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Ann Intensive Care. 2016 Dec;6(1):23. doi: 10.1186/s13613-016-0126-8. Epub 2016 Mar 22.

Hyperoxia toxicity after cardiac arrest: What is the evidence?

Author information

1
Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014, Paris, France. jllitjos@gmail.com.
2
Faculté de Médecine, Université Paris Descartes, Sorbonne Paris Cité, 15 rue de l'école de Médecine, 75006, Paris, France. jllitjos@gmail.com.
3
Medical Intensive Care Unit, Cochin Hospital, Hôpitaux Universitaires Paris Centre, Assistance Publique des Hôpitaux de Paris, 27 rue du Faubourg Saint-Jacques, 75014, Paris, France.
4
Faculté de Médecine, Université Paris Descartes, Sorbonne Paris Cité, 15 rue de l'école de Médecine, 75006, Paris, France.
5
Anesthesia and Intensive Care Department, Bicêtre Hospital, Assistance Publique des Hôpitaux de Paris, 94275, Le Kremlin-Bicêtre, France.
6
Université Paris Sud XI, Orsay, France.

Abstract

This review gives an overview of current knowledge on hyperoxia pathophysiology and examines experimental and human evidence of hyperoxia effects after cardiac arrest. Oxygen plays a pivotal role in critical care management as a lifesaving therapy through the compensation of the imbalance between oxygen requirements and supply. However, growing evidence sustains the hypothesis of reactive oxygen species overproduction-mediated toxicity during hyperoxia, thus exacerbating organ failure by various oxidative cellular injuries. In the cardiac arrest context, evidence of hyperoxia effects on outcome is fairly conflicting. Although prospective data are lacking, retrospective studies and meta-analysis suggest that hyperoxia could be associated with an increased mortality. However, data originate from retrospective, heterogeneous and inconsistent studies presenting various biases that are detailed in this review. Therefore, after an original and detailed analysis of all experimental and clinical studies, we herein provide new ideas and concepts that could participate to improve knowledge on oxygen toxicity and help in developing further prospective controlled randomized trials on this topic. Up to now, the strategy recommended by international guidelines on cardiac arrest (i.e., targeting an oxyhemoglobin saturation of 94-98 %) should be applied in order to avoid deleterious hypoxia and potent hyperoxia.

KEYWORDS:

Cardiac arrest; Cardiopulmonary resuscitation; Hyperoxia; Ischemia reperfusion; Oxidative stress; Reactive oxygen species

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