Determinants of cerebral perfusion during cardiopulmonary bypass

The risk of postoperative neurologic dysfunction in patients undergoing cardiac surgery remains high despite continued improvements in myocardial protective strategies. Part of this neurologic morbidity can be attributed to patients' increased age and underlying pathology, but other factors adversely affecting cerebral blood flow and cerebral metabolism during cardiopulmonary bypass may also contribute. Particulate microembolization during cardiopulmonary bypass appears to be a major cause of postoperative neurologic dysfunction and the pH-stat method of carbon dioxide management during hypothermia may potentiate neurologic damage by allowing a greater embolic load to be delivered to the brain. Echocardiography and transcranial Doppler methods may contribute to reducing the incidence of cerebral embolization by recognizing the timing and number of microemboli. Although hypothermia confers cerebral protection, rewarming may unmask and perhaps potentiate any ischemic damage that occurred with embolization during hypothermia. Both the degree and speed of rewarming may be important factors contributing to the extent of ischemic damage and ultimately neurologic function. In addition, many other factors related to cardiopulmonary bypass can alter cerebral perfusion and metabolism, such as nonpulsatile flow, hemodilution, pressure autoregulation, anesthetic and cerebroprotective drugs, and the neuroimmune response to bypass. In this review, the major factors affecting cerebral blood flow during cardiopulmonary bypass are discussed and their relative importance evaluated with regard to postoperative neurologic function.