RAPID INCREASE IN DESFLURANE CONCENTRATION IS ASSOCIATED WITH GREATERTRANSIENT CARDIOVASCULAR STIMULATION THAN WITH RAPID INCREASE IN ISOFLURANE CONCENTRATION IN HUMANS

Background: Increases in desflurane and isoflurane concentrations can transiently increase arterial blood pressure or heart rate or both dur ing induction of anesthesia. The current study tested the hypothesis t hat a rapid increase of desflurane concentration in humans increases s ympathetic activity and hormonal variables and heart rate and arterial blood pressure more than does an equivalent increase in isoflurane co ncentration. Methods: Twelve healthy male volunteers were assigned ran domly to receive desflurane and on a separate occasion isoflurane. Aft er Induction of anesthesia with propofol 2 mg/kg, anesthesia was maint ained at 0.55 MAC (desflurane, 4.0%; isoflurane 0.71% end-tidal) for 3 2 min. Mechanical ventilation maintained normocapnia throughout anesth esia. Mean arterial blood pressure and heart rate were recorded contin uously, and arterial blood was sampled for plasma catecholamine and va sopressin (AVP) concentrations, and plasma renin activity. Anesthetic concentration was increased rapidly to 1.66 MAC (desflurane, 12.0%; is oflurane 2.12% end-tidal), and maintained at this concentration for 32 min, and then rapidly decreased to and maintained at 0.55 MAC for an additional 32 min. Results: Neither anesthetic produced sympathetic or cardiovascular stimulation during their initial rapid wash-in to 0.55 MAC. The rapid increase to 1.66 MAC increased mean arterial blood pre ssure, heart rate, and plasma epinephrine and norepinephrine concentra tions, and plasma renin activity with both desflurane and isoflurane, the former usually producing a response of greater magnitude than the latter. Plasma AVP concentration increased with desflurane only. Incre ased mean arterial blood pressure returned to control In 4 min. Heart rate decreased 50% of the difference between its peak and the value at 32 min at 1.66 MAC in 2 min with desflurane and in 4 min with isoflur ane but did not return to the value at 0.55 MAC with either anesthetic . With desflurane, plasma epinephrine and AVP concentrations decreased quickly from their peak values, remaining elevated for 8 min. Decreas e of concentrations of desflurane and isoflurane from 1.66 MAC to 0.55 MAC rapidly decreased heart rate and increased mean arterial blood pr essure with both anesthetics. Thirty-two minutes after return to 0.55 MAC, with both anesthetics, only heart rate remained increased relativ e to the values at 32 min of the initial period of 0.55 MAC anesthesia . Conclusions: In healthy male volunteers, rapid increases of desflura ne or isoflurane from 0.55 to 1.66 MAC increase sympathetic and renin- angiotensin system activity, and cause transient increases in arterial blood pressure and heart rate. Desflurane causes significantly greate r increases than isoflurane, and also causes a transient increase in p lasma AVP concentration. The temporal relationships suggest that the i ncreased sympathetic activity increases mean arterial blood pressure a nd heart rate, with mean arterial blood pressure also increased by inc reased plasma AVP concentration, whereas the delayed, increased plasma renin activity is likely a response to the ensuing hypotension, or ea rlier inhibition by AVP, or both.