The authors could not determine whether interaction in blocking somatic responses in 50% of patients is additive. The MAC of xenon is in the range of the values that were predicted in a previous study.

The bispectral index (BIS) is derived empirically from the electroencephalogram database of patients receiving common anaesthetics, but it may not be valid for uncommon agents. Therefore, we investigated how xenon affects the BIS. Nine and 11 patients were anaesthetized with 0.8 of the minimal alveolar concentration (MAC) of isoflurane (0.92%) and xenon (56%), respectively. After the end of operation, these concentrations were decreased in decrements of 0.1 MAC (isoflurane 0.12% or xenon 7%) and each new concentration was maintained for 15 min. This was repeated until the patient first opened her eyes or squeezed the investigator's hand on command. Isoflurane and xenon at 0.8 MAC reduced the BIS to a median of 40 (range 36-53) and 36 (30-61), respectively. With decreasing concentrations of isoflurane, the BIS increased progressively and it reached a median of 96 (90-98) when the patients awoke. In contrast, four patients receiving xenon responded to verbal command while the BIS was below 50 [median 45 (range 41-49)]. The remaining seven patients in the xenon group awoke when their BIS was greater than 80 [median 96 (range 82-98)], but in four of them the BIS was no greater than 50 when the xenon concentration was only 0.1 MAC (7%) higher than that associated with awakening. We conclude that low BIS values (< 50) do not guarantee adequate hypnosis during xenon anaesthesia.

The MAC-awake of xenon is 33% or 0.46 times its MAC. In terms of the MAC-fraction, this is smaller than that for N2O but greater than those for isoflurane and sevoflurane. Unlike N2O, xenon interacts additively with isoflurane and sevoflurane on MAC-awake.

No abstract

SummaryXenon anaesthesia appears to have minimal haemodynamic effects. The purpose of this randomised prospective study was to compare the cardiovascular effects of xenon and nitrous oxide in patients with known ischaemic heart disease. In 20 patients who were due to undergo coronary artery bypass graft surgery, 30 min following induction of anaesthesia with fentanyl 30 lg.kg )1 and midazolam 0.1 mg.kg )1 but prior to the start of surgery, xenon or nitrous oxide 60% was administered for 15 min. The results showed that xenon caused a minimal decrease in the mean arterial pressure (from 81 (7) to 75 (8) mmHg, mean (SD)), but did not affect the systolic function of the left ventricle, as demonstrated by unchanged left ventricular stroke work index (LVSWI) and the fractional area change of the left ventricle (FAC) derived from transoesophageal echocardiography (TOE). However, in contrast, nitrous oxide was found to decrease the mean arterial pressure (from 81 (8) to 69 (7) mmHg), the LVSWI, and the FAC. The cardiac index, central venous and pulmonary artery occlusion pressures, systemic and pulmonary vascular resistances, and the TOE-derived E ⁄ A ratio through the mitral valve were unchanged by xenon or nitrous oxide. We conclude that xenon provides improved haemodynamic stability compared with nitrous oxide, conserving the left ventricular systolic function.