Airway Pressure Release Ventilation For Lung.143

CE: ; MCC/300106; Total nos of Pages: 9;
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REVIEW
C URRENT
OPINION Airway pressure release ventilation for lung
protection in acute respiratory distress syndrome:
an alternative way to recruit the lungs
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Luigi Camporota a,b, Louise Rose a,c, Penny L. Andrews d, Gary F. Nieman e
and Nader M. Habashi d
Purpose of review
Airway pressure release ventilation (APRV) is a modality of ventilation in which high inspiratory continuous
positive airway pressure (CPAP) alternates with brief releases. In this review, we will discuss the rationale
for APRV as a lung protective strategy and then provide a practical introduction to initiating APRV using the
time-controlled adaptive ventilation (TCAV) method.
Recent findings
APRV using the TCAV method uses an extended inspiratory time and brief expiratory release to first
stabilize and then gradually recruit collapsed lung (over hours/days), by progressively ‘ratcheting’ open a
small volume of collapsed tissue with each breath. The brief expiratory release acts as a ‘brake’ preventing
newly recruited units from re-collapsing, reversing the main drivers of ventilator-induced lung injury (VILI).
The precise timing of each release is based on analysis of expiratory flow and is set to achieve termination
of expiratory flow at 75% of the peak expiratory flow. Optimization of the release time reflects the changes
in elastance and, therefore, is personalized (i.e. conforms to individual patient pathophysiology), and
adaptive (i.e. responds to changes in elastance over time).
Summary
APRV using the TCAV method is a paradigm shift in protective lung ventilation, which primarily aims to
stabilize the lung and gradually reopen collapsed tissue to achieve lung homogeneity eliminating the main
mechanistic drivers of VILI.
Keywords
acute respiratory distress syndrome, airway pressure release ventilation, mechanical ventilation, ventilator-i-
nduced lung injury
INTRODUCTION primary disease causing this syndrome to resolve

&&
Acute respiratory distress syndrome (ARDS) devel- [3 ]. During this process, however, mechanical ven-
ops in response to various pulmonary or extrapul- tilation can cause ‘ventilation-induced’ lung injury
monary insults. It is characterized by disruption of (VILI), thereby worsening patient outcomes [4].
the lung endothelium and epithelium with pulmo-
nary microvascular permeability, resulting in alveo-
lar flooding and inflammatory pulmonary oedema a
Department of Critical Care, Guy’s & St Thomas’ NHS Foundation
[1]. Consequently, the ARDS lung becomes small, Trust, bCentre for Human & Applied Physiological Sciences, School of
unstable, and inhomogeneous. Regional volumes Basic & Medical Biosciences, cFlorence Nightingale Faculty of Nursing,
decrease heterogeneously following the gravita- Midwifery, and Palliative Care, King’s College London, London, UK,
d
Department of Critical Care, R Adams Cowley Shock Trauma Center,
tional gradient that is, from the inflated lung mainly University of Maryland Medical Center, Baltimore, Maryland and eDepart-
located in the nondependent regions, to the gasless ment of Surgery, Upstate Medical University, Syracuse, New York, USA
atelectatic or consolidated lung tissue found in the Correspondence to Luigi Camporota, Department of Critical Care,
most dependent regions [2]. Guy’s & St Thomas’ NHS Foundation Trust, London, UK.
The primary management option currently E-mail: Luigi.camporota@kcl.ac.uk
available for ARDS is supportive mechanical venti- Curr Opin Crit Care 2023, 30:000–000
lation to preserve life and buy time to enable the DOI:10.1097/MCC.0000000000001123
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Copyright © 2023 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
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Respiratory system
prone positioning [6]. Other interventions, such

KEY POINTS as recruitment manoeuvres [7,8], higher PEEP set-
tings [7,9], low or even ultralow tidal volumes [based
Loss of surfactant function with acute lung injury causes
on predicted body weight (PBW)] [10] delivered at a
regional alveolar instability (repetitive alveolar collapse
and expansion -- RACE) and overdistension-induced high rate [11,12], have demonstrated no effect on
stress-multipliers, which are the mechanisms of VILI at patient outcomes in comparison with more tradi-
the alveolar level. tional tidal volumes less than 12 ml/kg. Some inter-
ventions have even proven to increase the risk of

Surfactant dysfunction causes the lungs to become time-
harm or death in patients with moderate-to-severe
dependent and pressure-dependent.

ARDS [7,10,11]. Therefore lung-protective ventila-
Airway pressure release ventilation using the TCAV tion could be considered more of a ‘damage control’
method, based on this pathophysiologic knowledge, method of ventilation, as its primary stated aim is to
adjusts inspiratory and expiratory time to first stabilize limit injury, but not to reverse the main drivers of
and then gradually reopen collapsed lung units,
VILI (i.e. loss of inflated lung, alveolar heterogene-
counteracting the main drivers of VILI.
ity, and alveolar instability) [13].
The TCAV method is a paradigm shift in protective lung It seems logical, therefore, that stabilizing the
ventilation, that is, from the current low VT to protect the lung and preventing further atelectasis may preserve
‘baby lung’ from overdistension approach, and the lung volume, avert VILI progression, and gradually
open lung approach, to a novel Stabilize the
return the lungs to their previous state that is,
Lung Approach.
inflated and homogeneous. The initial catalyst of
VILI may be development of micro-atelectasis [14]
and formation of fluid-filled alveoli (oedema) scat-
Airway pressure release ventilation (APRV) is a tered throughout the lung [15]. These changes gen-
modality of ventilation in which higher inspiratory erate a physical interface between areas with
continuous positive airway pressure (CPAP) alter- different respiratory system elastance (ERS) [15–
nates with brief releases with the aim of first stabi- 17]. This in turn causes a two-fold to four-fold con-
lizing and then recruiting the lung. APRV can be centration and amplification of local mechanical
provided as a completely mandatory mode, in spon- forces [15,18–21], eventually leading to volutrauma
taneously breathing patients, and during weaning and stress failure [21–24] perpetuating lung injury.
and liberation from mechanical ventilation. Atelectatic areas may progress to consolidation and
In this review, we will briefly discuss the ration- then fibrosis, leading to prolonged mechanical ven-
ale for APRV as a lung protective strategy and tilation [25–27].
then provide a practical introduction to initiating
APRV according to the time-controlled adaptive
ventilation (TCAV) method. This method incorpo-
RATIONALE FOR AIRWAY PRESSURE
rates an extended inspiratory time (Thigh) so that the
RELEASE VENTILATION USING THE TIME
inspiratory pressure (Phigh), and volumes can be
CONTROLLED ADAPTIVE VENTILATION
distributed more uniformly within the lung, and a
METHOD
brief expiratory time (Tlow) to prevent collapse of Heterogeneous oedema and loss of surfactant make
fast emptying regions, and these settings are the affected alveoli ‘sticky’ [28], with alveolar open-
adjusted based on dynamic changes in lung ela- ing becoming time-dependent and pressure-
stance. dependent. This means that the lungs collapse rel-
atively quickly (<0.5 s) once a threshold closing
pressure is reached [29–33]. They also require a
CONCEPTUAL LIMITATIONS OF CURRENT longer inspiratory time above the opening pressure
LUNG-PROTECTIVE STRATEGIES to fully inflate given wide heterogeneity in the
The prevalent ventilatory strategy for ARDS involves distribution of alveolar opening (and closing) time
delivering low tidal volumes (to avoid excessive constants. To counterbalance these pathological
strain of the nondependent lung); at least moderate changes, a mechanical respiratory cycle should
positive-end expiratory pressure (PEEP) to counter- include a sufficiently extended inspiratory time to
balance gravitational forces and minimize atelecta- inflate regions with a longer inspiratory time-con-
sis [5], with prone position to achieve both the stant. It should also constitute a sufficiently brief
above goals, while most importantly achieving expiratory time (<0.5 s) [34] to prevent rapid col-
&&
greater lung homogeneity [3 ]. The only interven- lapse of lung units with a short expiratory time
tion that has proven to ameliorate excessive constant [35]. This is particularly important in
strain, gravitational forces, and atelectasis is severe disease with greater presence of inadequately
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APRV for lung protection in ARDS Camporota et al.

FIGURE 1. Flow chart illustrating setting airway pressure release ventilation using the time-controlled adaptive ventilation
method during different phases of ventilation: transition from a conventional mode to APRV (transition), optimisation of settings
in the hours that follow application of APRV; and stabilisation in the hours to days and finally weaning and liberation. PEF,
peak expiratory flow; Phigh, inspiratory pressure; Plow, expiratory pressure; PPLAT, plateau pressure; RR, respiratory rate; TEF,
termination of expiratory flow; Thigh, inspiratory time; Tlow, expiratory time; VT, tidal volume.
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Respiratory system
aerated lung regions and higher elastance (i.e. fast The brief duration of the Release Phase using the
recoil). TCAV method acts as a ‘brake’ to prevent newly
Although the ARDSNet recommendations fol- recruited tissue from re-collapsing. Furthermore,
low the logic of protecting the small baby lung, the the brief Release Phase is sufficiently short so that
combination of a relatively short inspiratory time the lung does not fully depressurize maintaining a
and longer expiratory time is incongruous with a ‘time-controlled’ PEEP (TC-PEEP). This dual method
strategy that stabilizes the alveoli and over time of time [brief release phase and pressure (TC-PEEP)]
achieves recruitment, re-inflation, and homogene- is effective for stabilizing the lung and obtaining
ity [36]. This is particularly incongruous given that
the recommended PEEP levels required to maintain

tidal recruitment are 24–25 cmH2O [37]. This level
of PEEP would generally lead to unacceptable pla-
teau pressures and significant adverse cardiovascular
consequences. Importantly, APRV is one of three
interventions for ARDS that are not currently stand-
ard of care, despite evidence of potential effective-
ness [38]. Recent systematic reviews suggest that
APRV might reduce the time spent on mechanical
ventilation and mortality [39–43]. However, evi-
dence certainty is low because of methodological
limitations and trial heterogeneity.
APRV using the TCAV method consists of a CPAP
inspiratory phase periodically interrupted by releases
brief enough to achieve a set reduction in end-expir-
atory flow compared with its peak [36,44,45]. The
TCAV method rapidly achieves lung stability with
this brief expiratory time and then progressively and
gradually recruits alveoli through an ‘inflate and
brake ratchet-like’ mechanism while preventing
&&
expiratory collapse [46 ]. This concept of rachet
and brake mechanism is equivalent to a system that
allows motion in only one direction and prevents
movement to slide back to the previous position (like
a car handbrake). In this sense, the ventilator during
inspiration inflates and recruits the lung thanks to
the Phigh and the longer inspiratory time (Thigh),
whereas the short Tlow will not allow sufficient time
for derecruitment to occur, and therefore Tlow acts as
a brake to deflation. The next breath will start the
cycle from the previous lung volume to achieve
further recruitment and stabilization. This is different
from other modes of ventilation when recruitment–
derecrutiment can occur with consequent tidal infla-
tion and deflation. A crucial aspect of the TCAV
method is that it is achieved by optimizing the timing
of each breathing phase. A longer inspiratory time
recruits more lung tissue without large transient
increases in airway pressure and mechanical power,
such as occurs during a conventional recruitment
manoeuvre. Once lung units begin to open, alveolar FIGURE 2. (a) Ventilator screen of a patient ventilated using
interdependence drives aeration of adjacent col- airway pressure release ventilation using the time-controlled
lapsed regions [62] and the cycle of stabilization– adaptive ventilation method. The settings include high and
reaeration–homogenisation can occur. In addition, low pressures (Phigh and Plow) at time spent at high and low
once the opening threshold pressure is reached and (Thigh and Tlow). In panel (b), the continuous positive airway
the collapsed airway inflates, pressure then propa- pressure (CPAP) and release phases are highlighted with the
gates, inflating more airways and alveoli. respective settings of pressure and time.
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optimal end-expiratory lung volume [29–31,45,47]. controlled and time-cycled mode, in which sponta-
This method may be superior to traditionally neous breathing can (although does not have to)
applied PEEP [48], provided that Tlow is appropri- occur throughout the breathing cycle (i.e. both the
ately set (see below) to prevent deflation [49], and is inspiratory and expiratory phases). APRV has essen-
adapted according to changes in elastance as the tially four settings. Two determine the inspiratory
lungs recover or deteriorate. cycle: inspiratory pressure (i.e. high pressure –
Phigh), and inspiratory time (i.e. time at high pres-
sure – Thigh) and make up the inspiratory or CPAP

HOW TO USE AIRWAY PRESSURE Phase. Two determine the expiratory cycle: expira-
RELEASE VENTILATION WITH THE TIME- tory pressure (i.e. Plow), and expiratory time (i.e.
CONTROLLED ADAPTIVE VENTILATION time at low pressure – Tlow) and make up the expir-
METHOD AIRWAY PRESSURE RELEASE atory or Release Phase (Fig. 2a and b). Once set, these
VENTILATION SETTINGS settings should be reviewed periodically, minimum
Setting APRV based on the TCAV method (Fig. 1) once very 12 h, when clinical conditions change, or
requires an understanding that APRV is a pressure- when certain events (e.g. disconnection from
FIGURE 3. Ventilator screen of a patient ventilated using airway pressure release ventilation using the time-controlled adaptive
ventilation method. The criterion for setting Tlow expiratory flow-time waveform. The Tlow is set to achieve a termination of
expiratory flow (TEF) 75% of peak expiratory flow (PEF). For example, if the PEF is 80 l/min, the Tlow should be set to achieve
an end-expiratory flow (TEF) of 60 l/min (i.e. 80 0.75 ¼ 60).
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Respiratory system
ventilator, transfer outside ICU, bronchoscopy or PEF. The Tlow can then be adjusted so that the TEF is
physiotherapy) occur. 75% of the PEF (Fig. 3). A Tlow that is too long may
decrease the end-expiratory pressure leading to der-
ecruitment and atelectrauma. A Tlow that is too brief
Setting of Phigh may cause overinflation and volutrauma. As lung
The initial Phigh is generally set to match the plateau mechanics change, the expiratory flow character-
pressure achieved by the conventional mode prior istics change and importantly the Tlow will need
to transition. For patients who receive APRV imme- titration to maintain the same expiratory flow %
diately following intubation, Phigh is set starting at and, therefore, end-expiratory lung volume (Fig. 4).
25 cmH2O. It is then titrated upwards or downwards

by 1–2 cmH2O at a time to a minimum of 20 and a
maximum of 30 cmH2O to achieve minimum tidal Setting of Thigh
volumes greater than 4–5 ml/kg PBW. As with all When transitioning to APRV, a Thigh less than 4 s
settings in APRV, Phigh requires titration over time in may be needed initially to maintain the respiratory
response to changes in lung volume and compli- rate and tidal volume (i.e. minute ventilation) close
ance. This ensures optimal volumes and lung infla- to that of the conventional ventilation mode used
tion pressures. For example, a flat diaphragm before transition. This is because APRV may initially
appearance on chest-radiograph and large release drop the VE resulting in hypercapnia if the Thigh is
volumes can indicate excessive Phigh. set between 4 and 6 s and the lung has not yet
recruited to sufficiently exchange CO2. As the lungs
recruit slowly, the Thigh can be increased. This low-
Setting of Plow ers the respiratory rate but does not negatively
The Plow is the set level of external pressure applied impact PaCO2 as the increased diffusion area with
during expiration. Plow does not determine the end- lung recruitment greatly accelerates gas exchange.
expiratory pressure. This is because the brief Tlow As lung units are recruited (Fig. 5), the lung effi-
does not allow complete expiration and, therefore, ciency (VCO2/VE) improves. This will maintain
does not equilibrate with the mouth pressure result- PaCO2 while increasing lung stability and maintain-
ing in TC-PEEP. Instead, end-expiratory pressure is ing alveolar stability-inflation-recruitment.
determined by the interaction between lung To select a Thigh necessary to maintain the same
mechanics, Phigh, and Tlow. Therefore, Plow is best respiratory rate as used on conventional ventilation,
set at 0 cmH2O to maximize pressure gradient and calculate the current respiratory cycle time using 60/
expiratory flow.
Setting of Tlow
The setting of Tlow is one of the most important and
distinctive features of the TCAV method. This sep-
arates it from pressure control ventilation using an
inverse ratio or other methods to set APRV [50]. In
APRV using the TCAV method, Tlow is set based on
lung mechanics and the patient’s expiratory flow
rate. The Tlow should be set to correspond to a
termination expiratory flow (TEF; i.e., the point at
which expiration is terminated) that is 75% of the
initial peak expiratory flow (PEF) (Fig. 3). Lastly, lung
volume may be more precisely controlled with the
brief Tlow as flow and time are integrals of volume.
Using time control of flow directly regulates end-
expiratory lung volume (EELV) as opposed to setting
a pressure (i.e. PEEP) to indirectly control EELV,
avoiding volume loss from differences between FIGURE 4. An expiratory flow wave and how changes in
the minimum and maximum closing volume [51]. compliance lead to a different recoil of the respiratory
We recommend first setting the Phigh as system (faster in patients with worse compliance, and more
described above, then using an initial Tlow of 0.5 s acute expiratory flow) are shown. Changes in compliance
for one to three breaths. Using the ventilator ‘freeze require a change in the Tlow to maintain termination of
waveform’ function, it is possible to quantify the expiratory flow (TEF) 75% of peak expiratory flow (PEF).
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FIGURE 5. Electrical impedance tomograms showing regional ventilation during conventional lung protective ventilation (a);
after a short recruitment manoeuvre (b) and on airway pressure release ventilation (APRV) after 5 min (c), 45 min (d), and
90 min (e) from transitioning. The figure shows progressive recruitment following airway pressure release ventilation (APRV).
respiratory rate then subtract the set Tlow. Once the neural time and Thigh will represent the time spent
patient is fully transitioned to APRV, the Thigh is at CPAP.
generally titrated between 4.0 and 6.0 s as the lung
fully reopens. It is important to highlight that the
setting of Thigh is one of the main determinants of TRANSITION CHALLENGES
mean airway pressure and minute ventilation – and Transitioning from a conventional ventilation
therefore, CO2 clearance – when APRV is used as a mode may result in a decrease in mean arterial
mandatory mode. Later, when patients are able to pressure (MAP). This may be because of unrecog-
breathe spontaneously, Thigh determines the time nized hypovolemia despite an acceptable blood
the patient spends breathing at higher CPAP. There- pressure prior to transition. Ensuring optimal vol-
fore, while during mandatory ventilation, Thigh is ume status and a cautious Phigh up-titration is gen-
the inspiratory time, during spontaneous breathing, erally sufficient to blunt the magnitude and
the true inspiratory time will be the patient’s own duration of hypotension.
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Respiratory system
Weaning airway pressure release ventilation Financial support and sponsorship

When the patient is ready for weaning based on G.F.N. has received financial support from the US
readiness criteria [52], a ‘stretch test’ can be per- Department of Defence Grant W81XWH-20-0696.
formed by increasing Thigh to 30 s for 5–6 min to
ascertain the presence of a satisfactory spontaneous Conflicts of interest
breathing rate, rhythm, and volume. In some cases, L.C. has received educational grant and honoraria from
patients with satisfactory spontaneous breathing Drager, Medtronic, Fisher and Paykel. The remaining
and no signs of increased work of breathing, a fast authors have no conflicts of interest.
track wean to CPAP can be used without the need for
progressive extension of Thigh and reduction of

Phigh. In other cases, APRV weaning is achieved REFERENCES AND RECOMMENDED
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&& of outstanding interest
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CE: ; MCC/300106; Total nos of Pages: 9;

INTRODUCTION primary disease causing this syndrome to resolve

prone positioning [6]. Other interventions, such

ventions have even proven to increase the risk of

dependent and pressure-dependent.

2 www.co-criticalcare.com Volume 30 Number 00 Month 2023

APRV for lung protection in ARDS Camporota et al.

the recommended PEEP levels required to maintain

4 www.co-criticalcare.com Volume 30 Number 00 Month 2023

APRV for lung protection in ARDS Camporota et al.

sure – Thigh) and make up the inspiratory or CPAP

25 cmH2O. It is then titrated upwards or downwards

6 www.co-criticalcare.com Volume 30 Number 00 Month 2023

APRV for lung protection in ARDS Camporota et al.

Weaning airway pressure release ventilation Financial support and sponsorship

progressive extension of Thigh and reduction of

8 www.co-criticalcare.com Volume 30 Number 00 Month 2023

APRV for lung protection in ARDS Camporota et al.

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