[ Contemporary Reviews in Critical Care Medicine ]

Low Tidal Volumes for Everyone?

Craig R. Rackley, MD; and Neil R. MacIntyre, MD

Since the first description of mechanical ventilation, our understanding of the positive and
negative effects of this form of life support has continued to evolve. To maintain “normal”
aeration of the lungs and “normal” blood gas measurements, patients often require much
higher airway pressures and tidal volumes than would be expected in a healthy, spontaneously
breathing adult. In the early days of mechanical ventilation, the goal was to normalize the blood
gas levels, but over the last several decades, we have developed a much better appreciation for
the deleterious effects of mechanical ventilation. We have found that lower tidal volumes, which
may actually worsen oxygenation and reduce clearance of CO2, can decrease the level of harm
caused by mechanical ventilation. This scenario is best described and agreed upon in the setting
of ARDS, but a growing body of evidence suggests that the use of higher tidal volumes is
harmful in patients with normal lungs undergoing general anesthesia or in patients with lung
diseases other than ARDS requiring mechanical ventilation. Finally, the concept of self-induced
lung injury has emerged as a mechanism through which patients generating large negative
intrathoracic pressures to achieve larger tidal volumes can contribute to worsened lung injury.
Given a growing supportive evidence base, we suggest that efforts be made to achieve low tidal
volume ventilation in all patients with lung injury or undergoing mechanical ventilation for any
reason. CHEST 2019; 156(4):783-791

KEY WORDS: ARDS; low tidal volumes; lung-protective ventilation; ventilator-induced lung injury

The goal of positive pressure ventilation
(PPV) is to safely provide adequate alveolar
ventilation for life support. Current
approaches to delivering PPV are generally
patterned after the normal breathing pattern
in which tidal volume (VT) values are
delivered at a certain respiratory rate.
Historically, however, VT settings were often
two or more times normal in an effort to
eliminate atelectasis and/or increase minute
ventilation to overcome effects of disease-
induced dead space, impaired ventilation-
perfusion matching, and shunting. In the last
decade of the 20th century, it became
increasingly apparent that excessive VT
settings had the potential to produce
significant lung injury. Beginning with a
focus on ARDS, a number of clinical trials
(described in detail later in this article) have
clearly shown that VT settings in the
physiologic range (6-8 mL/kg predicted body
weight [PBW]) produced significantly better
outcomes than VT settings twice that size.
This notion of “protecting” the lung (and
sometimes accepting worsened gas exchange
in trade-off) has now spread to other lung

ABBREVIATIONS: HFNC = high-flow nasal cannula; NIV = noninva-
sive ventilation; PBW = predicted body weight; PEEP = positive
end-expiratory pressure; PPV = positive pressure ventilation; SILI = self-
induced lung injury; VILI = ventilator-induced lung injury; VT = tidal
volume
AFFILIATIONS: From the Department of Medicine, Division of Pul-
monary, Allergy, and Critical Care Medicine, Duke University Medical
Center, Durham, NC.
CORRESPONDENCE TO: Craig R. Rackley, MD, Division of Pulmonary,
Allergy, and Critical Care Medicine, Box 102355, Duke University
Medical Center, Durham, NC 27710; e-mail: craig.rackley@duke.edu
Copyright Ó 2019 American College of Chest Physicians. Published by
Elsevier Inc. All rights reserved.
DOI: https://doi.org/10.1016/j.chest.2019.06.007

chestjournal.org 783
diseases and even to normal lungs (eg, anesthetized
patients). The current review explores the hypothesis
that a physiologic VT value is the best approach for
virtually anyone receiving PPV.
Evolution of PPV and VT Settings: Early
Concepts
Andreas Vesalius was one of the first to describe
artificial ventilation in 1543 when he reported the use of
a “tube or reed of cane” being inserted directly into the
trachea that could be blown into, thus allowing the lungs
to “rise again and take air.”1 Despite this early
description of PPV, no significant progress was made in
mechanical ventilation until the mid-1800s, when
negative pressure ventilation was described.2 The first
widespread use of mechanical ventilation was with the
negative pressure “iron lung” during the polio epidemics
beginning in 1928.3
Positive pressure ventilators were first used in the early
1900s as noninvasive devices (Pulmotor; Draeger) for
short-term rescue use for gas poisoning in coal miners.4
However, it was not until the 1940s and 1950s that
invasive PPV became widely available, and it largely
replaced negative pressure ventilation by the 1960s for
supporting patients with respiratory failure.5
The goals of early PPV were to mimic the normal
human respiratory pattern and restore near-normal gas
exchange. This goal required the development of
accurate blood gas analyzers6,7 and characterization of
normal human lung volumes and breathing patterns.
The clear relation of vital capacity to height was first
thoroughly described through experiments performed
by Hutchinson in 1846.8 However, it was another
century before resting VT values were measured by
Needham et al9 and first reported in 1954 to be 9.7 mL/
kg PBW for adult men and 10.5 mL/kg PBW in adult
women. In subsequent years, derivation nomograms
based on CO2 production predicted the basal VT value
for an adult breathing 12 to 18 breaths/minute to be w6
to 8 mL/kg.10 In 1967, Stahl11 showed, through
prediction models, that VT values were highly correlated
to body weight across different mammalian species
ranging in size from rat to man with an average of
7.69 mL/kg.
By the mid-20th century, much of the literature on the
management of PPV was originating from the operating
room.12 It was clear at the time that anesthetized,
paralyzed patients were prone to atelectasis and
hypoxemia. Although positive end-expiratory pressure
784 Contemporary Reviews in Critical Care Medicine
(PEEP) could ameliorate this situation, hemodynamic
concerns limited its use. As a consequence, anesthesia
recommendations in the mid-20th century were to
minimize PEEP and ventilate patients undergoing
general anesthesia with VT values of 10 to 15 mL/kg
PBW, often with “sigh” breaths.13
As ICUs were developed, operating room PPV strategies
were transferred into these units to manage a variety of
patients with respiratory failure.13,14 Accordingly, from
the early 1970s to the 1990s, it was recommended to
apply these same larger VT values using the justification
that this had been done in “several thousand ventilated
patients with no evidence of development of pulmonary
damage.”13
The Paradigm Shift: From “Normalizing”
Blood Gases to Lung Protection
From the infancy of artificial respiration methods, it was
clear that providing indiscriminate VT settings could be
harmful. In 1744, John Fothergill15 expressed concern
that using fireplace bellows to support respiration could
be harmful and recommended mouth-to-mouth support
instead to assure that the delivered volume of a breath
would not exceed that of the rescuer. In 1829, Leroy of
Paris noted that “bellows in the hands of an ignorant
person might become a lethal weapon.”16 As part of the
early research of Hutchinson8 measuring lung volumes
(noted earlier), he showed that applying increasing
volume through bellows led to extreme leakage of air
from the lungs (pneumothorax).
In 1987, Kolobow et al17 found that ventilating normal
sheep at VT settings of 50 to 70 mL/kg led to rapid
deterioration and death from severe lung injury, whereas
those ventilated at 10 mL/kg remained stable. This high
VT setting actually approximated a normal inspiratory
capacity and produced an end-inspiratory lung volume
equivalent to total lung capacity. Although it may seem
absurd to use such high VT settings given modern
practice, the potential for harm from this value was
certainly not clear at the time. In later studies involving
normal sheep (described later in more detail),
Mascheroni et al18 also reported that VT settings only
slightly larger than normal (9-15 mL/kg PBW) led to
severe lung injury relative to VT settings approximating
normal resting VT.
In an elegant group of studies, Dreyfuss et al19 clearly
showed that it was the volume change and not the
applied pressure that caused the lung injury. Animals
subjected to high airway pressures and normal chest wall
[ 156#4 CHEST OCTOBER 2019 ]
mechanics developed high VT values and severe injury.
In contrast, control animals had chest wall strapping
that prevented excessive VT values despite similar high
airway pressures, and they experienced no injury. These
observations led to the concepts of stress and strain with
PPV.20 Stress is the pressure applied to alveolar
structures (ie, transpulmonary pressure), and strain is
the resulting stretch or volume change. Ventilator-
induced lung injury (VILI) was now believed to be a
consequence of both excessive dynamic strain (VT) and
excessive static strain (end-inspiratory lung volume).
Research has also implicated acceleration forces,
respiratory frequency, inadequate expiratory pressure
(PEEP), and vascular factors in promulgating this
injury.21-23 In addition, VILI is associated with cytokine
production that can produce systemic inflammation and
multiorgan dysfunction (biotrauma).24 These concepts
have driven a paradigm shift in management
recommendations away from “normalizing” blood gas
measurements to lung-protective ventilation.
The Patient With ARDS
Much of the literature focusing on lung-protective
ventilation strategies in humans has come from studies
on ARDS. ARDS is characterized by the acute onset of
tachypnea, hypoxia, and loss of lung compliance and
was first described in adults in 1967.25 Interestingly, this
initial description commented on the apparent benefit of
PEEP; however, there was no discussion of the VT values
these patients were receiving, which ranged from 167 to
1,000 mL.
Over the next 2 decades, recommendations from various
professional groups and clinical trial consortiums
addressing sepsis and ARDS continued to recommend
large VT settings (Fig 1).26 However, as noted earlier,
over this same time, the experimental evidence in
animals with acute lung injury/ARDS was emerging
showing the deleterious effects of high inspiratory
pressures and large VT values. Thus, by the early 1990s,
there was a growing body of evidence to support the
hypothesis that limiting end-inspiratory plateau
pressures (a surrogate for end-inspiratory
transpulmonary pressure in the setting of near-normal
chest wall mechanics), reducing lung overdistention by
using VT settings, and allowing “permissive”
hypercapnia reduces VILI and improves outcomes in
severe ARDS.27-29
In 1998, Amato et al30 published a small, randomized
trial showing a significant survival benefit to ventilating
with VT values of 6 mL/kg vs 12 mL/kg in patients with
chestjournal.org
16
14
Tidal Volume (mL/kg PBW)
12
10
8
6
4
2
0
1989 1992 1994 1995 1996 1996 1996
Year Study Began
Figure 1 – Tidal volume settings during the 1990s. This graph illustrates
that tidal volumes used during several large clinical trials that began
during the late 1980s through the 1990s ranged from 10.3 to 13.7 mL/kg
PBW (shaded area). PBW ¼ predicted body weight. (Data from
Thompson et al.26)
ARDS. In contrast, several other small trials evaluating
VT strategies with less VT separation showed no
significant benefits.31-33 In 2000, the landmark National
Institutes of Health ARDS Network randomized trial of
861 patients with ARDS was reported; it compared
ventilation with 6 mL/kg PBW and a plateau pressure <
30 cm H2O as opposed to 12 mL/kg PBW and a plateau
pressure < 40 cm H2O. In this trial, the lower VT
group had a 9% absolute reduction in mortality.34
Importantly, it seemed that it was both high VT values
and high end-inspiratory plateau pressures that drove
the increased mortality.35
ARDS was originally viewed through the lens of the chest
radiograph and was believed to be a relatively
homogeneous disease characterized by uniform damage to
the alveolar capillary membrane causing the lungs to
become heavy and stiff. However, by the mid-1980s, CT
scans were able to better characterize the distribution of
injury and showed patchy infiltrates, worse in dependent
lung zones, interspersed with areas of normal-appearing
lung.36 This brought about the concept of the “baby lung”
in which, radiographically, the aerated portion of lung in
a patient with severe ARDS is similar in volume to that of a
5- to 6-year-old child.37 This finding, in turn, led to the
notion that VILI was a regional phenomenon wherein the
delivered positive pressure breath preferentially went to
healthier regions. A “normal” global VT value could thus
produce excessive regional VT values with excessive
regional dynamic and static strain.38
The approach to optimal VT settings continues to
evolve. Indeed, given the aforementioned “baby lung”
785
concept, it would make sense that targeting a VT setting
that matches the functioning aerated lung rather than an
ideal normal lung would be the best approach. One way
to do this would be to visually or physiologically
measure the functional lung size and set the VT value as
a fraction of functional lung.39 A simpler strategy is to
assume that lung compliance correlates with functional
lung size and use it to scale the VT. The relationship of
VT value to static lung compliance (CRS) is the driving
pressure (DP ¼ VT/CRS ¼ plateau pressure – PEEP). In
retrospective reanalyses of several clinical trials
evaluating mechanical ventilation management
strategies, driving pressure was more strongly associated
with survival than VT value, plateau pressure, or PEEP.40
It would then follow that even a normal VT setting of 6
to 8 mL/kg PBW may be excessive if the driving pressure
was excessive (eg, > 15-19 cm H2O).40,41
How are these concepts being applied to patients with
ARDS in the 21st century? Extensive guidelines
emphasize the need for VT settings of 4 to 8 mL/kg PBW
and plateau pressures < 30 cm H2O.42 However, a large
survey of 2,813 patients with ARDS worldwide revealed
that only about two-thirds received VT settings < 8 mL/
kg PBW, and nearly 10% had VT settings > 10 mL/kg
PBW. Furthermore, 10% had plateau pressures > 30 cm
H2O, and 50% had driving pressures > 15 cm H2O
(Fig 2).43
The Non-ARDS Patient
Although there is consensus opinion regarding the use
of low VT settings in patients with ARDS, what about
100%
> 30 cm H2O
90%
80%
> 8 mL/kg
> 15 cm H2O
70%
60%
50%
≤ 30 cm H2O
40%
≤ 8 mL/kg
30%
≤ 15 cm H2O
20%
10%
0%
Tidal Plateau Driving
Volume Pressure Pressure
Figure 2 – Lung-protective ventilation in 2014. Data are from a large
cross-sectional survey of patients receiving mechanical ventilation with
ARDS; the data show the fraction of patients receiving recommended
lung-protective ventilation strategies. (Data from Laffey et al.43)
786 Contemporary Reviews in Critical Care Medicine
patients who have normal lungs or non-ARDS lung
injury and are undergoing mechanical ventilation?
Importantly, in virtually all of these clinical scenarios,
underlying injury is usually heterogeneous and thus the
potential for regional overdistention from PPV
described earlier for ARDS is likely present. In essence,
the need for mechanical ventilation in and of itself may
be a risk factor for ARDS, and thus preemptively
managing these patients with lower VT settings may be
prudent.
In the Operating Room
General anesthesia affects pulmonary physiology largely
through the loss of respiratory muscle tone. As described
earlier, this loss of muscle tone, coupled with controlled
tidal breathing at normal VT settings, leads to
progressive atelectasis, physiologic shunting, and
decreased arterial oxygen tension in the blood.44
Periodic large volume breaths that use pressures
sufficient to reopen collapsed air spaces restore
oxygenation, and when patients are ventilated at
constant large VT settings, the gradual decrease in
oxygen tension goes away.12
As our understanding of VILI evolved, and the body of
evidence implicating the benefits of low VT settings in
ARDS grew, the common anesthesia practices that used
larger VT settings were called into question.45,46
Beginning in the mid-2000s, it was becoming evident
that there was a similar benefit to using low VT settings
in the operating room. One of the early reports involved
patients undergoing surgery for pneumonectomy. The
investigators found that patients who developed
postoperative respiratory failure were ventilated at larger
intraoperative VT settings (8.3 vs 6.7 mL/kg PBW).47 In
another group of patients undergoing cardiac surgery,
VT settings > 10 mL/kg PBW was a significant risk
factor for organ failure, multiple organ failure, and
prolonged stay in the ICU.48
Following several other smaller reports, the
Intraoperative Protective Ventilation (IMPROVE) trial
showed that patients who were ventilated with VT
settings of 10 to 12 mL/kg and no PEEP compared with
those receiving 6 to 8 mL/kg with PEEP of 6 to 8 cm
H2O had a greater risk of postoperative respiratory
failure and longer hospital stays.49 Subsequently, a large
meta-analysis of patients undergoing general surgery
found a dose-response relationship between the rate of
postoperative pulmonary complications and increasing
VT settings.50 A corollary to these observations is a study
showing that using a lung-protective strategy (VT setting
[ 156#4 CHEST OCTOBER 2019 ]
of 6-8 mL/kg PBW and PEEP of 8-10 cm H2O) in
potential organ donors increases the number of lungs
available for transplantation compared with a
conventional strategy (VT setting of 10-12 mL/kg PBW
and PEEP of 3-5 cm H2O).51
Each year, > 300 million surgeries are performed
worldwide.52 Therefore, any incremental benefit
achieved in optimizing lung protection during general
anesthesia will have an enormous potential reduction in
harm. Fortunately, the use of PEEP and lower VT
settings for intraoperative ventilation has increased
significantly through 2013.53
In the ICU
It would make sense that if larger VT settings for the
short duration of a surgery can cause VILI in patients
without any acute pulmonary process that the same
would also be true for patients in the ICU who do not
have ARDS. In a study from the early 1990s, intubated
patients in a surgical ICU were randomly assigned to
VT settings of 12 mL/kg vs 6 mL/kg PBW. The
investigators found that the routine use of low VT
settings seemed to be safe.54 Indeed, among patients
without ARDS who were ventilated, protective
ventilation with lower VT settings was associated with
better clinical outcomes.55 In another cohort of patients
without ARDS, the average VT setting in the lung-
protective group was 6.45 mL/kg vs 10.60 mL/kg PBW
in the control strategy. In this study, the main risk
factor for development of ARDS was large VT settings
with an OR of 1.3 for each milliliter above 6 mL/kg
PBW.56 Two subsequent reviews reaffirmed these
conclusions.57,58
A recent large trial noted no benefit to targeting small
vs intermediate VT settings in non-ARDS patients who
were mechanically ventilated.59 Because the mean
difference between the VT values in the two groups was
small, caution should be used extrapolating these results
to the potential impact of larger VT differences.
Overall, the bulk of the evidence favors the use of lower
VT settings to improve outcomes in patients who are
mechanically ventilated and who have a variety of
diseases that are not ARDS. It thus makes sense to limit
VT settings in virtually all forms of respiratory failure.
Self-Induced Lung Injury
An increasingly recognized clinical challenge is the
patient who is mechanically ventilated with a high
ventilatory demand who is generating spontaneous or
chestjournal.org
assisted VT settings greater than what is believed to be
safe (generally > 8-9 mL/kg PBW). This scenario is
often coupled with excessive maximal transpulmonary
pressures (generally > 25-30 cm H2O).60-62 Although
this can be iatrogenically induced (or magnified) by
excessive ventilator pressure settings in response to
patient efforts,61 the causes for an excessive patient
ventilatory demand can be multifactorial. Among these
are metabolic demands, pain (including presence of
endotracheal tube), anxiety, neurologic injury, patient-
ventilator asynchronies, and deranged respiratory
system mechanics/irritant receptor activity inducing
dyspnea. The systemic inflammatory response syndrome
may also be involved through inflammatory effects on
the behavior of the ventilatory control system and
through compromise of protective brainstem reflexes
designed to limit excessive tidal stretch (ie, Hering-
Breuer reflex).63,64
To help better understand whether spontaneously
unassisted breaths could cause lung injury similar to that
seen in VILI, Mascheroni et al18 gave sheep a mild acid
infusion in the brainstem, which increased their minute
ventilation by w300%. VT settings increased transiently
to 15.7 mL/kg following each injection and remained
> 9.1 mL/kg during the study. A control group of sheep
were given a similar acid infusion but were paralyzed to
prevent hyperinflation and ventilated at 8 mL/kg. Those
in the high VT group developed progressively worsening
hypoxia and severe lung injury, and those with normal
VT settings developed no injury. In a rabbit model of
ARDS, combined with increased respiratory rate and VT
settings, high transpulmonary pressure generated by
strong spontaneous breathing effort led to worsened
lung injury.65
In patients, it is becoming clearer that excessive tidal and
maximal inflations (dynamic and static strain) on the
alveolar tissue can induce injury even when generated
largely by spontaneous efforts (self-induced lung injury
[SILI]).66 However, the pattern of injury may be
different in the presence of spontaneous effort.67,68
Positive airway pressure distributes gas according to
regional lung mechanics and against a passive
diaphragm that moves preferentially in nondependent
regions. In contrast, spontaneous efforts lead to more
uniform contraction of the diaphragm and pleural
pressure reductions, with gas distribution being affected
by regional pleural and alveolar mechanics. Thus,
although global transalveolar pressures may be similar
during spontaneous or full machine breaths, regional
transalveolar pressures may vary considerably in
787
spontaneously breathing patients, especially those with
marked heterogeneity of lung injury.
The distributional effects of spontaneous efforts can be
beneficial in improving ventilation-perfusion matching
in milder forms of lung injury. However, in more severe
lung injury, these distributional efforts can also produce
pendelluft.66 This scenario can lead to significant tidal
recruitment and local overstretch of the involved
dependent region, as well as rapid deflation of the
corresponding nondependent region. Importantly, it
may occur without causing a significant change in
overall VT value, and it is believed that this rapid cyclic
inflation-deflation contributes to lung injury.69
Vigorous inspiratory efforts can have other negative
effects as well.60 Excessive VT values can produce air
trapping if the respiratory rate is too rapid to allow for
complete emptying between breaths, which contributes
to further alveolar overdistention. The accompanying
increased diaphragm stimulation with vigorous efforts,
especially in the presence of ventilator-patient
asynchronies, can lead to respiratory muscle fatigue and
injury. Finally, the increase in transmural pulmonary
vascular pressure swings caused by inspiratory efforts
may worsen vascular leakage.
Inadequate PEEP can contribute to SILI through
regional atelectasis that produces cyclic alveolar
opening/collapse injury during VT delivery. Vigorous
efforts in the presence of negative regional expiratory
transalveolar pressures can further worsen this
injury.69,70 Alveolar collapse also can increase
respiratory drive, create large negative intra-alveolar
pressures that can draw edema fluid into these alveoli,
and subsequently worsen the heterogeneity of injury.
Taken together, these concepts and a growing evidence
base suggest that SILI is a real phenomenon driven not
only by excessive VT settings but also by other effects of
vigorous negative pleural pressure swings.
The potential for SILI exists not only in intubated
patients but also in patients receiving noninvasive
ventilation (NIV). With NIV, it is almost impossible to
control the VT that patients receive, and in patients with
ARDS, a high expired VT value is independently
associated with NIV failure.71 Patients with lung injury
often have an increased dead space fraction, which leads
to a higher minute ventilation requirement to achieve
adequate alveolar ventilation. NIV fails to reduce this
dead space, but heated, humidified high-flow nasal
cannula (HFNC) has been proposed as a way to wash
out and reduce the physiologic dead space. Indeed,
788 Contemporary Reviews in Critical Care Medicine
patients with ARDS receiving oxygen via HFNC had
reduced dyspnea and respiratory rate compared with
those receiving NIV.72 Furthermore, they had a reduced
rate of intubation and death. It is unclear whether these
findings represent better tolerance of the device and
fewer ventilator-associated complications, or whether
the reduction in dead space led to lower VT settings and
less SILI.
Is it possible for the lungs to adapt to seemingly
excessive stretch and reduce injury potential? For
example, residents at high altitude thrive with average
alveolar ventilation 25% or more above that of sea level
residents and VT in excess of 8 mL/kg PBW.73 Similarly,
patients with chronic spinal cord injury also seem to
tolerate high VT patterns for decades. Another
interesting observation in animal experiments is that
high VT settings delivered at very low flows have far less
injury potential than high VT settings delivered with
physiologic inspiratory flows.74 This finding perhaps
suggests a capability of the alveolar capillary structures
to adapt to a larger stretch if given time and/or
appropriate ventilatory pattern. Although it is an
attractive concept, evidence for adaptation to high VT in
a short-term ICU setting is lacking.
What should clinicians do in the setting of a patient who
is mechanically ventilated demanding high VT settings
during an assisted breath? First and foremost, the
clinician should fix the fixable: reduce unnecessary
inspiratory pressures, synchronize the delivered VT
setting with patient effort as much as possible, optimize
PEEP, and reduce causes of excessive drive (eg, pain,
agitation, endotracheal tube irritation, metabolic
demands, acidosis). In the nonintubated patient, the use
of HFNC may be preferable to NIV to reduce dead space
ventilation and thereby reduce respiratory drive.
Once all of these issues have been addressed, the clinical
choice is then to either blunt (or eliminate) the
respiratory drive pharmacologically (eg, sedatives,
opioids, neuromuscular blockade) or else “live with” the
high VT settings. Pharmacologic blunting (or
elimination) of respiratory drive carries with it another
set of complications that may prolong mechanical
ventilation and compromise long-term muscle function.
Thus, the choice is essentially determining the lesser of
two evils. If the underlying injury is not severe, the
plateau and driving pressures are low, and VT elevation
is modest (ie, # 10 mL/kg PBW), the choice may be to
tolerate the excessive VT settings. In contrast, severe
lung injury with high transpulmonary driving or plateau
[ 156#4 CHEST OCTOBER 2019 ]
pressures and/or VT settings $ 12 mL/kg PBW might be
indications for blunting of respiratory drive. Another
approach under investigation is the use of low-flow
extracorporeal CO2 removal systems to reduce the need
for alveolar ventilation.75
Conclusions
Mechanical ventilation can sustain life in patients with
acute respiratory failure. A major concern in patients
who are mechanically ventilated, however, is the risk of
VILI driven in large part by excessive dynamic and static
strain. Limiting VT settings ameliorate this injury but
may actually lead to worsened gas exchange. Evidence to
date indicates that this low VT trade-off is clearly
favorable in ARDS and likely favorable in other forms of
respiratory failure and even normal lungs (eg,
anesthetized surgical patients). The “default” setting for
VT settings today in virtually all patients should thus be
in the normal physiologic range (6-8 mL/kg PBW).
Exceptions likely exist, and an example would be
patients with excessive driving or plateau pressures in
whom even lower VT settings may be indicated. In
contrast, patients with vigorous respiratory drives
demanding higher VT settings may be permitted to have
modest VT increases to avoid sedation/paralysis if
transpulmonary pressures are not excessive.
Acknowledgments
Financial/nonfinancial disclosures: None declared.
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