CRITICAL CARE PERSPECTIVE

FIFTY YEARS OF RESEARCH IN ARDS

Spontaneous Breathing during Mechanical Ventilation
Risks, Mechanisms, and Management
Takeshi Yoshida1,2,3,4, Yuji Fujino4, Marcelo B. P. Amato5, and Brian P. Kavanagh1,2,3
1
Translational Medicine, 2Department of Critical Care Medicine, and 3Department of Anesthesia, Hospital for Sick Children, University of
Toronto, Toronto, Ontario, Canada; 4Intensive Care Unit, Osaka University Hospital, Suita, Japan; and 5Laboratório de Pneumologia
LIM-09, Disciplina de Pneumologia, Heart Institute (InCor) Hospital das Clı́nicas da Faculdade de Medicina da Universidade de São
Paulo, São Paulo, Brazil

Abstract Notwithstanding the central place of spontaneous breathing in

Spontaneous respiratory effort during mechanical ventilation has
long been recognized to improve oxygenation, and because
oxygenation is a key management target, such effort may seem
beneficial. Also, disuse and loss of peripheral muscle and
diaphragm function is increasingly recognized, and thus
spontaneous breathing may confer additional advantage.
Reflecting this, epidemiologic data suggest that the use of partial
(vs. full) support modes of ventilation is increasing.
mechanical ventilation, accumulating evidence indicates that it
may cause—or worsen—acute lung injury, especially if acute
respiratory distress syndrome is severe and spontaneous effort is
vigorous. This Perspective reviews the evidence for this
phenomenon, explores mechanisms of injury, and provides
suggestions for clinical management and future research.
Keywords: mechanical ventilation; acute respiratory distress
syndrome; spontaneous breathing; ventilator-induced lung injury

Spontaneous respiratory effort during
mechanical ventilation has long been
recognized to improve oxygenation (1, 2),
and because oxygenation is a key
management target, such effort may seem
beneficial. Also, disuse and loss of peripheral
muscle and diaphragm function is
increasingly recognized (3), and thus
spontaneous breathing may confer additional
advantage. Of course, all patients will need to
transition to spontaneous effort if they are
to become independent of the ventilator.
Finally, epidemiologic data suggest that the
use of partial (vs. full) support modes of
ventilation—reflecting more overall patient
effort—is increasing (4). Notwithstanding
the central place of spontaneous breathing
in mechanical ventilation, accumulating
evidence indicates that this may cause—or
worsen—acute lung injury, especially if acute
respiratory distress syndrome (ARDS) is
severe (5–11). This Perspective reviews the
evidence for this phenomenon, explores
mechanisms of injury, and provides
suggestions for clinical management and
future research.
Spontaneous Breathing
Causes Injury during
Mechanical Ventilation
The most direct evidence comes from
experimental studies. In mechanically
ventilated rabbits with established lung
injury, vigorous spontaneous effort did
not change plateau pressure (Pplat) but
did worsen injury (8, 9). In a clinical study,
strong spontaneous effort can injure
not only the injured lung but also the
diaphragm (12). Data from three
randomized trials support this concept
in demonstrating that neuromuscular
blockade (to prevent spontaneous effort)
results in improved lung function, and
increased survival in severe ARDS (13–15).
In the largest study (340 patients), early
use of neuromuscular blockade in severe
ARDS reduced barotrauma (4 vs. 11.7%)
and mortality at 90 days (30.8 vs. 44.6%)
(15). In addition, mortality in ventilated
patients with severe sepsis was up to 12%
lower among those who received
neuromuscular blockade in the first two
hospital days (16). Finally, individual case
reports suggest that in pressure-targeted
ventilation, spontaneous breathing will

( Received in original form April 12, 2016; accepted in final form October 27, 2016 )
Supported by a RESTRACOMP training award from the Research Institute of the Hospital for Sick Children (Toronto, ON, Canada) (T.Y.). B.P.K. is funded by
the Canadian Institutes of Health Research, and holds the Dr. Geoffrey Barker Chair in Critical Care Research.
Correspondence and requests for reprints should be addressed to Brian P. Kavanagh, M.B., Department of Critical Care Medicine, Hospital for Sick Children,
500 University Avenue, Toronto, ON, M5G 1X8 Canada. E-mail: brian.kavanagh@utoronto.ca
Am J Respir Crit Care Med Vol 195, Iss 8, pp 985–992, Apr 15, 2017
Copyright © 2017 by the American Thoracic Society
Originally Published in Press as DOI: 10.1164/rccm.201604-0748CP on October 27, 2016
Internet address: www.atsjournals.org

Critical Care Perspective 985


increase VT and can be associated with
barotrauma (10, 11).
How Does a Spontaneous
Breath Combine with a
Ventilator Breath?
The lung tissue stress during a tidal
inhalation is the pressure distending the
lung, or the transpulmonary pressure (PL)
(17), that is, the difference between the
airway pressure (Paw) and the pleural
pressure (Ppl): PL = Paw 2 Ppl. In positive-
pressure ventilation under muscle paralysis,
Paw constitutes the bulk of PL (Ppl is a
minor contributor) unless chest wall
compliance is seriously impaired (17, 18),
and at end-inspiration is termed Pplat (19).
Also, Pplat is readily recorded, whereas Ppl
is not; thus, Pplat is the common indicator
of inspiratory lung stress during mechanical
ventilation (19). This is sufficiently accurate
where changes in Ppl are minor under
passive conditions; however, when
spontaneous effort occurs during positive-
pressure ventilation, Pplat no longer
approximates to PL, and because negative
changes in Ppl are far greater with
spontaneous effort, the risk of lung injury is
increased (8, 9). Several lines of evidence
support this reasoning.
Although the PL (i.e., Paw 2 Ppl) is the
static pressure that holds the lung at any
volume, its nature is better understood by
decomposing Ppl into two parts: static and
dynamic. Paw is zero (atmospheric) during
spontaneous ventilation, and has a positive
value during mechanical ventilation.
However, Ppl is either static (e.g., at end-
expiration) or dynamic (the magnitude of
its change during inspiration). In the supine
position, the static value of Ppl varies
according to the vertical height (more
negative, nondependent; more positive,
dependent), and this is determined by the
interaction between the shape of the lung
and the (slightly different) shape of the
thorax, as well as by lung density and the
weights of mediastinal and abdominal
contents (20).
A dynamic change in PL results from
a change in Paw or a change in Ppl.
Inspiration is driven by an increase in Paw
(positive pressure) or a decrease in Ppl
(spontaneous effort). In the healthy lung,
changes in local Ppl, are evenly transmitted
across the lung surface; this phenomenon is
called “fluid-like” behavior (21, 22). Here,
986 American Journal of Respiratory and Critical Care Medicine Volume 195 Number 8 | April 15 2017
CRITICAL CARE PERSPECTIVE
the change in PL is uniform, and therefore to lung injury (10, 11). However, the
inflation is homogeneous across all lung increase in VT may be less than predicted
regions (21, 22). This principle explains, from the change in PL. There are several
in part, why the changes in esophageal reasons for this discrepancy. First, if
pressure (Pes) are used as a surrogate of spontaneous effort causes pendelluft
overall Ppl changes. In contrast, injured (see below), the local inflation is facilitated
lungs exhibit “solid-like” behavior, where by corresponding deflation of aerated
a nonaerated lung region impedes the rapid (nondependent) lung, without a significant
generalization of a local change in PL; in increase in overall VT (6, 7). Second,
such cases, the lung expansion is intrinsic positive end-expiratory pressure
heterogeneous (7). (PEEP) associated with high respiratory
Superimposing a spontaneous effort drive can lower VT (23). Third, PL has
onto a ventilator breath has an additive two components: resistive (generates
effect on the distending PL and therefore airflow) and transalveolar (expands alveoli).
on the resulting VT (Figure 1). If PL measured during spontaneous
breathing includes the resistive pressure
due to flow (e.g., incomplete inspiration)
Mechanisms of Injury from and the resistive component of PL is high
Spontaneous Breathing (e.g., status asthmaticus), an elevated
PL would inflate the alveoli less than
There are several mechanisms whereby predicted from the PL, and the net VT will
spontaneous breathing during mechanical thus be lower than predicted. However,
ventilation may worsen lung injury. airway (inspiratory) resistance is rarely
increased in ARDS (24). Finally, if
spontaneous effort worsens lung injury over
Distending Pressure and Tidal
time, the compliance will progressively lessen
Volumes
and the VT will be less for a given PL (8, 9).
Spontaneous effort during a ventilator
breath reduces Ppl and increases PL
(Figure 1), and if the mechanical properties Pendelluft
of respiratory system have not changed, The exchange of air from one lung region
the resulting VT will be increased to another without causing a significant
proportionally (17, 23); this may contribute change in overall VT (i.e., pendelluft), has
Paw
+30
Paw
+30
Ppl PCap
–20 +8
Ppl PCap
Interstitial
+10 +12
Fluid
Figure 1. Spontaneous effort and transpulmonary and transvascular pressures. During a mechanical
breath (left), the transpulmonary pressure (Paw 2 Ppl = PL) distending the lung is 120 (30 2 10); the
pulmonary blood vessels are compressed by the positive-pressure breath and the transvascular
pressure (Pcap 2 Ppl) is low (assume 12 2 10 = 2). When spontaneous effort is added (right), the
PL (30 1 20 = 150) is greater, thereby increasing the VT and causing lung injury. In addition, the
negative Ppl (220) distends the pulmonary blood vessels and increases perfusion; the transvascular
pressure is greater (assume 8 2 220 = 128), increasing fluid shift to the interstitium. In the presence
of injury, permeability (and therefore propensity to alveolar edema) is increased. Paw = airway
pressure; Pcap = capillary hydrostatic pressure; Ppl = pleural pressure.
CRITICAL CARE PERSPECTIVE

been observed with spontaneous breaths
during mechanical ventilation. Although
first observed in a patient with ARDS, the
mechanisms and characteristics have been
determined in a large-animal (pig) model
(6, 7). The rapid tissue deformation results
in tidal recruitment and local overstretch of
the involved dependent region, as well as
rapid deflation (followed by reinflation) of
the corresponding nondependent region.
This phenomenon occurs because the
negative Ppl changes generated by
diaphragmatic contraction have localized
effects in dependent regions, and the Ppl
changes are not uniformly transmitted
(i.e., solid-like behavior) (Figure 2). Thus
a large vertical pressure gradient of Ppl
“swings” from nondependent (less negative)
to dependent (more negative) regions causes
pendelluft. Although pendelluft has not
been proved to cause injury, the rapid
inflation–deflation is an injurious pattern.
Increased Lung Perfusion
Spontaneous effort generates a more
negative Ppl, which in turn increases
transvascular pressure (difference between
intravascular pressure and pressure outside
the vessels); this distends thoracic and
pulmonary vessels, and increases lung
perfusion (25, 26); in injured lungs it may
cause edema (27). Clinical data indicate
that inspiratory effort in the setting of
volume-controlled ventilation (27) or
upper airway obstruction (28) (i.e., no
change in VT or PL) can result in elevated
transvascular pressure, thereby increasing
perfusion and propensity to edema.
Finally, because pulmonary edema can
reduce lung compliance and increase
the heterogeneity of ventilation, it can
ultimately contribute to injury (29).
Patient–Ventilator Asynchrony
Asynchrony between the patient’s
(spontaneous) effort and the ventilator
can worsen lung injury. “Double triggering”
is the occurrence of two consecutive
inspirations after a single respiratory effort
(30), and is injurious because the delivered
(total) VT is the sum of the two consecutive
tidal volumes (Figure 3). Double triggering
may be common (sometimes more than
twice per minute) when a protective lung
strategy in ARDS is facilitated by heavy
sedation, and may lead to higher VT (.150%
preset VT) (30, 31). Second, in heavily sedated
patients reverse triggering (entrainment) can
occur, in which the diaphragm is “triggered”
by ventilator-driven inspiration (32). Although
the mechanism of initiation is unclear, the
phenomenon is identified by a slight decrease
in Paw and Pes (corresponding to increased
PL), and an increase in delivered VT. The
increases in PL and VT are potentially harmful.
Finally, as noted previously, inability of the
patient to receive the desired VT can result in
more negative Ppl, contributing to edema and
injury (see above) (27).
The adverse impact of these (and other)
patient–ventilator asynchronies is
increasingly recognized, and data from 50
ventilated patients suggest an association
between increased incidence of asynchrony
and higher mortality (33).
Spontaneous Effort: Expiration
Spontaneous effort activates expiratory (as
well as inspiratory) muscles. Forced expiration
shifts the diaphragm cephalad and lowers the
end-expiratory lung volume; this leads to
hypoxemia, and may necessitate more
injurious ventilator settings (5, 34).
Opioids—frequently used in patients
with ARDS with preserved spontaneous
effort—may potentially facilitate this
phenomenon by increasing abdominal muscle
tone (35). Lower lung volume also increases the
intrinsic risk of lung injury (36), and because
the volume of aerated lung is reduced (35), will
increase the injury caused by a given VT.
Risk Factors for Injury
Severity of ARDS
Spontaneous effort added to mechanical
ventilation in established experimental
lung injury significantly worsens the

Pes Ppl
(Global) (Regional)
(cmH2O) 5

–5

Esophageal
Pressure –10
(Sec.) (Sec.)

Regional Pleural
Pressure

HU
–1000 –900 –500 –200 +100

Figure 2. Spontaneous effort and distribution of regional ventilation and pleural pressure. Dynamic computed tomographic scan in end-expiration (left)
demonstrates that the aerated lung (blue) is nondependent, while the dependent lung is densely atelectatic (red). At end-inspiration during a spontaneous
breath (middle), there is little change in the nondependent aerated lung (blue); the dependent lung, previously densely atelectatic (red), is now partially
aerated (green/red) (i.e., tidal recruitment). The inspiratory pleural pressure traces (right), measured at the arrow tips, show the negative deflections
(“swings”) in regional Ppl and global Pes during inspiration. However, the “swing” in regional Ppl is greater (by twofold) than the “swing” in Pes, indicating
that diaphragm contraction results in greater distending pressure applied to the regional lung near the diaphragm, compared with the pressure transmitted
to the remainder of the lung (i.e., Pes). A = anterior; HU = Hounsfield units; I = inferior; L = left; P = posterior; Pes = esophageal pressure; Ppl = pleural
pressure; R = right.

Critical Care Perspective 987

 CRITICAL CARE PERSPECTIVE

26 force of contraction; this results in more

negative ΔPpl changes to the lung surface,
and it increases the positive appositional
(cm H2O)
Pressure

pressure to the abdominal rib cage (6, 41).

Increased Respiratory Drive

Greater respiratory drive is caused by
0 several factors including hypercapnia,
acidemia, hypoxemia, pain, fever, and
50 pulmonary and systemic inflammation—all
of which are common in ARDS, and to a
greater extent in more severe disease. If
(L/min)
Flow

respiratory neuromuscular function is

intact, then increased drive translates into
stronger diaphragm contraction and
larger “swings” of Ppl. This has been
–40 demonstrated in laboratory studies, in
which spontaneous effort (and negative
900 deflections in Pes) was greater in more
Double-Trigger VT severe lung injury (9). Stronger
spontaneous effort is linearly related to
Volume

Regular Trigger VT larger degrees of pendelluft, as well as

(L)

greater tidal recruitment and local

volutrauma (6, 7). In addition, strong
spontaneous effort can injure not
only the injured lung but also the
0
diaphragm (12).
Figure 3. Impact of double triggering on tidal volume. Double triggering occurs when a spontaneous Enhanced respiratory drive also
effort triggers a (second) ventilator breath before the initial breath has been completely exhaled (arrow). impacts on patient–ventilator interaction.
The pressure–time trace (top) and flow–time trace (middle) demonstrate the occurrence of the additional
For example, double triggering (breath
breath but do not give a sense that both inspirations are summed; this is apparent from the volume–time
trace (bottom) indicating that the double triggering results in a substantially larger (potentially injurious) VT
stacking) is more frequent in patients with
(red) compared with regular triggering (blue). Adapted by permission from Reference 56. higher respiratory drive (42); thus, in
more severe disease tidal volumes
significantly larger than intended may
injury if severe to begin with (8, 9); Loss of Lung Volume
be delivered.
however, in mild lung injury, spontaneous Loss of aerated lung volume has two
It is possible (although not proven) that
effort improves function (e.g., gas exchange, principal effects: less lung available for
increased respiratory drive explains in
lung compliance, aeration), but does not tidal distension and increased force of
part why spontaneous ventilation worsens
worsen injury (2, 9, 37). diaphragmatic contraction. For any
injury in severe (but not mild) ARDS,
This pattern of susceptibility is given VT (or Paw), a lung with lower
because the increased drive results in greater
reflected in clinical studies. In the major end-expiratory volume is inherently
swings in Ppl and these occur at a higher
clinical trial examining the impact of more susceptible to injury from tidal
rate.
early neuromuscular blockade in ARDS, inflation (36, 39). With mechanical
only patients with severe disease breaths, this is distributed to (and
(PaO2/FIO2 , 150 mm Hg) were recruited overstretches) already aerated regions Injurious Ventilator Settings
(15); by contrast, enrollment in most trials (e.g., the “baby” lung) (40); in Mechanical ventilation in more severe
in ARDS specifies a lesser degree of contrast, a spontaneous breath appears ARDS usually provides higher Pplat
hypoxemia (PaO2/FIO2 , 300 mm Hg) (38). to be distributed mostly to zones and driving pressure (43), and this is
Although the unadjusted analysis suggested of atelectatic lung, resulting in probably due to lower respiratory system
benefit from neuromuscular blockade, transient (“tidal”) recruitment and compliance. When spontaneous effort is
this was significant in patients with severe local volutrauma in the dependent added to a higher Pplat, the resultant PL
disease (PaO2/FIO2 , 120 mm Hg), in whom lung (6, 7) (Figure 2). would be injuriously high, reflecting the higher
survival was increased by 13.8% (15). Reduced lung volume has important Pplat plus the added negative Ppl (9).
Of course, increased severity of effects on diaphragm position and function. Driving pressure predicts survival in
ARDS is inherently linked to greater loss Cephalad displacement results in greater ARDS, but the initial analysis excluded
of lung volume, more injurious ventilator curvature of the diaphragm and patients with spontaneous effort (18).
settings (Paw), and increased respiratory an increase in the size of the zone of Conventional calculation of driving
drive (and effort); these issues are apposition (41). In addition, diaphragm pressure takes into account measurement
considered individually. fibers are lengthened, augmenting its of (positive) airway pressures only

988 American Journal of Respiratory and Critical Care Medicine Volume 195 Number 8 | April 15 2017
CRITICAL CARE PERSPECTIVE
(i.e., Pplat 2 PEEP), and not any
contribution from Ppl. However, in the
presence of spontaneous effort, two
different types of pressure are combined to
inflate the respiratory system: positive
airway pressure (i.e., Pplat 2 PEEP) applied
by the ventilator, and the negative change
in Ppl generated by respiratory muscles. In
this case, the true driving pressure across
the respiratory system should be calculated
as Pplat 2 PEEP 1 DPpl; thus spontaneous
effort preserved in severe ARDS would
increase considerably the true driving
pressure (9), especially if spontaneous effort
is prolonged. Conventional calculation of
driving pressure (using an end-inspiratory
hold) can be accurately performed
provided spontaneous effort has ended
before the end of inspiration, and muscle
relaxation has occurred (44). It is likely
that higher driving pressure due to added
spontaneous effort will be associated with
greater injury.
In severe ARDS, Pplat may remain
elevated (e.g., .30 cm H2O) even after
the reduction of VT to low levels
(e.g., 4 ml$kg–1); in such cases, decreasing
PEEP to lower Pplat (15), this may increase
spontaneous effort and driving pressure,
and with spontaneous breathing, may
also increase the severity of pendelluft (6).
Benefits of Spontaneous
Effort Added to Mechanical
Ventilation
Spontaneous breathing during mechanical
ventilation has been recommended for more
than four decades because of important
short-term benefits (1, 2, 45).
Diaphragm Muscle Tone
Controlled mechanical ventilation
(i.e., no spontaneous breathing) induces
diaphragmatic muscle dysfunction and
atrophy (3). This is a serious problem,
especially for subsequent weaning; it is
detectable in patients within as little as
18 hours (3), and can be ameliorated by
preservation of spontaneous effort (46).
Cardiovascular Effects
Whereas positive-pressure ventilation
reduces transvascular pressure and
ventricular preload (elevated intrathoracic
pressure) (47), as well as reducing
ventricular afterload, spontaneous
Critical Care Perspective
respiration does the opposite. Increased
preload and afterload might reduce
cardiac output where ventricular function
is impaired; this may be important in
ARDS where impaired right ventricular
function is present in 30% of patients (48).
The net effect of spontaneous effort on
cardiac output reflects a balance of
intrathoracic pressure, baseline ventricular
filling, and the ventricular contractile
function.
Pulmonary Function
Spontaneous breathing increases aeration
in dependent lung (37), as well as
increasing lung perfusion (see below) (49).
Thus : intrapulmonary
:
shunt is reduced
and V/Q matching and oxygenation
increased (1, 2, 49). Indeed, spontaneous
breathing is considered to be the least
invasive means to maintain lung
recruitment (5).
Although diaphragm movement
effectively recruits the lungs, diaphragmatic
tone is also important. Continuous
phrenic nerve stimulation during general
anesthesia (i.e., deep sedation, healthy
lungs) lessens the development of atelectasis
because transmission of abdominal
pressure to the pleural space is impeded by
the increased diaphragmatic tone (50).
Benefit from addition of spontaneous
breathing has been described in several
clinical and laboratory studies, where
improved oxygenation is consistently
reported; however, in each of these studies
the lung injury was mild (modest
impairment of oxygenation, low Paw)
(1, 2, 9, 37, 49). These data may be the
basis for recommendations to preserve
spontaneous breathing in patients with
mild ARDS (45).
Outcome
In addition to reports of physiological
benefit associated with spontaneous
ventilation, Putensen and colleagues
reported reduced length of intensive care
unit stay (2). However, experimental and
clinical data suggest a common theme. In
severe ARDS, avoidance of spontaneous
effort reduces injury (9) and improves
outcome (15). By contrast, in milder
disease, the presence of spontaneous effort
has little impact on outcome, but may
prevent worsening of lung injury, improve
pulmonary function (1, 2, 9, 37, 49), and in
some patients, reduce duration of
mechanical ventilation (2).
Detection of Spontaneous
Effort
Spontaneous effort is usually apparent by
observing spontaneous breaths (i.e., chest
movement or ventilator waveforms) that are
out of sequence with the ventilator breaths.
In addition to the timing, it is usually
possible to observe the patient effort, which
is apparent from accessory muscle use.
Although indirect, additional signs of
respiratory distress, such as anxiety or nasal
flaring, indicate a high likelihood of
independent respiratory effort. Standard
ventilator monitoring will confirm increased
respiratory rate (above the ventilator “set”
rate), and demonstrate negative deflection
in Paw at the start of inspiration, as well as
higher minute ventilation, VT, and
inspiratory flow. It will help us to evaluate
whether respiratory drive is vigorous over
the appropriate range (e.g., respiratory
rate . 35 breaths/min, VT . 8 ml/kg).
Importantly, airway occlusion pressure
(i.e., P0.1) can represent a more precise
respiratory drive measurement than
respiratory rate, VT, and minute ventilation
(51). A high value of P0.1 was observed in
the early stage of acute respiratory failure
as reflecting vigorous spontaneous effort,
but its value decreased as conditions of patients
improved (52). Such standard ventilator
monitoring is helpful to detect high respiratory
drive and, if necessary, further monitoring
including esophageal balloon manometry or
electrical impedance topography (EIT) will be
considered to evaluate PL or ventilation pattern.
Thus, detection of spontaneous effort is usually
straightforward.
However, three aspects of spontaneous
breathing during mechanical ventilation
might not be appreciated. First, Pes, which
is considered to reflect changes in overall
Ppl, might not reliably detect changes in
regional Ppl in the injured lung. Because
atelectatic or consolidated lung regions are
solid-like, they poorly transmit dynamic
regional changes in Ppl and changes in local
Ppl at dependent lung might be
underestimated by changes in Pes (7). Thus,
esophageal manometry may underestimate
spontaneous effort if the lung overlying
the diaphragm is densely consolidated or
atelectatic (Figure 2). Second, spontaneous
breathing often leads to better oxygenation,
and this may be interpreted by the clinician
as an improvement in the patient’s status
rather than recognized as a potential
989
 CRITICAL CARE PERSPECTIVE

contributor to worsening lung injury (i.e., tidal
recruitment and local volutrauma in the
dependent lung). Third, pendelluft cannot be
detected by standard monitoring of airway
flow, Paw, or Pes, and can be reliably detected
only by EIT (accessible) or dynamic CT (less
accessible).
Approach to Management
Minimize Spontaneous Effort
The definitive way to prevent harm from
spontaneous effort is to use neuromuscular
blockade. Papazian and colleagues
demonstrated that early (and short-term)
use of neuromuscular blockade reduced
mortality and barotrauma in severe ARDS
(15). Because most physiological
parameters were similar in both groups, the
presence of spontaneous effort seems to
have been responsible for the difference in
outcome (i.e., lung injury); however, the
specific mechanism is uncertain. When
using neuromuscular blockade it is
important to avoid awareness, provide
sufficient analgesia, and detect and manage
potentially lethal causes of dyspnea (e.g.,
endotracheal tube displacement). Providing
adequate sedation and analgesia (and
perhaps buffering acidosis) may reduce
breathing effort; indeed, spontaneous effort
can be successfully reduced by maintaining
normal PaCO2 during extracorporeal support
(53). In addition, because increased lung
volume flattens the curvature of the diaphragm,
the diaphragmatic fiber length is lessened
and its force of contraction reduced (41). Thus,
optimal recruitment may reduce spontaneous
effort and lessen pendelluft (6).
Tidal Volume
Limitation of VT might reduce effort-
associated lung injury, but this is difficult
to accomplish where spontaneous effort
is vigorous, especially with pressure-preset
modes. If respiratory effort is great,
restriction to a small VT by means of
volume-controlled ventilation can
cause the patient to develop highly
negative Ppl with forced inspiration, and this
can contribute to increased pulmonary
edema (see above) and increased frequency
of double triggering (27, 30, 31).
Limitation of VT might fail to protect
for additional reasons. A ventilator breath
is introduced through already aerated lung,
thus inflating already aerated lung and the
atelactatic lung that borders the aerated
lung. In contrast, a spontaneous effort may
be introduced largely through atelectatic
lung; because this exhibits solid-like
behavior, the impact of the diaphragmatic
effort may be in part restricted to this
atelectatic lung, causing pendelluft and
contributing less to the overall VT (Figure 2).
However, the usefulness of VT limitation
during spontaneous effort is unproven.
Ventilator Mode
First, in patient–ventilator asynchrony,
double triggering is frequently observed
during volume-controlled ventilation (30,
31). Switching to ventilator mode with
better patient–ventilator interaction such as
pressure support may better reduce the
frequency of double triggering than
increasing sedatives and analgesia (31).
Thus, it is important to adapt the ventilator
mode to patients to decrease
patient–ventilator asynchrony. Second, the
presence of spontaneous effort while using
inspiratory synchronization (e.g., assist-
control, pressure support), is likely to cause
high PL because each spontaneous breath
will initiate—and augment—the
corresponding positive pressure from the
ventilator. In contrast, during
nonsynchronized ventilation (e.g., airway
pressure release ventilation), a spontaneous
breath will infrequently combine with a
ventilator breath; when not combined (the
usual case), the ventilator and spontaneous
volumes are not added and the VT or PL
therefore is not increased (54). However, use
of nonsynchronized modes has not been
associated with improved outcome (55).
Optimal Lung Recruitment
Lung recruitment—and maintenance with
adequate PEEP—increases compliance,
thereby lessening driving pressure for a
given VT. Moreover, optimal lung
recruitment can reduce the intensity of
respiratory drive (as reflected in reduced
negative “swings” in Pes) (6). Recruitment
also lessens the degree of solid-like behavior
of the lung, and could mitigate injury from
spontaneous effort because solid-like behavior
contributes to inhomogeneous inflation,
and causes underestimation by Pes of
swings in Ppl and development of pendelluft
(7). Theoretically, optimal recruitment
could facilitate benefit from spontaneous
breathing (e.g., preservation of muscle
tone, less sedation or paralysis), while
minimizing injury.
Conclusions
There are protective and deleterious
consequences of spontaneous breathing
during mechanical ventilation in ARDS.
Accumulating evidence has revealed that
the net impact depends on the severity of
lung injury. Ventilator strategies allowing
spontaneous breathing and mechanical
ventilation with muscle paralysis during
ARDS should both be integrated into
management strategies. Restoration of
ventilated fluid-like lung may be key to
preventing the deleterious effects of
spontaneous breathing and to render
Pes a more accurate reflector of local
lung stress. n
Author disclosures are available with the text
of this article at www.atsjournals.org.

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