Comparison of the Effect of Etomidate and Desflurane on Brain Tissue Gases and pH during Prolonged Middle Cerebral Artery Occlusion

TLDR: The results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion, and treatment with desflurane significantly increases tissue P (O)2 alone and attenuates acidotic changes to prolongedmiddle cerebral artery Occlusion.

Abstract: Background: The authors compared the effects of etomidate and desflurane on brain tissue oxygen pressure (Po 2 ), carbon dioxide pressure (Pco 2 ), and pH in patients who had middle cerebral artery occlusion for >15 min. Methods: After a craniotomy, a probe that measures Po 2 , Pco 2 and pH was inserted into cortical tissue at risk for ischemia during middle cerebral artery occlusion. A burst suppression pattern of the electroencephalogram was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) started before middle cerebral artery occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. Results: During baseline conditions, tissue Po 2 , Pco 2 , and pH were similar between the two groups (Po 2 = 15 mmHg, Pco 2 = 60 mmHg,pH = 7.1). During administration of etomidate before middle cerebral artery occlusion, tissue Po 2 decreased in five of six patients without a change in Pco 2 or pH. During administration of 9% desflurane, tissue Po 2 and pH increased before middle cerebral artery clipping. Middle cerebral artery occlusion for an average of 33 min with etomidate and 37 min with desflurane produced a decrease in pH with etomidate (7.09 to 6.63, P < 0.05) but not with desflurane (7.12 to 7.15). Conclusion: These results suggest that tissue hypoxia and acidosis are often observed during etomidate treatment and middle cerebral artery occlusion. Treatment with desflurane significantly increases tissue Po 2 alone and attenuates acidotic changes to prolonged middle cerebral artery occlusion.