Journal of Intensive Care Medicine

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Hemodynamic Consequences of Auto-PEEP

David Berlin
J Intensive Care Med published online 15 May 2012
DOI: 10.1177/0885066612445712

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 Journal of Intensive Care Medicine
00(0) 1-6
Hemodynamic Consequences of ª The Author(s) 2012
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Auto-PEEP DOI: 10.1177/0885066612445712
http://jicm.sagepub.com

David Berlin, MD1

Abstract
Auto–positive end-expiratory pressure (PEEP) is a common but frequently unrecognized problem in critically ill patients. It has
important physiologic consequences and can cause shock and cardiac arrest. Treatment consists of relieving expiratory airflow
obstruction and reducing minute ventilation delivered by positive pressure ventilation. Sedation and fluid management are impor-
tant adjunctive therapies. This analytic review discusses the prevalence, pathophysiology, and hemodynamic consequences of
auto-PEEP and an approach to its treatment.

Keywords
Auto–positive end-expiratory pressure, dynamic hyperinflation, shock, mechanical ventilation

Received November 3, 2011, and in revised November 29, 2011. Accepted December 13, 2011.

Positive end-expiratory pressure (PEEP) is the distention of the
lungs with air above atmospheric pressure prior to the onset of
inspiration. Clinicians can intentionally apply extrinsic PEEP
with mechanical ventilation. This is a positive pressure target
the ventilator maintains in the airway circuit during exhalation.
PEEP can also arise as an intrinsic consequence of a patient’s
ventilatory pattern. Pepe and Marini coined the term auto-
PEEP in 1982 to describe this phenomenon.1 Extrinsic PEEP
is a therapy set by a clinician on a ventilator. Auto-PEEP is
unintentional. It can occur in people with expiratory airflow
obstruction who are breathing without the assistance of
mechanical ventilation but is more commonly associated with
positive pressure ventilation.2 By convention, auto-PEEP is
defined as the magnitude of the end-expiratory pressure in
excess of the set extrinsic PEEP. High minute ventilation and
expiratory airflow obstruction are the most important risk fac-
tors for the development of auto-PEEP. Intrinsic and extrinsic
PEEP have similar effects on respiratory mechanics, gas
exchange, and hemodynamics.3 Auto-PEEP is a common cause
of dyspnea, patient–ventilator dysynchrony, and the inability to
trigger mechanical ventilation.4 Since its first description, auto-
PEEP is increasingly recognized as an important but treatable
cause of shock and cardiac arrest.1,5-12
postmortem examination cannot detect its presence.8 There are
a few reports of its prevalence in specific critically ill populations.
In one series, 47% of patients on mechanical ventilation had evi-
dence of at least minimal auto-PEEP.13 In another series, it was
observed in the majority of critically ill patients on mechanical
ventilation. All the patients in this series with chronic obstructive
pulmonary disease had auto-PEEP.14 In a series of patients with
the acute respiratory distress syndrome (ARDS), most of whom
had stable hemodynamics and high levels of extrinsic PEEP, there
was a low prevalence of auto-PEEP,15 while others have noted a
higher prevalence.16 Since it is defined as the excess pressure
above the set PEEP, the prevalence of auto-PEEP will be lower
with ventilatory strategies that use high levels of extrinsic
PEEP.17 Prone ventilation may reduce the prevalence of auto-
PEEP in ARDS.18 Trauma is a major risk factor for developing
auto-PEEP, likely due to hyperventilation from metabolic acido-
sis and shock.13,19 Hyperventilation during cardiopulmonary
resuscitation (CPR) is another common cause.20,21
Pathophysiology of Auto-PEEP
One form of auto-PEEP is caused by activation of the muscles
of exhalation. Normal exhalation during unassisted breathing

Prevalence of Auto-PEEP 1
Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical
The prevalence of auto-PEEP is unknown and is likely more com- College, New York, NY, USA
mon than realized. There are no clear diagnostic criteria and the
Corresponding Author:
threshold for the magnitude of auto-PEEP that has significant car- David Berlin, Weill Cornell Medical College, 1300 York Avenue, New York,
diorespiratory effects varies with different clinical situations. NY 10023, USA
Even when auto-PEEP is the immediate cause of death, Email: berlind@med.cornell.edu

Downloaded from jic.sagepub.com at BROWN UNIVERSITY on October 24, 2012

2 Journal of Intensive Care Medicine 00(0)
or positive pressure ventilation is accomplished by passive
elastic recoil of the lungs. A patient may use muscles of exha-
lation to enhance intrathoracic pressure to accelerate expiratory
airflow. This may occur when tidal volumes are large or there is
expiratory airflow limitation due to bronchospasm or obstruc-
tion of the ventilator circuit.22 Patient effort raises pleural pres-
sure, but not the transpulmonary gradient, which limits the
physiologic consequences of auto-PEEP.4,23
The more important cause of auto-PEEP is dynamic hyper-
inflation. Also called breath stacking, it occurs when a patient
inhales successive tidal volumes despite incomplete exhala-
tion. Progressively larger volumes of air become trapped in the
lungs. This commonly occurs when there is insufficient time
for completion of expiratory flow due to rapid respiratory rates,
large inflation volumes, and short expiratory times.24 Expira-
tory airflow limitation exacerbates dynamic hyperinflation, and
it commonly complicates mechanical ventilation in patients
with asthma and chronic obstructive pulmonary disease.
Dynamic hyperinflation can occur with any mode of mechani-
cal ventilation although theoretically it is more likely to occur
with strategies that intentionally limit expiratory time such as
inverse ratio and airway pressure release ventilation. It can
occur when the patient or the ventilator initiates the breaths
or during manual mask bag ventilation. Since inadequate time
for expiratory flow contributes to dynamic hyperinflation,
auto-PEEP is common whenever there is increased minute ven-
tilation. Examples of clinical scenarios include metabolic
acidosis and large alveolar dead-space fraction.14
Auto-PEEP may create dysynchrony by impeding a
patient’s ability to trigger mechanical ventilation. The patient
must generate sufficient negative inspiratory force to overcome
the auto-PEEP.4 Improved synchronization with inspiratory
efforts may paradoxically worsen dynamic hyperinflation in
patients with a powerful respiratory drive. This is a potential
limitation of increasing the trigger sensitivity or using neural
adjusted ventilation.
Dynamic hyperinflation results in lung recruitment and ele-
vation of end-expiratory lung volumes. Exhaled tidal volumes
may fall in the presence of dynamic hyperinflation, as there is
insufficient time for exhalation. The hyperinflation can alter
lung compliance as well as airway caliber. The transpulmonary
expiratory pressure rises with increasing end-expiratory lung
volumes. During volume-targeted ventilation, dynamic hyperin-
flation can elevate the plateau pressure. In pressure-targeted
modes, the delivered tidal volume may fall in the presence of
auto-PEEP.14,25
Diagnosis of Auto-PEEP
Auto-PEEP is also called occult PEEP because it is difficult to
diagnose.1 Careful examination, however, can detect its pres-
ence. Auscultation may reveal the persistence of expiratory
flow up to the onset of cycling over to inspiration.26 Activation
of the muscles of exhalation is found by palpating the transver-
sus abdominus.27 The presence of dynamic hyperinflation can
be identified by observation of the flow–time curve on
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Figure 1. Flow–time curves from a patient on mechanical ventilation.
There is a normal decay in expiratory flow to zero prior to the onset
of the second breath. The second exhalation is incomplete due to
rapid cycling to inspiration resulting in dynamic hyperinflation.
ventilator graphics. Ventilators typically display inspiratory
flow as a positive deflection and expiratory flow as a negative
deflection with zero flow as the x-axis. In the normal situation,
there is a pause at end exhalation during which there is no fur-
ther expiratory flow. This is seen as zero flow on the flow–time
curve. In the presence of dynamic hyperinflation, however, the
ventilator graphics will demonstrate the rapid onset of inspira-
tory flow prior to the expiratory flow curve returning to the
x-axis. This generates a vertical line rising up from the negative
(expiratory) portion of the flow–time curve (Figure 1).28 The
ventilator may display exhaled tidal volumes that are less than
expected due to dynamic hyperinflation and air trapping.4
The aforementioned maneuvers demonstrate the presence
but not the magnitude of auto-PEEP. The airway pressure most
ventilators display reflects the pressure at the interface between
the ventilator and the tubing of the ventilator circuit (ie, the air-
way opening). The pressure displayed on ventilator graphics,
therefore, will not reflect the intra-alveolar pressure unless
there is equilibration of pressure between the distal airways and
the ventilator circuit. For equilibration to occur there must be
sufficient expiratory time and no significant obstruction to air-
flow between distal airways and the ventilator. Performing a
pause maneuver at end expiration will prevent cycling over
to inspiration for a short duration (typically <1 second) and
allow the pressure to better equilibrate between alveoli and
ventilator circuit tubing. During an expiratory pause, the venti-
lator displays a pressure that better approximates the actual
PEEP. The amount of pressure above the set extrinsic PEEP
is the auto-PEEP.25,28 Accurate measurement of auto-PEEP
requires passive ventilation without significant patient effort.
For an individual patient, the presence and magnitude of
auto-PEEP will vary over time as the respiratory pattern
changes.29
Auto-PEEP may be difficult to detect by analysis of ventila-
tor graphics if there is significant airway closure and the
obstructed airways do not equilibrate with the airway opening.
Heterogeneous airflow obstruction can lead to slower emptying
from certain lung units and localized areas of dynamic hyper-
inflation that are difficult to detect. This phenomenon is
Berlin
common in asthma and obesity but also occurs in ARDS, par-
ticularly in the recumbent position.4,30,31
Presently, there are no reliable automated diagnostic sys-
tems to detect the presence of auto-PEEP. Research techniques
such as esophageal balloon manometry may not provide useful
clinical information.4 Physical examination and evaluation of
ventilator graphics are the cornerstones of diagnosis. If auto-
PEEP is present, the clinician should determine whether there
is expiratory airflow limitation due to bronchospasm or
obstruction of the ventilator circuit.
Auto-PEEP as a Cause of Shock
The cardiovascular effects of PEEP are similar whether it is
extrinsic or intrinsically generated.3 These effects have been
known for more than 60 years.32 PEEP can decrease left ventri-
cular afterload; the wall tension required to eject blood into the
extrathoracic arteries.33,34 Lung hyperinflation by positive
pressure may also cause bradycardia and vasodilation via auto-
nomic reflexes.35,36
PEEP exerts its most powerful hemodynamic effects on the
right side of the circulation. Normally, venous return to the
heart is driven by the pressure gradient between the systemic
veins (estimated by mean systemic filling pressure) and the
right atrium. The total venous return to the right heart is the
same as the cardiac output. PEEP increases the juxtacardiac
right atrial pressure and decreases the gradient for venous
return and the cardiac output.37 Studies using transesophageal
echocardiography demonstrate that positive airway pressure
can create a barrier to venous return by causing mechanical
compression and obstruction of the intrathoracic portion of the
superior vena cava.38 In a study of postoperative patients, a
central venous pressure of less than 10 mm Hg always resulted
in a fall in stroke volume and systemic hypotension after treat-
ment with 10 cm H2O continuous positive airway pressure.39
The effects of positive pressure on impedance to venous return
are attenuated by volume expansion which distends the venous
capacitance vessels and transmission of the positive pressure to
the blood reservoir in the mesenteric venous system.40
Excessive PEEP can also precipitate acute right ventricular
failure by hyperinflation of the lungs.41 The thin-walled right
ventricle must eject the entire cardiac output into the pulmonary
circulation. This system depends on low pulmonary vascular
resistance (PVR). Excessive PEEP will increase end-expiratory
lung volume. In the presence of hyperinflation, PVR rises dra-
matically.23 This may be especially important when there is
focal lung disease that diverts airflow into more compliant lung
regions causing progressive hyperinflation. The right ventricle
has a limited capacity to compensate for acute elevation in PVR.
As a result, the right ventricular pressure rises dramatically,
reducing the perfusion gradient for right coronary blood flow
leading to right ventricular ischemia. As cardiac output falls, sys-
temic hypotension worsens right ventricular ischemia.42
Through the phenomenon of interventricular dependence, eleva-
tion of right ventricular pressure impairs left ventricular filling
further reducing cardiac output.43 In short, elevation of PVR
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3
Hemodynamic Instability
from Auto-PEEP
Treat Dynamic Hyperinflation Support Circulation
Relieve airflow
Right ventricular
overload?
obstruction
No Yes
Decrease respiratory rate
and delivered tidal volume Fluid
Prolong time for exhalation
resuscitation
Suppress spontaneous respiratory drive Consider vasopressors
Consider trial of apnea or
disconnecting ventilator
circuit
Figure 2. Treatment of hemodynamic instability due to auto–positive
end-expiratory pressure.
by hyperinflation can unleash a vicious cycle of right ventricular
failure. Importantly, volume loading will be deleterious in this
scenario as blood dams up in the failing right ventricle which
is unable to eject its large preload into the high resistance pul-
monary circuit.23,44
The hemodynamic effects of positive pressure ventilation
are cyclical and more pronounced when airway pressures are
highest during inspiration. Since expiratory times are gener-
ally longer than inspiration, low expiratory pressures preserve
cardiac output.32 However, in the presence of significant
auto-PEEP, the hemodynamic consequences of positive pres-
sure ventilation will persist throughout the entire respiratory
cycle.23
The hemodynamic effects of auto-PEEP may be profound.
Shock and cardiac arrest may occur. It is likely that occult
auto-PEEP is a common cause of pulseless electrical activity
in patients treated with positive pressure ventilation.8 It is an
explanation for the unexpectedly high mortality rate of patients
with status asthmaticus treated with mechanical ventilation.45
However, the true incidence of death due to auto-PEEP is
unknown. Auto-PEEP during CPR can prevent return of spon-
taneous circulation.20
Treatment
There are highly effective therapies for auto-PEEP (Figure 2).
The general principle is to allow more complete exhalation.
The first step is to relieve bronchospasm or obstruction of the
ventilator circuit.14 Dynamic hyperinflation will improve with
a reduction of inspired tidal volume or prolongation of the time
available for exhalation. If the patient is being passively venti-
lated, the clinician can reduce the targeted volume or inspira-
tory pressure.46,47
With most modes of mechanical ventilation, decreasing the
set respiratory rate will prolong total expiratory time. If the
patient is undergoing mandatory ventilation, the clinician can
decrease the set ventilator frequency. If the patient is sponta-
neously triggering the ventilator breaths, opiates (which
decrease air hunger) can suppress the respiratory drive.
4 Journal of Intensive Care Medicine 00(0)
Sedation and, ultimately, neuromuscular blockade can also
prevent the patient from triggering the ventilator and help
reduce delivered minute ventilation.14,48 Other measures to
decrease minute ventilation such as avoiding over-feeding,
correcting metabolic acidosis, and suppressing fever should
theoretically reduce auto-PEEP.14,45 To avoid dynamic hyper-
inflation during CPR, the clinician should provide 2 breaths for
every 30 compressions and 8 to 10 breaths/min after endotra-
cheal intubation.21,49,50
The clinician can directly set a longer expiratory time using
pressure-targeted time-cycled ventilation (pressure control).
With ventilator modes that cycle to exhalation after delivering
a targeted volume, setting a higher peak inspiratory flow rate or
square wave inspiratory flow pattern will shorten inspiratory
time. Reducing set tidal volume will also allow more time for
exhalation to reduce dynamic hyperinflation.14 However,
reducing a tidal volume low enough to generate a rapid shallow
breathing pattern can also produce auto-PEEP.51 On pressure-
targeted flow-cycled ventilation (pressure support), increasing
expiratory flow sensitivity will facilitate early cycling over to
exhalation.52 Matching the auto-PEEP by increasing the set
extrinsic PEEP may decrease the patient work required to trig-
ger the ventilator. Since this maneuver has little effect on the
total amount of PEEP, however, it has insignificant cardiovas-
cular effects.53-55 There is a theoretical benefit of adding a low
level of extrinsic PEEP even in the presence of dynamic hyper-
inflation if there is heterogeneous airflow obstruction in ARDS.
In this scenario, extrinsic PEEP can stent open slower emptying
lung units to limit focal dynamic hyperinflation and improve
impedance to right ventricular outflow.31 Switching to high fre-
quency jet ventilation appears to have no benefit for patients
with auto-PEEP.56
If the patient is in shock or cardiac arrest due to auto-PEEP,
the clinician should consider a brief trial of apnea or temporar-
ily disconnect the endotracheal or tracheostomy tube from the
ventilator circuit to allow more complete exhalation.8,9,57
Obviously, the fraction of inspired oxygen will fall during the
maneuver. However, there are multiple reports of full circula-
tory arrest spontaneously reversing by detaching the patient
from the ventilator circuit. This has been called the ‘‘Lazarus
effect’’ and is thought to be a mechanism of ‘‘auto-resuscita-
tion.’’ In 1 case, a young woman with status asthmaticus had
cardiac arrest each time the positive pressure ventilation was
resumed and auto-resuscitated each time her physicians
detached her from the circuit to allow declaration of death.11
If severe consequences of auto-PEEP develop, the clinician
may need to limit the patient’s minute ventilation and permit
hypercapnia. This may be particularly important in cases of sta-
tus asthmaticus.47 Since both hypercapnia and dynamic hyper-
inflation can raise PVR, the clinician must monitor the
hemodynamic consequences of changing minute ventilation.58
Even if the ventilator changes relieve auto-PEEP, the hemody-
namic instability will persist if the extrinsic PEEP is set too
high. Moreover, a prolonged and high-pressure inspiratory
phase may limit the hemodynamic benefit of reducing auto-
PEEP.
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If shock from auto-PEEP persists, the clinician should
consider adjunctive fluid management. If auto-PEEP impairs
venous return, fluid resuscitation may help restore the pressure
gradient and recruit stroke volume via the Starling mechan-
ism.40 Fluids may be deleterious, however, if auto-PEEP con-
tributes to right ventricular failure by increasing PVR.44
Diagnostic studies may help to determine whether or not fluid
resuscitation will be beneficial. Unfortunately, significant auto-
PEEP may impair accurate measurement of pulmonary artery
occlusion pressure since airway pressure may exceed pulmon-
ary venous pressure.23 In general, static measures of cardiac
filling pressures are poor predictors of whether fluid resuscita-
tion will recruit stroke volume. Variability of stroke volume or
pulse pressure induced by the positive pressure respiratory
cycle can predict the response to fluid resuscitation.59 The pres-
ence of significant auto-PEEP, however, may affect the
results of these dynamic tests. The tests rely on the cyclic
decline of left ventricular stroke volume following an
inspiratory decline in right-sided venous return. High
expiratory pressure, especially when accompanied by rela-
tively small tidal volumes, diminishes the stroke volume
variability during the cardiac cycle. High respiratory rates
commonly associated with auto-PEEP also limit the respira-
tory variability of stroke volume. Therefore, the false nega-
tive rate of the pulse pressure and stroke volume variability
tests are likely higher in the presence of auto-PEEP.60,61
Stroke volume variability with the respiratory cycle, more-
over, will not reliably predict fluid responsiveness in the
presence of right ventricular failure.62 Auto-PEEP can pre-
cipitate acute right heart failure and create false positive
results of the dynamic tests. All tests of fluid responsiveness
that assess the cyclical circulatory effects of passive positive
pressure ventilation, including inferior vena cava variability,
are also invalid when there is a strong spontaneous ventila-
tory drive.59
Auto-PEEP does not limit the echocardiographic prediction
of the right ventricular response to fluid resuscitation. If the
right ventricle is markedly dilated with flattening of intraven-
tricular septum and dilation of the inferior vena cava, further
fluid resuscitation will not improve stroke volume.43 Auto-
PEEP is also unlikely to affect the ability of a passive leg raise
study to predict stroke volume response to a fluid bolus. Diag-
nostic passive leg raise has been validated in multiple settings
including high inflation pressures.63,64
Exogenous catecholamines may be useful to support a circu-
lation failing from auto-PEEP. Alpha-receptor-mediated veno-
constriction may mobilize blood from venous capacitance
vessels and increase cardiac output from augmented venous
return. In the setting of right ventricular failure from auto-
PEEP-induced elevation of PVR, catecholamine vasopressors
can augment systemic arterial pressure to restore the perfusion
gradient to the right ventricle and augment its contractility.42,44
There is currently no automated diagnostic testing that can
reliably diagnose and manage significant auto-PEEP. Only the
presence of a trained clinician can mitigate the severe hemody-
namic consequences of this common problem.
Berlin
Declaration of Conflicting Interests
The author declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author received no financial support for the research, authorship,
and/or publication of this article
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