Airway Pressure Release Ventilation

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Airway Pressure Release Ventilation

• Muhammad Asim Rana

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• 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-associat
  ed lung injury and may improve outcomes from
  ALI/ARDS.

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• 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

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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

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CPAP Inhalation
CPAP Exhalation
APRV Exhalation
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• 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

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• 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.

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• 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.

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• 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.

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

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• 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.

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• 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.

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• Mean air way pressure on APRV is calculated using
  this formula
• (P High ? T High) (P Low ? T Low)
• (T High T Low)

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• 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.

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• 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 IE ratio, thus
  improving patient comfort patient-ventilator
  synchrony with reduction in the amount of
  sedation necessary.

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• 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

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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

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Advantages of APRV
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•  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.

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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.

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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.

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• 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

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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

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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

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Duration of ICU stay

• The decreased use of sedatives neuromuscular
  blockade may translate into decreased length of
  mechanical ventilation ICU length of stay

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Indications

• ARDS/ALI
• Atelactasis after major surgery
• Pulmonary edema
• Obesity/Ascities
• PIPgt35 PEEPgt 10 cm of water

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Contraindications

• Increased Air way resistance
• Patients of COPD Asthma

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

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• 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)

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• Likewise use of APRV has not been investigated in
  patients with neuromuscular disease is not
  supported by any evidence

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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.

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• 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

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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

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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

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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

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TROUBLESHOOTING
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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.

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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.

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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

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Thank you

• For patient listening