Propofol Does Not Ameliorate Cerebral Venous Oxyhemoglobin Desaturation During Hypothermic Cardiopulmonary Bypass

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Abstract
Reductions in cerebral venous oxyhemoglobin saturation (SjO2) occur during the rewarming phase of hypothermic cardiopulmonary bypass (CPB). We prospectively investigated the effects of propofol on these reductions in SjO2 (SjO2 <50%). Fiberoptic jugular bulb catheters were inserted in 30 patients undergoing coronary artery bypass grafting. Patients were randomly allocated to a test or control group. Test group patients (n = 15) received a propofol IV infusion titrated to electroencephalographic burst suppression during CPB. No significant differences in SjO2 <50% were found between the groups either by blood sampling and bench oximetry or fiberoptic oximetry. The arteriovenous difference in lactate concentration became negative in 59 of 120 samples. Propofol was associated with an increased incidence of hypotension (mean arterial pressure <50 mm Hg) (P = 0.023), an increased requirement for vasoconstrictor therapy (P = 0.025), and increases in the lactate oxygen index (P < 0.01). Propofol, when administered in doses that produce electroencephalographic burst suppression, does not attenuate the frequency or extent of reductions of SjO2 below 50% during rewarming from hypothermic CPB. However, it is associated with arterial hypotension and an increase in cerebral anaerobic metabolism. Reductions in cerebral venous oxyhemoglobin saturation during the rewarming phase of cardiopulmonary bypass may be related to brain injury. When administered in doses sufficient to produce electroencephalographic burst suppression, propofol did not attenuate the frequency or extent of such reductions in cerebral venous oxyhemoglobin saturation.