Respiratory systemHyperoxia in the intensive care unit: why more is not always betterAltemeier, William Aa; Sinclair, Scott EbAuthor Information aDepartment of Medicine, University of Washington, Seattle, Washington, USA bDepartment of Medicine, University of Tennessee, Memphis, Tennessee, USA Correspondence to William A. Altemeier, MD, Pulmonary & Critical Care Medicine, University of Washington, Box 356522, Health Sciences Building, 1959 NE Pacific St, Seattle, WA 98195-6522, USA Tel: +1 206 616 6140; fax: +1 206 685 8673; e-mail: [email protected] This work was funded by NIH grants HL71020 and HL004479. Current Opinion in Critical Care: February 2007 - Volume 13 - Issue 1 - p 73-78 doi: 10.1097/MCC.0b013e32801162cb Buy Metrics Abstract Purpose of review Hyperoxic inspired gas is essential for patients with hypoxic respiratory failure; it is also suspected, however, as a contributor to the pathogenesis of acute lung injury. Several recent studies in humans, animals, and cell culture have identified mechanisms by which hyperoxia may exert deleterious effects on critically ill patients. This review identifies relevant new findings regarding hyperoxic lung injury in the context of providing guidance for future clinical studies. Recent findings Recent studies have clarified the roles of both receptor-mediated and mitochondrial cell death pathways in experimental hyperoxic lung injury. Studies in animals demonstrate that hyperoxia interacts with mechanical stretch to augment ventilator-induced lung injury. Finally, studies in humans implicate hyperoxia in impairment of host defense responses to infections. Summary Although hyperoxia has not been conclusively identified as a clinically important cause of lung injury in humans, animal data strongly implicate it. Reports of interaction effects between hyperoxia and both mechanical ventilation and host defense suggest that clinical studies of hyperoxia must take these variables into account. Accumulating data about how hyperoxia initiates cell death provide guidance for development of both biomarkers to identify hyperoxia-induced injury and pharmacological interventions to limit hyperoxia's adverse effects. © 2007 Lippincott Williams & Wilkins, Inc.