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Ann Thorac Surg 1987;43:391-396
© 1987 The Society of Thoracic Surgeons

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Articles

The Effect of Low-Flow Cardiopulmonary Bypass on Cerebral Function: An Experimental and Clinical Study

Divisions of Cardiovascular Surgery and Neurology and Department of Pathology, The Hospital for Sick Children, the Department of Clinical Biochemistry, The Toronto General Hospital, and the Departments of Surgery, Pathology, Clinical Biochemistry, The University of Toronto, Ontario, Canada

Accepted for publication June 20, 1986.

^* Address reprint requests to Dr. Coles, Division of Cardiovascular Surgery, The Hospital for Sick Children, 555 University Ave, Toronto, Ont, Canada M5G 1x8

Systemic flow rates (Q) during nonpulsatile hypothermic cardiopulmonary bypass (CPB) that are consistent with preservation of cerebral function have not to our knowledge been objectively denned. The effect of a sequential reduction in flow rates on cerebral cortical metabolism and function was evaluated in 6 mongrel dogs during hypothermic (25°C) CPB. Cerebral function was assessed using somatosensory cortical evoked potentials (SSEP); cerebral metabolism was assessed by adenosine triphosphate (ATP) and lactate content of snap-frozen gray matter biopsies taken from the hemisphere contralateral to that monitored for SSEP. A progressive decline in ATP levels was observed during flow reduction with virtually complete depletion of ATP at 0.25 L min^–1 m^–2 (p = .0003). The significant (p = .028) dependence of cortical ATP levels on perfusion pressure was no longer evident after adjusting for the effects of flow rate. Lactate levels increased during flow reduction (p = .028), especially at flow rates less than 0.5 L min^–1 m^–2. Somatosensory neural transmission remained intact until flow was reduced to 0.25 L min^–1 m^–2 in 5 animals and until total circulatory arrest in 1, at which time loss of the signal occurred. In addition, 5 patients were subjected to brief periods of low-flow CPB (Q = 1.0 L min^–1 m^–2) at 21° to 25°C. SSEPs remained intact during flow reduction, and postoperative neurologic evaluation was normal in all patients. We conclude that, in the absence of cerebral vascular disease, the flow rate threshold for incurring functional cerebral injury during hypothermic (25°C) nonpulsatile CPB is less than 1.0 L min^–1 m^–2. Preservation of cortical function during flow reduction, however, occurs at the expense of a reduction in cerebral metabolic reserve. Finally, flow rate rather than perfusion pressure per se appears primarily to influence cerebral function during low-flow bypass.

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