Mj. Souter et al., PROPOFOL DOES NOT AMELIORATE CEREBRAL VENOUS OXYHEMOGLOBIN DESATURATION DURING HYPOTHERMIC CARDIOPULMONARY BYPASS, Anesthesia and analgesia, 86(5), 1998, pp. 926-931
Reductions in cerebral venous oxyhemoglobin saturation (Sjo(2)) occur
during the rewarming phase of hypothermic cardiopulmonary bypass (CPB)
. We prospectively investigated the effects of propofol on these reduc
tions in Sjo(2) (Sjo(2) <50%). Fiberoptic jugular bulb catheters were
inserted in 30 patients undergoing coronary artery bypass grafting. Pa
tients were randomly allocated to a test or control group. Test group
patients (n = 15) received a propofol IV infusion titrated to electroe
ncephalographic burst suppression during CPB. No significant differenc
es in Sjo(2) <50% were found between the groups either by blood sampli
ng and bench oximetry or fiberoptic oximetry. The arteriovenous differ
ence in lactate concentration became negative in 59 of 120 samples. Pr
opofol was associated with an increased incidence of hypotension (mean
arterial pressure <50 mm Hg) (P = 0.023), an increased requirement fo
r vasoconstrictor therapy (P = 0.025), and increases in the lactate ox
ygen index (P < 0.01). Propofol, when administered in doses that produ
ce electroencephalographic burst suppression, does not attenuate the f
requency or extent of reductions of Sjo(2) below 50% during rewarming
from hypothermic CPB. However, it is associated with arterial hypotens
ion and an increase in cerebral anaerobic metabolism. Implications: Re
ductions in cerebral venous oxyhemoglobin saturation during the rewarm
ing phase of cardiopulmonary bypass may be related to brain injury. Wh
en 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.