EFFECT OF DEEP HYPOTHERMIA AND CIRCULATORY ARREST ON CEREBRAL BLOOD-FLOW AND METABOLISM

The primary goal of monitoring cerebral blood flow and metabolism is to improve our understanding of the association with cardiopulmonary bypass and deep hypothermic circulatory arrest so that effective brain protection strategies can be developed and employed. A review of our cerebral blood flow/cardiopulmonary bypass database, presently totaling 275 neonates and infants, for the purposes of this publication, reveals certain trends and some conclusions that can be drawn. Deep hypothermic circulatory arrest continues to be a factor in the delayed recovery of cerebral blood flow and metabolism in these patients. Examining now and metabolism serially in the postoperative period shows that in the majority of patients, flow, metabolism and autoregulation return to normal within 24 hours after operation. Some patients' cerebral oxygen metabolism is unable to exert a protective response of increasing extraction in the setting of low cerebral blood flow. We have also observed that in the setting of low cardiac output after cardiac repair, cerebral blood flow is low. It is therefore likely that low cardiac output and pressure-passive cerebral blood flow potentiate brain ischemia after cardiopulmonary bypass and operation in some patients. We have also examined in our series of 275 patients selective neuroprotection strategies for their potential for improving recovery of cerebral blood flow and cerebral metabolism. Duration of cooling on cardiopulmonary bypass correlates directly with suppression of metabolism due to hypothermia. Low-flow cardiopulmonary bypass instead of deep hypothermic circulatory arrest, and topical brain cooling with ice during deep hypothermic circulatory arrest, improve cerebral blood flow and cerebral metabolic recovery.