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Review
. 2020 Aug 12:8:60.
doi: 10.1186/s40560-020-00477-w. eCollection 2020.

Oxygen administration in patients recovering from cardiac arrest: a narrative review

Ryo Yamamoto  1 , Jo Yoshizawa  1
Affiliations
Review

Oxygen administration in patients recovering from cardiac arrest: a narrative review

Ryo Yamamoto et al. J Intensive Care. .

Abstract

High oxygen tension in blood and/or tissue affects clinical outcomes in several diseases. Thus, the optimal target PaO2 for patients recovering from cardiac arrest (CA) has been extensively examined. Many patients develop hypoxic brain injury after the return of spontaneous circulation (ROSC); this supports the need for oxygen administration in patients after CA. Insufficient oxygen delivery due to decreased blood flow to cerebral tissue during CA results in hypoxic brain injury. By contrast, hyperoxia may increase dissolved oxygen in the blood and, subsequently, generate reactive oxygen species that are harmful to neuronal cells. This secondary brain injury is particularly concerning. Although several clinical studies demonstrated that hyperoxia during post-CA care was associated with poor neurological outcomes, considerable debate is ongoing because of inconsistent results. Potential reasons for the conflicting results include differences in the definition of hyperoxia, the timing of exposure to hyperoxia, and PaO2 values used in analyses. Despite the conflicts, exposure to PaO2 > 300 mmHg through administration of unnecessary oxygen should be avoided because no obvious benefit has been demonstrated. The feasibility of titrating oxygen administration by targeting SpO2 at approximately 94% in patients recovering from CA has been demonstrated in pilot randomized controlled trials (RCTs). Such protocols should be further examined.

Keywords: Cardiac arrest; Hyperoxia; Hypoxic brain injury; Oxygen; Post cardia arrest syndrome.

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Conflict of interest statement

Competing interestsThe authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Pathophysiology of hyperoxia. The redundant oxygen resulting from hyperoxia causes overproduction of ROS, which has pathophysiological consequences. ROS induces lipid peroxidation, protein oxidation, DNA damage, which result in neural cell dysfunction. Hyperoxia also causes cerebral vascular constriction, decreased cardiac output, and pulmonary dysfunction, which introduce reductions in oxygen delivery to the brain
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