Expert answer:Nava functions as a mode of mechanical Ventilation
Expert answer:Explain how NAVA functions as a mode of mechanical ventilation, what are its trigger, limits and control variables?Explain PAV as a mode of mechanical ventilation.Will either of these modes be the future of mechanical ventilation, justify your response?Explain APRV as a mode of mechanical ventilation, does your hospital use this mode, how do you set Phigh, Plow, Thigh, Tlow?How is Pes, Ppl and PL calculated/measured?What perspective value does knowing these values provide for patient care?Create your own question based upon the readings that you would like to pose to your fellow classmates which demonstrates you did more than simply skim the articles provided.
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EDUCATIONAL OBJECTIVE: Readers will enumerate the advantages and disadvantages of airway pressure release
ventilation as an alternative mode of mechanical ventilation in acute respiratory distress syndrome
ARIEL MODRYKAMIEN, MD
Assistant Professor of Medicine,
Pulmonary, Sleep and Critical Care
Medicine Division, Creighton University
School of Medicine, Omaha, NE
ROBERT L. CHATBURN, MHHS, RRT-NPS
Clinical Research Manager,
Department of Respiratory Therapy, Cleveland Clinic
RENDELL W. ASHTON, MD
Respiratory Institute, Cleveland Clinic
Airway pressure release ventilation:
An alternative mode of mechanical
ventilation in acute respiratory
distress syndrome
■ ■ABSTRACT
Acute respiratory distress syndrome (ARDS) results in
collapse of alveoli and therefore poor oxygenation. In
this article, we review airway pressure release ventilation
(APRV), a mode of mechanical ventilation that may be
useful when, owing to ARDS, areas of the lungs are collapsed and need to be reinflated (“recruited”), avoiding
cyclic alveolar collapse and reopening.
■ ■KEY POINTS
The advantages and disadvantages of APRV are related
to its two components: high mean airway pressure and
spontaneous ventilation.
Several studies show APRV to have physiologic benefits
and to improve some measures of clinical outcome, such
as oxygenation, use of sedation, hemodynamics, and
respiratory mechanics.
No study has reported that fewer patients die if they
receive APRV compared with conventional protective
ventilation.
APRV is a promising mode, and further research is needed to strengthen support for its more widespread use.
n the early stages of acute respiratory
Iof the
distress syndrome (ARDS), multiple areas
lung collapse, most often in the depen-
dent regions. A factor involved in this process
is the loss of functional surfactant, creating a
condition in which alveolar units are unstable
and prone to collapse due to unopposed surface tension. This situation, similar to that in
premature infants, results in a reduced volume
of aerated lung, intrapulmonary shunting, and,
therefore, poor oxygenation.
The treatment of this alveolar collapse is
lung reinflation (or “recruitment,” a term first
used by Lachmann).1 Gattinoni et al2 showed
that the percentage of recruitable lung could
range from a negligible fraction to 50% or more.
There are various means of reopening injured lungs and keeping them open. The choice
of recruitment maneuver is based on the individual patient and the ventilatory mode.3
In this article, we review airway pressure release ventilation (APRV), a mode of mechanical ventilation that may be useful in situations
in which, due to ARDS, the lungs need to be
recruited and held open. APRV was developed
as a lung-protective mode, allowing recruitment while minimizing ventilator-induced
lung injury.
■■ BASIC PRINCIPLES
OF PROTECTIVE VENTILATION
doi:10.3949/ccjm.78a.10032
If we draw a graph with the pressure in the
lung on the horizontal axis and the volume on
CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 78 • NUM BE R 2 F E BRUARY 2011
101
Airway pressure release ventilation
Compliance curve of the lung with its lower and upper inflection points
Collapse
Recruitment
Overdistention
Alveoli
1,000
Upper inflection point
Volume (mL)
800
600
Airway
pressure release
ventilation (APRV)
Volume-controlled
continuous
mandatory
Mean
ventilation
lung
volume
400
200
Lower inflection point
0
10
20
30
40
APRV may be
Pressure (cm H2O)
useful when
Reprinted from Papadakos PJ, Lachmann B. The open lung concept of mechanical ventilation: the role of recruitment and stabilization.
the lungs need
Crit Care Clin 2007; 23:241–250, with permission from Elsevier.
to be recruited FIGURE 1
and held open the vertical axis, the result is called the com- ing with each inspiration, as this cycle of
pliance curve (FIGURE 1).
This curve has two inflection points between which its slope is steep, indicating
greater compliance or elasticity. Below the
lower inflection point, the alveoli may collapse; above the upper inflection point, the
lung loses its elastic properties and the alveoli
are overdistended. To protect the lungs, the
challenge in mechanical ventilation is to keep
the lungs between these two points throughout the respiratory cycle.
Avoiding lung collapse by using PEEP
During mechanical ventilation, the pressure in
the lungs is lowest, and thus the alveoli are most
prone to collapse, at the end of expiration.
We want to prevent the alveoli from collapsing with each expiration and reopen-
102
opening and closing damages them (causing
atelectrauma, ie, cyclical atelectasis).4 Preventing it prevents the release of inflammatory mediators and the perpetuation of lung
injury (biotrauma).5
The solution is to apply positive end-expiratory pressure (PEEP), taking into account
the value of the lower inflection point when
setting the PEEP level.
Villar et al6 compared outcomes in an intervention group that received a PEEP level 2
cm H2O above the lower inflection point plus
low tidal volumes, and in a control group that
received higher tidal volumes and low PEEP
(5 cm H2O). The study was stopped early, after significantly more patients had died in the
control group than in the intervention group
(53% vs 32%, P = .04).
CLEV ELA N D C LI N I C JOURNAL OF MEDICINE VOL UME 78 • N UM BE R 2 F E BRUARY 2011
MODRYKAMIEN AND COLLEAGUES
Avoiding overdistention
by keeping the tidal volume low
Tidal volumes that exceed the upper inflection point overstretch the lung and induce
volutrauma, which can manifest as pneumothorax or pneumomediastinum, or both—the
lungs rupture like a balloon. Also, overdistention produces liberation of inflammatory mediators in the blood (biotrauma). High tidal
volumes should therefore be avoided or limited as much as possible.
The ARDS Network,7 in a multicenter,
randomized, controlled trial, showed that
fewer patients die if they receive mechanical
ventilation with low tidal volumes rather than
higher, “conventional” tidal volumes. Patients
were randomized to receive either a tidal volume of 6 mL/kg and a plateau pressure lower
than 30 cm H2O or a tidal volume of 12 mL/kg
and a plateau pressure lower than 50 cm H2O.
They were followed for 180 days or until discharged home, breathing without assistance.
A total of 861 patients were enrolled. The
mortality rate was significantly lower in the
low tidal volume group than in the group with
conventional tidal volumes, 31% vs 40%.
Lower tidal volumes were also associated
with faster attenuation of the inflammatory
response.8
Amato et al9 randomized 58 patients to
receive mechanical ventilation with tidal volumes of either 6 mL/kg or 12 mL/kg. The PEEP
level was maintained above the lower inflection point. At 28 days, 62% of the patients in
the intervention group were still alive, compared with only 29% in the control group.
However, many concerns were expressed over
the high mortality rate in the control group.
Based on these studies, the use of low tidal
volumes with appropriate levels of PEEP to
ensure lung recruitment is the current standard of care in mechanical ventilation of patients with ARDS.10
■■ APRV: A pressure-controlled mode
that allows spontaneous breaths
Airway pressure release ventilation (APRV),
first described by Stock et al in 1987,11 is essentially a pressure-control mode—ie, the clinician sets a high and a low pressure. However,
it also allows spontaneous breathing through
the entire breathing cycle (FIGURE 2).12,13
A baseline high pressure (P high) is set
first. Mandatory breaths are achieved by releasing the high baseline pressure in the circuit very briefly, usually to 0 cm H2O (P low),
which allows the lungs to partially deflate, and
then quickly resuming the high pressure before the unstable alveoli can collapse.
In theory, the optimal release time (the
very short time in low pressure, or T low) in
APRV should be determined by the time constant of the expiratory flow. The time constant
(t) is the time it takes to empty 63% of the
lung volume. It is calculated as:
t=C×R
where C is the combined compliance of the
lung and chest wall, and R is the combined
resistance of the endotracheal tube and the
natural airways. In diseases that lead to lower
lung compliance (such as ARDS), the time
constant is shorter. A practical equilibrium
time—or the time it takes for the lung volume
in expiration to reach steady state (no expiratory flow)—is about 4 time constants.14
Since the release time in APRV is much
shorter than the equilibrium time, a residual
volume of air remains in the lung, creating intentional auto-PEEP. Ideally, this intentional
auto-PEEP should be high enough to avoid
derecruitment (optimally above the lower
inflection point). In APRV the auto-PEEP is
controlled by the settings, and this intentional restriction of the expiratory flow is critical
to avoid derecruitment of unstable alveolar
units.
The amount of time spent at the higher
pressure (T high) is generally 80% to 95% of
the cycle (ie, the lungs are “inflated” 80% to
95% of the time), and the amount of time at
the lower pressure (T low) is 0.6 to 0.8 seconds.
Thus, APRV settings provide a relatively
high mean airway pressure, which prevents
collapse of unstable alveoli and over time
recruits additional alveolar units in the injured lung. The major difference between this
mode and more conventional modes is that in
APRV the mean inspiratory pressure is maximized and end-expiratory pressure is due to
intentional auto-PEEP. In addition, spontane-
Repeated
opening
and closing of
the alveoli
damages them,
in processes
called
atelectrauma
and biotrauma
CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 78 • NUM BE R 2 F E BRUARY 2011
103
Airway pressure release ventilation
Airway pressure release ventilation with spontaneous breathing
P high
35
T high
Mean airway
pressure
Airway pressure
(cm H2O)
30
25
20
15
10
5
P low
0
1
2
3
T low
4
5
Time
(seconds)
6
7
8
9
10
FIGURE 2
Reprinted from FRAWLEY PM, Habashi NM. Airway pressure release ventilation: theory and practice. AACN Clinical Issues 2001; 12:234–246,
with permission from Wolters Kluwer Health/Lippincott, Williams & Wilkins.
ous breathing is allowed throughout the entire
cycle (FIGURE 2).13
Although APRV does not approximate
the physiology of spontaneous breathing with
healthy lungs, it is nonetheless relatively comfortable and well tolerated. Its theoretical advantage in patients with lung injury is its ability
to maximize alveoli recruitment by maintaining a higher mean inspiratory pressure, while
the peak alveolar pressure remains lower than
with conventional ventilation (FIGURE 1).
Low tidal
volumes
with PEEP
is the standard
of care in ARDS Other modes that are similar to APRV
Other modes of mechanical ventilation very
similar to APRV are biphasic positive airway
pressure (BiPAP) and bilevel ventilation.
BiPAP differs from APRV only in the timing of the upper and lower pressure levels. In
BiPAP, T high is usually shorter than T low.
Therefore, in order to avoid derecruitment, P
low has to be set above zero with both a high
and a low PEEP level.13
No studies have demonstrated one mode
to be more beneficial than the other, although
BiPAP might be more predictable, as both
pressures are known.
Bilevel ventilation works like APRV but
incorporates pressure support to spontaneous
breathing. The use of pressure support may
affect the positive physiologic effects (see
section below) of unsupported spontaneous
104
breathing. Nevertheless, this strategy might
be useful to address severe hypercapnia in the
context of APRV.
■■ Initial ventilator settings IN APRV
As we described in the previous section, P high
and T high are set to increase end-inspiratory
lung volume, recruitment, and oxygenation.
P low and T low regulate end-expiratory lung
volume, and their settings should prevent
derecruitment but ensure adequate alveolar
ventilation (TABLE 1).
P high. In selecting an initial P high, we
measure the plateau pressure in a conventional mode using an accepted protective strategy,
such as volume-control mode. If the plateau
pressure is lower than 30 cm H2O, we use this
pressure as our initial P high. If the plateau
pressure is higher than 30 cm H2O, we select
30 cm H2O as an initial P high to minimize
peak alveolar pressure and reduce the risk of
lung overdistention.
P low is set at 0 cm H2O.
T high is set at 4 seconds and is then adjusted if necessary.
T low is probably the most difficult variable to set because it needs to be short enough
to avoid derecruitment but still long enough
to allow alveolar ventilation. We usually start
with a T low of 0.6 to 0.8 seconds.
CLEV ELA N D C LI N I C JOURNAL OF MEDICINE VOL UME 78 • N UM BE R 2 F E BRUARY 2011
MODRYKAMIEN AND COLLEAGUES
■■ ADJUSTING THE VENTILATOR SETTINGS
TABLE 1
For hypoxemia. Physician-controlled variables that affect oxygenation in APRV are:
• Mean airway pressure (dependent primarily on P high and T high)
• Fraction of inspired oxygen (Fio2).
Inadequate oxygenation usually requires
increasing one or both of these settings.
Physician-controlled variables that affect
alveolar ventilation in the APRV mode are:
• Pressure gradient (P high minus P low)
• Airway pressure release time (T low)
• Airway pressure release frequency.14 Frequency is related to total cycle time of mandatory breaths by the following equation3:
Airway pressure release ventilation (APRV)
bedside guide
frequency = 60/cycle time = 60/(T high + T low).
Note that if T low remains constant, adjusting T high will adjust frequency (the more
time the lung remains inflated, the lower the
respiratory frequency). Conversely, some ventilators allow adjustment of frequency, making T high the dependent variable. The goal
of this mode is to recruit alveoli and improve
oxygenation, so we usually do not modify the
pressure gradient to improve ventilation.
In practice, physicians rarely calculate the
time constant for each patient to set T low.
Hence, T low is usually adjusted according to
the flow-time curve on the ventilator, so that
the pressure release ends when expiratory flow
reaches approximately 40% of the peak expiratory flow, ie, approximately 1 time constant
(FIGURE 3).13
For hypercapnia. A frequent and expected
consequence of lung-protective ventilation
strategies is hypercapnia, termed “permissive” hypercapnia because it is allowed to
some extent. In APRV, some degree of CO2
retention is not unusual. When the measured
Paco2 becomes extreme, we usually increase
the frequency of releases by shortening T
high, recognizing that this adjustment may affect recruitment by lowering the mean airway
pressure.
Spontaneous breaths. A positive aspect of
APRV that contributes to its tolerability for
patients is that it allows for spontaneous respiration. In some studies of patients with ARDS
ventilated with APRV, spontaneous breathing
CRITERIA FOR APRV
Acute respiratory distress syndrome, and
Fio2 > 60%, and
Positive end-expiratory pressure > 10 cm H2O
INITIAL SETTINGS
Mandatory breaths
P high Same as plateau pressure in volume-control mode
(maximum of 30 cm H2O)
P low 0 cm H2O
T high 4 seconds
T low
40% of peak expiratory flow (around 0.6–0.8 seconds)
Spontaneous breaths
Titrate sedation so that spontaneous breathing is at least 10%
of total minute ventilation
ADJUSTMENTS
Hypoxemia
Prolong T high by 0.5–1 second
Increase P high by 2–5 cm H2O
If no response, consider other alternative modes
(eg, high-frequency oscillatory ventilation)
Hypercapnia
Tolerate “permissive hypercapnia,” with pH as low as 7.15
If severe hypercapnia, reduce T high by 0.5–1 second
(this will increase frequency of releases)
Add pressure-support APRV to bilevel
Weaning
Decrease P high by 2 cm H2O, and
prolong T high by 0.5–2 seconds
When P high is about 16 cm H2O, and T high is about 15 seconds,
switch to continuous positive airway pressure
(may add pressure support)
accounted for 10% to 30% of the total minute ventilation and was responsible for an improvement in ventilation-perfusion matching
and oxygenation.15,16 We titrate our patients’
sedation to a goal of spontaneous breathing of
at least 10% of total minute ventilation.
■■ WEANING FROM APRV
Weaning from APRV is done carefully to
avoid derecruitment. Some authors recom-
CL EVEL AND CL I NI C J O URNAL O F M E DI CI NE V O L UM E 78 • NUM BE R 2 F E BRUARY 2011
105
Airway pressure release ventilation
Inspiratory and expiratory flows in airway pressure release ventilation
Peak inspiratory gas flow
100
Inspiratory 80
Spontaneous
breaths
60
Release
phase
begins
Flow of gas
(L/min)
40
20
0
0
1
2
3
4
5
6
20
25%
40
50%
Expiratory 60
75%
80
100%
100
T high
7
8
9
T low terminates
at 40% of the peak
expiratory flow
Peak expiratory
gas flow
T low
Time
(seconds)
FIGURE 3
Reprinted from FRAWLEY PM, Habashi NM. Airway pressure release ventilation: theory and practice. AACN Clinical Issues 2001; 12:234–246,
with permission from Wolters Kluwer Health/Lippincott, Williams & Wilkins.
APRV does not
approximate
normal
breathing, but
it is relatively
comfortable
and well
tolerated
mend lowering P high by 2 to 3 cm H2O at a
time and lengthening T high by increments of
0.5 to 2.0 seconds.13,17
Once P high is about 16 cm H2O, T high is
at 12 to 15 seconds, and spontaneous respiration
accounts for most or all of the minute volume,
the mode can be changed to continuous positive
airway pressure (CPAP) and titrated downwards.
Usually, when CPAP is at 5 to 10 cm H2O, the
patient is extubated, provided that mental status
or concerns about airway protection or secretions are not contraindications.
■■ PHYSIOLOGIC EFFECTS OF APRV
WITH SPONTANEOUS BREATHING
Effects on the respiratory system
During spontaneous breathing, the greatest
displacement of the diaphragm is in dependent regions. These regions are the best ventilated.18 Compared with spontaneously breathing patients, mechanically ventilated patients
have a smaller inspiratory displacement of the
dependent part of the lung.19
A study using computed tomography demonstrated that the reduction of lung volume
106
observed in patients with acute lung injury
(ALI) predominantly affects the lower lobes
(dependent areas).20 Causative mechanisms
could be an increase in lung weight related to
ALI and a passive collapse of the lower lobes associated with an upward shift of the diaphragm.
In a preliminary study, the topographic
distribution of lung collapse was different in
spontaneously breathing ARDS patients than
in patients who were paralyzed. In particular,
lung densities were not concentrated in the
dependent regions in the former group.21
Oxygenation is better with APRV with
spontaneous breathing than with mechanical
ventilation alone. This effect is at least partly
attributable to recruitment of collapsed lung
tissue and increased aeration of the dependent
areas of the lung.22
Putensen et al15 compared ventilation-perfusion distribution in 24 patients with ARDS
who were randomized to APRV with spontaneous breathing (more than 10% of the total
minute ventilation), APRV without spontaneous breathing, or pressure-support ventilation. Spontaneous breathing during APRV
improved ventilation-perfusion matching and
CLEV ELA N D C LI N I C JOURNAL OF MEDICINE VOL UME 78 • N UM BE R 2 F E BRUARY 2011
MODRYKAMIEN AND COLLEAGUES
increased systemic blood flow.
Neumann et al23 recently compared the
effect of APRV with spontaneous breathing
vs APRV without spontaneous breathing in
terms of ventilation perfusion in an animal
model of lung injury. APRV with spontaneous breathing increased ventilation in juxtadiaphragmatic regions, predominantly in dependent areas. Spontaneous breathing had a
significant effect on the spat …
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