Cerebral physiology of hypothermia and hypothermic acid-base management during cardiopulmonary bypass

Abstract

Cerebral hypothermia is the principal means of protecting the brain during cardiac surgery, permitting periods of reduced perfusion and/or circulatory arrest. For example, at 10–20°C, circulatory arrest for 45–75 minutes is tolerated in animals without subsequent behavioral or histopathologic evidence of neurologic injury. Nevertheless, clinically, die protective effect of hypothermia is far from complete. In children undergoing hypothermic circulatory arrest under equivalent conditions, coma, seizures, choreoathetosis, and developmental retardation are recognized as potential neurologic sequels, occurring widi a combined incidence of 10-30%. Neurologic complications (stroke, neuropsychologic change) also occur with distressing frequency in adults undergoing cardiac surgery, even in the absence of circulatory arrest. An improved understanding of the physiology of cerebral hypothermia during cardiopulmonary bypass and hypothermic arrest is needed to improve upon these results. This review will address current concepts and controversies regarding flow of blood to the brain and its metabolism during hypothermic cardiopulmonary bypass and their relationship to current techniques for cerebral protection.