Cerebral function and preservation during cardiac arrest

Abstract

Neurologic impairment remains a serious consequence of cardiac arrest. While current investigations are difficult to compare due to their lack of standardization, our understanding of the pathophysiology of CNS ischemia has been greatly increased. Ion fluxes, especially K and Ca, may contribute to injury by initiating a cascade of events culminating in free fatty acid, prostaglandin, and free radical formation, with their related pathogenetic potential. Treatment measures currently consist of CPR (although disagreement exists as to which form of CPR), standard supportive measures, and attention to intracranial pressure control. There is some experimental evidence to support the use of calcium channel-blockers, phenytoin, prostaglandin inhibitors, and free-radical scavengers or inhibitors; however, no human trials have been performed. Steroids and barbiturates have been investigated in human trials and do not appear to be efficacious in ameliorating CNS injury after cardiac arrest.