Abstract

The heart is incapable of storing significant oxygen or substrates and thus is entirely dependent on a continuous delivery of flow in order to support its high metabolic state. Following cardiac arrest, myocardial tissue oxygen tension falls rapidly and aerobic production of ATP ceases. Without re-oxygenation of the ischemic myocardium, return of spontaneous circulation (ROSC) cannot be achieved. The oxygen paradox which has been described regarding other ischemia-reperfusion conditions seems to have application in cardiac arrest. It is clear that some level of oxygenation is necessary to achieve ROSC, however post ROSC there appears to be increased toxicity associated with hyperoxia. The optimal conditions for re-oxygenation in the setting of cardiac arrest remain ill defined at present.

Keywords: cardiac arrest, oxygen, myocard, oxygen delivery, Adenosine-5′-triphosphate (ATP), mitochondria, measurement of tissue oxygen, oxygen paradox

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