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J Thorac Cardiovasc Surg 1994;107:1006-1019
© 1994 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
New York, N.Y.
Supported by grant HL-45636-02 from the National Heart, Lung, and Blood Institute and in part by the Cardiothoracic Research Fund, Mount Sinai Medical Center, New York, N.Y.
Address for reprints: Craig Mezrow, MS, Department of Cardiothoracic Surgery, Mount Sinai Medical Center, P.O. Box 1028, New York, NY 10029.
Abstract
Although widely used for repair of complex cardiovascular pathologic conditions, long intervals of hypothermic circulatory arrest and low flow cardiopulmonary bypass may both result in cerebral injury. This study examines cerebral hemodynamics, metabolism, and electrical activity to evaluate the risks of cerebral injury after 60 minutes of hypothermic circulatory arrest at 8° C, 13° C, and 18° C, compared with 60 minutes of low flow cardiopulmonary bypass at 18° C. Thirty-two puppies were randomly assigned to one of four experimental groups and centrally cooled to the appropriate temperature. Serial evaluations of quantitative electroencephalography, radioactive microsphere determinations of cerebral blood flow, calculations of cerebral oxygen consumption, cerebral glucose consumption, cerebral vascular resistance, cerebral oxygen extraction, systemic oxygen metabolism, and systemic vascular resistance were done. Measurements were obtained at baseline (37° C), at the end of cooling, at 30° C during rewarming, and at 2, 4, and 8 hours after hypothermic circulatory arrest or low flow cardiopulmonary bypass. At the end of cooling, cerebral vascular resistance remained at baseline levels in all groups, but systemic vascular resistance was increased in all groups. Cerebral oxygen consumption became progressively lower as temperature was reduced: it was only 5% of baseline at 8° C; 20% at 13° C; and 34% and 39% at 18° C. Quantitative electroencephalography was silent in the 8° C and 13° C groups, but significant slow wave activity was present at 18° C. Systemic vascular resistance and cerebral oxygen consumption returned to baseline values in all groups by 2 hours after hypothermic circulatory arrest or low flow cardiopulmonary bypass, but cerebral vascular resistance remained elevated at 2 and 4 hours, not returning to baseline until 8 hours after hypothermic circulatory arrest or low flow cardiopulmonary bypass. All but two of the long-term survivors (27 of 32) appeared neurologically normal; after hypothermic circulatory arrest at 8° and 18° C two animals had an unsteady gait. Comparison of quantitative electroencephalography before operation and 6 days after operation showed a significant increase in slow wave activity (delta activity) after hypothermic circulatory arrest and low flow cardiopulmonary bypass at 18° C, a change that suggests possible cerebral injury. Although undetected after operation by simple behavioral and neurologic assessment, significant differences in cerebral metabolism, vasomotor responses, and quantitative electroencephalography do exist during and after hypothermic circulatory arrest and low flow cardiopulmonary bypass at various temperatures and may be implicated in the occurrence of cerebral injury. The data from this study suggest that for an interval of 60 minutes, hypothermic circulatory arrest at 8° C or 13° C may provide cerebral protection superior to hypothermic circulatory arrest or low flow cardiopulmonary bypass at 18° C. (J THORACCARDIOVASCSURG1994;107:1006-19)
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