Search

Sevoflurane anaesthesia was conducted using a totally closed circuit PhysioFlex anaesthesia machine (PhysioFlex group) or with a standard Modulus CD anaesthesia machine (Modulus group) (n = 8 in each group). The PhysioFlex was used under closed system conditions and the Modulus was used under low-flow system conditions (flow rate 1 litre min-1). Concentrations of sevoflurane degradation products and the temperature of soda lime were compared. Degradation products in the circuit were measured hourly, and the temperature of soda lime was monitored. The only degradation product detected was CF2 = C(CF3)-O-CH2F (compound A). Maximum concentrations of compound A were significantly lower (median 8.5 (range 5.4-15.9) ppm) in the PhysioFlex than in the Modulus group (21.2 (16.5-27.4) ppm) (P < 0.05). The maximum temperature of soda lime was also significantly lower in the PhysioFlex group (35.3 (32.1-36.3) degrees C vs 44.6 (43.0-47.1) degrees C, respectively) (P < 0.05). Hourly compound A concentrations were lower in the PhysioFlex group than in the Modulus group. End-tidal sevoflurane concentrations during measurement of degradation products were not different between groups. Therefore, use of the totally closed PhysioFlex system may significantly reduce compound A concentrations compared with low-flow anaesthesia using a standard anaesthesia machine.

We studied 61 healthy ASA 1 patients (aged 2-6 yr) to determine if fentanyl affects the minimum alveolar concentration which blocks adrenergic responses to skin incision (MAC-BAR) in 50% of children in the presence of 60% nitrous oxide. Patients were allocated randomly to one of three fentanyl groups to receive 0, 2 or 4 micrograms kg-1. Patients also received sevoflurane at a preselected end-tidal concentration according to an 'up-and-down' design. After a steady-state sevoflurane concentration had been maintained for at least 15 min, fentanyl was given i.v. Skin incision was performed 5 min after administration of fentanyl. The response was considered positive if heart rate (HR) or mean arterial pressure (MAP) increased by 15% or more. The MAC-BAR of sevoflurane was 1.45 MAC (95% confidence intervals 1.25-1.65 MAC), and this was reduced markedly to 0.63 MAC and 0.38 MAC by addition of fentanyl 2 and 4 micrograms kg-1, respectively. A ceiling effect was not observed and there was a significant difference between the 2 and 4 micrograms kg-1 groups.

We studied 80 healthy ASA 1 patients (aged 20-52 yr) to determine if fentanyl affects sevoflurane requirements for achieving 50% probability of no movement in response to laryngoscopy and tracheal intubation (MAC-TI). Patients were allocated randomly to one of four fentanyl dose groups (0, 1, 2 and 4 micrograms kg-1). Patients in each group received sevoflurane at a pre-selected end-tidal concentration according to an 'up-down' technique. After steady state sevoflurane concentration had been maintained for at least 10 min, fentanyl was administered i.v. Tracheal intubation was performed 4 min after administration of fentanyl, and patients were assessed as moving or not moving. Heart rate (HR) and mean arterial pressure (MAP) were recorded before induction of anaesthesia, just before administration of fentanyl, just before laryngoscopy for intubation, and after intubation. The MAC-TI of sevoflurane was 3.55% (95% confidence intervals 3.32-3.78%), and this was reduced markedly to 2.07%, 1.45% and 1.37% by addition of fentanyl 1, 2 and 4 micrograms kg-1, with no significant difference in the reduction between 2 and 4 micrograms kg-1, showing a ceiling effect. Fentanyl attenuated haemodynamic responses (HR and MAP) to tracheal intubation in a dose-dependent manner, even with decreasing concomitant sevoflurane concentration. Fentanyl 4 micrograms kg-1 suppressed the changes in HR and MAP more effectively than fentanyl 1 or 2 micrograms kg-1 at sevoflurane concentrations close to MAC-TI.

Low-flow (1 litre min-1) sevoflurane anaesthesia was used in 16 patients undergoing laparoscopic cholecystectomy (group LSC, n = 8) or tympanoplasty (group TP, n = 8), and concentrations of sevoflurane degradation products were measured. Degradation products in the circuit were measured hourly, and end-tidal carbon dioxide concentration, inspired and end-tidal sevoflurane concentrations, and carbon dioxide elimination were monitored. The only degradation product detected was CF2=C(CF3)-O-CH2F (compound A). The mean maximum concentrations of compound A were 21.6 (SEM 1.6) ppm and 19.6 (0.8) ppm in the LSC and TP groups, respectively (ns). The maximum temperatures of soda lime were 46.4 (0.5) degrees C and 44.8 (0.5) degrees C, respectively (P < 0.05). Hourly end-tidal sevoflurane concentrations and concentrations of sevoflurane degradation products were the same for both groups. Carbon dioxide elimination was the same for both groups 1 h after the start of anaesthesia, but was higher in group LSC after 2 h (P < 0.05). Intraperitoneal carbon dioxide insufflation associated with laparoscopic cholecystectomy had no effect on the concentration of sevoflurane degradation products.

We have compared concentrations of degradation products in the circle system during sevoflurane anaesthesia at different fresh gas flows. Twenty-four patients underwent sevoflurane anaesthesia with fresh gas flows of 1 litre min-1 (1L group), 3 litre min-1 (3L group), or 6 litre min-1 (6L group) (n = 8 in each group). During anaesthesia, the concentrations of degradation products were measured every hour, and the temperature of soda lime, end-tidal carbon dioxide concentrations, inspired and end-tidal sevoflurane concentrations, and carbon dioxide elimination were measured. CF2 = C (CF3)-O-CH2F (compound A) was the only degradation product detected. The mean maximum concentration of compound A was 19.7 (SD 4.3) ppm in the 1L group, 8.1 (2.7) ppm in the 3L group and 2.1 (1.0) ppm in the 6L group (P < 0.05). The maximum temperature of soda lime was 44.6 (1.5) degrees C in the 1L group, 37.0 (4.4) degrees C in the 3L group and 29.1 (5.1) degrees C in the 6L group (P < 0.05). There were no significant differences in end-tidal sevoflurane concentration or mean carbon dioxide elimination between the groups. Only compound A was detected following anaesthesia, with higher concentrations observed at lower flow rates.

We have studied 64 ASA I and II patients (aged 20-60 yr) to determine if nitrous oxide affects sevoflurane requirement for achieving 50% probability of no movement in response to verbal commands (MACawake). Patients were allocated randomly to one of four nitrous oxide concentration groups (0, 20, 40 and 60 vol.%). Patients in each group received sevoflurane at two different end-tidal concentrations according to a predetermined randomization table. After steady state sevoflurane and nitrous oxide concentrations had been maintained for at least 15 min, patients were assessed as being awake or asleep. The MACawake for sevoflurane was 0.63% and this was reduced significantly in a non-linear manner by increasing nitrous oxide concentration. A 50% reduction in MACawake was produced by a nitrous oxide concentration of 45%. The reduction in MACawake by nitrous oxide was non-linear; the interaction coefficient between nitrous oxide and sevoflurane being significantly less than zero (P = 0.0238), indicating that the reduction in MACawake by nitrous oxide was smaller than would be expected from simple additivity and that nitrous oxide antagonized the effects of sevoflurane in preventing response to verbal commands.