The Neurologic Sequelae of Cardiopulmonary Bypass-Induced Cerebral Hyperthermia and Cerebroprotective Strategies

Rush University, Department of Perfusion Technology, Rush Presbyterian St. Luke’s Medical Center, Chicago, Illinois

^* Address correspondence to: Todd Scheffer, BS, Rush University, College of Health Science, Department of Perfusion Technology, 600 S. Paulina Street, Chicago, IL 60612.E-mail: tschef@earthlink.net

Received: 22 March 2002
Accepted: 12 January 2003

Abstract

Cerebral hyperthermia during the rewarming phase of cardiopulmonary bypass (CPB) is associated with adverse outcomes. Cerebral hyperthermia can exacerbate a preexisting injury prior to rewarming, and may be damaging in itself. Temperature and cerebral metabolic rate (CMRO₂) play a vital role in cerebral autoregulation. Therefore, hyperthermia can have a strong impact on cerebral oxygen transfer, and neurologic outcome. Glutamate levels can increase during cerebral hyperthermia, leading to eventual cell death. Rapid rewarming decreases jugular venous hemoglobin saturation, creating a mismatch between cerebral oxygen consumption and delivery. With these ill effects in mind, cerebral protection during CPB is imperative. Special attention should be given during rewarming to prevent these harmful outcomes. Pharmacologic agents such as sodium nitroprusside can be used to assist the rewarming process. Temperature management is the key component during the rewarming phase of CPB in the prevention of cerebral hyperthermia.