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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 sedation.
Ventilator failure or accidental disconnection can be catastrophic in patients undergoing neuromuscular blockade. Neuromuscular blockade can eliminate patient-ventilator asynchrony but not with a mode of ventilation requiring a spontaneously breathing patient.
APRV is a time-triggered, pressure-limited, time-cycled mode of ventilation that allows unrestricted spontaneous breathing 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. 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 volume and promote alveolar recruitment. 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 obvious lung distention during P high and to avoid lung derecruitment and intrinsic positive end-expiratory pressure (PEEP) during P low.
Very few randomized controlled trials have been conducted to study APRV, and consensus among practitioners regarding initial APRV settings is limited.undefined#ref8">8 A time-controlled adaptive ventilation (TCAV) protocol should be used to establish appropriate APRV settings for each patient.6
Given the current focus on the deleterious side effects of sedation medication and neuromuscular blockade, including delirium,5 APRV may begin to gain favor among practitioners, particularly when compared with high-frequency oscillatory ventilation (HFOV), which requires far deeper sedation levels and, in many cases, neuromuscular blockade.7 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 allows for an increase in the mean airway pressure (MAP) and improvement in oxygenation. Increasing the T high and P high increases MAP and lengthens the time for gas mixing, thereby optimizing the gas exchange surface area to promote oxygenation.
When the measured arterial partial pressure of carbon dioxide (PaCO2) becomes extreme, shortening T high increases the frequency with which carbon dioxide is released. PaCO2 may increase if T high is increased, P high is decreased, or T low is decreased.
Patients who have obstructive lung disease with airflow obstruction and who require a prolonged expiratory time may not benefit from APRV because of patient-ventilator asynchrony (i.e., auto-PEEP and inverse inspiratory-to-expiratory [I:E] ratios).
Rationale: Limiting P high to 30 cm H
2O may minimize ventilator-associated lung injury.
Rationale: P low of 0 produces minimal expiratory resistance and facilitates rapid pressure drops, thus accelerating unimpeded expiratory flow rates.
Rationale: T high of less than 3 seconds begins to negatively impact mean airway pressure and recruitment. Extending the T high period may be required to enhance carbon dioxide clearance.
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 derecruitment and long enough to obtain a suitable tidal volume (V
Rationale: A shorter T high means more releases per minute.
T and peak inspiratory pressure, which is best below 30 cm H
Rationale: The primary method to wean support in APRV is the “drop and stretch method.” Increased P high and increased T high improves oxygenation. Manipulation of P low and T low regulates end-expiratory lung volume.
Rationale: Too long a time interval lengthens stay in the intensive care unit; too short a time interval promotes alveolar collapse.
Cairo, J.M. (Ed.). (2020). Chapter 17: Effects of positive pressure ventilation on the pulmonary system. In Pilbeam’s mechanical ventilation: Physiological and clinical applications (7th ed., pp. 307-332). St. Louis: Elsevier.
Mireles-Cabodevila, E. (2016). Should airway pressure release ventilation be the primary mode in ARDS. Respiratory Care, 61(6), 761-773. doi:10.4187/respcare.04653
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(1), 3. doi:10.1186/s13613-019-0619-3
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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