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Objective: To review the use of airway pressure release ventilation (APRV) in the treatment of acute lung injury/acute respiratory distress syndrome.Data Source: Published animal studies, human studies, and review articles of APRV.Data Summary: APRV has been successfully used in neonatal, pediatric, and adult forms of respiratory failure. Experimental and clinical use of APRV has been shown to facilitate spontaneous breathing and is associated with decreased peak airway pressures and improved oxygenation/ventilation when compared with conventional ventilation. Additionally, improvements in hemodynamic parameters, splanchnic perfusion, and reduced sedation/neuromuscular blocker requirements have been reported.Conclusion: APRV may offer potential clinical advantages for ventilator management of acute lung injury/acute respiratory distress syndrome and may be considered as an alternative "open lung approach" to mechanical ventilation. Whether APRV reduces mortality or increases ventilator-free days compared with a conventional volume-cycled "lung protective" strategy will require future randomized, controlled trials. [ABSTRACT FROM AUTHOR]

Competing Interests: Dr. Habashi disclosed that he has patents in the field of mechanical ventilation and airway pressure release ventilation. Dr. Bates’ institution received funding from the National Institutes of Health (NIH) (HL142702); he received funding from Oscillavent, Respiratory Sciences, and Johnson & Johnson; he disclosed that he is co-inventor on patents (US7945303 B2, WO2015127377 A1, and 20160007882 A1) and that he has a patent pending (PCT/US21/24537). Dr. Bates and Nieman received support for article research from the NIH. Dr. Nieman’s institution received funding from Drager Medical; he received support for article research from the Congressionally Directed Medical Research Programs Department of Defense. The remaining authors have disclosed that they do not have any potential conflicts of interest.

Objective: To review effects of the vehicle of lorazepam, propylene glycol, in regard to lactate, osmolarity, and renal dysfunction., Design: Case report., Setting: Intensive care unit of a Level I trauma center. Patient A 36-yr-old Hispanic man who developed severe respiratory failure and required high-dose lorazepam for sedation. The patient was ventilated with low tidal volumes in a lung-protective fashion, with resultant "permissive hypercapnia." Lactates and osmolalities rose on initiation and fell, as expected, on discontinuation of the lorazepam infusion. However, there was no renal compensation for the hypercapnia except while the patient was not receiving lorazepam., Measurements and Main Result: Serial osmolalities, lactates, serum bicarbonate, PaCO2, and pH were measured during lorazepam infusion. Rise and fall of serum lactate and osmolality closely correlated with lorazepam. Serum bicarbonate rose significantly while the patient was not receiving lorazepam in response to hypercarbia and failed to rise while the patient was receiving lorazepam., Conclusion: The vehicle of lorazepam, propylene glycol, can cause hyperlactatemia and elevated osmolar gaps. However, propylene glycol may also interfere with renal tubular function and may blunt renal compensation for respiratory acidosis.