Current guidelines emphasize the use of 100% oxygen during cardiopulmonary resuscitation after cardiac arrest. When patients are ventilated for variable periods after return of spontaneous circulation (ROSC), hyperoxia causes increased morbidity and mortality by overproduction of reactive oxygen species. Various patient, volunteer, and animal studies have shown the harmful effects of hyperoxia. This mini-review article aims to expand the potential clinical spectrum of hyperoxia on individual organ systems leading to organ dysfunction. A framework to achieve and maintain normoxia after ROSC is proposed. Despite the harmful considerations of hyperoxia in critically ill patients, additional safety studies including dose-effect, level and onset of the reactive oxygen species effect, and safe hyperoxia applicability period after ROSC, need to be performed in various animal and human models to further elucidate the role of oxygen therapy after cardiac arrest.
Keywords: cardiac arrest; end-organ damage; hyperoxia; normoxia protocol.
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