PROPOFOL DOES NOT AMELIORATE CEREBRAL VENOUS OXYHEMOGLOBIN DESATURATION DURING HYPOTHERMIC CARDIOPULMONARY BYPASS

Citation
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
Citations number
18
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00032999
Volume
86
Issue
5
Year of publication
1998
Pages
926 - 931
Database
ISI
SICI code
0003-2999(1998)86:5<926:PDNACV>2.0.ZU;2-#
Abstract
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.