Airway Pressure Release Ventilation is easy to set up and comfortable for patients. There is some research to show that it reduces alveolar inflammation and progression to lung injury for mechanically ventilated patients. The mechanisms behind Ventilator Induced Lung Injury (VILI) are still being studied. APRV appears beneficial due to decreased atelectatrauma.
PEEP is known to improve oxygenation and prevent alveolar collapse (derecruitment/atelectasis). However PEEP may not be as effective in preventing derecruitment as once thought. This is likely due to the lower Mean Airway Pressure in conventional I:E ratio mechanical ventilation. From a conceptual point of view, Airway Pressure Release Ventilation is somewhat similar to a sustained PEEP recruitment manoeuvre. However, instead of being a one-off manoeuvre, APRV is a mode of mechanical ventilation which supports alveolar recruitment over time and is more suited to keeping lung tissue open and stable.
If commenced early, rather than being called upon as last-ditch therapy, APRV (with specific time settings guided by expiratory flow) may reduce the progression to ARDS compared with a low-tidal-volume strategy. This has already been researched in animal (pig) models of sepsis and shock. There is also single-centre trial comparing a version of APRV with ARDSnet with improved liberation from the ventilator in the APRV arm.
APRV should not be used in patients with high intrinsic PEEP (such as patients with severe asthma or COPD-related bronchoconstriction). If they have an “obstructive capnograph” they are not suitable for APRV. This group represents a minority of intubated ED patients.
The inspiratory time (“T high”) makes up the bulk of the breath cycle such that the expiratory (“T low” or “release”) phase is less than 1 second (usually 0.5-0.8sec). On the Hamilton C1 this means choosing the PSIMV+ mode (which is pressure-cycled), setting a respiratory rate of 8-15 breaths per minute, an inspiratory pressure of 18-30cm, and turning the inspiratory time as high as it will go (inverse I:E ratio). PEEP on the machine is set to zero but because the expiratory phase is short (0.8second) the alveoli haven't time to collapse. The intellisync button should be set to “off”. As of 2020, Hamilton have released an APRV module which renders the method here described obsolete.
Titrate the inspired oxygen to the patient's saturations.
To encourage the patient to take spontaneous breaths sedation should be kept at the lowest comfortable level and neuromuscular blockers avoided if possible. In the post-intubation period in ED repeat-dose neuromuscular blockade is to be avoided. A Fentanyl infusion is preferred for patient comfort and to help tailor the patient's respiratory drive. The main options for sedation are propofol if it is well tolerated from a haemodynamic point of view, or ketamine. In ICU dexmedetomidine is sometimes used.
Stepping up the Inspiratory Pressure in increments of 1-2cm and increasing the RR to 16-20/min should allow the patient to blow off more CO2. Also try lightening the patient's sedation to permit spontaneous breaths. In the patient who is too unwell for spontaneous breathing some degree of respiratory acidosis is generally well tolerated. Certain patients may be considered for bicarbonate infusion aiming for high normal levels on blood gas analysis.
Assess the CXR appearance and bring the Inspiratory Pressure down in increments of 2 if the lung fields appear hyperinflated. Look at the volumes being released in expiration and ensure the patient doesn't have bronchoconstriction or airway collapse.
Generally the pressures involved in APRV will not cause haemodynamic issues as long as patient's volume status and vascular tone are managed in the usual ways.
This is an area where different practices exist - one reasonable method is to give patients who have improved clinically a trial of spontaneous breathing on CPAP at 10cm H2O once their P(high) has come down to about 20 and their FiO2 is acceptable. More traditionally, drop the inspiratory pressure in increments of 2cm and stretch the time between releases by lowering the respiratory rate on the ventilator. The pre-extubation target is a P(high) of 15cm and a breath rate of 8. It is also important to ensure that the patient's oxygen requirement is at a manageable level (eg lower than 40%). The other usual criteria for extubation still apply.
Probably not as much as in other modes but yes the ventilator will alarm from time to time. You may get an alert that the tidal volume is “too high”. Since you are not really delivering a tidal volume (in the standard sense) in APRV you can adjust the alarm limits to suit your patient's respiratory dynamics while still achieving a Tidal Volume between 6 and 10ml/kg.
One method is to find the patient's plateau pressure on a normal ventilator breath and use that. Alternatively start at 18cm in patients with healthy lungs. Use a higher pressure (up to 30cm or even 35cm) in obese patients, or those with alveolar consolidation / collapse.
Even if APRV is not proven to be beneficial in all patients, familiarity with the mode will allow better use in critically ill respiratory patients such as those with MODS, severe influenza, aspiration pneumonitis or COVID-19.