Objective: To review the theoretical benefits of airway pressure release ventilation (APRV), summarize the evidence for its use in clinical practice, and discuss different titration strategies. Data Source: Published randomized controlled trials in humans, observational human studies, animal studies, review articles, ventilator textbooks, and editorials. Data Summary: Airway pressure release ventilation optimizes alveolar recruitment, reduces airway pressures, allows for spontaneous breathing, and offers many hemodynamic benefits. Despite these physiologic advantages, there are inconsistent data to support the use of APRV over other modes of ventilation. There is considerable heterogeneity in the application of APRV among providers and a shortage of information describing initiation and titration strategies. To date, no direct comparison studies of APRV strategies have been performed. This review describes 2 common management approaches that bedside providers can use to optimally tailor APRV to their patients. Conclusion: Airway pressure release ventilation remains a form of mechanical ventilation primarily used for refractory hypoxemia. It offers unique physiological advantages over other ventilatory modes, and providers must be familiar with different titration methods. Given its inconsistent outcome data and heterogeneous use in practice, future trials should directly compare APRV strategies to determine the optimal management approach.

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A 27-year-old male patient presented to Mitchell's Plain Hospital on 4 December 2017 with 50% total body surface area (TBSA) burns and an inhalational injury. He was brought in by the paramedics, and no other past medical history was obtained prior to intubation for airway protection (rapid sequence intubation). Areas involved included superficial and middermal burns to his face, occiput, neck and right arm. He had mid-dermal burns to his left foot and right leg. The remainder to his back, left arm and thigh were deep dermal and full-thickness burns. His left arm had circumferential full-thickness burns, and escharotomies were performed. He had an abbreviated burn severity index of 9. His fluid requirement, according to the modified Parkland formula, was calculated as 14 L required in the first 24 hours, at a rate of 875 mL/hr for the first 8 hours, then 437.5 mL/hr for the next 16 hours. He had a full-body scrub-down, and wounds were dressed with ACTICOAT. Morphine and midazolam sedation was started as an infusion. During the resuscitative phase, he required frequent crystalloid boluses, owing to drops in urine output and mean arterial pressures (MAPs). These were associated with increased heart rates of 130-145 bpm, and serum lactate of ~3. Inotropes were not needed at this stage. Albumin was also not obtainable after-hours in the unit, and therefore not given to the patient. After an 80 mg dose of furosemide, calculated at 1 mg/kg, he passed more than 2 mL/kg urine. Furosemide is usually given half an hour after starting albumin, and in this case the rationale for giving the furosemide is not clear. At this time, he had clear air entry, with no evidence of pulmonary oedema. He was ventilating easily on lung protective settings. His acidosis improved. He did, however, receive 17 L of fluid in total in the first 24 hours, 3 L more than the calculated need. Preoperatively he had a pH of 7.24 (from 6.9) with PaCO 2 7.1 kPa, PO 2 20.5 kPa, lactate of 3.6 mmol/L (from >15 mmol/L) and standard bicarbonate of 21.5 mmol/L. His peak airway pressure at this point was