EVALUATION OF CEREBRAL METABOLISM AND QUANTITATIVE ELECTROENCEPHALOGRAPHY AFTER HYPOTHERMIC CIRCULATORY ARREST AND LOW-FLOW CARDIOPULMONARYBYPASS AT DIFFERENT TEMPERATURES

Although widely used for repair of complex cardiovascular pathologic c onditions, long intervals of hypothermic circulatory arrest and low fl ow cardiopulmonary bypass may both result in cerebral injury. This stu dy examines cerebral hemodynamics, metabolism, and electrical activity to evaluate the risks of cerebral injury after 60 minutes of hypother mic circulatory arrest at 8 degrees C, 13 degrees C, and 18 degrees C, compared with 60 minutes of low flow cardiopulmonary bypass at 18 deg rees C. Thirty-two puppies were randomly assigned to one of four exper imental groups and centrally cooled to the appropriate temperature. Se rial evaluations of quantitative electroencephalography, radioactive m icrosphere determinations of cerebral blood how, calculations of cereb ral oxygen consumption, cerebral glucose consumption, cerebral vascula r resistance, cerebral oxygen extraction, systemic oxygen metabolism, and systemic vascular resistance mere done. Measurements were obtained at baseline (37 degrees C), at the end of cooling, at 30 degrees C du ring rewarming, and at 2, 4, and 8 hours after hypothermic circulatory arrest or low flow cardiopulmonary bypass. At the end of cooling, cer ebral vascular resistance remained at baseline levels in all groups, b ut systemic vascular resistance was increased in all groups. Cerebral oxygen consumption became progressively lover as temperature was reduc ed: it was only 5 % of baseline at 8 degrees C; 20% at 13 degrees C; a nd 34% and 39 % at 18 degrees C. Quantitative electroencephalography w as silent in the 8 degrees C and 13 degrees C groups, but significant slow wave activity was present at 18 degrees C. Systemic vascular resi stance 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 ele vated 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 degrees and 18 degr ees C two animals had an unsteady gait. Comparison of quantitative ele ctroencephalography before operation and 6 days after operation showed a significant increase in slow wave activity (delta activity) after h ypothermic circulatory arrest and low flow cardiopulmonary bypass at 1 8 degrees C, a change that suggests possible cerebral injury. Although undetected after operation by simple behavioral and neurologic assess ment, significant differences in cerebral metabolism, vasomotor respon ses, and quantitative electroencephalography do exist during and after hypothermic circulatory arrest and low how cardiopulmonary bypass at various temperatures and may be implicated in the occurrence of cerebr al injury. The data from this study suggest that for an interval of 60 minutes, hypothermic circulatory arrest at 8 degrees C or 13 degrees C may provide cerebral protection superior to hypothermic circulatory arrest or low flow cardiopulmonary bypass at 18 degrees C.