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Don appropriate personal protective equipment (PPE) based on the patient’s signs and symptoms and indications for isolation precautions.
Airway pressure release ventilation (APRV) is not recommended in patients who require deep or heavy sedation.
Neuromuscular blockade should not be used with APRV that requires a spontaneously breathing patient.
APRV is a time-triggered, pressure-limited, time-cycled mode of ventilation that uses extreme inverse inspiratory-to-expiratory (I:E) ratios that allows unrestricted spontaneous breathing with or without pressure support throughout the entire ventilatory cycle. By allowing patients to spontaneously breathe during APRV, dependent lung regions may be preferentially recruited without the need to raise applied airway pressure. There are several modes that are like APRV but use different manufacturer names, including but not limited to BiVent™ and DuoPAP™. Setting options, terminology, and abbreviations may be brand specific based on the mechanical ventilator specifications.undefined#ref3">3 APRV is a lung-protective strategy that helps to meet the goals of acute respiratory distress syndrome (ARDS) management and to diffuse pneumonia and atelectasis by maximizing alveolar recruitment while limiting the transalveolar pressure gradient and barotrauma.
Conceptually, APRV applies a high continuous positive airway pressure (CPAP) (P high) identical to CPAP for a prolonged time (T high) to maintain adequate lung volumes that promote alveolar recruitment and oxygenation. However, APRV adds a time-cycled release phase to a lower set CPAP (P low) for a short period of time (T low, or release time) where most of the ventilation and carbon dioxide removal occurs (Figure 1). The goal is to maintain adequate oxygenation and ventilation without alveolar overdistention at P high or intrinsic positive end-expiratory pressure (PEEP) at P low.
Very few randomized controlled trials have been conducted to study APRV, and consensus among practitioners regarding initial APRV settings is limited.6 A time-controlled adaptive ventilation (TCAV) protocol should be used to establish appropriate APRV settings for each patient.5
Given the current focus on the deleterious side effects of sedation medication and neuromuscular blockade, including delirium,2,6 APRV may be a good option to improve patient-ventilator synchrony without the need for heavy sedation or neuromuscular blockade. APRV has been shown to improve oxygenation, achieve a better ventilation–perfusion match, and decrease dead space compared with conventional mechanical ventilation.4
In APRV, the extended inspiratory time increases the mean airway pressure (MAP). Increasing the T high and P high increases MAP and lengthens the time for gas mixing, thereby optimizing the gas exchange surface area that promotes oxygenation.
In APRV, ventilation may be optimized by the T high, P high, and T low settings. Arterial partial pressure of carbon dioxide (PaCO2) levels may rise if T high is increased, P high is decreased, or T low is decreased. If the measured PaCO2 becomes excessively high, incremental adjustments to decrease T high, increase P high, or increase T low should allow for more carbon dioxide release that should bring the PaCO2 down to the desired level.
Patients who have obstructive lung disease with airflow obstruction and who require a prolonged expiratory time may not tolerate APRV because of patient-ventilator asynchrony caused by auto-PEEP and inverse I:E ratios.
Rationale: Limiting P high to 30 cm H2O may minimize ventilator-associated lung injury.7
Rationale: P low of 0 produces minimal expiratory resistance and facilitates rapid pressure drops, thus accelerating unimpeded expiratory flow rates.3
Rationale: T high of less than 3 seconds may result in lower MAP that may not achieve alveolar recruitment.7 T high of greater than 6 seconds may cause carbon dioxide retention.7
Rationale: The goal is to terminate expiratory gas flow at about 75% to 50% of the peak expiratory flow rate to prevent the peak expiratory flow from returning to a zero baseline.3 T low should be short enough to prevent alveolar derecruitment and long enough to obtain a suitable tidal volume (VT).4
Rationale: A shorter T high means more releases per minute.
Monitor VT and peak inspiratory pressure, which is best below 30 cm H2O.3
Monitor oxygenation because increasing T low may cause alveolar derecruitment.1
Monitor oxygenation and avoid alveolar derecruitment.1
Rationale: Pressure support augments spontaneous breathing efforts and volumes.
Carsetti, A. and others. (2019). Airway pressure release ventilation during acute hypoxemic respiratory failure: A systematic review and meta-analysis of randomized controlled trials. Annals of Intensive Care, 9(44), 1-9. doi:10.1186/s13613-019-0518-7
Fredericks, A.S. and others. (2020). Airway pressure release ventilation: A review of the evidence, theoretical benefits, and alternative titration strategies. Clinical Medicine Insights: Circulatory, Respiratory and Pulmonary Medicine, 14, 1-9. doi:10.1177/1179548420903297
Nieman, G.F. and others. (2020). Prevention and treatment of acute lung injury with time-controlled adaptive ventilation: Physiologically informed modification of airway pressure release ventilation. Annals of Intensive Care, 10(3), 1-16. doi:10.1186/s13613-019-0619-3
Othman, F. and others. (2021). The efficacy of airway pressure release ventilation in acute respiratory distress syndrome adult patients: A meta-analysis of clinical trials. Annals of Thoracic Medicine, 16(3), 245-252. doi:10.4103/atm.ATM_475_20
Shelledy, D.C., Peters, J.I. (2020). Chapter 7: Patient stabilization: Adjusting ventilatory support. In D.C. Shelledy, J.I. Peters (Eds.), Mechanical ventilation (3rd ed., pp. 367-400). Burlington, MA: Jones & Bartlett Learning.
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