Effects of 1 MAC desflurane on cerebral metabolism, blood flow and carbon dioxide reactivity in humans

Abstract

We investigated the cerebral haemodynamic effects of 1 MAC desflurane anaesthesia in nine male patients scheduled for elective coronary bypass grafting. For the measurement of cerebral blood flow (CBF) a modified Kety-Schmidt saturation technique with argon as inert tracer gas was used. Measurements of CBF were made before induction of anaesthesia and 30 min after induction under normocapnic, hypocapnic and hypercapnic conditions in sequence. Changes in mean arterial pressure after induction of anaesthesia and during the course of the study were minimized using norepinephrine infusion. In comparison with the awake state under normocapnic conditions, desflurane reduced mean cerebral metabolic rate of oxygen (CMRO2) by 51% and mean cerebral metabolic rate of glucose (CMRglc) by 35%. Concomitantly, CBF was significantly reduced by 22%; jugular venous oxygen saturation (SjvO2) increased from 58 to 74%. Hypo- and hypercapnia caused a 22% decrease and a 178% increase in CBF, respectively. These findings may be interpreted as the result of two opposing mechanisms: cerebral vasoconstriction induced by a reduction of cerebral metabolism and a direct vasodilator effect of desflurane. CBF alterations under variation of PaCO2 indicate that cerebrovascular carbon dioxide reactivity is not impaired by application of 1 MAC desflurane.

Cerebrovascular reactivity to carbon dioxide is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane

“…Therefore, what is measured clinically is the result of a subtle balance between these two antagonizing effects. It is possible that at the higher desflurane concentration the cerebral vasconstriction as a result of the decreased CMRO 2 becomes more prominent, as suggested by Mielck et al 3 In that study, CCO 2 R was preserved at 1.0 MAC desflurane.…”

“…Studies in adults have reported that CCO 2 R is preserved during desflurane anesthesia. [2][3][4] In children, the effects of desflurane on CCO 2 R are not as well defined. In a study of ten children, 4 cerebral blood flow velocity (CBFV) was recorded during the first ten minutes of desflurane administration while the EtCO 2 was changed from 40 to 30 mmHg.…”

“…2 Although the authors only examined the CCO 2 R at 25 and 35 mmHg P a CO 2 , they reported that CCO 2 R at 1.0 MAC desflurane and isoflurane is maintained at about 1.3 to 1.6 %/mmHg. Mielck et al 3 used a modified Kety-Schmidt saturation technique with argon as inert tracer gas to measure CBF in adults and suggested that CCO 2 R is preserved at 1.0 MAC desflurane between an EtCO 2 of 30 and 50 mmHg.…”

Gas exchange with a reflecting system for inhalational anaesthesia

“…In clinical concentrations, desflurane and isoflurane preserve reactivity of cerebral circulation and coupling of changes in CO 2 and metabolism to blood flow in the brain. 16 In the presence of sevoflurane autoregulation of cerebral blood flow is preserved below 1.5 MAC. 17 …”

Wpływ stopniowo narastających stężeń desfluranu na mózgowe ciśnienie perfuzyjne u królika

“…The cardiovascular effects of desflurane manifest themselves mostly as a dose-dependent increase in heart rate and a reduction in arterial pressure, resulting mainly from dilatation of the vascular bed with the resultant decrease in peripheral resistance, and from negative inotropic action, albeit to a lesser extent [1, [5][6][7][8][9]. As in the peripheral circulation, desflurane dilates the cerebral vessels, which results in increased cerebral blood volume (CBV) likely to lead to increases in intracranial pressure (ICP) [6,10,11]. The factors determining intracranial homeostasis include cerebral blood flow (CBF), cerebral metabolic rate (CMR), autoregulation and reactivity of the cerebral vessels to PaCO 2 .…”