Ventilator strategies for posttraumatic acute respiratory
distress syndrome: airway pressure release ventilation
and the role of spontaneous breathing
in critically ill patients
Nader Habashia and Penny Andrewsb
Purpose of review
Patients who experience severe trauma are at increased risk
for the development of acute lung injury and acute respiratory
distress syndrome. The management strategies used to treat
respiratory failure in this patient population should be
comprehensive. Current trends in the management of acute
lung injury and acute respiratory distress syndrome consist of
maintaining acceptable gas exchange while limiting
ventilator-associated lung injury.
Recent findings
Currently, two distinct forms of ventilator-associated lung injury
are recognized to produce alveolar stress failure and have
been termed low-volume lung injury (intratidal alveolar
recruitment and derecruitment) and high-volume lung injury
(alveolar stretch and overdistension). Pathologically, alveolar
stress failure from low- and high-volume ventilation can
produce lung injury in animal models and is termed
ventilator-induced lung injury. The management goal in acute
lung injury and acute respiratory distress syndrome challenges
clinicians to achieve the optimal balance that both limits the
forms of alveolar stress failure and maintains effective gas
exchange. The integration of new ventilator modes that include
the augmentation of spontaneous breathing during mechanical
ventilation may be beneficial and may improve the ability to
attain these goals.
Summary
Airway pressure release ventilation is a mode of mechanical
ventilation that maintains lung volume to limit intra tidal
recruitment /derecruitment and improves gas exchange while
limiting over distension. Clinical and experimental data
demonstrate improvements in arterial oxygenation,
ventilation-perfusion matching (less shunt and dead space
ventilation), cardiac output, oxygen delivery, and lower airway
pressures during airway pressure release ventilation.
Mechanical ventilation with airway pressure release ventilation
permits spontaneous breathing throughout the entire
respiratory cycle, improves patient comfort, reduces the use of
sedation, and may reduce ventilator days.
Keywords
acute lung injury, acute respiratory distress syndrome,
ventilator-associated lung injury, ventilator-induced lung injury,
airway pressure release ventilation, spontaneous breathing
Curr Opin Crit Care 10:549–557. © 2004 Lippincott Williams & Wilkins.
a
Multi-trauma Intensive Care Unit, R Adams Cowley Shock Trauma Center,
Baltimore, Maryland; and bNeuro-trauma Intensive Care Unit, R Adams Cowley
Shock Trauma Center, Baltimore, Maryland, USA
Correspondence to Nader Habashi, MD, FACP, FCCP, Medical Director
Multi-trauma ICU, 22 South Greene Street, Baltimore, MD 21201, USA
Tel: 410 328 2359; fax: 410 328 7175; e-mail: [email protected]
Current Opinion in Critical Care 2004, 10:549–557
Abbreviations
ALI
APRV
ARDS
CPAP
PEEP
PSV
VALI
VILI
V/Q
acute lung injury
airway pressure release ventilation
acute respiratory distress syndrome
continuous positive airway pressure
positive end-expiratory pressure
pressure support ventilation
ventilator-associated lung injury
ventilator-induced lung injury
ventilation-perfusion
© 2004 Lippincott Williams & Wilkins
1070-5295
Introduction
Respiratory failure after traumatic injury leads to significant disruption in pulmonary integrity. Over the past 20
years, significant physiologic data have helped characterize and improve the fundamental understanding of acute
lung injury (ALI) and acute respiratory distress syndrome
(ARDS). Although attempts to clearly define optimal
ventilator strategies remain a clinical challenge, new insights have improved the overall approach to respiratory
failure from ALI/ARDS.
Airway pressure release ventilation (APRV) is a ventilator mode that allows unrestricted spontaneous breathing
and has been shown to improve gas exchange, in addition to improving patient tolerance to mechanical ventilation in ALI/ARDS. In the past, the focus of ventilation
was to control and adapt the patient to the ventilator.
Alternatively, APRV accommodates the patient’s breathing pattern and superimposes native ventilation onto a
pressure framework that supports spontaneous breathing. APRV differs from other modes of positive pressure
ventilation in that it applies a form of continuous positive
airway pressure (CPAP), which is released periodically,
augmenting CO2 clearance. The patient’s spontaneous
breaths are unrestricted and independent of the ventilator cycle.
549
550 Trauma
Mechanical ventilation
Mechanical ventilation may lead to ventilator-induced
lung injury (VILI) or ventilator-associated lung injury
(VALI).
Ventilator-induced lung injury and
ventilator-associated lung injury
In addition to maintaining organ support during respiratory failure, current ventilation strategies focus on limiting the potentially harmful effects of mechanical ventilation. Studies continue to suggest that mechanical
ventilation may produce, sustain, or potentiate ALI
[1–9].
In animal models, VILI has been recognized as an acute
lung injury caused directly by mechanical ventilation.
The appearance of diffuse alveolar damage produced
with animal models sustaining VILI is indistinguishable
pathologically from the diffuse alveolar damage of other
forms of ALI [1–9]. The severity and rapidity of VILI
varies with the intensity of the lung inflammation that
develops and ventilation strategies that are used [10–12].
Recent data suggest that positive end-expiratory pressure (PEEP) may protect and even delay the onset of
VILI [13]. Although a direct cause-and-effect relation for
a human form of VILI has yet to be established, an
association between mechanical ventilation and ALI has
been suggested and termed VALI. Although the normal
lung is designed to withstand significant transpulmonary
pressures and lung volume changes such as those occurring during exercise, the injured lung may have limited
ability of lung protection [1–9].
Mechanisms of ventilator-induced lung injury
and alveolar stress failure
Ventilator-induced lung injury is a form of alveolar stress
failure that can extend through the alveolar epithelium,
interstitium, and endothelium. The lung normally redistributes stress and uses elasticity, a large surface area,
and nearly uniform inflation to dissipate the forces associated with ventilation. Pressure and volume (ventilation
stress) are absorbed by the lung/chest wall elasticity, and
energy is distributed three-dimensionally over the large
surface area of the lung (70 m2) [14]. However, ALI/
ARDS results in an alteration in lung micromechanics,
leading to an uneven distribution of ventilation and resulting in a chaotic pattern of pressure and volume distribution as the lung inflates and deflates [15]. Alveolar
instability leads to out-of-phase recruitment, derecruitment, and overdistension during cyclic ventilation.
microscopy, documented alveolar instability after producing acute lung injury. Direct video microscopy suggested that during ALI, alveoli exhibited three distinct
types of mechanical behavior and were classified as
Types I, II, and III.
Type I: air spaces displaying no visible change in size
or shape during tidal ventilation.
Type II: air spaces demonstrating changes in size and
shape without evidence of collapse at end-expiration.
Type III: air spaces that cyclically “pop” open during
inspiration, increasing in size and shape, then collapse at end-expiration.
These altered mechanics result in regional repeated alveolar collapse and expansion. Although PEEP has been
proposed to limit cyclic alveolar collapse, Schiller et al.
[16] were unable to document any correlation between
complete alveolar stability and PEEP levels above the
lower inflection point.
Computed tomography of ARDS patients demonstrates
ALI to be heterogeneous, documenting a predominantly
dependent lung distribution [20]. CT scans performed
with incremental increases in levels of PEEP characterize the pathoanatomy of lung injury into three compartments similar to those demonstrated during in vivo video
microscopy [20a].
1. Aerated lung regions demonstrating preservation of
normal lung architecture. These lung regions retain
normal gas/tissue density on CT scan and typically
have a nondependent distribution. High PEEP/airway pressures further inflate these previously aerated lung units and can progress to overdistension.
2. Lung regions where alveolar gas volume remains unchanged throughout dynamic airway pressure changes
(ventilation). These lung regions are typically in a
dependent distribution and appear dense radiographically. These lung regions are not recruitable by
increasing airway pressures and are presumed to be
consolidated with an alveolar filling process.
3. Lung regions that are collapsed by interstitial expansion and have alveolar gas volume loss without alveolar filling. These collapsed lung regions are potentially recruitable by increasing airway pressure.
Once recruited and stabilized, gas/tissue density ratio
increases toward normal.
Alveolar instability and heterogeneity
Alveolar instability in ALI/ARDS results from loss/inactivation of surfactant, loss of functional residual capacity,
and gas absorption [16–19]. Additionally, alveolar instability affects gas exchange, recruitment, and alveolar
stress distribution. Schiller et al. [16], using in vivo video
The heterogeneity of lung regions in ALI/ARDS produces a range of opening and closing pressures. The net
result is nonuniform distribution of ventilation, which
affects gas exchange and potential alveolar stress distribution and failure [21,22].
Ventilator strategies in critically ill patients Habashi 551
Regional effects of diffuse acute lung injury
Although lung injury in ARDS is characterized by diffuse
alveolar damage, regional response to injury leads to variable mechanics throughout the lung [23]. Compressible
lung tissue, gravity, and the effect of other intrathoracic
organs exaggerate dysfunction in dependent lung regions. In early hyperdynamic ARDS, dependent lung
regions receive greater perfusion. Vascular exudation
from pulmonary capillaries leads to rising interstitial
pressures, producing interstitial expansion, alveolar collapse, and flooding. Increased pulmonary capillary exudation generates a fluid column, superimposing a hydrostatic pressure gradient along the dorsal/ventral axis of
the lung. Further collapse of dependent lung regions
ensues and manifests on CT scan as dependent lung
densities (Fig. 1).
The heart and mediastinal structures impose additional
hydrostatic pressure on dependent lung regions. The
weight of the blood-filled heart results in additional compression of the broad middle and dependent lung regions
toward the posterior thorax and spine [24–30]. Compression of lung regions leads to additional airway closure and
alveolar collapse. The heart and mediastinum remain
mobile within the thorax. CT scans demonstrate a 2- to
6-cm dorsal-ventral shift with supine-to-prone position
changes. When the patient is placed in the prone position, decompression of underlying lung tissue occurs as
the heart and mediastinum displace toward the sternum
[24]. Clinical and animal data demonstrate improved
ventilation of dependent lung regions with prone positioning through modification of dependent pleural pressure [24–30].
Frequently, ALI /ARDS patients are condemned to the
supine position. Hypoxemia and hemodynamic instabilFigure 1. CT scan of patient with acute lung injury and acute
respiratory distress syndrome
Figure 2. Gravity and compressive forces (lung edema,
hydrostatic pressure, weight of heart, and cephalad
displacement of the diaphragm from abdominal contents) on
dependent lung regions alter ventilation (V)/perfusion (Q)
matching and stress distribution
The altered distribution of ventilation results in low V/Q and shuts in the
dependent lung region and high V/Q or dead space ventilation in the
nondependent regions.
ity often discourage medical staff from repositioning patients. In general, hospital beds are designed specifically
to accommodate the tradition of minimizing patient mobilization. The supine position maximizes the compressive effect of the heart, mediastinal structures, and chest
wall onto the lungs. Supine positioning concentrates the
weight of the abdominal organs posteriorly and cephalad.
As a result, the abdominal contents displace the posterior
portion of the diaphragm cephalad, encroaching upon
the thoracic cavity [31–37].
Traditionally, spontaneous breathing in ALI /ARDS patients is discouraged, forcing the patient to adapt to predetermined ventilator settings. Controlled ventilation
frequently mandates heavy sedation or neuromuscular
blocking agents, which eliminate the diaphragm’s potential to facilitate dependent lung ventilation [32,33]. Furthermore, lack of diaphragmatic tone compounds the
cephalad displacement of the diaphragm [31–35]. The
summation of these forces results in disproportionate
underventilation of dependent lung regions (Fig. 2).
Therefore, initial lung injury combined with traditional
management practices may further amplify lung heterogeneity [31–37].
In summary, the regional effects of lung injury potentiate the mechanical difference between dependent and
nondependent lung regions. This heterogeneity of lung
regions in ALI/ARDS creates a complex volume to pressure relation, subjecting distribution of ventilation to regional micromechanics [15,16,20a].
CT scan demonstrates dependent densities
Beyond the initial lung injury, subsequent ventilation
strategies, patient positioning, and the presence of spontaneous ventilation further affect the regional distribution of ventilation.
552 Trauma
Implications for ventilation
Although applied airway pressures (peak and plateau) are
monitored clinically, transalveolar pressures more accurately reflect regional volume and pressure distribution
within the alveoli. Transalveolar pressure is the differential pressure measured across the alveolar wall. Gas
flow and volume distribution occur as intraalveolar pressure changes in relation to pressure surrounding the alveolus (pleural pressure). A greater transalveolar pressure
differential yields larger regional alveolar volume. Clinically, additional factors such as chest and abdominal wall
compliance affect lung volume change and reflect a decreased transpulmonary pressure differential (differential
pressure across the alveolus and chest wall) [38,39].
Regional transpulmonary pressure gradients exist
throughout the normal lung and are exaggerated in
ALI/ARDS [40]. Forces directed dorsally and cephalad
progressively increase pleural pressure in dependent
lung regions. Ventilation decreases as pleural pressure
surrounding these regions lowers the transpulmonary
pressure differential. As dependent transpulmonary
pressure differential decays, regional differences in compliance and resistance induce further nonuniform volume distribution as progressive airway closure ensues.
Consequently, lung units begin inflation from variable
end-expiratory lung volumes. As inflation progresses,
disproportionate pressure and volume changes develop
throughout the lungs. Such “malventilation” produces
regional overdistension and shearing forces simultaneously as airway pressure elevates toward end inspiration.
Gas/tissue densities obtained from CT scans performed
at end-expiration and end-inspiration demonstrate nonuniform tidal volume distribution in ARDS patients [41].
Tidal volume distributes predominantly to nondependent lung regions. Nonuniform ventilation limits gas exchange to a fraction of the total lung surface area.
Although the precise cause of barotrauma/volutrauma is
not known, several factors have been suggested [1–9].
Alveolar instability creates an opportunity for both forms
of alveolar stress failure—stretch from overdistension
and repeated airway opening–to generate shear forces.
The alveolar instability in ALI regionalizes pressure and
volume changes within a lung structurally weakened by
intense inflammation and edema.
Early stages of VILI develop at commonly used airway
pressures (transalveolar pressure > 35 cm H2O) in animals with normal lungs. The threshold for lung injury
may occur at lower pressures in injured lungs. Substantial evidence from animal investigations demonstrates lesions histopathologically before clinical manifestations
are evident [1–9]. CT scans demonstrate both dependent and nondependent distributions of VILI and VALI
[7,8,42]. Overdistension or stretch is more likely to occur
in healthier, nondependent regions where the bulk of
ventilation is delivered. Shear forces develop in dependent lung regions as airspaces are tidally recruited and
derecruited. However, VILI, either from overdistension
or shear forces, is intensified by volume and pressure
maldistribution from unequal lung inflation. Consequently, regional overinflation of healthy lung units results in alveolar stress fractures, continued lung tissue
injury, increased pulmonary edema formation, and persistence of the inflammation cascade [3–8,43]. In clinical
practice, VALI is typically monitored by chest radiographs. Radiographically, VILI includes interstitial emphysema, intraparenchymal bleb formation, pneumothoraces, and pneumomediastinum. However, radiographic
manifestations occur late, often after VALI has reached
advanced stages of tissue destruction [42]. Recent data
suggest that cellular stress deformation causing biotrauma results in subsequent receptor activation and signal pathways activating local inflammatory response. Additional data suggest that disruption of the alveolar
membrane barrier may orchestrate the systemic inflammatory response, promoting bacterial translocation and
providing the “engine” for multisystem organ failure
[3,43,44].
Ventilatory management
During the initial stages of ALI, increased capillary permeability results in increased extravascular lung water/
pulmonary edema. As exudation from the intravascular
space accumulates in the interstitium, superimposed
pressures on dependent lung regions increase and compress small airways and alveolar spaces. Compressive atelectasis progresses unless counterbalanced by applied
positive airway pressure. The required positive pressure
to reinflate the lung must exceed the sum of superimposed hydrostatic pressure within the lung and additional force exerted by the mediastinal structures, chest
wall, abdomen, and gravity [24,40].
In the initial days after injury, the lung is capable of
effectively withstanding and redistributing pressures.
The response to recruitment is favorable as edema fluid
is displaced and airways reopen. However, after the initial phase of injury, alveolar edema becomes organized.
As edema is replaced by fibrinous material, recruitment
maneuvers become less effective as responses to pressure increases are blunted and begin to favor overdistension. Therefore, lung recruitment should be considered
early in the course of respiratory failure [45].
The contradiction of minimizing overdistension and
eliminating shear forces while maintaining acceptable
blood gases can be arduous. Ideally, ventilator management should distribute pressure and volume to dependent and nondependent lung regions proportionally. PEEP
should be applied to sustain recruitment (prevent dere-
Ventilator strategies in critically ill patients Habashi 553
cruitment) of as many air spaces as possible, maximizing
gas exchange and improving alveolar stress distribution.
The PEEP levels required to maintain end-expiratory
lung volume in ALI and limit shear forces may be substantial (> 20 cm H2O). Although the exact level of
PEEP required to eliminate cyclic airway closure and
shear force completely is unknown, the data suggest that
a wide spectrum of airway pressures exists within the
acutely injured lung [20a–22,45a–47c]. These studies
suggests that recruitment is a “paninspiratory” phenomenon and may require pressures of 30 cm H2O or greater
to fully recruit lung regions, and prevent tidal shear stress
and limit lung inflation [49]. Therefore, the attempt to
precisely define one level of PEEP at which all airways
remain open at end-expiration may result in a gross oversimplification [50]. Unfortunately, if adequate PEEP
levels are used to prevent derecruitment, the potential to
produce overdistension is greater.
Tidal ventilation superimposed on high levels of PEEP
(> 30 cm H2O) reduces the differential pressure (pressure above PEEP for ventilation) and volume delivered
to accomplish ventilation if it is desired to limit plateau
airway pressures. Conventional ventilation must use
lower tidal volumes in an attempt to prevent overdistension. Although tidal volume reductions and airway pressure limits have been proposed for lung protective strategies during conventional ventilation, tidal inflation must
still elevate applied airway pressure and lung volume
toward overdistension. Furthermore, lower tidal volume
strategies may result in less distension per breath; however, the increase in frequency results in additional exposure to repetitive stress injury [51].
Airway pressure release ventilation
Airway pressure release ventilation may present several
advantages for ventilator management of ALI/ARDS.
APRV may provide a balanced approach, minimizing overdistension while maximizing recruitment (decreasing intratidal recruitment/derecruitment) [52]. APRV can be
described as CPAP with an intermittent release phase.
Conceptually, APRV applies continuous airway pressure
(P High), identical to CPAP, to maintain lung volume
and aid in recruitment and diffusive respiration. In addition, because the applied airway pressure is a form of
CPAP, spontaneous breathing can occur independently
of the ventilator cycle (Fig. 3). CPAP breathing mimics
the distribution of spontaneous breaths and is in opposition to mechanical breaths associated with controlled,
assisted, or supported breaths, which have less physiologic distribution [52–54].
In patients with decreased functional residual capacity,
the elastic work of breathing is effectively reduced with
the application of CPAP. As functional residual capacity
is restored, inspiration begins from a more favorable pres-
Figure 3. Airway pressure release ventilation (APRV) is a form
of continuous positive airway pressure (CPAP)
CPAP level is determined by P High; duration of CPAP is determined by T High.
CPAP is intermittently released to a P Low for a brief duration during T Low;
CPAP level is reestablished on subsequent breath. APRV allows unrestricted
spontaneous breathing to be superimposed throughout this pressure framework.
sure to volume relation, facilitating spontaneous ventilation and improving oxygenation [55].
However, in ALI/ARDS, the surface area available for
gas exchange may be significantly reduced. Despite optimal lung volume, spontaneous breathing during CPAP
mandates unloading the entire CO2 production through
spontaneous breathing. CPAP alone may be inadequate
to accomplish necessary CO2 removal without producing
excessive work of breathing. During APRV, ventilation is
augmented by releasing airway pressure to a second
CPAP level (P Low). Therefore, in contrast to CPAP,
APRV interrupts airway pressure briefly to augment
spontaneous minute ventilation. The intermittent release in airway pressure during APRV augments ventilation by enhancing CO2 removal, thus partially or completely unloading the metabolic burden of pure CPAP
breathing.
By using a release phase for ventilation, APRV uncouples the association of ventilation with alveolar distension. Rather than producing a tidal volume by elevating airway pressure above the preset PEEP (as in
traditional ventilation), tidal volumes during APRV are
generated by releasing the airway pressure from P High
to P Low (a lower CPAP level). During APRV, release
ventilation lowers airway pressure and lung volume, reducing the risk of overdistension. APRV does not require
an increase in airway pressure above P High to augment
ventilation allowing the process of ventilation to be directed away from lung inflation and distension. (Fig. 4).
By contrast, conventional ventilation increases airway
pressure, elevating lung volumes and potentially increasing the risk of overdistension.
The use of tidal volumes generated during the release
phase may have additional advantages in ALI/ARDS.
554 Trauma
Figure 4. Ventilation during airway pressure release
ventilation is augmented by release volumes and is associated
with reducing airway pressure and lung distention
Tidal volumes during traditional ventilation are associated with increasing airway
pressure and lung distention.
Increased elastic recoil is common to restrictive lung diseases such as ALI/ARDS, resulting in increased expiratory gas flow. With APRV, pressure is interrupted to release tidal volume and is driven by lung recoil stored
during the P High period (T High) and gas compression.
During traditional ventilation, inspiratory tidal volumes
must overcome airway impedance and elastic forces of
the restricted lung from its resting volume, increasing
the energy or pressure required to distend the lung and
chest wall. Furthermore, as compliance decreases, the
inspiratory limb of the volume/pressure curve shifts to
the right; that is, more pressure is required to deliver a
set tidal volume. However, the expiratory limb remains
unaffected by the prevailing volume/pressure relation
and extends throughout all phases of injury [45]. APRV
uses the more favorable volume/pressure relation of the
expiratory limb for ventilation.
Recruitment is an inspiratory phenomenon and occurs
after airway pressure exceeds the threshold opening
pressure of the lung. Once alveolar expansion develops,
the duration above threshold opening pressure is vital for
sustained recruitment and alveolar stability [45a]. Traditional volume ventilation limits recruitment to brief cyclic intervals at end-inspiration. Lung regions that are
recruited only during brief end-inspiratory pressure
cycles produce inadequate mean alveolar volume and
generate shear forces. Because alveolar volume is not
maintained, compliance does not improve, requiring the
same inflation pressure on subsequent breaths. Conversely, sustained recruitment is associated with increased compliance, allowing successful sequential airway pressure reduction and improved gas exchange [56].
Gas exchange during airway pressure
release ventilation
Gallagher et al. [57] demonstrated a direct correlation
between mean airway pressure, lung volume, and oxy-
genation. The use of APRV to optimize mean airway
pressure/lung volume provides a greater surface area
for gas exchange. Allowing sustained duration of P high
(T high) and limiting duration and frequency of the release phase of P low (T low) permits only partial emptying, limiting lung volume loss during ventilation. As
lung recruitment is sustained, gas redistribution and diffusion along concentration gradients have time to occur.
This results in a mixture of alveolar gas and inspired gas
with anatomic dead space, resulting in a greater equilibration of gas concentrations in all lung regions, improved oxygenation, and less dead space ventilation [58].
(Fig. 5)
Spontaneous breathing during airway
pressure release ventilation
Spontaneous breathing may play a vital role during mechanical ventilation. Improvements in ventilation-perfusion (V/Q) matching, alveolar recruitment, and cardiac
output are often seen when effective spontaneous breathing is introduced during mechanical ventilation [31–
37,52–54,58,58a].
Historically, mechanical ventilation has been used in an
attempt to provide total support for the patient until the
underlying respiratory failure resolves. Predetermined
inspiratory flow rates, respiratory frequencies, tidal volumes, and inspiratory/expiratory ratios conform patients
to the ventilator. Frequently, mechanical ventilation
locks dynamic and metabolically active critically ill patients into predetermined settings that lead to patientventilator dyssynchrony. As a result, for patients to become synchronous with the ventilator, heavy sedation
may be necessary to eliminate spontaneous efforts.
Figure 5. Gas exchange during airway pressure
release ventilation
(A) Mean airway pressure (lung volume) provides sustained mean alveolar
volume for gas diffusion. (B) Alveolar volume provides continuous diffusive gas
exchange between alveolar and blood compartments despite the cyclic nature of
ventilation. (C) CO2-enriched gas is released to accommodate oxygen-enriched
gas delivered with the subsequent inspiratory cycle. Fresh inspiratory volume is
reintroduced, renewing diffusion gradients.
Ventilator strategies in critically ill patients Habashi 555
Extreme cases of dyssynchrony may require the use of
neuromuscular blocking agents or, more recently, highdose continuous propofol infusions.
quently in trauma patients, higher airway pressure may
be associated with lower transpulmonary pressure as a
result of reduced thoracic and abdominal compliance
[38,39].
Ignoring patient comfort or masking ventilator dyssynchrony with sedation and neuromuscular blocking agents
may lead to increased ventilator days, adverse hemodynamic effects, ventilator-associated complications, and
cost [60–62].
Prone positioning, diaphragmatic tone, and generation of
spontaneous breaths modify pleural pressure [23,28,29,
36,39,40]. By lowering pleural pressure, transalveolar
pressure gradients increase in dependent lung regions,
improving ventilation without additional airway pressure. Spontaneous breathing improves transalveolar pressure gradients, augmenting dependent lung ventilation.
Increased ventilation in the dependent lung regions during spontaneous breaths recruits alveoli, improving V/Q
matching by improving ventilation [52,53,58,58a].
Because APRV applies airway pressure in the form of
CPAP, the patient can control the frequency and the
duration of inspiration and expiration. During mechanical ventilation with APRV, the patient is not confined to
a preset inspiratory/expiratory ratio, and tidal volumes
maintain a sinusoidal flow pattern that is typical of normal spontaneous breaths. The ability of APRV to “flex”
with a critically ill patient’s changing metabolic needs
may improve the patient’s tolerance to mechanical ventilation [62a,62b].
Fundamentally, mechanical breaths during controlled,
assisted, or supported ventilation differ from spontaneous or CPAP breaths by altering the normally optimized
distribution of ventilation. Mechanical breaths shift ventilation to the nondependent lung regions as the passive
respiratory system accommodates the “push” of gas into
the lungs [64,65]. However, spontaneous breathing during mechanical ventilation results in a more dependent
gas distribution when the active respiratory system
“pulls” gas into the lung as pressure change and flow
have a similar time course [36,64,65].
In addition, the descent of the diaphragm into the abdomen during a spontaneous breathing effort simultaneously decreases pleural pressures and increases abdominal pressure. This effectively lowers the right atrial
pressure while compressing abdominal viscera and propels blood (preload) into the inferior vena cava. Coupling
the thoracic and cardiac pumps increases venous return,
improving cardiac output and decreasing dead space ventilation [72,73].
Conversely, when spontaneous breathing is limited or
the diaphragm is paralyzed, the passive descent of the
diaphragm is no longer linked to pleural/right atrial pressure reduction, minimizing the inferior vena cava to right
atrial pressure gradient and limiting venous return and
cardiac output.
Data from patients transitioned from spontaneous
breathing to assisted breathing through the induction of
anesthesia demonstrate worsening gas exchange with increased dead space and shunt [31–33,36,37,69]. Furthermore, the appearance of rim-shaped dependent atelectasis on CT scan have been demonstrated to occur with
minutes of anesthetic induction [34–36]. These studies
suggest rapid alteration of ventilation distribution when
the respiratory systems become passive. Conversely, several studies have demonstrated improved V/Q matching
during spontaneous breathing [52,58,58a].
Currently, some ventilator manufacturers incorporate
pressure support ventilation (PSV) above P High. However, the use of PSV above P High may lead to significant elevation in transpulmonary pressure. When PSV is
triggered during the P High phase, the higher baseline
lung volume distends further as the sum of P High, PSV,
and pleural pressure raise the transpulmonary pressure.
The additional lung distension above the P High and the
transpulmonary pressure will not be completely reflected
in the airway pressure because the pleural pressure remains unknown [73a]. This effect negates the purpose of
APRV, which is to reduce airway pressure and limit lung
distension during ventilation.
Comprehensive respiratory care is incomplete if mechanical ventilation and the pressure applied to the airways remain the only focus. Ventilator management
should encompass all factors adversely affecting the
lungs. Most mechanical ventilators monitor airway pressures; however, transpulmonary pressures ultimately determine lung volume change. Although they are difficult
to monitor clinically, transpulmonary pressures should
not be excluded from management principles. Fre-
The major advantage of APRV is the preservation and
promotion of spontaneous breathing. The addition of
PSV to APRV eliminates the benefits of spontaneous
breathing by altering sinusoidal spontaneous breaths to
decelerating assisted mechanical breaths as flow and
pressure development are uncoupled from the patient’s
effort. Ultimately, the addition of PSV during APRV defeats improvements in the distribution of ventilation and
V/Q matching associated with unassisted spontaneous
breathing [73,74–77].
556 Trauma
Conclusion
Clinical and experimental studies demonstrate improvements in gas exchange, cardiac output, and systemic
blood flow with spontaneous breathing during APRV
[53–54,58,58a]. APRV facilitates spontaneous breathing
and improves patient tolerance to mechanical ventilation
by decreasing patient-ventilator dyssynchrony. Additional studies document reduction in sedation and neuromuscular blocking agents with APRV and suggest lower
ventilator days and length of stay in the intensive care
unit [52,53,58a,62a,62b]. Reducing ventilator days may
lessens the risk of nosocomial infections and ventilatorassociated complications. Finally, APRV maintains lung
volume to minimize low volume lung injury while limiting lung distension during mechanical ventilation, providing an alternative lung protective strategy.
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The authors thank Dr. John Downs for reviewing this manuscript.
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