APRV (Airway Pressure Release Ventilation) is a ventilation mode that applies continuous positive airway pressure (CPAP) for a prolonged high-pressure phase (T high) to recruit and maintain lung volume. It then has a brief low-pressure release phase (T low) where most ventilation and CO2 removal occurs. Compared to conventional ventilation, APRV may cause less ventilator-induced lung injury due to maintaining higher end-expiratory lung volumes without repetitive opening/closing of alveoli. It also allows for spontaneous breathing which improves patient comfort and outcomes. While APRV does not reduce mortality, it can improve other outcomes such as shorter ventilation times and ICU stays.

1. Airway Pressure
Release Ventilation
Dr Muhammad Asim Rana

2. 
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 end-expiratory lung
volumes (EELVs) may be protective from these
forms of ventilator-associated lung injury and may
improve outcomes from ALI/ARDS.

3. 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

4. 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

7. 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

8. 
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.

9. 
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 inflationdeflation cycle lasting 15
seconds. This allows 4
inflations and deflations to
be completed each minute.

10. 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.

12. If the patient has no spontaneous respiratory
effort, APRV becomes typical to “inverse ratio
pressure limited, time cycle-assisted mechanical
ventilation (pressure control ventilation).

13. 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
pressure-volume relationship, facilitating
spontaneous ventilation & improve oxygenation.

14. 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.

15. 
Mean air way pressure on APRV is calculated
using this formula:
(P High х T High) + (P Low х T Low)
(T High + T Low)

16. Minute ventilation & CO2 removal in APRV
depend on lung compliance, airway resistance,
the magnitude & duration of pressure release
and the magnitude of patient’s spontaneous
breathing efforts.

17. 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 & patient-ventilator
synchrony with reduction in the amount of
sedation necessary.

18. 
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

19. 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

20. Advantages of APRV

21. 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.

22. 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.

23. 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 opre load and
consequently increasing the cardiac out put.

24. 

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

25. 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

26. Effects on sedation


The level of sedation & analgesia required in
CMV is usually equivalent to Ramsay score of 45, 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

27. Duration of ICU stay

The decreased use of sedatives & neuromuscular
blockade may translate into decreased length of
mechanical ventilation & ICU length of stay

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

29. Contraindications

Increased Air way resistance
Patients of COPD & Asthma

30. Theoretically, using short release time is not
beneficial for patients who require long
expiratory time

31. 
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)

32. 
Likewise use of APRV has not been investigated
in patients with neuromuscular disease & is not
supported by any evidence

33. 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 end-inspiration in patients with ARDS. This is
lung protective strategy.

34. 

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

35. Setting Pressures

P high should be below the high inflection point
on the static volume-pressure curve, while P low
should be above the low inflection point on the
same curve

37. 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

39. 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

40. TROUBLESHOOTING

41. 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.

42. 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 patient’s
contribution to minute ventilation.

43. Thank you