourth power in the denominator, resistance
increases rapidly as diameter decreases.
the ventilator setting (Table 3). Minute ventilation is

equal to the product of tidal volume and respiratory
rate. The set respiratory rate must take into
consideration the patients ability to exhale in order
to avoid lung overdistention. The typical starting
respiratory rate for a healthy adult is 814 bpm.
auto-PEEP. Sedation is key because expiratory muscle

contraction and chest and abdominal wall contributions
to ventilation can alter the measurements of autoPEEP and produce falsely elevated levels of autoPEEP.44,45 This can worsen dynamic hyperinflation and
overdistention by leading to a mistakenly higher level of
applied PEEP.
Alveolar overdistention is a precursor to the
development of acute lung injury (ALI). Plateau
pressure is the pressure equilibration between the
airways and alveoli. Plateau pressure is a measurement
of alveolar overdistention; its clinical value can provide
helpful information in determining appropriate tidal
volumes for each patient. Plateau pressure is achieved
by pausing flow at end-inspiration by initiating an
inspiratory hold (Figure 8). Patients must be heavily
sedated or paralyzed to obtain reliable measurements.
Measurement Of Lung Mechanics

Valuable information can be obtained for optimal
settings of mechanical ventilation based on your
patients respiratory mechanics (Figures 6 and 7).
The assessment of lung mechanics is essential for
the effective management of ventilated patients.
Failure to obtain the right data can be dangerous for
your patient. Common dynamic changes and their
associated sequelae are: alveolar overdistention that
can result in VILI, increased flow resistance occurring
with bronchospasm in asthma, decreased lung
compliance in acute pulmonary edema, and dynamic
hyperinflation in emphysema.
One of the first parameters to measure is autoPEEP. This will determine the appropriate PEEP
level42 and uncover any air trapping.43 To do this,
auto-PEEP must be determined; this is accomplished
by first setting the PEEP to zero to measure the actual
auto-PEEP with an exhalation hold maneuver (Figure
8). The intrinsic (auto-) PEEP may not be accurately
detected if the extrinsic PEEP is set greater than the
Specific Disease Processes: Asthma,

Emphysema, And Acute Pulmonary Edema
Asthma
Airway resistance is not simply a flow inward problem.
Asthmatics must struggle both to inhale and to exhale.
Longer expiratory times are necessary for the entire
volume of gas to be released. Air trapping occurs
when an asthmatic either cannot fully exhale before
the next breath or cannot overcome the frictional
resistance in their own airways to empty their alveoli.
Either mechanism leads to retained air in the alveoli
and increased alveolar pressures. This is referred to
as air trapping. This additional pressure at the end of
expiration is referred to as intrinsic PEEP or auto-PEEP.
Mechanical ventilation can lead to or worsen gas
trapping if insufficient expiratory times are provided.
In this situation, the lungs become hyperinflated
(dynamic hyperinflation) and overdistended. Excessive
dynamic hyperinflation can lead to hypotension and
volutrauma during mechanical ventilation of severe
asthma as demonstrated in the comparative study of
95 patients by Williams et al.46 Since this increases
the chances of morbidity and mortality,47 strategies
must be employed to avoid this complication. The
most effective way to reduce the worsening effects of
Figure 8: Mechanical Maneuvers

INSPIRATORY Occlusion Maneuver
Plateau Pressure: Inspiratory pause for at least 3
seconds after ventilator initiates a breath. During the
inspiratory hold, flow stops; the VT is trapped inside the
lung, and static airway pressure (plateau pressure) is
measured.
Inspiratory Pause
(no flow)
Press
Plateau
Pressure
Time
EXPIRATORY Occlusion Maneuver
auto-PEEP: Expiratory pause for at least 3 seconds
during the exhalation phase. PEEP must be turned
to zero for accurate results. In a normal subject,
alveolar pressure is nearly zero. When air trapping is
present, the pressure difference associated with the
trapped volume is auto-PEEP.
Press
Figure 9. Decreasing Minute Ventilation By Reducing Air

Trapping In Asthmatics
Prolong E-time
VE = VT x RR
Expiratory
Pause
auto-PEEP
Decrease tidal volume

Decrease pressure control
Decrease respiratory rate

Shorten I-time
Increase flow rate
Time
lung hyperinflation is through a reduction in minute

ventilation (VT x RR) (Figure 9).4850
The deliberate use of alveolar hypoventilation to
reduce pulmonary overdistention and acceptance of
hypercapnia has been termed permissive hypercapnic
ventilation.48,51 Well-designed studies (such as
a prospective randomized controlled trial of 53
patients with ARDS performed by Amato et al52 and
a retrospective controlled study of 34 cases involving
status asthmaticus by Darioli et al53) have shown the
resulting acidosis and increased carbon dioxide in the
setting of controlled hypoventilation to be generally
well tolerated. In a systematic review of over 20
clinical studies, Bigatello et al found that although
hypoventilation is a reasonable alternative to invasive
ways of limiting VILI, there is no clear evidence
that demonstrates a safe level of hypercapnia and
acidemia.54 The reduction in minute ventilation has the
potential for lowering serum oxygenation. The use of
supplemental oxygen during permissive hypercapnia
ventilation allows for the substantial reduction of
minute ventilation without jeopardizing oxygenation.
Fundamental to permissive hypercapnia is
sedation and possibly paralysis. The prolonged use
of neuromuscular-blocking agents in combination
with corticosteroid therapy increases the risk of the
development of protracted muscle weakness.55 In a
retrospective cohort study, Leatherman et al evaluated
107 consecutive episodes of mechanical ventilation
for severe asthma to assess the incidence of myopathy
in patients treated with corticosteroids alone versus
corticosteroids with neuromuscular paralysis.56 The
use of corticosteroids and a neuromuscular-blocking
agent was associated with a higher incidence of muscle
weakness as compared with the use of corticosteroids
alone (20 of 69 versus 0 of 38). Eighteen of the 20
weak patients had been paralyzed for more than 24
hours. However, this is not a concern in the initial
management of the acute asthmatic in the ED. Having
said that, paralytic agents should be used only if
adequate control of mechanical ventilation cannot be
achieved by sedation alone. Minimizing the use of
paralytic agents may decrease the risk of critical illness
myopathy and other adverse consequences of muscle
paralysis.57
Rate
Reduced respiratory rates and shortened I-times will
allow longer exhalation times, reduce air trapping, and
help minimize VILI caused by alveolar overdistention.48
Adjusting inspiratory time versus reducing respiratory
rate is summarized in Table 4. Prolongation of
expiratory time has been shown to decrease dynamic
hyperinflation in patients with severe asthma; this was
demonstrated in an observational study by Leatherman
et al of 12 mechanically ventilated patients.59 The
reduction in respiratory rate allowed for longer
E-times, and the decrease in dynamic hyperinflation
was evidenced by a reduction in plateau pressure. This
is accomplished by beginning with a rate between 6
bpm and 8 bpm with the main goal of ensuring low
minute ventilation (VE) and an expiratory time long
enough to allow lung emptying; lung emptying is
observed on the flow verses time waveform on the
ventilator. The expiratory flow waveform optimally
should return to baseline before the next breath begins
(Figure 10).
Finally, auscultation of the intubated asthmatic
is critically important. While the ventilator can
offer significant information, listening for complete
expiration (end of wheezing) before the next breath
begins is paramount to preventing air trapping and
dynamic hyperinflation.
PEEP
The presence of air flow at end-expiration indicates
that the alveolar pressure is higher than the applied
PEEP.44 The challenge at the bedside is to select the
appropriate amount of PEEP to counterbalance autoPEEP (also called intrinsic PEEP). To do this, autoPEEP must be determined by the expiratory occlusion
maneuver (Figure 8). PEEP can have a significant
positive effect in the care of an asthmatic and should
not be overlooked. Well-designed prospective studies
of over 60 patients have shown that the addition
of PEEP in the setting of auto-PEEP will prevent
gas-trapping by holding the airways open.6062 The
appropriate use of PEEP will provide alveolar stability
and reduce potential injury that occurs during
recruitment and decruitment of atelectatic alveoli.63
However, PEEP levels of 10 cm H2O or higher can
increase lung volume in patients with asthma and lead
to lung overdistention.64 The use of PEEP during total
Tidal Volume
Since the most effective method of decreasing dynamic
hyperinflation is by reducing the minute ventilation
Figure 10. Air Trapping On Flow Wave Form
(VE = RR x VT), patients with asthma will benefit from
Air Trapping Versus Prolonged Exhalation
reduced tidal volumes. Protective lung ventilation
starts at 6 mL/kg predicted body weight (PBW) and
Flow
increases to 810 mL/kg PBW as long as the plateau
I-time too short
L/min
58
pressure remains < 30 cm H2O. Similarly, if the
plateau pressure is above 30 cm H2O at a VT of 6 mL/
Longer E-time
kg PBW, then VT should be decreased to 45 mL/kg
to keep the plateau pressure below 30 cm H2O. This
strategy will minimize the potential of developing VILI
Time
injury.
Flow returns to
baseline
ventilatory support of a patient who has dynamic

hyperinflation with airflow obstruction due to acute
asthma and without airway collapse is controversial.
should be adjusted for each individual patients lung

mechanics rather than assuming that one VT will suit
all patients. For patients with emphysema, a reasonable
VT to begin with is 8 mL/kg PBW followed by a plateau
pressure measurement. Plateau pressure is a reliable
bedside indicator for alveolar overdistention. If plateau
pressure is > 30 cm H2O, the VT should be reduced to
6 mL/kg PBW. Petrucci et al reported in a systematic
review of 8 randomized controlled trials that tidal
volumes adjusted up to 10 mL/kg PBW are acceptable if
plateau pressure is < 30 cm H2O.72 As with an asthmatic
on a ventilator, auscultation of the lungs during
expiration is key to managing the ventilator and making
adjustments to best match the patients needs.
Emphysema
The loss of elastic recoil differentiates emphysema
from asthma. Patients with emphysema experience
both airway collapse and flow limitation during
normal tidal breathing.45,65
Since elastic recoil of the lungs is key to outward
flow of air, emphysematous patients have prolonged
expiratory times and reduced outward flow. If the
tidal volume is not completely exhaled, then a certain
amount of air will be trapped in the alveoli. On x-ray,
this hyperinflated lung appears lucent and is the
characteristic picture for a COPD patient or the pink
puffer. The functional residual capacity (FRC) is the
volume of gas remaining in the lungs at the end of
normal exhalation; it is increased in this population.
The overall result of all these effects is increased
dead space, severe ventilation-perfusion mismatch
related to atelectasis, marked airflow limitation
(bronchospasm, mucus, edema), air trapping (autoPEEP), and hyperinflation (alveolar overdistention).66
Dynamic hyperinflation has the most deleterious
effects, such as decreased cardiac output and increased
risk of barotrauma.6771 Therefore, when managing
a decompensated emphysematous patient on a
ventilator, close attention must be paid to managing
dynamic hyperinflation. This can be achieved by a
combination of reduced respiratory rates (prolonged
expiratory times), limited tidal volume, and shortened
I-times.
Rate
Acute respiratory failure in patients with emphysema is
associated with significant expiratory obstruction and
hyperinflation. Decreasing the amount of auto-PEEP on
mechanical ventilation requires a decreased respiratory
rate and prolonged expiratory phase. Since these
patients often have less structural airflow obstruction
than patients with asthma, initial rate settings can begin
at 1012 bpm. An end-expiratory occlusion maneuver
should then be performed to measure auto-PEEP (air
trapping). The exhalation phase can be expanded by
decreasing the mechanical respiratory rate or shortening
the I-time (Table 4).
An increase in respiratory rate proceeded by a
decrease in expiratory time will worsen dynamic
hyperinflation.
PEEP
PEEP provides a fixed positive airway pressure at the
end of expiration and opens previously unrecruited
alveolar units. In the case of auto-PEEP due to flow
Tidal Volume (VT)
On a ventilator, progressive hyperinflation results from limitation, increasing the PEEP setting on the ventilator
either excessive tidal volume or insufficient expiratory should be set to counterbalance the auto-PEEP based on
individualized lung mechanics.6264,73 In emphysema,
time. Overinflated alveoli will increase dead space;
the different parts of the lungs are not affected to the
this increases residual air within the lungs, reduces
exchange of gases, and lowers alveolar ventilation. VT same degree. Certain lung units may have longer
time constants and therefore be more predisposed to
Table 4. Adjusting I-Time Versus Respiratory Rate
hyperinflation than others.74 This increases the intricacy
of determining optimal PEEP levels. Unfortunately,
Example: RR: 10 breaths per minute
there is insufficient data to support a generalized PEEP
Total Cycle Time: 6 seconds (60 seconds divided by 10 breaths
setting to prevent or minimize ventilator-associated
= 6 seconds/breath)
lung injury while simultaneously preventing alveolar
I-time = 1.0 seconds
collapse. Evidence-based data is lacking to prove that
E-time = 5.0 seconds
high levels of PEEP are better.
I:E ratio = 1:5 (expiratory time divided by
inspiratory time)
RR:
Decreasing
I-Time
Decreasing
Respiratory Rate
10 breaths per minute
Decreased to 6
breaths per minute
Total Cycle Time:
6 seconds
10 seconds
I-Time:
Decreased to 0.75
seconds
Stays the same at 1.0

seconds
E-Time:
Now is 5.25 seconds
Now is 9.0 seconds
I:E Ratio:
1:7
1:9
Figure 11. Hyperinflation

Dynamic Hyperinflation
Volume
Air Trapping
Normal Lungs
Time
Clinical Pathway Of Ventilator Management

ASTHMATICS:
INITIAL VENTILATOR SETTINGS
MODE: Pressure Control or Assist Control
If PC, set PC for target tidal volume desired
If AC, set actual tidal volume
FIO2: 1.0
RR: 68 bpm
VT: 6 mL/kg PBW
PEEP: auto-PEEP measurement on PEEP of 0
Is patient adding rate?
EMPHYSEMA:
FIO2: 1.0
RR: 1012 bpm
VT: 8 mL/kg PBW
NO
Is air trapping present on flow waveform?
YES
Patient requires
more sedation and
analgesia.
Consider
increased
sedation/paralysis.
Key:
FIO2: Fraction of Inspired Oxygen
VT: Tidal Volume
RR: Respiratory Rate
PEEP: Positive End-Expiratory Pressure
Pplat: Plateau Pressure
PC: Pressure Control
AC: Assist Control
PULMONARY EDEMA:
FIO2: 1.0
RR: 1214 bpm
VT: 8 mL/kg PBW
YES
Decrease RR to allow longer

exhalation times
Keep Pplat < 30 cm H2O. May
need to decrease VT but not
< 45 mL/kg
Decrease I-time to allow
longer exhalation times
Measure auto-PEEP; if
present, follow auto-PEEP
pathway
(Class I)
NO
Is auto-PEEP present?
YES
NO
Add PEEP in 2 cm H2O

increments until auto-PEEP
resolves
Decrease RR to allow longer
exhalation times
Keep Pplat < 30 cm H2O. May
need to decrease VT but not <
4 5 mL/kg
Decrease I-time to allow
longer exhalation times
(Class I)
Set
PEEP to
5 cm H2O
(Class IIb)
Is plateau pressure < 30 cm H2O?

YES
Obtain ABG
Is CO2 80?
Is PH 7.20?
(Class Indeterminate)
YES
Wean FIO2 to maintain PaO2
6080 mm Hg
Continue aggressive medical
therapy
Monitor therapy goal
(Class IIa)
NO
Decrease VT but not
< 45 mL/kg
Decrease PC to
decrease target VT
(Class I)
NO
Consider increasing RR if absence of air
trapping
May increase VT to 810 mL/kg if plateau
pressure is < 30 cm H2O
Consider methods of decreasing carbon
dioxide production, such as fever control
(Class IIb)
The evidence for recommendations is graded using the following scale: Class I: Definitely recommended. Definitive, excellent evidence provides
support. Class IIa: Acceptable and useful. Very good evidence provides support. Class IIb: Acceptable and useful. Fair to good evidence provides
support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a patients
individual needs. Failure to comply with this pathway does not represent a breach of the standard care.
Copyright 2008 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of
EB Practice, LLC.
10
FIO2
Oxygen therapy provides benefits to patients who are
hypoxemic. Oxygen should be administered in doses
sufficient to raise the partial pressure of oxygen greater
than 60 mm Hg8 or a pulse oximeter reading greater
than 90%. The risk of oxygen-induced respiratory
acidosis and hypercapnic respiratory failure associated
with COPD is no longer a concern once the patient
is intubated, sedated, and on controlled mechanical
ventilation. However, prolonged use of high oxygen
concentrations can lead to alveolar-capillary membrane
changes and absorption atelectasis.75 Set the FIO2 at
100% upon the initiation of mechanical ventilation, and
wean as early as possible to avoid extended uses as
long as adequate serum partial pressure of oxygen is
maintained.
Acute Pulmonary Edema

Pulmonary edema is one of the most common
causes of absolute capillary shunting. The overall
result is reduced serum oxygen tension and relative
hypercarbia. Patients presenting with capillary
shunting respond poorly to oxygen therapy alone
because the inspired oxygen cannot adequately reach
the circulating blood. Positive pressure ventilation,
either noninvasive or invasive, can help reverse the
decompensated physiologic state and push fluid back
out of the lungs.63,76
Tidal Volume
In congestive heart failure, lung compliance is
markedly reduced secondary to engorged capillaries
surrounding the alveoli, alveolar flooding, and
alveolar collapse. Low compliance means that volume
change is small per unit pressure change (C = Vol/
Press). The decrease in lung compliance restricts the
expansion of the lungs and physiologically functions
as a restrictive defect. As such, patients with acute
pulmonary edema will benefit from a reduction in
their tidal volumes.
Normal VT in a less compliant lung may cause
alveolar overdistention and lead to an increase in
plateau pressure. An initial 6 mL/kg PBW should be
a starting point to reduce the risk of iatrogenic acute
lung injury. Since plateau pressure is an indicator of
alveolar overdistention, the VT can be adjusted up
or down based on the patients lung mechanics. If
plateau pressure can be maintained < 30 cm H2O,
the likelihood of ventilator-induced lung injury is
minimal.60
Rate
Since smaller tidal volumes are employed, higher
respiratory rates must be used to maintain a sufficient
minute ventilation (VE = VT x RR). Remember: the
goal for plateau pressure is < 30 cm H2O. Patients
with a restrictive lung disease, such as pulmonary
edema, tolerate a respiratory range between 12 bpm
and 20 bpm since they typically do not experience the

obstructive components associated with air trapping.
FIO2
The PaO2/FIO2 can be used as an index of pulmonary
oxygen exchange efficiency (Table 5). A low PaO2/
FIO2 ratio on a high FIO2 > .60 is evidence of a poor
response to oxygen therapy and of absolute shunting.
A high FIO2 is ineffective in improving PaO2 in the
presence of a large intrapulmonary shunt because
oxygen cannot reach the blocked alveoli. This is
referred to as refractory hypoxemia. High FIO2 levels
predispose patients to the development of absorption
atelectasis77 and exacerbate the capillary shunting
process. Decreases in lung volume, alveolar collapse,
and hypoxia stimulate an increased pulmonary
vasomotor tone by the process of hypoxic pulmonary
vasoconstriction.77 Therefore, the appropriate use of
oxygen to relieve hypoxic pulmonary vasoconstriction
and right heart strain will lessen myocardial ischemia,
improve cardiac output, and improve oxygen delivery
to other critical organs.
PEEP
The role of PEEP cannot be stressed enough in acute
pulmonary edema. An optimal level of PEEP will help
splint open water-logged airways as well as reverse
continued hydrostatic fluid flow into alveoli. PEEP
will recruit and prevent alveolar collapse, increase lung
compliance, and reduce the intrapulmonary shunt.63,78
PEEP improves functional residual capacity. For
every change in PEEP, compliance and plateau pressure
should be assessed to avoid alveolar overdistention
and the risk of barotrauma. Since there is no data that
supports a minimal level of PEEP for this population,
start with a PEEP between 8 cm H2O and 10 cm H2O
and adjust accordingly to keep both plateau pressures
< 30 cm H2O and PaO2 between 60 mm Hg and 80 mm
Hg.
PEEP affects cardiac function from increased
lung volumes and intrathoracic pressure.78,79 An
optimal level of PEEP improves the hemodynamics of
congestive heart failure by 5 primary components:80,81
Decreased venous return
Decreased right ventricular output
Decreased left ventricular filling
Decreased left ventricular output
Decreased left ventricular afterload
Table 5. Oxygen Ratio

PaO2/FIO2
Normal: 80100 = 400500 mm Hg
.21
PaO2/FIO2 < 200 = absolute shunt*
*A low PaO2/FIO2 on higher FIO2 > 60% is evidence of absolute
shunt and will have a poor response to oxygen therapy alone.
PEEP is needed.
Note: Not accurate on low FIO2 requirements.
11
In patients with cardiac dysfunction, Fellahi

et al reported in a randomized controlled study of
12 patients that PEEP of 9.6 +/- 0.2 cm H2O could
improve rather than impair cardiac output by
decreasing left ventricle afterload in a manner similar
to systemic vasodilator therapy; however, it cannot be
recommended in patients with dilated cardiomyopathy
and poor left ventricular function.82 The analogous
manner to treat CHF with PEEP, as with vasodilators,
was also supported in a well-designed randomized
study of 39 patients. This study demonstrated a rise in
cardiac output when PEEP was appropriately applied
to patients with poor myocardial function.83 Cardiac
output showed curvilinear changes with an increase
in PEEP from 0 cm H2O to 7 cm H2O, but it dropped
markedly when PEEP was increased to 13 cm H2O.
Primum Non NocereFirst, Do No Harm

If the ventilator is not used properly, the patient can be
injured. Physicians must be keenly aware of not only
the post-intubation period and appropriate ventilator
set up, but also of the dynamic nature of the disease
they are managing. VILI describes a compilation of
complications associated with the use of a ventilator.
Ventilator strategies that minimize air trapping,
dynamic hyperinflation, and auto-PEEP can be
achieved by decreasing the set mechanical respiratory
rate, prolonging the expiratory phase of ventilation,
reducing VT, and shortening I-time.48,64,69,84 Elimination
of patient effort through sedation and, if necessary,
paralysis is employed to avoid patient-ventilator
dyssynchrony. These strategies will reduce the risks
for barotrauma and VILI caused by auto-PEEP and
alveolar overdistention; see Ten Pitfalls To Avoid.
Air Trapping And Pulmonary Hyperinflation

High breathing rates shorten the time available for
expiration. Expiratory resistance develops when
airways are narrowed by bronchospasm, mucus
hypersecretion and plugging, mucosal or interstitial
edema, airway inflammation, airway collapse, or
loss of elastic recoil of the lung. Patients with severe
airflow obstruction and impaired expiratory flows
may not have enough expiratory time to exhale all of
the air from the lungs. If expiratory time is not long
enough, air is trapped in the alveoli. This is known as
air trapping. When this continues over several breaths,
breath stacking will occur until a new end-expiratory
lung volume is achieved. As this volume increases,
the functional residual capacity (FRC) of the lung
increases, forcing normal tidal breathing to occur at
higher lung volumes. The lungs become overdistended
and hyperinflated. This is referred to as dynamic
pulmonary hyperinflation. Pulmonary hyperinflation
can worsen gas exchange by increasing physiologic
dead space, reducing oxygen delivery to the tissues,
and increasing the risk of barotrauma (Figure 11).48
Alveolar Overdistention
Normal physiologic VT is typically around 68 mL/
kg PBW throughout life. Until recently, most patients
with acute respiratory failure were managed with
VT of 1015 mL/kg PBW. VILI can occur when the
lungs and alveoli overdistend.85 It is quite clear in the
evidence of 2 randomized, controlled trials of over
900 patients60,86 that VT 12 mL/kg PBW in acutely
ill patients is associated with increased mortality and
that smaller tidal volumes of 68 mL/kg PBW were
effective in the management of acute lung injury as
they avoided excessive alveolar distention. Along
similar lines, patients with obstructive and restrictive
processes who are at risk for VILI may also benefit
from lung-protective ventilation.87,88 However, there
is insufficient data to recommend a VT of 6 mL/kg
PBW as a standard for every patient who requires
mechanical ventilation.
Plateau pressures are determined by static
measurement of pulmonary distention pressures. In
the prospective, randomized, controlled trial reported
by the ARDS Network, 861 patients were placed on
either low VT (6 mL/kg PBW) with plateau pressures
< 30 cm H2O or on higher VTs (12 mL/kg PBW) with

plateau pressures up to 50 cm H2O.60 The results
showed a significant decrease in mortality from 39.8%
to 31% (P = 0.007) in patients receiving lower tidal
volumes and plateau pressures. If VT is limited, fewer
patients reach higher plateau pressures so that alveolar
overdistention and excessive stretch is minimized.
Since plateau pressure is a better indicator of
transpulmonary pressure and alveolar overdistention,
it is a better target for determining appropriate VT
settings (Figure 8). Comparative systematic reviews of
lung-protective ventilation studies suggest that plateau
pressures rather than tidal volumes are the most
accurate bedside indicator of alveolar overdistention
for patients with ARDS and those at risk for VILI.74,89
Patients who require smaller tidal volumes to
minimize plateau pressures and reduce lung injury
have other potential adverse effects including
hypercarbia and respiratory acidosis. However,
respiratory acidosis without a co-existing severe
metabolic acidosis is generally safe and well tolerated.90
Intrinsic PEEP/Auto-PEEP
The presence of airflow at end-expiration indicates that
the alveolar pressure is higher than the atmospheric
pressure or higher than the applied PEEP.44,45 The
pressure difference associated with the trapped volume
is called intrinsic PEEP or auto-PEEP. Auto-PEEP is the
average pressure inside the alveoli at end-exhalation.
Elevated intrathoracic pressure due to auto-PEEP
can decrease cardiac output and blood pressure by
impeding venous return and right ventricular filling.
This will result in increasing pulmonary vascular
resistance and increasing preload and afterload of the
left ventricle (Figure 8).91
12
Ten Pitfalls To Avoid When Troubleshooting The Ventilator

1. My patients peak inspiratory pressure alarm
kept beeping, so I decided to decrease the tidal
volume.
Did you check the plateau pressure first? Plateau
pressure represents the force required to overcome
the lungs elastic recoil. It will increase with
decreased compliance, overdistention of the lungs,
or hyperinflation. It is important to note the
difference between overdistention (too much tidal
volume and subsequent alveolar stretching) and
hyperinflation (trapped air in the lungs). If the
plateau pressure did not change then the lungs
recoil force did not change, and the ventilator
alarmed for another reason.
Peak inspiratory pressure (PIP) also reflects
the total force required to flow air through the
lungs. Increases in PIP without change in plateau
pressure may be due to an obstruction to airflow
or an increase in airway resistance. In this case,
higher PIP levels would not indicate overdistention.
Consider increased secretions (suction the airway),
bronchospasm (give bronchodilators), and
obstruction (check ETT placement).
trapping and hyperinflation. Setting the ventilator

to deliver a high inspiratory flow rate shortens
I-time (thus, longer exhalation time). This will
increase inspiratory flow and increase PIP. The
severe airway resistance seen in asthmatics actually
prevents the complete transference of this pressure
to the alveoli (Poiseuilles law) thus averting alveoli
from experiencing the full effect of the PIP. Recall
the difference between PIP and plateau pressures. If
you raise the PIP, there may not be a corresponding
change in the plateau pressure after you shorten the
I-time and lengthen the expiration because youve
reduced the auto-PEEP somewhat. As a result, the
plateau pressure will tend to decrease. A high peak
airway pressure is not necessarily dangerous unless
it corresponds to a dangerously high transalveolar
pressure (Pplat).
2. My patients peak inspiratory alarm kept

beeping, and I couldnt find the silent button.
What if the increase in PIP was the result of
decreased compliance? If the plateau pressure
increased to the same extent that peak pressure
increased without a difference between the two (no
change in resistance: R = PIP Pplat/Flow) then
decreased compliance is to blame. Factors that
decrease compliance include alveolar collapse/
atelectasis (measure auto-PEEP and apply PEEP),
lung collapse (decompress the pneumothorax),
overdistention of the lung (decrease tidal volume),
air trapping (reduce I-time or rate), and right
mainstem intubation (confirm with CXR).
Please compare pitfall 1 and 2. Note that the
PIP alarm in pitfall 1 resulted from increased
airway resistance whereas it represents an increase
in plateau pressure due to decreased compliance
in this example. While these events may appear
similar and the alarms sound the same, understand
that their etiologies and management are quite
different.
3. Since my asthmatic had extremely high
inspiratory resistance, I chose to use a lower
inspiratory flow rate.
While a high inspiratory flow may exaggerate the
high resistance in asthma and result in increased
peak inspiratory pressures, a short inspiratory time
is necessary to allow for a prolonged expiratory
time. The expiration phase of breathing must be
extended so air trapping is avoided. A careful
balance must be obtained between adequate
inspiratory flow, PIP, and sufficient expiratory
times. Longer E-times are necessary to minimize air
4. After applying PEEP of 8 cm H2O to overcome

auto-PEEP in the pressure control mode, my COPD
patient became hypotensive. I simply turned off
the PEEP since I figured it was the problem.
Understanding a ventilator patient interface often
involves thinking through what is happening
between the person and the machine.
1) In pressure control, tidal volumes vary in relation
to compliance.
2) PEEP that corrects auto-PEEP will result in
an increased functional residual capacity and
compliance.
3) If pressure control remains the same, the tidal
volume will increase along with this increase in
compliance. (C = Vol/ Press)
4) If the pressure control (PC) dial was originally set
to achieve a target tidal volume of 500 mL, your
patient may now get a higher VT of 800 mL as a
result of improved compliance.
5) This increase in VT may cause overdistention
and hyperinflation. This can result in decreased
right ventricular output, cardiac output, and
subsequently reduced blood pressure.
Therefore, before taking away the PEEP that was
effective in recruiting collapsed alveoli, consider
decreasing the PC setting to achieve the original
desired target VT of 500 mL and assuring that Pplat
remains < 30 cm H2O. The suspicion of dynamic
hyperinflation should also prompt you to listen to
the lungs and assess for auto-PEEP (air trapping).
The effects of PEEP on decreasing right
ventricular output, cardiac output, and blood
pressure directly relate to how PEEP changes total
lung volume and intra-alveolar pressures (Pplat).
The question to keep in mind is to what extent
did the PEEP change your patients lung volumes
and plateau pressure and to not simply assume the
effect was a direct result of PEEP.
13
Ten Pitfalls To Avoid When Troubleshooting The Ventilator (cont.)

5. The plateau pressure was < 30 cm H2O, so I was
able to increase my patients tidal volume to 15
mL/kg.
Normal physiologic tidal volume is 68 mL/kg
PBW. So why push a VT between 1215 mL/kg
when a patient is sick? Clearly, if a healthy person
does not require such a large tidal volume then
it would be wise to avoid such a stress on our
critically ill patients.
Always take care to treat your patient and not a
number. In a severely compromised patient with
low compliance lungs, plateau pressures of 40
cm H2O may only establish a VT of 5 mL/kg PBW
and induce lung injury because of high alveolar
pressures. The rule of thumb is to adjust VT up
to 10 mL/kg PBW as long as plateau pressure is <
30 cm H2O and adjust respiratory rate to achieve
desired minute ventilation.
for equal bilateral chest expansion. If the ETT

has been pushed into the right mainstem, slowly
withdraw it until equal chest expansion and
breath sounds are present. If still in doubt, use a
laryngoscope blade and visualize directly.
Obstruction: Does the patient need suctioning?
Secretions in the airway can plug the ETT. Another
cause could be the ventilator tubing. Check the
ventilator to ensure no kinking in the circuit.
Pneumothorax: Absent breath sounds may
indicate a pneumothorax. Treatment requires
decompression.
Equipment: While unusual, this complication can
occur. Decipher where the problem has occurred by
systematically approaching the ventilator from the
patient back to the machine. Under any suspicion of
mechanical failure, the patient should be removed
from the ventilator and manually bagged on 100%
O2.
6. Even though my emphysema patient was

bucking the vent, I was relieved to see the
improvement in his mental status.
Your patient is more awake because he is miserable!
While your goal of intubation may have been
to protect your patient, the lack of sedation and
agitation is harming him.
After intubation, it is often necessary to use
smaller tidal volumes as a protective lung strategy
in patients at risk for VILI. Forcing a low VT of
5 mL/kg (when necessary) on a patient without
sedation can result in marked cardiovascular
instability as the patient will be fighting for
larger tidal volumes. This increases the patients
discomfort, oxygen consumption, and carbon
dioxide production. This and agitation will make
the patient more active.
9. My asthmatic developed hypotension on pressure

control. He was only on 5 cm H2O of physiologic
PEEP.
At the initiation of mechanical ventilation, asthmatics
may require higher pressures to overcome increased
resistance caused by bronchospasm, persistent
airway secretions, plugging, and inflammation.
However, as bronchodilators and steroid therapy
lead to clinical improvement and bronchospasm
and inflammation clears, your patients will require
lower set airway pressures to ventilate the lungs
appropriately.
If this improvement is not recognized and
initial pressure settings are not decreased, these
high intrathoracic pressures are transmitted to the
mediastinum. The resulting compression of superior
and inferior venae cavae leads to decreased cardiac
output and hypotension. Since the increased tidal
volume delivered led to the hypotension, the best
management would be to reduce the tidal volume;
in this case, do so by lowering the pressure control
setting. Checking the plateau pressure to assure it
is < 30 cm H2O should be done with any change in a
patients target tidal volume.
7. I wanted to check for auto-PEEP on my patient

receiving 10 cm H2O of PEEP. After performing
the expiratory occlusion maneuver on the 10 cm
H2O of PEEP, I discovered there was no auto-PEEP
present so I decreased it to 0 cm H2O.
The 10 cm H2O of PEEP was actually counterbalancing the auto-PEEP. If you fail to decrease the
PEEP to zero before performing the expiratory hold
maneuver, you would have measured 10 cm H2O
of auto-PEEP instead. If the set PEEP overcomes
auto-PEEP, the true amount of auto-PEEP will be
falsely low. As a minimum, physiologic PEEP is
considered to be between 5 cm H2O and 8 cm H2O.
8. The peak pressure alarm still continued to beep
despite all my efforts.
The mnemonic DOPE (tube Displacement, tube
Obstruction, Pneumothorax, and Equipment
failure) covers 4 of the most common causes of postintubation hypoxia or other deterioration.
Displacement: Check for endotracheal tube
placement by auscultating the chest and watching
14
10. My CHF patient remained hypoxic on 100% FIO2.

In acute pulmonary edema, a high FIO2 alone is
ineffective in improving PaO2 in the presence of
a large intrapulmonary shunt. The reason for the
persistent hypoxemia is that there is no transmission
of oxygen to the red blood cells perfusing collapsed
alveoli. This condition is known as refractory
hypoxemia. In this case, PEEP is needed to splint
open the airways so more alveoli can participate in
oxygenation.
Cutting Edge
Measuring And Applying The P-Flex
change in pressure results in significant volume change.

The inspiration between LIP and UIP represents
optimal lung usage. In clinical terms, the goal is to keep
patients inspiring between the LIP and UIP. Setting
the appropriate PEEP will allow the start of inspiratory
cycle at the LIP. Determining this number is done
through a P-flex calculation.
Gattinoni et al introduced P-flex as the
intersection point between the slopes of the low
compliance segment and high compliance segments
(Figure 13).92 The intersection of these 2 slopes was
defined as the P-flex and corresponds to the optimal
PEEP for the patient. Alveolar recruitment is maximized
at this point.
By using the P-flex, PEEP can be optimized. This
will help reduce the need for high inspiratory pressures
(which were being used to overcome the static resistance
of the alveoli) and help avoid barotrauma to the patient.
In simple terms, the P-flex helps us to determine the
appropriate pressure to keep our alveoli moving (open)
and to avoid repeatedly overcoming the static resistance
of collapse and re-recruited alveoli.
In a randomized controlled study of 52 patients
by Amato et al,88 setting PEEP 2 cm H2O above the LIP
had less barotrauma and a lower mortality rate when
compared to conventional strategies without P-V curve
analysis. The rationale for setting PEEP 2 cm H2O
above the LIP was to completely avoid any chance of
recruitment and decruitment of alveoli that would cause
lung injury.
Unlike the expiratory-hold occlusion maneuver,
the advantage of a P-V curve is that auto-PEEP can
be measured without reducing the PEEP to 0, thus
minimizing the shear forces of opening and closing
alveoli. However, adequate sedation and/or paralysis is
still required since the patients flow rate must be
< 10 L/min to eliminate resistive changes in the lung.93,94
PEEP titration by P-flex and P-V curve analysis is still an
ongoing investigational process simply due to the range
in variability of subjective interpretation.9597 Further
studies in the overall use of its clinical capabilities when
combined with other techniques will be a helpful tool in
decreasing the risks of barotrauma and VILI.
Managing a ventilated patient involves obtaining the

correct information and maximizing your ventilator
settings. Having the right PEEP setting is very
important. PEEP serves to splint open small airways
and to recruit alveoli. Determining a patients optimal
PEEP is done through the clinical procedure known as
the P-flex.
To understand P-flex we need to recall some basic
physics. To move a body at rest requires overcoming
friction (a type of resistance). There is static and
dynamic resistance; the difference is very important.
The initial movement of an object (static friction)
requires significant energy to overcome the static
forces holding the object in place. Once the object
begins to move, less but continuous force must be
exerted to continue the objects movement (overcoming
dynamic friction).
Inside the lungs of an ill patient, the alveoli tend
to collapse secondary to reduced patient effort to keep
them open. One goal of ventilator management is
to pop (static friction) alveoli open and to use them
for ventilation (alveolar recruitment). This can be
facilitated by optimizing PEEP. The P-flex helps select
the appropriate PEEP setting to open the collapsed
alveoli. On a ventilator, pressure volume curves can
be created. Compliance represents the proportion of
change in volume to that of change in pressure. (C =
Vol/ Press). The pressure volume-curve (P-V curve)
plots the two components (inspiration and expiration)
throughout the respiratory cycle. With regards to
alveolar recruitment, inspiration is key. Applying
this to collapsed alveoli and static/dynamic resistance
is demonstrated in Figure 12. On the left side of the
plots (just below the lower inflection point [LIP]),
compliance is low and a significant amount of pressure
must be exerted to obtain a relatively small change
in volume. However, the forces required to change
volume (i.e., high compliance) change dramatically at
the lower inflection point up to the upper inflection
point (UIP). Between these points, a relatively small
Figure 13: P-Flex
Figure 12. Pressure-Volume Curve (P-V Curve)
The steepest part of the curve reflects the best recruitable lung.
Upper Inflection
Point (UIP)
V
O
L
Volume
Low compliance
decreased Volume/
pressure
P-flex
High compliance
Increased Volume/
pressure
Low compliance
decreased Volume/
pressure
Lower Inflection
Point (LIP)
10
15
20
25
30
Pressure
Press
15
Pressure-Regulated Volume Control Mode (PRVC)

Pressure-regulated volume control is a mode that
allows the physician to use pressure control ventilation
with a constant tidal volume. One way to look at
PRVC is that it combines assist control volume mode
and pressure control mode. This approach helps us
to maintain adequate ventilation (tidal volume) while
avoiding excessive alveolar pressures.
The tidal volume is the key setting, but the
ventilator delivers a pressure-controlled breath. The
pressure to deliver the breath will automatically
adjust to changes in a patients compliance and airway
resistance until the set tidal volume is achieved. If
the delivered volume is insufficient on one breath, the
ventilator increases inspiratory pressure for the next
breath. Additionally, the ventilator will decrease the
pressure delivered if tidal volume is too high.
The maximum amount of pressure the ventilator
is allowed to deliver in PRVC is determined by the
high-pressure alarm setting. The peak pressure
allowed is 5 cm H2O below this setting. For example,
the high-pressure alarm should be set at 35 cm H2O to
assure that the patient will not exceed a PIP > 30 cm
H2O. Since pressure-controlled breaths equal plateau
pressure, recall that it is recommended to keep plateau
pressures < 30 cm H2O to avoid lung overdistention.
The advantage of PRVC is that minute ventilation
and tidal volume are guaranteed with controlled peak
airway pressures, thus reducing the risk for VILI.
Mandatory settings for PRVC are:
Target tidal volume
High pressure alarm
I-time
Rate
FIO2
PEEP
Summary
Ventilators are life-saving machines, but they must
be used properly. Just as they can save lives, they can
cause significant and irreparable damage to a patient if
used improperly. In this article, the basics of ventilator
management were discussed for 3 common causes
of respiratory failure in the ED. While respiratory
decompensation was the common theme, each disease
process is marked by unique pathophysiology. An
understanding of the diseases, their pathophysiology,
and the ventilator basics presented here will allow for
confident management of difficult patients.
Asthma is a major health concern in the United
States. This disease affects both young and old, and it
can rapidly lead to respiratory insufficiency and arrest.
The underlying issue involves obstruction of the lower
airway with inflammation, mucous, and airway spasm.
Ventilatory management must be approached carefully
and individualized to each case. Adequate sedation
is the first step. This will allow a tired patient to rest
16
and allow accurate lung mechanics measurements to be

obtained. Ensuring adequate expiratory times as well
as avoiding excessive airway pressures (plateau not
inspiratory pressures) is key. Auscultation and frequent
assessment of patients will help clinicians manage these
difficult cases correctly.
Emphysema involves a weakened distal airway.
The normal elastic recoil is significantly impaired and
the alveolar walls are thin and weakened. Be diligent
in managing patients with alveolar recruitment while
avoiding pressure-induced lung trauma. As with the
asthmatic, expiratory times must be monitored closely
to ensure complete expiration and to avoid air trapping.
Congestive heart failure is becoming a common
problem. Unfortunately, stress on an already weakened
heart can lead to infarction, dysrhythmias, and
reduced flow to multiple organ systems. Caring for
the decompensated patient in acute pulmonary edema
involves managing multiple problems at once. The
first step is an appropriately set ventilator. Mechanical
ventilation can reduce the stress on the heart by
reducing preload and afterload. You can maximize
oxygenation while avoiding absorption atelectasis.
While the task of stabilizing a truly ill CHF patient can
be daunting, recognizing the utility of the ventilator is
your first step to providing the appropriate care.
5 Key Concepts To Remember

Keep plateau pressures < 30 cm H20 to avoid alveolar
overdistention.
Avoid air trapping (assessed on expiratory flow
waveform) when setting respiratory rate.
Apply PEEP to overcome auto-PEEP.
Wean FIO2 to maintain PaO2 between 60 mm Hg and
80 mm Hg.
Use adequate sedation to allow for passive
ventilation.
Case Conclusions
Case #1: You intubate the young asthmatic and start her
on pressure control ventilation. She is adequately sedated
and paralyzed as you obtain your initial settings. Because
of severe obstruction and prolonged expiratory phase, you
have the following settings: FIO2 100% and PCAC to achieve
target tidal volume of 400 mL. The inspiratory occlusion
maneuver reveals an acceptable plateau pressure of 27 cm
H2O. After initial PEEP of 5, the P-flex suggests you set the
PEEP at 8 cm H2O. The patient is adequately sedated with
ketamine and morphine and therefore tolerates a respiratory
rate of 6 breaths per minute and a short inspiratory time with
a prolonged expiratory time. With these settings, you get an
ABG of pH 7.28, PaO2 85, and PaCO2 of 110. The nurses
are uncomfortable and ask to increase the respiratory rate
and oxygen. Instead, you recognize the role of permissive
hypercapnia and lung protective strategies. The whistling
of the continuous nebs comforts you as you arrange an ICU
admission.
Case #2: Your frail COPD patient deteriorated soon

after you stabilized the asthmatic. You wondered if this
man would ever come off the vent as you deftly slid the 8.0
ETT through the cords. After airway stabilization, you
set your ventilator as follows: PCAC, FIO2 100%, PIP
22 (corresponds to volumes between 600 cc and 800 cc),
PEEP 14 (based on P-flex), sedated with midazolam drips
and morphine, short inspiratory time with a prolonged
expiratory time, and a respiratory rate of 8. This gives you
an ABG of pH 7.40, PaO2 170, and PaCO2 of 30. You ask
the respiratory therapist to reduce the FIO2 based on the
oxygenation pleth (there is a good wave) and to reduce the
PIP. She remarks that the plateau pressures are already
below 30, but you explain that the corresponding volumes
are a bit too large for a 60 kg man.
Case #3: Stabilizing this patient was a chore that
involved management of her myocardial infarction, flash
pulmonary edema, and new onset seizure (either hypoxic
or a run of ventricular tachycardia). Her short neck, large
size, and frothy pink sputum made intubation difficult. She
ended up with a 7-0 ETT tube, volume control ventilation,
FIO2 100%, set tidal volumes of 400 (corresponding plateau
pressure 35), initial PEEP of 5, sedated with morphine
and propofol, and a respiratory rate of 14. A P-flex shows
an optimal PEEP of 15. You set this and notice, with
satisfaction, that her plateau pressures come down as you
recruit more lung volume. You adjust her tidal volumes up
to 500 as you maintain her plateau pressures < 30. You also
reduce your FIO2 to 50% to avoid absorption atelectasis.
References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology
and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.
To help the reader judge the strength of each
reference, pertinent information about the study,
such as the type of study and the number of patients
in the study, will be included in bold type following
the reference, where available. In addition, the
most informative references cited in this paper, as
determined by the authors, will be noted by an asterisk
(*) next to the number of the reference.
1. American Lung Association. Epidemiology and statistics Unit, Research
and Program Services. Trends in Asthma Morbidity and Mortality May
2005. (Consensus opinion)
2. Pappas G, Hadden W, Kozak L, et al. Potentially avoidable
hospitalizations: inequalities in rates between US socioeconomic
groups. Am J Public Health 1997;87:811-816 (Retrospective; 192,734
hospitalizations)
3. Weiss KB, Gergen PG, Hodgson TA. An economic evaluation of asthma
in the United States. N Engl J Med 1992;326:862-866 (Retrospective)
4. New Asthma Estimates: tracking Prevalence, Health Care and
Mortality, NCHS, CDC, 2001 (Consensus opinion)
5. Centers for Disease Control and Prevention. Forecasted state-specific
estimates of self-reported asthma prevalence- Unites States 1998.
MMWR Morb Mortal Wkly Rep 1998; 47:1022-1025 (Retrospective)
6. Pendergraft T, Stanford R, Beasley R, et al. Rates and characteristics
of intensive care unit admissions and intubations among asthmarelated hospitalizations. Ann Allergy Asthma Immunol 2004;93:29-35
(Comparative analysis)
17
7. Kearney SE, Graham DR, Atherton ST: Acute severe asthma treated by
mechanical ventilation: a comparison of the changing characteristics over
a 17 year period. Respir Med 1998;92:716-721 (Comparative analysis)
8. Pauwels R, Buist A, Ma P, et al. Global strategy for the diagnosis,
management, and prevention of chronic obstructive pulmonary disease:
National Heart, and Lung Blood Institute and world Health Organization
Global Initiative for COPD(GOLD):executive summary. Respir Care
2001;46(8):798-825 (Consensus development conference, review)
9. National Center for Health Statistics. National Health Interview Survey:
Research for the 1995-2004 redesign. Hyattsville, MD: U.S. Department of
Health and Human Services, CDC, NCHS Vital and Health Stat 1999;2:126
(Consensus opinion)
10. National Center for Health Statistics. National Hospital Ambulatory
Medical Care Survey. Hyattsville, MD: U.S. Department of Health and
Human Services, CDC, NCHS 1995-2000 (Consensus opinion)
11. National Heart, Lung, and Blood Institute. Chronic obstructive pulmonary
disease. Bethesda, MD: U.S. Department of Health and Human Services,
NIH, NHLBI March 2003 (Expert guidelines)
12. National Heart, Lung, And Blood Institute. Morbidity and Mortality: 2002
Chartbook on Cardiovascular, Lung, and Blood Diseases. Bethesda, MD:
U.S. Department of Health and Human Services, NIH, NHLBI May 2002
(Textbook)
13. National Heart, Lung, and Blood Institute. Congestive Heart Failure Data
Fact Sheet: NHLBI 2001 (Review)
14. National Center for Chronic Disease Prevention & Health Promotion.
Facts about congestive heart failure.CDC, Division of Media Relations
2001 (Retrospective)
15. Burt C, Schappert S. Ambulatory care visits to physician offices, hospital
outpatient departments and emergency departments: United Sates 2000.
Vital Health Stat 2004;(13)157:1-70 (Review)
16. Centers for Medicare and Medicaid Services. Health Care Financing
Review: Medicare and Medicaid Statistical Supplement. Baltimore, MD:
Centers for Medicare and Medicaid Services 2003 (Cost analysis)
17. Bott J, carroll MP, Conway JH, et al. Randomized, controlled trial of nasal
ventilation in acute ventilatory failure due to chronic obstructive airway
disease. Lancet 1993;341:1555-1557 (Prospective, randomized, control, 60
patients)
18. Brochard L, Mancebo J, Wysocki M, et al. Non-invasive ventilation for
acute exacerbations of chronic obstructive pulmonary disease. N Engl J
Med 1995;333:817-822 (Prospective, randomized, control 85 patients)
19. Kramer N, Meyer TJ, Meharg J, et al. Randomized, prospective trial of
non-invasive positive pressure ventilation in acute respiratory failure. Am
j Respir Crit Care Med 1995;151:1799-1806 (Prospective, randomized, 31
patients)
20. Martin T, Hovis J, Costantino J, et al. A randomized, prospective
evaluation of non-invasive ventilation for acute respiratory failure.
Am J Respir Crit Care Med 2000;161:807-813 (Prospective, comparative,
randomized, control, 61 patients)
21. Antonelli M, Conti G, Rocco M, et al. A comparison of non-invasive
postive pressure ventilation and conventional mechanical ventilation
in patients with acute respiratory failure. N Engl J Med 1998;339:429-435
(Randomized control 64 patients)
22. Masip J, Roque M, Sanchez B, et al. Noninvasive ventilation in acute
cardiogenic pulmonary edema; systematic review and meta-analysis.
JAMA 2005;294(2):3124-3130 (Randomized, control, 40 patients)
23. Meduri G, Cook T, Turner R, et al. Noninvasive positive pressure
ventilation in status asthmaticus. Chest 1996;110(3):767-774 (Prospective,
17 patients)
24. Soroksky A, Stav D, Shipirer I. A pilot prospective, randomized placebocontrolled trial of bilevel positive airway pressure in acute asthmatic
attack. Chest 2003;123(4):1018-1025 (Prospective, randomized control, 30
patients)
25. Peter J, Moran J, Phillips-Hughes J, et al. Noninvasive ventilation in acute
respiratory failure- a meta-analysis update. Crit Care Med 2002;30:555-562
(Meta-analysis, 15 articles)
26. Evans T. International consensus conferences in intensive care medicine:
non-invasive positive pressure ventilation in acute respiratory failure.
Intensive Care Med 2001;27:166-178 (Consensus, conference review)
27. Meduri G, Turner R, Abou-Shala N, et al. Noninvasive positive pressure
ventilation via face mask: first-line intervention in patients with acute
hypercapnic and hypoxemic respiratory failure. Chest 1996;109:179-193
(Prospective, uncontrolled, 158 patients)
28. Mehta S, Hill N. Noninvasive ventilation. Am J Respir Crit Care Med
2001;163: 540-577 (Review)
29 Lightowler JV, Wedzicha JA, Elliot MW, Ram FS. Noninvasive
positive pressure ventilation to treat respiratory failure resulting from
exacerbations of chronic obstructive pulmonary disease: Cochrane
systematic review and meta-analysis. BMJ 2003;326:185-187 (Systematic
review, 8 articles)
30. Wood K, Lewis L, VonHarz B, et al. The use of noninvasive positive
pressure ventilation in the emergency department: results of a
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
randomized clinical trial. Chest 1998;113:1339-1346 (Randomized, 27

patients)
Merlani P, Pasquina P, Granier J, et al. Factors associated with failure of
noninvasive positive pressure ventilation in the emergency department.
Acad Emerg Med 2005:12(12)1206-1215 (Retrospective, 104 patients)
Confalonieri M, Garuti G, Cattaruzza M, et al. A chart of failure risk for
noninvasive ventilation in patients with chronic obstructive disease. Eur
Respir J 2005;25(2)348-355 (Meta-analysis, 1,033 patients)
Anton A, Guell R, Gomez J, et al. Predicting the result of noninvasive
ventilation in severe acute exacerbations of patients with chronic airflow
limitation. Chest 2000;117(3):828-833 (Prospective, 44 patients)
Keenan S, Sinuff T, Cook D, et al. Which patients with acute
exacerbation of chronic obstruction pulmonary disease benefit from
noninvasive positive-pressure ventilation? A systematic review of the
literature. Ann Intern Med 2003;138(11):861-870 (Meta-analysis, 15 trials)
Phua J, Kong K, Lee K, et al. Noninvasive ventilation in hypercapnic
acute respiratory failure due to chronic obstructive pulmonary disease
vs. other conditions: effectiveness and predictors of failure. Intensive Care
Med 2005;31(4):533-539 (Prospective, 111 patients)
Antonelli M, Conti G, Moro M, et al. Predictors of failure of
noninvasive positive pressure ventilation in patients with acute
hypoxemic respiratory failure: a multi-center study. Intensive Care Med
2001:27(11):1718-1728 (Prospective, multicenter cohort, 354 patients)
Rana S, Jenad H, Gay P, et al. Failure of noninvasive ventilation in
patients with acute lung injury: observational cohort study. Crit Care
2006;10(3):R79 (Comparative analysis, 54 patients)
Honrubia T, Garcia-Lopez F, Franco N, et al. Noninvasive versus
conventional mechanical ventilation in acute respiratory failure. Chest
2005;128:3916-3924 (Multicenter, randomized controlled trial 64
patients)
Branson R, Chatburn R. Classification of mechanical ventilators. In
MacIntyre NR, Branson RD. Mechanical ventilation. Philadelphia: WB
Saunders; 2000:1-33 (Textbook)
Register SD, Downs JB, Stock MC et al. Is 50% oxygen harmful? Crit Care
Med 1987;15(6):598-601
Zakynthinos S, VassilaKopoulous T, Zakynthinos E, et al. Measuring
dynamic PEEP. Am J Respir Crit Care Med 2000;162:1633-1640.
(Randomized, control, 15 patients)
Rossi A, Polese G, Brandi G, et al. Intrinsic positive end-expiratory
pressure. Intensive Care Med 1995;21(6):522-536 (Review)
Brochard L. Intrinsic (or auto-) positive end-expiratory pressure
during spontaneous or assisted ventilation. Intensive Care Med
2002;28(10):1376-1378 (Prospective, randomized)
Lessard MR, Lofaso F, Brochard L. Expiratory muscle activity increases
intrinisic posititve end-expiratory pressure independently of dynamic
hyperinflation in mechanically ventilated patients. Am J Respir Crit Care
Med 1995;151:562-569 (Prospective, randomized, 8 patients)
Leatherman J, Ravenscraft S. Low measured auto-positive endexpiratory pressure during mechanical ventilation of patients with
severe asthma: Hidden auto-positive end-expiratory pressure. Crit Care
Med 1996;24:541-546 (Observational, 4 patients)
Williams T, Tuxen D, Scheinkestel C, et al. Risk factors for morbidity
in mechanically ventilated patients with acute sesvere asthma. Am Rev
Respir Dis 1992;146:607-615 (Comparative study, 95 patients)
Mansel JK, Stogner SW, Petrini MF, et al. Mechanical ventilation in
patients with acute severe asthma. Am J Med 1990;89:42-49 (Review)
Tobin M, Jubran A, Laghi F. Patient-ventilatory interaction. Am J Respir
Crit Care Med 2001;163(5):1059-1063 (Retrospective, 17 patients)
Kondili E, Prinianakis G, Georgopoulos D. Patient-ventilator interaction.
Br J Anaesth 2003;91(1):106-119 (Review)
Bellomo R, McLauglin P, Tai E, et al. Asthma requiring mechanical
ventilation. A low morbidity approach. Chest 1994;105:891-896 (Metaanalysis 35 patients)
Fiehl F, Perrett C. Permissive hypercapnia. How permissive should we
be? Am J Resp Crit Care Med 1994;150:1722-1737 (Review)
Amato M, Barbas C, Medeiros D, et al. Effect of a protective-ventilation
strategy on mortality in the acute respiratory distress syndrome. N Engl
J Med 1998;338(6):347-354 (Prospective, randomized, controlled trial 53
patients)
Darioli R, Perret C: Mechanical controlled hypoventilation in status
asthmaticus. Am Rev Respir Dis 1984;129:385-387 (Retrospective, 34
cases)
Bigatello L, Patroniti N, Sangalli F. Permissive hypercapnia. Curr Opin
Crit Care 2001;7:34-40 (Systematic review)
Douglass JA, Tuxen DV, Horne M. Myopathy in severe asthma. Am Rev
Respir Dis 1992;146:1136 (Retrospective 25 patients)
Leatherman J, Fluegel W, David W, et al. Muscle weakness in
mechanically ventilated patients with severe asthma. Am J Respir Crit
Care Med 1996;153(5):1686-1690 (Retrospective, 94 patients)
57. Corbridge T, Hall J. The assessment and management of adults with

status asthmaticus. Am J Respir Crit Care Med 1995;151:1296 (Review, 22
articles)
*58. The Acute Respiratory Distress Syndrome Network. Ventilation with
lower tidal volumes as compared with traditional tidal volumes for
acute lung injury and the acute respiratory distress syndrome. N Eng
J Med 2000;342(18):1301-1308 (Multicenter, randomized trial, 861
patients)
59. Leatherman JW, McArthur C, Shapiro RS. Effect of prolongation of
expiratory dynamic hyperinflation in mechanically ventilated patients
with severe asthma. Crit Care Med 2004;32(7):1542-1545 (Observational,
12 patients)
60. Caramez M, Borges J, Mauro R. Paradoxical responses to postive
end-expiratory pressure in patients with airway obstruction during
controlled ventilation. Crit Care Med 2005;33(7):1519-1528 (Randomized,
control; 8 patients)
61. Armaganidis A, Stavrakaki-Kallergi K, Koutsoukou A, Lymberis A et
al. Intrinsic positive end-expiratory pressure in mechanically ventilated
patients with and without tidal expiratory flow limitation. Crit Care Med
2000;28(12):3837-3842 (Prospective, 32 patients)
62. Leatherman J, Ravenscraft S. Low measured auto-positive endexpiratory pressure during mechanical ventilation of patients with
severe asthma: Hidden auto-positvie end-expiratory pressure. Crit Care
Med 1996;24:541-546 (Observational 16 patients)
63. Marini JJ, Gattinoni L. Ventilatory management of acute respiratory
distress syndrome. Crit Care Med 2004;32:250-255 (Systematic Review)
64. Patel H, Yang K. Variability of intrinsic positive end-expiratory
pressure in patients receiving mechanical ventilation. Crit Care Med
1995;23:1074-1079
65. Smith TC, Marini JJ. Impact of PEEP on lung mechanics and
work of breathing in severe airflow obstruction. J Appl Physiol
1988;65(4):1488-1499 (Randomized, control 10 patients)
66. Yang SC, Yang SP. Effects of Inspiratory flow waveforms on lung
mechanics, gas exchange, and respiratory metabolism in COPD patients
during mechanical ventilation. Chest 2002;122:2096-2104 (Randomized,
comparative 54 patients)
67. Tuxen DV, Lane S. The effects of ventilatory pattern on hyperinflation,
airway pressures, and circulation in mechanical ventilation of patients
with severe airflow obstruction. Am Rev Respir Dis 1987;136(4):872-879
(Randomized, control; 9 patients)
68. Franklin C, Samuel J, Hu TC. Life-threatening hypotension associated
with emergency intubation and the initiation of mechanical ventilation.
Am J Emerg Med 1994;12(4):425-428 (Review)
69. Ranieri V, Giuliani R, Cinnella G, et al. Physiologic effects of positive
end-expiratory pressure in patients with chronic obstructive pulmonary
disease during acute ventilatory failure and controlled mechanical
ventilation. Am Rev Respir Dis 1993;147(1):5-13 (Review)
70. MacNee W. Pathophysiology of cor pulmonale in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 1994;150(3):833-852
(Review)
71. ODonnell DE, Laveneziana P. Physiology and consequences of lung
hyperinflation in COPD. Eur Resp Rev 2006;15:61-67
72. Petrucci N, Iacovelli W. Ventilation with lower tidal volumes versus
traditional tidal volumes in adults for acute lung injury and adult
respiratory distress syndrome. Cochrane Database Syst Rev 2004;(2)
CD003844 (Systematic review of 8 randomized controlled trials)
73. Ranieri M, Mascia L, Fiore T, et al. Cardiorespiratory effects of positive
end-expiratory pressure during progressive tidal volume reduction
(permissive hypercapnia) in patients with acute respiratory distress
syndrom. Anesthesiology 1995;83(4):710-720 (Randomized, control; 9
patients)
74. Gay PC, Rodarte JR, Hubmayr RD. The effects of positive expiratory
pressure on isovolume flow and dynamic hyperinflation in patients
receiving mechanical ventilation. Am Rev Respir Dis 1989;139:621-626
75. Jackson RM. Pulmonary oxygen toxicicty. Chest 1985;88(6):900-905
(Review)
76. Koutsoukou A, Armaganidis A, Stavrakaki-Kallergi K, Vassilakopoulos
T, et al. Expiratory flow limitation and intrinsic positive end-expiratory
pressure at zero positive end-expiratory pressure in patients with
adult respiratory distress syndrome. Am J Respir Crit Care Med
2000;161(5):1590-1596 (Randomized, controlled, 10 patients)
77. Pinsky M. Cardiovascular issues in respiratory care. Chest
2005;128(5):592-597 (Review)
78. Pinsky M. The hemodynamic consequences of mechanical ventilation;
an evolving story. Intensive Care Med 1997;23:493-503 (Review)
79. Naughton M, Rahman M, Hara K, et al. Effects of continUous positive
airway pressure on intrathoracic and left ventricular transmural
pressures in patients with CHF. Circulation 1995;91(6):1725-1731
(Prospective; 24 patients)
18
80. Bradley T, Holloway R, McLaughin P, et al. Cardiac output response to

continuous positive airway pressure in congestive heart failure. Am Rev
Respir Dis 1992;145(2):377-382 (Controlled, prospective; 22 patients)
81. Montner P, Greene E, Murata G, et al. Hemodynamic effects of nasal
and face mask continuouos positive airway pressure. Am J Respir Crit
Care Med 1994;149(6):1614-1618 (Comparative; 6 patients)
82. Fellahi J, Valtier B, Beauchet A, et al. Does positive end-expiratory
pressure ventilation improve left ventricular function? Chest
1998;114:556-562 (Prospective comparative; 12 patients)
83. Zhang W, Huang L, Qin Y, et al. Clinical study of the setting of
positive end expiratory pressure in patients with acute cardiogenic
pulmonary edema during mechanical ventilation. Chin Crit Car Med
2006;18(6):367-369 (Randomized, control, 39 patients)
84. Georgopoulus D, Mitrouska I, Markopoloulou K, et al. Effects of
breathing patterns on mechanically ventilated patients with chronic
obstructive lung disease and dynamic hyperinflation. Intensive Care Med
1995;21(11):880-886 (Randomized, controlled trial, 9 patients)
85. Slutsky, AS. Lung injury caused by mechanical ventilation. Chest
1999;116:9-15 (Review)
86. Amato M, Barbas C, Medeiros D, et al. Effect of a protective-ventilation
stragegy on mortality in the acute respiratory distress syndrome. N
Engl J Med 1998;338:37-354 (Randomized, prospective, control; 52
patients)
87. Gajic O, Dara SI, Mendez JL, Adesanya AO et al. Ventilatorassociated lung injury in patients without acute lung injury at the
onset of mechanical ventilation. Crit Care Med 2004;32(9):1817-1824
(Retrospective, 332 patients)
88. Gajic O, Frutos-Vivar F, Esteban A, Hubmyr RD, Anzueto A. Ventilator
settings as a risk factor for acute respiratory distress syndrome in
mechanically ventilated patients. Intensive Care Med 2005;31(7):922-926
89. Kallet RH, Corral W, Silverman HF, Luce JM. Implementation of a low
tidal volume ventilation protocol for patients with acute lung injury or
acute respiratory distress syndrome. Resp Care 2001;46(10):1024-1037
(Review)
90. Hickling KG. Permissive hypercapnia. Resp Care Clin N Am
2002;8(2):155-169 (Retrospective, 50 patients)
91. Luecke T, Pelosi P. Clinical review: positive end-expiratory pressure
and cardiac output. Critical Care 2005;9:607-621 (Systematic review)
92. Gattinoni L, Presenti A, Avalli L, et al. Pressure volume curve of total
respiratory system in acute respiratory failure: computed tomographic
scan study. Am Rev Respir Dis 1987;136(3):730-736
93. Kallet R. Pressure volume curves in management of adult respiratory
distress syndrome. Respir Care Clin Am 2003;9:321-341 (Review)
94. Lu Q, Vieira S, Richecoeur J, et al. A simple automated method for
measuring pressure volume curves during mechanical ventilation. Am J
Respir Crit Care Med 1999;159(1):275-282 (Review)
95. Johnson B, Richard J Straus C, et al. Pressure-volume curves and
compliance in acute lung injury: evidence of recruitment above the
lower inflection point. Am J Respir Crit Care Med 1999;159(4):1172-1178
(Review)
96. Ward N, Lin D, Nelson D. Successful determination of lower inflection
point and maximal compliance in a population of patients with
adult respiratory distress syndrome. Crit Care Med 2002;30(5):963-968
(Prospective, 28 patients)
97. Mehta S, Stewart T, MacDonal R, et al. Temporal change,
reproducibility, and interobserver variability in pressure-volume
curves in adults with acute lung injury and adult respiratory distress
syndrome. Crit Care Med 2003;31(8):2118-2125 (Prospective, 11 patients)
CME Questions
4. What therapy is most beneficial to improve

hypoxia in patients with an intrapulmonary
shunt caused by pulmonary edema?
a. Hyperoxygenation
b. Applied PEEP
c. Hypoventilation
d. Hyperventilation
5. Which type of measurement can provide helpful
information in determining an appropriate tidal
volume that may reduce the likelihood of VILI?
a. Resistance
b. Flow
c. Minute ventilation
d. Plateau pressure
6. What may indicate that the pulmonary
compliance of a patient on a controlled volume
cycled ventilator has decreased?
a. Decrease in minute ventilation
b. Decrease in VT
c. Increase in PIP
d. Decrease in PIP
7. Another name for air trapping is:
a. Bronchospasm
b. Auto-PEEP
c. Hypercapnia
d. Extrinsic PEEP
8. The use of alveolar hypoventilation to reduce
pulmonary overdistention is also known as:
a. Dynamic hyperinflation
b. Air trapping
c. Alveolar overdistention
d. Permissive hypercapnia
9. The O in the mnemonic DOPE, which covers
4 of the most common causes of post-intubation
hypoxia or other deterioration, stands for:
a. Oxygen
b. Overdistention
c. Obstruction
d. Obesity
10. What is the I:E ratio for a patient receiving
mechanical ventilation with a RR of 10 bpm and
an I-time of .75 seconds?
a. 1:3
b. 1:4
c. 1:5
d. 1:7
1. What is the equation to calculate minute

ventilation?
a. Tidal volume resistance
b. Respiratory rate x peak inspiratory pressure
c. Tidal volume x respiratory rate
d. Tidal volume respiratory rate
11. Which of the following parameters can

determine auto-PEEP?
a. End-inspiratory pause
b. End-expiratory occlusion maneuver
c. Plateau pressure measurement
d. PEEP applied to the ventilator
2. Auscultation of a chest reveals persistent

expiratory airflow at the initiation of the next
ventilator breath. This may result from:
a. Decreased minute ventilation
b. Shortened I-time
c. Respiratory rate is too high
d. Prolonged exhalation phase
3. What are ways to eliminate air trapping seen on

a flow waveform?
a. Increase I-time
b. Increase E-time
c. Increase VT
d. Increase respiratory rate
19
12. A patient is being ventilated in pressure control/

assist control mode. Which of the following
cannot be manually set by the physician?
a. Pressure
b. Flow
c. I-time
d. PEEP
Physician CME Information
13. The P-flex helps select the appropriate _______

setting to open collapsed alveoli.
a. PEEP
b. Tidal volume
c. Respiratory rate
d. Flow
14. What is constant in pressure control/assist control
mode?
a. Flow
b. I-time
c. Volume
d. A and C
15. The most effective method to decrease the risk
for dynamic hyperinflation associated with air
trapping is:
a. Add PEEP
b. Reduce minute ventilation
c. Increase VT
d. Increase minute ventilation
Coming In Future Issues

Severe TBI
Hypothermia
Announcements
We have now launched the

Emergency Medicine Practice blog.
Let your voice be heard!
This is your chance to weigh in on key aspects
of care and controversial topics.
Voice your opinion today at
www.empractice.wordpress.com
Date of Original Release: August 1, 2008. Date of most recent review: June 11,
2008. Termination date: August 1, 2011.
Accreditation: This activity has been planned and implemented in accordance
with the Essentials and Standards of the Accreditation Council for Continuing
Medical Education (ACCME) through the joint sponsorship of Mount Sinai School
of Medicine and Emergency Medicine Practice. The Mount Sinai School of
Medicine is accredited by the ACCME to provide continuing medical education
for physicians.
Credit Designation: The Mount Sinai School of Medicine designates this
educational activity for a maximum of 48 AMA PRA Category 1 Credit(s) per
year. Physicians should only claim credit commensurate with the extent of their
participation in the activity.
ACEP Accreditation: Emergency Medicine Practice is approved by the American
College of Emergency Physicians for 48 hours of ACEP Category 1 credit per
annual subscription.
AAFP Accreditation: Emergency Medicine Practice has been reviewed and is
acceptable for up to 48 Prescribed credits per year by the American Academy of
Family Physicians. AAFP Accreditation begins August 1, 2008. Term of approval
is for two years from this date. Each issue is approved for 4 Prescribed credits.
Credits may be claimed for two years from the date of this issue.
AOA Accreditation: Emergency Medicine Practice has been approved for 48
Category 2B credit hours per year by the American Osteopathic Association.
Needs Assessment: The need for this educational activity was determined by a
survey of medical staff, including the editorial board of this publication; review
of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and
evaluation of prior activities for emergency physicians.
Target Audience: This enduring material is designed for emergency medicine
physicians, physician assistants, nurse practitioners, and residents.
Goals & Objectives: Upon completion of this article, you should be able to: (1)
demonstrate medical decision-making based on the strongest clinical evidence;
(2) cost-effectively diagnose and treat the most critical ED presentations; and (3)
describe the most common medicolegal pitfalls for each topic covered.
Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that is
outside Food and Drug Administration-approved labeling. Information presented
as part of this activity is intended solely as continuing medical education and is
not intended to promote off-label use of any pharmaceutical product. Disclosure
of Off-Label Usage: This issue of Emergency Medicine Practice discusses no
off-label use of any pharmaceutical product.
Faculty Disclosure: It is the policy of Mount Sinai School of Medicine to ensure
objectivity, balance, independence, transparency, and scientific rigor in all
CME-sponsored educational activities. All faculty participating in the planning
or implementation of a sponsored activity are expected to disclose to the
audience any relevant financial relationships and to assist in resolving any conflict
of interest that may arise from the relationship. Presenters must also make
a meaningful disclosure to the audience of their discussions of unlabeled or
unapproved drugs or devices.
In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty
for this CME activity were asked to complete a full disclosure statement. The
information received is as follows: Dr. White, Dr. DeGiorgi, Dr. DeBlieux, and
Dr. Weingart report no significant financial interest or other relationship
with the manufacturer(s) of any commercial product(s) discussed in this
educational presentation. Dr. Murphy is a shareholder in The Airway Site.
Method of Participation:
Print Subscription Semester Program: Paid subscribers who read all CME
articles during each Emergency Medicine Practice six-month testing period,
complete the post-test and the CME Evaluation Form distributed with the June
and December issues, and return it according to the published instructions are
eligible for up to 4 hours of CME credit for each issue. You must complete both
the post test and CME Evaluation Form to receive credit. Results will be kept
confidential. CME certificates will be delivered to each participant scoring higher
than 70%.
Online Single-Issue Program: Current, paid subscribers who read this
Emergency Medicine Practice CME article and complete the online post-test
and CME Evaluation Form at ebmedicine.net are eligible for up to 4 hours of
Category 1 credit toward the AMA Physicians Recognition Award (PRA). You
must complete both the post-test and CME Evaluation Form to receive credit.
Results will be kept confidential. CME certificates may be printed directly from
the website to each participant scoring higher than 70%.
Hardware/Software Requirements: You will need a Macintosh or PC to access the
online archived articles and CME testing. Adobe Reader is required to view the
PDFs of the archived articles. Adobe Reader is available as a free download at
www.adobe.com.
Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.

CEO: Robert Williford
President and Publisher: Stephanie Williford Associate Editor & CME Director: Jennifer Pai
Director of Member Services: Liz Alvarez
Direct all editorial, subscription-related,

customer service, or copyright/reprint questions to:
EB Medicine
1-800-249-5770
Outside the U.S.: 1-678-366-7933
Fax: 1-770-500-1316
5550 Triangle Parkway, Suite 150
Norcross, GA 30092
E-mail: ebm@ebmedicine.net
Web Site: ebmedicine.net
Subscription Information:
1 year (12 issues) including evidence-based print issues, 48
AMA/ACEP Category 1, AAFP Prescribed, or AOA Category 2B
CME credits, and full online access to searchable archives and
additional CME: $329
1 year institutional/hospital/library rate: $899
Individual issues, including 4 CME credits: $30
(Call 1-800-249-5770 or go to www.empractice.com to order)
Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and
is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions.
The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright 2008 EB
Practice, LLC. All rights reserved. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. This publication is intended for the use of the
individual subscriber only, and may not be copied in whole or part or redistributed in any way without the publishers prior written permissionincluding reproduction for educational purposes
or for internal distribution within your hospital, library, group practice, or other entity.
20

Ventilator Management Asthma, COPD, and Pulmonary Edema

Diunggah oleh

Informasi Dokumen

Judul Asli

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Ventilator Management Asthma, COPD, and Pulmonary Edema

Diunggah oleh

Hak Cipta:

Format Tersedia

Ventilator Management: Maximizing

Outcomes In Caring For Asthma,

Volume 10, Number 8

Michael A. Gibbs, MD, FACEP

Charles V. Pollack, Jr, MA, MD,

Corey M. Slovis, MD, FACP,

Jenny Walker, MD, MPH, MSW

rips her CPAP mask aside and screams, I cant

overcome the frictional forces of respiration is primarily

BC or Airway, Breathing, Circulation is a mantra

Critical Appraisal Of The Literature

Acute Pulmonary Edema

EBMedicine.net August 2008

results following the alveolar consolidation (alveolar

management of acute respiratory distress. There are

Confalonieri et al analyzed prospective data

Non-Invasive Positive Pressure

The primary use of mechanical ventilation is to assist

August 2008 EBMedicine.net

Emergency Medicine Practice 2008

and oxygenation. Key to the successful management

Table 2. Abbreviations Associated With Mechanical Ventilation

Mode that delivers each breath with

Positive end-expiratory pressure

Constant pressure maintained at

The period from the start of

The percentage of oxygen delivered

Time constant determined by total

While this mnemonic may be simplistic, attention

The period from the start of

Males: 50 kg + 0.91 (Height in cm

Mode that delivers each breath with

Positive pressure is held in the lungs

Pressure recorded at end

The static transalveolar pressure

Number of preset mechanical

The average volume of gas entering

Volume Control (AC) (Figure 2)

Lung injury resulting from

The volume of gas inhaled or

Flow = Tidal Volume/Inspiratory Time

EBMedicine.net August 2008

the total respiratory rate. When using a volume

breathe spontaneously between mandatory breaths

Figure 3. Flow In Pressure Control Mode

INCREASE SEDATION IF SPONTANEOUS BREATHS PRESENT

Figure 5. Factors For Increasing Peak Inspiratory Pressure

With in Volume or in Resistance

Pressure Control Mode

August 2008 EBMedicine.net

VOLUME CONTROL MODE

Emergency Medicine Practice 2008

machine breathing cycle. A couple of caveats must

Adequate sedation is also necessary to determine

Positive End-Expiratory Pressure (PEEP)

Table 3. Key Features Of Ventilator Settings And Mechanics

Variable with changes

Control of peak airway

Adjust minute ventilation

Adjust FIO2 and

Adjust FIO2 and PEEP

Emergency Medicine Practice 2008

Normal compliance for a normal subject on mechanical ventilation