CASE CONFERENCES

The Clinical Physiologist

Section Editors: John Kreit, M.D., and Erik Swenson, M.D.

Can the Plateau Be Higher Than the Peak Pressure?

Hassan Sajjad1, Gregory A. Schmidt1, Roy G. Brower2, and Michael Eberlein1
1
Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa Hospitals and Clinics, Iowa City, Iowa; and 2Division of
Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland

The Clinical Challenge 40 cmH2O A) Ppeak (cmH2O)

A 30-year-old woman was admitted to B) B) 28

the medical intensive care unit with Pmean
(cmH2O) 16
multisystem organ failure, severe anion
PEEP 14
gap metabolic acidosis, and hypoxemic (cmH2O)
respiratory failure requiring intubation. RR (b/min)
100 I/min
Within 24 hours, the patient progressed to
17
severe acute respiratory distress syndrome C)
(ARDS), with an arterial oxygen pressure/ O2 (%)
fraction of inspired oxygen ratio of 70.
81
She was placed in the prone position,
and a neuromuscular blocking agent –100 Ti/Ttot 0.12
600 ml
was administered. After 48 hours, the MVe (l/min)
paralytic was stopped. Volume-control lung-
protective mechanical ventilation was 6.5
continued (tidal volume, 270 ml; respiratory VTi
382
(ml)
rate, 32; positive end-expiratory pressure VTo D) 444
[PEEP], 14 cm H2O; fraction of inspired (ml)
oxygen, 0.6; peak inspiratory pressure, 36 cm
H2O; plateau pressure, 29 cm H2O). Despite Figure 1. Ventilator screenshot during end-inspiratory hold performed immediately after peak
heavy sedation, progressive patient–ventilator inspiratory pressure was achieved. (A) Plateau pressure (39 cm H2O) exceeds the (B) peak-inspiratory
dyssynchrony developed, as manifested by pressure (28 cm H2O). The high initial inspiratory flow-rates (C) indicate strong inspiratory drive.
frequent breath stacking and auto-PEEP. This (D) Indicates expiratory tidal volume of 444 ml. This figure is a redrawn graphic of the ventilator screen
did not respond to increasing the respiratory shot; the original ventilator screenshot is available as Figure E1 in the online supplement. A continuous
video recording of a series of end-inspiratory hold maneuvers is available as Video E1.
rate or shortening the inspiratory time. To
improve patient–ventilator synchrony, H2O (Figure 1; see Video E1 in the online 2. Can the plateau pressure be higher than
pressure-support ventilation was attempted supplement). the peak pressure?
(pressure-support, 14 cm H2O; PEEP, 14 cm
H2O). The patient–ventilator interaction 3. Is there concern for patient self-inflicted
improved. However, an end-inspiratory hold Questions lung injury?
maneuver performed while the patient was
completely passive showed a plateau pressure 1. Was the inspiratory hold airway pressure [Continue onto next page for answers]
of 39 cm H2O, which was significantly higher during pressure-support ventilation an
than the peak inspiratory pressure of 28 cm accurate representation of the plateau pressure?

(Received in original form July 13, 2017; accepted in final form April 6, 2018 )
Correspondence and requests for reprints should be addressed to Michael Eberlein, M.D., Ph.D., Division of Pulmonary, Critical Care, and Occupational
Medicine, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, C 33 GH, Iowa City, IA 52242. E-mail: michael-eberlein@uiowa.edu.
This article has an online supplement, which is accessible from this issue’s table of contents at www.atsjournals.org.
Ann Am Thorac Soc Vol 15, No 6, pp 754–759, Jun 2018
Copyright © 2018 by the American Thoracic Society
DOI: 10.1513/AnnalsATS.201707-553CC
Internet address: www.atsjournals.org

754 AnnalsATS Volume 15 Number 6 | June 2018

 CASE CONFERENCES
Clinical Reasoning
We reasoned that our patient had a strong
respiratory drive and strong inspiratory
effort. This was evident from high initial
inspiratory flow rates during pressure-
support ventilation (Figure 1C) and the
increase in tidal volume from 270 ml during
volume-control ventilation to 444 ml during
pressure-support ventilation (Figure 1D).
Strong inspiratory effort leading to very
negative pleural pressures can occur in patients
with ARDS, raising the transpulmonary
pressure, tidal volume, and driving pressure.
For our patient, during volume-
control ventilation the respiratory system
compliance was calculated to be 18 ml/cm
H2O: compliance = [tidal volume]/[plateau
pressure 2 PEEP] = 270 ml/15 cm H2O =
18 ml/cm H2O.
Assuming there was no change in
respiratory compliance, a tidal volume of
444 ml during pressure-support ventilation
correlates with a driving pressure of 25 cm H2O:
driving pressure = tidal volume/compliance =
444 ml/18 ml/cm H2O = 25 cm H2O.
Adding the driving pressure of 25 cm
H 2 O to the PEEP of 14 cm H2 O would
correlate to a plateau pressure of 39 cm
H 2 O, the same as measured during the
end-inspiratory hold maneuver (Figure 2).
The distending pressure of the lung is
the transpulmonary pressure, which is the
alveolar pressure minus the pleural pressure.
In our patient, during pressure-support
ventilation, peak inspiratory pressure was
28 cm H2O; however, our patient must have
generated a pleural pressure of at least
211 cm H2O, in addition to the pressure
supplied by the ventilator, at end-inspiration
(Figure 3). Our patient had normal weight,
there was no chest wall or abdominal
restriction, and she was fully passive during
the plateau pressure measurement of 39 cm
H2O, suggesting there was an injurious
transpulmonary pressure.
Clinical Solution
Although there was better patient–ventilator
synchrony on pressure-support ventilation,
the high plateau pressure measurement
of 39 cm H2O suggested that there were
injurious transpulmonary pressures. The
patient was therefore switched back to
volume-control ventilation in an effort
to prevent likely injurious increases in
tidal volume, driving pressures, and
Case Conferences: The Clinical Physiologist
Volume
VT 444 ml
VT 270 ml
P 15 cmH2O
P 25 cmH2O
Airway
Pressure
PEEP +14 Pplat +29
PEEP +14 Pplat +39
Figure 2. Compliance curve of the respiratory system. Parameters during volume-control mechanical
ventilation are shown in green (tidal volume [VT], 270 ml; positive end-expiratory pressure [PEEP], 14 cm
H2O; plateau pressure [Pplat], 29 cm H2O; driving pressure [ΔP], 15 cm H2O). Parameters during
pressure-support mechanical ventilation are shown in red (VT , 444 ml; PEEP, 14 cm H2O; Pplat. 39 cm
H2O; driving pressure, 25 cm H2O).
transpulmonary pressure. She was positive-pressure mechanical ventilation. A
reparalyzed to prevent auto-PEEP, breath plateau pressure can be measured during
stacking, and pendelluft from her high any mode of positive pressure ventilation.
respiratory drive with very negative pleural However, measuring the plateau pressure
pressures with inspiration. Switching to can be challenging, as it requires the patient
volume-control ventilation and paralysis to be completely passive during the
allowed limiting the tidal volume at 270 ml, maneuver. If a patient is not completely
the plateau pressure at 29 cm H2O, and the passive during the end-inspiratory hold
driving pressure at 15 cm H2O to meet lung- maneuver, this measurement is unreliable.
protective ventilation targets. It can be falsely high if the patient is
actively trying to exhale into the closed
ventilator circuit or falsely low if the
Science behind the Solution patient is actively trying to inhale from the
closed ventilator circuit. This, however,
Mechanical ventilation is central in ARDS was not the case with our patient, for the
management. Lung-protective strategies following reasons:
such as volume-control ventilation with low
d Our patent was deeply sedated with
tidal volumes, higher levels of PEEP, plateau
continuous infusions of propofol,
pressure less than 30 cm H2O, and driving
lorazepam, and dexmedetomidine and
pressure less than 15 cm H2O are associated
was completely passive during the plateau
with improved survival (1).
pressure measurement.
d The plateau pressure measurement was
The Plateau Pressure
repeated several times with reproducible
The plateau pressure is measured as the
results (Video E1).
pressure at the airway opening during
d Cardiac oscillations were seen on the
an end-inspiratory pause at a no-flow
ventilator wave-form during the end-
state, where the pressures across the
inspiratory hold, which again suggests
respiratory system and the ventilator can
that patient was passive during this
equilibrate from alveoli to the ventilator
maneuver (Figure 1A, Video E1).
circuit (2). The plateau pressure reflects the
average pressure applied to airways and The ARDS network tidal volume trial (3)
alveoli at the end of inspiration during showed that a lung-protective mechanical
755
 CASE CONFERENCES

A End Expiration B Early Inspiration C End Inspiration

(Plateau pressure measurement)

PEEP +14 PEEP +14

PEEP +14 TV 444 ml
PS +14 PS +14 P +25
PIP +28 PPlateau +39

PAW +14 PAW +28 PAW +39

Flow at
No Flow 90 No Flow
L/min

PAlv PAlv
+14 PAlv +39
+14

0 –11 +4
PPleura [–4 to +4]† PPleura [–15 to –7]† PPleura [0 to +8]†

PL = PAlv – PPleura PL = PAlv – PPleura PL = PAlv – PPleura

PL = 14 – [–4 to +4]† PL = 14 – [–15 to –7]† PL = 39 – [0 to +8]†
PL = +10 to +18 PL = +21 to +29 PL = +31 to +39

Transpulmonary pressure estimates (PL)

Figure 3. Lung mechanics during (A) end expiration, (B) early inspiration, showing peak inspiratory pressure of 128 cm H2O applied by ventilator and the
patient’s respiratory effort leading to a negative pleural pressure and a high inspiratory air flow rate of 90 L/min. Lung mechanics during (C) end-inspiratory
hold maneuver (plateau pressure measurement), while the patient was fully passive, showing a plateau pressure of 139 cm H2O. †Pleural pressure estimates
as discussed in the “Science behind the Solution” section on transpulmonary pressure. ΔP = driving pressure; PAlv = alveolar pressure; PAW = pressure at the
airway opening; PEEP = positive end-expiratory pressure; PIP = peak inspiratory pressure; PL = transpulmonary pressure; PPlateau = plateau pressure; PPleura =
pleural pressure; PS = pressure support; TV = tidal volume.

ventilation approach of low tidal volume of compared with a tidal volume of 12 ml/kg less than 30 cm H2O in this trial was that the
6 ml/kg predicted body weight and limiting predicted body weight and a plateau pressure transpulmonary pressure is approximately
plateau pressure to less than 30 cm H2O limit of 50 cm H2O (Figure 4A). Part of the 30 cm H2O in a normal lung at inflation to
improved survival in patients with ARDS, rationale for limiting the plateau pressure to total lung capacity. However, a secondary

A B
1
1.0
.9
0.9
Mortality Proportion
Proportion of Patients

.8
0.8
.7
0.7
.6
0.6
.5
0.5
.4
0.4
0.3 .3
Lower tidal volumes Traditional tidal volumes .2
0.2 Survival Survival
0.1 .1
Discharge Discharge
0.0
0 20 40 60 80 100 120 140 160 180 0 20 40 60
Days after Randomization Day 1 Plateau Pressure (cm H2O)

Figure 4. (A) Probability of survival and of being discharged home and breathing without assistance during the first 180 days after randomization in patients
with acute lung injury and the acute respiratory distress syndrome. Reprinted by permission from Reference 3. (B) Association between risk of mortality and
Day 1 plateau pressure among patients enrolled in the Acute Respiratory Distress Syndrome Network tidal volume study (n = 787) (2). Reprinted from
Reference 4.

756 AnnalsATS Volume 15 Number 6 | June 2018

 CASE CONFERENCES

analysis of the trial data (4) addressed the
question “Is there a safe upper limit to
inspiratory plateau pressure in patients with
ARDS below which there is no beneficial
effect of tidal volume reduction?”. This analysis
could not identify such a safe upper limit
(Figure 4B).
The Transpulmonary Pressure
The true distending pressure of lung is the
transpulmonary pressure (2–6), which is
the pressure inside of the lung (alveolar
pressure) minus the pressure outside of the
lung (pleural pressure): transpulmonary
pressure = [alveolar pressure] 2[pleural
pressure]. Because the transpulmonary
pressure cannot be measured directly (2–6),
the plateau pressure on volume-targeted
modes or peak inspiratory pressure on
pressure-targeted modes is often used as
a surrogate. This simplification assumes
that the contribution of pleural pressure
is minimal. If the pleural pressure is
much different from normal values, the
transpulmonary pressure can be very
different from the plateau and peak
inspiratory pressures (Figures 5C–5E) (7).
In our patient with strong respiratory
drive and active inspiratory effort, the peak
inspiratory pressure on a pressure-targeted
mode of ventilation did not reflect the
transpulmonary pressure during inspiration.
We estimated that our patient generated a
pleural pressure of approximately 211 cm
H2O (estimated range, 215 to 27 cm H2O;
Figure 3B) during inspiration, in addition to
the peak inspiratory pressure of 28 cm H2O.
This was unmasked during the end-
inspiratory pause maneuver as a plateau
pressure of 39 cm H2O (Figure 3C). Our
patient had normal weight, there was no
chest wall or abdominal restriction, and she
was fully passive during the plateau pressure
measurement, suggesting that the plateau
pressure likely was an accurate measure of
the transrespiratory system pressure at end-
inspiration and suggestive of an injurious
transpulmonary pressure. From the very

A Normal spontaneously breathing B Normal anesthetized, paralyzed C Patient with stiff chest wall, on
person, at end inspiration patient on mechanical ventilati
ventilation, mechanical ventilation, at end
at end inspiration inspiration

Palv = 0 cm
m H2O Palv = 9 cm H2O Palv
alv = 30 cm H2O

Ppl = –8 cm H2O Ppl = 1 cm H2O

Ppl = 25 cm H2O

Ptp = 0 – (–8) = +8 cm H2O Ptp = 9 – 1 = +8 cm H2O Ptp = 30 – 25 = +5 cm H2O

D Trumpet player whilee playing a note th marked respiratory distress, on noninvasive

E Patient with
ventilation,, at end inspiration

Palv = 150 cm H2O Palv = 10 cm H2O

Ppl = 140 cm H2O

Ppl = –15 cm H2O

Ptp = 150 – 140 = +10 cm H2O Ptp = 10 – (–15) = +25 cm H2O

Figure 5. Intrathoracic pressures and lung stretching. Reprinted by permission from Reference 7. Palv = alveolar pressure; Ppl = pleural pressure;
Ptp = transpulmonary pressure.

Case Conferences: The Clinical Physiologist 757


severe ARDS, our patient likely had a severe
reduction in functional residual capacity
(FRC), which the PEEP of 114 cm H2O
likely restored toward a normal FRC;
however, it is unlikely that the PEEP of
114 cm H2O increased her FRC above the
normal range, as on chest X-rays with a
PEEP of 114 cm H2O she had evidence of
low lung volumes. On the basis of this
consideration, we estimate a pleural
pressure in the range of 24 to 14 cm H2O
at end-expiration (Figure 3A). With early
inspiration, we estimated her possible
pleural pressure range to be between 215
to 27 cm H2O, reflective of her significant
inspiratory effort. The pressure support of
114 cm H2O together with the significant
inspiratory effort of our patient generated
a high inspiratory airflow at 90 L/min
(Figures 1 and 3B). Our patient likely
had normal chest wall compliance of
100 ml/cm H2O, and with the added tidal
volume of 444 ml at end-inspiration, we
estimated her pleural pressure to increase
by approximately 4 cm H 2 O to an
estimated pleural pressure range of 0 to
18 cm H2O at the end of inspiration
(Figure 3C). Our patient’s pleural pressure
at the end of inspiration would have
to be 110 cm H2O or greater for the
transpulmonary pressure to be less than
30 cm H2O, which, on the basis of the
above consideration, would be unlikely.
Under these circumstances, our
patient’s transpulmonary pressure at end-
inspiration was likely injurious.
2.5
P<0.001
Multivariate Relative Risk
of Death in the Hospital
2.0
1.5
1.0
0.5
0.0
Median VT 5 10
(10th–90th percentile) —
mg/kg of predicted
body weight
6.0 (5.9–7.5)
Figure 6. Relative risk of death in the hospital versus driving pressure (DP) in the combined cohort after
multivariate adjustment. Reprinted by permission from Reference 8. VT = tidal volume.
758
The Driving Pressure
To minimize ventilator-induced lung injury,
most studies have scaled tidal volume to
predicted body weight to normalize tidal
volume to lung size. In patients with ARDS,
the decrease in the volume of lung available
for ventilation can vary from patient to
patient. The decrease in proportion of lung
available for ventilation in patients with
ARDS is reflected by lower respiratory
system compliance. Therefore, the concept
of driving pressure was developed by
normalizing tidal volume to respiratory
system compliance and using that ratio as an
index indicating the “functional” size of the
lung receiving the tidal volume (8). This
driving pressure can be routinely calculated
for patients who are not making inspiratory
efforts as the plateau pressure minus PEEP.
In an analysis of individual patient data
from nine ARDS Network studies, among
all ventilation variables, driving pressure
was most strongly associated with survival
(8). Each 7–cm H2O increase in driving
pressure was associated with a 41% increase
in mortality (relative risk, 1.41; 95%
confidence interval, 1.31–1.51; P , 0.001).
Furthermore, decreases in driving pressure
owing to changes in ventilator settings were
strongly associated with increased survival.
These data suggested that limiting driving
pressure to less than 15 cm H2O could be an
important target to improve outcomes in
patients with ARDS (Figure 6).
For our patient, during volume-control
ventilation the respiratory system
15 20 25 30 35
P (cm of water)
6.1 (5.8–9.2) 8.0 (5.7–12.1)
AnnalsATS Volume 15 Number 6 | June 2018
CASE CONFERENCES
compliance was calculated to be 18 ml/cm
H2O (Figure 2). Thus, for the tidal volume
during volume-control ventilation of 270 ml,
a driving pressure of 15 cm H2O was
needed. Assuming there was no change in
respiratory compliance, during pressure-
support ventilation for the tidal volume of
444 ml generated by the patient, a driving
pressure of 25 cm H2O is needed. Adding
this driving pressure of 25 cm H2O to the
PEEP (14 cm H2O) is 39 cm H2O, the same
as the measured plateau pressure.
Patient Self-inflicted Lung Injury
Vigorous spontaneous inspiratory efforts
can significantly lower pleural pressures
and substantially increase transpulmonary
pressures (9), which in animal models of severe
ARDS worsened existing lung injury (10).
Inspiratory and expiratory airflows in
healthy lungs are relatively uniform throughout
the bronchial tree and the lung. In a healthy
lung, the changes in pleural pressure are
transmitted equally across the lung surface,
causing homogenous expansion; this
is termed “fluid-like behavior.” In
injured lungs, however, the pleural pressure
changes are not equally distributed, causing
heterogeneous lung expansion known as
“solid-like behavior.” Under the abnormal
conditions of ARDS, the pattern of gas flow
and lung inflation can be disturbed;
inhomogeneous inflation or deflation of
the lungs can cause dynamic pressure
differences between regions, which in turn
lead to interregional airflow. This effect is
referred to as pendelluft or “swinging air,”
because gas is passed back and forth between
the different regions of the lungs. Yoshida
and colleagues reported on patients with
ARDS receiving mechanical ventilation in
whom pendelluft during early inflation was
caused by spontaneous breathing effort (11).
The transient intrapulmonary gas flow caused
inflation of dependent lung, with concomitant
deflation of nondependent lung (11).
In addition to excessive tidal volume
and transpulmonary pressure, pendelluft
points to another potential mechanism
of patient self-inflicted lung injury (11).
Clinical trials demonstrating benefit of
neuromuscular blockade in patients with
severe ARDS (12) suggest that a strategy of
avoiding spontaneous breaths could be the
mechanism by which paralysis mediates
improved clinical outcomes. In our patient,
cisatracurium was used as a paralytic.
Studies have shown that cisatracurium and
 CASE CONFERENCES

other related drugs may also act in an
antiinflammatory mode, possibly by altering
nicotinic neuronal pathways (13).
In addition to the effects on
transpulmonary pressures, spontaneous
breathing also increases the transvascular
pressure (14). This leads to distention
of thoracic aorta and pulmonary
vasculature, predisposing patients to
development of pulmonary edema. Several
studies have shown the injurious effects of
pulmonary edema in the setting of ARDS.
Answers
1. Was the inspiratory hold airway
pressure during pressure-support ventilation
an accurate representation of the plateau
pressure?
Yes. Our patient was completely passive
during the measurement, as evidenced by
reproducibility of the test and cardiac
oscillations seen on the ventilator
waveform. In addition, similar plateau
pressure value was obtained by using the
driving pressure calculation (as described
above).
2. Can the plateau pressure be higher than
the peak pressure?
Yes. In pressure-regulated modes of
ventilation, plateau pressures can be higher
than peak pressures if inspiratory efforts of
the patient generate larger tidal volumes and
significantly negative pleural pressures.
3. Is there concern for patient self-inflicted
lung injury?
Yes. Accumulating evidence suggests that
in certain patients with ARDS with high
respiratory drive, spontaneous breaths can
increase tidal volumes and transpulmonary
and driving pressures and induce pendelluft—
all of which could contribute to lung injury.
Summary
This case highlights that patients with
severe ARDS can have a significant
respiratory drive. In this circumstance, it is
important to recognize that in pressure-
regulated modes of ventilation, the peak
inspiratory pressure may not be a good
surrogate of the transpulmonary pressure. n
Author disclosures are available with the text
of this article at www.atsjournals.org.

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