Airway Pressure

Release
Ventilation
Muhammad Asim Rana

In patients with acute lung injury (ALI) and

ARDS, conventional mechanical ventilation
(CV) may cause additional lung injury from
overdistention of the lung during
inspiration, repeated opening and closing of
small bronchioles and alveoli, or from
excessive stress at the margins between
aerated and atelectatic lung regions.
Increasing evidence suggests that smaller
tidal volumes (VTs) and higher endexpiratory lung volumes (EELVs) may be
protective from these forms of ventilatorassociated lung injury and may improve
outcomes from ALI/ARDS.

APRV was introduced to clinical

practice about 2 decades ago as an
alternative mode for mechanical
ventilation; however, it had not
gained popularity until recently as
an effective & safe alternative for
difficult to ventilate/oxygenate
patients of ALI/ARDS

What is APRV

APRV was introduced initially by Stock &

Down in 1987 as a CPAP with an
intermittent release phase
APRV applies CPAP (P high) for a prolonged
time (T high) to maintain adequate lung
volume & alveolar recruitment, with a time
cycled release phase to a lower set of
pressure (P low) for a short period of time
(T low) or (release time) where most of the
ventilation & CO2 removal occurs

The transition from

P high to P low
deflates the lungs
and eliminates
carbon dioxide.
Conversely, the
transition from P
low to P high
inflates the lungs.
Alveolar recruitment
is maximized by the
high continuous
positive airway
pressure

The difference
between P high and P
low is the driving
pressure. Larger
differences are
associated with
greater inflation and
deflation, while smaller
differences are
associated with
smaller inflation and
deflation. The exact
size of the tidal volume
is related to both the
driving pressure and
the compliance.

T high and T low

determine the
frequency of inflations
and deflations. As an
example, a patient
whose T high is set to
12 seconds and whose
T low is set to 3
seconds has an
inflation-deflation
cycle lasting 15
seconds. This allows 4
inflations and
deflations to be
completed each
minute.

Spontaneous
breathing is possible
at both P high and P
low, although most
spontaneous
breathing occurs at
P high because the
time spent at P low
is brief. This is a
novel feature that
distinguishes APRV
from other types of
IRV.

If the patient has no spontaneous

respiratory effort, APRV becomes
typical to inverse ratio pressure
limited, time cycle-assisted
mechanical ventilation (pressure
control ventilation).

In ARDS the functional residual

capacity & lung compliance are
reduced, & thus the elastic work of
breathing is elevated. By applying
CPAP, the FRC is restored & inspiration
starts from a more favorable pressurevolume relationship, facilitating
spontaneous ventilation & improve
oxygenation.

Applying P high for a T high (80-95%

of the cycle time), the mean airway
pressure is increased insuring almost
constant lung recruitment (open lung
approach), in contrast to the repetitive
inflation & deflation of the lung using
conventional ventilatory methods (which
could ventilator induced lung injury), or
the recruitment maneuvers which have
to be done frequently to avoid
derecruitment.

Mean air way pressure on APRV is

calculated using this formula:

(P High T High) + (P Low T Low)

(T High + T Low)

Minute ventilation & CO2 removal in

APRV depend on lung compliance,
airway resistance, the magnitude &
duration of pressure release and the
magnitude of patients spontaneous
breathing efforts.

Spontaneous breathing plays a very

important role in APRV allowing the
patient to control his/her respiratory
frequency without being confined to
an arbitrary preset I:E ratio, thus
improving patient comfort & patientventilator synchrony with reduction
in the amount of sedation necessary.

Additionally, spontaneous breathing

helps derive the inspired gas to the
nondependent lung regions by using
patients own respiratory muscles &
through pleural pressure changes
without raising the applied airway
pressure to a rather dangerous level, as
in conventional mechanical ventilation,
producing more physiological
distribution to the non dependent lung
regions & improving V/Q matching

Adding Pressure Support to

APRV

The addition of PSV above P High to add

spontaneous breaths is feasible, but this
addition contradicts limiting the airway
pressure & may cause significant lung
distention.
Furthermore, the imposition of PSV to
APRV reduces the benefits of spontaneous
breathing by altering the normal
sinusoidal flow of spontaneous breathing

Advantages of
APRV

APRV has not been shown to improve

mortality. However, it may improve
alternative important clinical outcomes
compared to other modes of ventilation. In
one trial, 30 patients being mechanically
ventilated because of trauma were
randomly assigned to receive APRV alone
or pressure-limited ventilation for 72 hours
followed by APRV. The APRV alone group
had a shorter duration of mechanical
ventilation, a shorter ICU stay, and required
less sedation and pharmacologic paralysis.
Mortality did not differ between groups.

Effects on Oxygenation

The improved oxygenation parameters

i.e., PaO2/FiO2 & lung compliance are
attributed to the beneficial effects of
spontaneous breathing through better
gas distribution & better V/Q
matching to the poorly aerated dorsal
regions of the lungs, along with
higher mean airway pressure obtained
compared to conventional ventilation.

Effects on hemodynamics

During spontaneous breathing the

pleural pressure decreases leading
to a decrease in intra thoracic & Rt
atrial pressure thus improving
venous return & improving o\pre
load and consequently increasing
the cardiac out put.

Kaplan compared the hemodynamics

effects in patients with ALI/ARDS on
patients APRV vs IRV PCV; they found
significantly higher cardiac index,
oxygen delivery, mixed venous oxygen
saturation, urine output & significantly
lower vasopressors & inotropes usage,
lactate concentration & CVP while on
APRV
Putnsen found same results in a
separate study

Effects on regional blood

flow & organ perfusion

In a study by Hering APRV improved

respiratory muscle blood flow in 12
pigs with ALI
In a similar study by same author
APRV showed improved blood flow to
stomach duodenum, ileum & colon
Kaplan found significant improvement
in GFR in pts on APRV

Effects on sedation

The level of sedation & analgesia

required in CMV is usually equivalent
to Ramsay score of 4-5, but during
APRV a Ramsay score of 2-3 can be
targeted
APRV has shown to decreased the need
of neuromuscular blockade use by 70%
& use of sedation by about 40%
compared to conventional ventilation

Duration of ICU stay

The decreased use of sedatives &

neuromuscular blockade may
translate into decreased length of
mechanical ventilation & ICU length
of stay

Indications

ARDS/ALI
Atelactasis after major surgery
Pulmonary edema
Obesity/Ascities
PIP>35 & PEEP> 10 cm of water

Contraindications

Increased Air way resistance

Patients of COPD & Asthma

Theoretically, using short release time

is not beneficial for patients who
require long expiratory time

Because of lower levels of sedation

used to allow spontaneous breathing
APRV should not be used in patients
who require deep sedation for
management of their underlying
disease (e.g.cerebral edema with
increased ICP or status epilepticus)

Likewise use of APRV has not been

investigated in patients with
neuromuscular disease & is not
supported by any evidence

Setting APRV

Mechanical ventilation with PEEP

titrated above the lower infliction
point of the static pressure volume
curve & a low tidal volume at 6 ml/kg
are thought to prevent alveolar
collapse at end expiration and over
distension of lung units at endinspiration in patients with ARDS.
This is lung protective strategy.

The setup at the bed side is simple

and the goals are same:
To maintain adequate oxygenation &
ventilation without overt lung
distention during P high & avoiding
lung derecruitment during P low

Setting Pressures

P high should be below the high

inflection point on the static volumepressure curve, while P low should
be above the low inflection point on
the same curve

Setting Time

T high should allow complete

inflation of the lungs, as indicated by
end-respiratory phase of no flow
when spontaneous breathing is
absent, & T low should allow for
complete exhalation with no flow at
the end to assure absence of
intrinsic or auto PEEP

Initial setup & transition

from conventional
ventilation

P high is usually set between 20 &

30
P low is set between 0 & 5 cm of
H2O
T high is 4 to 6 seconds
T low is 0.2 to 0.8 seconds

TROUBLESHOOTI
NG

Maneuvers to correct poor

oxygenation

1) increase either P high, T high

or both to increase mean airway
pressure;
2) change the patient position to the
prone position along with the APRV.

Maneuvers to correct poor

ventilation

1) increase P high and decrease T high

simultaneously to increase minute
ventilation while keeping stable mean
airway pressure (preferred method);
2) increase T low by 0.05-0.1 s
increments;
3) decrease sedation to increase the
patients contribution to minute ventilation.

Acknowledgements

Dr. Mostafa Adel

Dr. Omar Alsayed
Dr. Ahmed fouad
Dr. Ahmed Hossam

Dr. Ahmed Rajab

Dr. Sameer
Ibrahim
Dr. Bashir Ahmed
Dr. Sayed Afzal

Thank you
For patient listening