More than 2,500 patients per year suffer severe strokes following coronary artery bypass surgery. Twenty thousand (20,000) patients or more experience transient cerebral dysfunction. More than half of all patients undergoing heart surgery demonstrate enzymatic evidence of neurologic insult. Prevention of neurological deficits following coronary artery bypass graft surgery would increase the safety of this frequently-performed operation. The etiology of neurological deficits after cardiac surgery may be embolic in origin or may be related to cerebral hypoperfusion. Nevertheless, despite the fact that cerebral perfusion is impaired either in a global or a diffuse, multifocal fashion, there is very little data available regarding the functional characteristics of the human cerebral circulation during cardiopulmonary bypass. This proposal is intended to further characterize the physiologic responses of the cerebral circulation during cardiopulmonary bypass and to formulate hypotheses regarding potentially effective prophylactic or therapeutic strategy which may then be subjected to clinical testing. This proposal will study two questions. First, the changes in cerebral blood flow and cerebral metabolism produced by changes in carbon dioxide tension during cardiopulmonary bypass will be defined. Two strategies for the management of carbon dioxide tension and pH during cardiopulmonary bypass will be compared in terms of their effects on cerebral blood flow and metabolism. Second, the effects of a reduction in mean arterial pressure on cerebral blood flow and metabolism will be studied. Three different, commonly employed methods for avoiding high mean arterial pressure during cardiopulmonary bypass will be studied in relationship to their interaction with changes in acid-base management. The interventions to be studied include a reduction in blood flow through the pump-oxygenator, the effects of the vasodilator sodium nitroprusside, and the effects of the anesthetic isoflurane, a drug which reduces systemic blood pressure and also causes a reduction in the cerebral metabolic rate for oxygen.
Showing the most recent 10 out of 12 publications
