• W L Young.
• Department of Anesthesiology, Columbia University, New York, New York 10032.
• Anesth. Analg. 1992 Oct 1; 75 (4 Suppl): S32-7.

AbstractDesflurane causes dose-dependent decreases in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption (CMRO2), suggesting that desflurane is a cerebral arteriolar dilator with global flow-metabolism coupling similar to halothane and isoflurane. Desflurane is also similar to isoflurane in that cerebrovascular responsivity to carbon dioxide appears to be maintained. In the dog, arterial hypotension to 40 mm Hg induced with 2.4 MAC desflurane resulted in global decreases in cerebral blood flow of 60% and CMRO2 of 20%. Concentrations of cerebral metabolites of high-energy phosphates were not significantly deranged. The intracranial pressure data from humans are controversial. Desflurane and oxygen at 1 MAC caused sustained increases in cerebrospinal fluid pressure (maximum of 19 +/- 6 mm Hg) in patients undergoing craniotomy for mass lesion, despite prior establishment of hypocapnia. In a more recent study, the same investigators reported similar cerebrospinal fluid pressures before and after 0.5 MAC of either isoflurane or desflurane in 50% N2O. The electroencephalographic effects of desflurane are similar to those of isoflurane in humans, and burst suppression is easily achieved. There are no data available concerning possible interactions between desflurane and the outcome of a cerebral ischemic event. Similar to other potent volatile agents, desflurane can cause cerebral vasodilation and may result in intracranial pressure changes in vulnerable patients, but if adequate hyperventilation and depth of anesthesia are maintained, it is probably safe to use desflurane in a manner similar to isoflurane in patients with decreased intracranial compliance.

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