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Background: We evaluated the effect of low-flow sevoflurane anaesthesia, in which compound A is generated, and isoflurane anaesthesia, in which compound A is not generated (n=13 in each group), on hepatocellular integrity using a glutathione S-transferase (GST). a GST is a more sensitive and specific marker of hepatocellular damage than is aminotransferase activity and correlates better with hepatic histology. Methods: Sevoflurane or isoflurane were delivered without nitrous oxide with a fresh gas flow of 1 l/min. Concentrations of compound A in the circuit were measured hourly, and plasma a GST concentrations were measured perioperatively. Results: Mean duration of anaesthesia was 338±92 min in the sevoflurane group and 320±63 min in the isoflurane group. Mean compound A concentration in the sevoflurane group was 28.6±9.0 ppm. There was no significant difference in a GST concentrations between the sevoflurane and isoflurane groups during or after anaesthesia. Conclusion: These results indicate that low-flow sevoflurane and isoflurane anaesthesia have the same effect on hepatic function, as assessed by plasma a GST concentrations.

Background: Bispectral index (BIS) monitoring has been found to decrease the requirements for propofol, sevoflurane and desflurane and to improve recovery. We wanted to assess the effect of BIS monitoring on intraoperative isoflurane utilisation, and the early recovery profile. Methods: Eighty patients undergoing various surgical procedures were studied. In the first phase of the study, patients were anaesthetised without the use of BIS, the anaesthetists being blinded to the BIS readings, and isoflurane being administered according to standard clinical practice (control group). In a second phase, isoflurane was titrated to maintain a BIS value between 40 and 60 during surgery, and then 60–70 during 15 min prior to the end of surgery (BIS group). Isoflurane consumption was measured. Recovery times and the time to achieve a modified Aldrete score of 9 were recorded. Results: Despite similar mean BIS levels during maintenance of anaesthesia, the cumulative time spent with BIS values between 40 and 60 during maintenance of anaesthesia was significantly longer in the BIS group as compared with the control group (P

Background: Sevoflurane has a lower blood:gas partition coefficient than isoflurane and thus should be associated with a more rapid recovery from anaesthesia. Methods: A review and meta-analysis were employed to examine the recovery profiles of adult patients following anaesthesia, comparing sevoflurane to isoflurane and sevoflurane to propofol. Results: There were significant differences in times to several recovery events that favoured sevoflurane to isoflurane anaesthesia, including time to emergence, response to commands, extubation, and orientation. Likewise, there were significant differences in times to the same recovery events following anaesthesia with sevoflurane versus propofol. There were no differences in time to recovery room discharge when comparing sevoflurane to isoflurane or propofol. Conclusion: The observed differences between sevoflurane and isoflurane or propofol anaesthesia support the postulate that the use of sevoflurane is associated with a more rapid recovery from anaesthesia than either isoflurane or propofol.

Background: Electroencephalogram (EEG) and somatosensory evoked potentials (SEPs) are altered by inhalation anaesthesia. Nitrous oxide is commonly used in combination with volatile anaesthetics. We have studied the effects of nitrous oxide on both EEG and SEPs simultaneously during isoflurane burst-suppression anaesthesia. Methods: Twelve ASA I-II patients undergoing abdominal or orthopaedic surgery were anaesthetized with isoflurane by mask. After intubation and relaxation the isoflurane concentration was increased to a level at which an EEG burst-suppression pattern occurred (mean isoflurane end-tidal concentration 1.9 (SD 0.2) %. With a stable isoflurane concentration, the patients received isoflurane-air-oxygen and isoflurane-nitrous oxide-oxygen (FiO2 0.4) in a randomized cross-over manner. EEG and SEPs were simultaneously recorded before, and after wash-out or wash-in periods for nitrous oxide. The proportion of EEG suppressions as well as SEP amplitudes for cortical N20 were calculated. Results: The proportion of EEG suppressions decreased from 53.5% to 34% (P< 0.05) when air was replaced by nitrous oxide. At the same time, the cortical N20 amplitude was reduced by 69% (P < 0.01). Conclusion: The results suggest that during isoflurane anaesthesia, nitrous oxide has a different effect on EEG and cortical SEP at the same time. The effects of nitrous oxide may be mediated by cortical and subcortical generators.

Background: The pharmacodynamic profile of muscle relaxants is usually changed by volatile anaesthetics. These changes seem to be time-dependent, even though few data are available to substantiate this. Methods: We studied neuromuscular effects of a single dose of mivacurium (0.2 mg kg -1 ) during short and intermediate duration of isoflurane anaesthesia. Forty-five children 1-10 years of age were randomized to receive 1.5% end-tidal concentration of isoflurane in N 2 O/O 2 for 10 or 30 min (groups Iso-10 and Iso-30, respectively) or to receive nitrous oxide in oxygen for 10 min (Group N 2 O) before 0.2 mg. kg -1 of mivacurium was given. Neuromuscular response was recorded by adductor pollicis electromyogram. Results: The onset time of mivacurium was shorter in Group Iso-30, 1.7 (1.0-2.3) min than in Group Iso-10, 2.3 (1.7-3.3) min or Group N 2 O, 2.3 (1.7-3.3) min (median with 10-90% percen-tiles) (P

R/T-wave amplitude ratio of electrocardiogram (ECG), heart rate (HR) and systolic arterial pressure (SAP) were recorded in 15 patients awake, at 1 minimal alveolar concentration of isoflurane before and during surgery, and in deep anaesthesia (electroencephalogram burst suppression) during surgery. R/T-wave amplitude ratio and HR were sensitive to both surgery and changes in the level of isoflurane anaesthesia; induction of anaesthesia, skin incision and the rapid increase in the concentration of isoflurane all significantly decreased the T-wave amplitude, without influence on the R-wave. Changes in the T-wave amplitude correlated directly to HR. SAP increased at skin incision and decreased when the anaesthesia was deepened. The authors conclude that the R/T-wave amplitude ratio of ECG provides a reliable method for monitoring the sympathetic tone during isoflurane anaesthesia.

Fifty unpremedicated patients scheduled for outpatient restorative dentistry and/or oral surgery lasting 2 to 4 h were anaesthetized with either propofol infusion or isoflurane inhalation. Before induction of anaesthesia with propofol (2.5 mg.kg-1), all patients were given 75 mg of diclofenac and 0.01 mg.kg-1 vecuronium intravenously. Intubation was facilitated with suxamethonium (1.5 mg.kg-1) and anaesthesia was maintained in random order either with propofol infusion (12 mg.kg-1.h-1 for the first 20 min, 9 mg.kg-1.h-1 for the next 20 min, and 6 mg.kg-1.h-1 for the rest of the anaesthesia) or with isoflurane (inspired concentration 1-2.5%), both with nitrous oxide and oxygen (30%). The patients breathed spontaneously using a non-rebreathing circuit. Patients given propofol infusion became re-orientated faster (11.0 +/- 5.5 min vs. 16.5 +/- 7.5 min; P less than 0.01) and at 30 min walked along a straight line better (P less than 0.01). At 60 min, none of the propofol patients displayed an unsteady gait, whereas 11 of the 25 isoflurane patients did (P less than 0.001). None of the patients receiving propofol had emesis at the clinic, compared with 10 of the 25 patients receiving isoflurane (P less than 0.001). The overall incidence of emesis was 2 of 25 and 14 of 25 in the propofol and isoflurane groups, respectively (P less than 0.01). Patients receiving propofol were discharged home earlier than patients receiving isoflurane (80 +/- 14 min and 102 +/- 32 min, respectively; P less than 0.01). It is concluded that propofol allows early discharge of patients, even after long anaesthesias.

In order to evaluate the difference between poikilo-capnic (no CO2 added to inspired gas) and iso-capnic (CO2 added to keep end-tidal CO2 constant) hypoxic ventilatory responses (HVR) awake and during 0.6 MAC isoflurane anaesthesia, seven cardio-pulmonary healthy patients were investigated. Pneumotachography and capnography were used before and during hypoxia (end-tidal O2 tension approx. 7 kPa). In the awake stale, poikilo-capnic hypoxic challenges resulted in an increased HVR as indicated by a VE that on average increased by 1.4 ± 1.0 (mean ± s.d.) 1 · min−1, whereas the iso-capnic hypoxic challenges resulted in a VE increase that was 4.7 ± 2.3 1 · min−1 on average. In the anaesthetized state, the corresponding value during poikilocapnia was 1.3 ± 0.8 1 · min−1 (88% of the awake responses, n.s.) and during iso-capnia 2.3 ± 1.4 1 · min−1 (49% of the awake, P < 0.02). Awake HVR was achieved by greater tidal volumes during poikilocapnia as well as during isocapnic challenges, while respiratory rates were unchanged. In the anaesthetized state, during poikilocapnia, however, HVR was mediated by an increased respiratory rate, (from 17.5 ± 1.7 breath · min−1 to 20.2 ± 2.2) and during isocapnia by a combination of increased rate (from 17.1 ± 1.9 breath · min−1 to 19.1 ± 1.8) and tidal volume (from 496 ± 80 to 560 ± 83 ml). It is concluded that poikilocapnic HVR is maintained at 0.6 MAC isoflurane whereas iso-capnic HVR is depressed by 50%. In addition, both poikilo- and iso-capnic HVR were accomplished by greater tidal volumes at unchanged respiratory rates in the awake state while the opposite occurred during isoflurane anaesthesia. The more dominating chronotropic HVR during hypoxic challenge under anaesthesia will have to be further clarified in experimental studies.

Short latency somatosensory evoked potentials (SEPs) to median nerve stimulation during isoflurane anaesthesia were recorded in 12 elective-surgery patients. The effect of isoflurane on the shape, amplitude and latency of SEPs was evaluated. SEPs were recorded at awake, 1 MAC, 1.5 MAC, at electroencephalogram (EEG) burst suppression and at continuous suppression levels. Finally, SEPs were recorded when anaesthesia was lightened back to 1 MAC. The peak latency and amplitude of the first cortical N20 wave were measured. The latencies increased with increasing isoflurane concentrations. At high concentrations only an almost monophasic N20 wave was recorded, reduced in shape and amplitude. No specific changes could be correlated with the burst suppression or suppression patterns. This suggests that EEG and SEP generators are differently affected with increasing isoflurane concentration. The results indicate that SEPs can also be recorded in drug-induced EEG suppression.

The effect of isoflurane administration on diaphragmatic activity was investigated in six anaesthetized mechanically ventilated dogs. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure (Pdi) generated during supramaximal stimulation of both cervical phrenic nerves at frequencies of 0.5, 10, 20, 50 and 100 Hz under partially isometric conditions at 1, 1.5 and 2 minimum alveolar anaesthetic concentrations (MAC), after maintaining 1 h of stable conditions. Pdi measurements were made at the start of the stimulation (initial) and at the end of a 2-s period (2-s). The force-frequency relationship was compared at each anaesthetic level. For single twitch (0.5 Hz) stimulation, the time constant of diaphragmatic relaxation was also assessed. The sequence of changing anaesthetic depth was altered in random fashion between animals. Pdi amplitude at single twitch stimulation was unchanged at the three anaesthetic concentrations. There was no significant difference in initial Pdi at various stimulus frequencies with increasing depth of isoflurane anaesthesia. In addition, no change in 2-s Pdi during low frequency stimulation (10 and 20 Hz) was noted during any of the three levels of anaesthesia. By contrast, 2-s Pdi with 50 Hz stimulation during 2 MAC isoflurane exposure decreased significantly below Pdi levels seen at 1 and 1.5 MAC (P < 0.01). Furthermore, 2-s Pdi at 100 Hz stimulation decreased significantly in a dose-dependent fashion. From these results, we conclude that isoflurane reduces diaphragmatic activity at higher stimulation frequencies of 50 and 100 Hz.

EEG burst suppression pattern was recorded during propofol and isoflurane anaesthesia. Using a long time constant, i.e. a high-pass filter with low cut-off frequency, revealed slow potentials, DC shifts, during bursts. These have been extensively studied in conjunction with cognitive-evoked potentials and epileptic discharges, but not previously in burst suppression EEG.

The costs of anaesthetic drugs, intravenous agents as well as gases, were studied for different anaesthetic techniques in a medium-sized operative procedure, cholecystectomy. Three anaesthetic breathing systems were used: a non-rebreathing system, a circle absorber system with medium fresh gas flows of 3-6 l/min, and a low-flow circle system. Anaesthesia without volatile inhalation agents used with a low-flow technique was the least expensive, and anaesthesia with isoflurane in a non-rebreathing system was the most expensive. The costs of anaesthesia without volatile inhalation agents in a non-rebreathing system, enflurane anaesthesia in a circle system with medium fresh gas flows, and isoflurane anaesthesia with low-flow technique were similar.

Brainstem auditory evoked potentials (BAEP) were determined in 12 volunteers. The effect of isoflurane anaesthesia on BAEP was determined in six patients. Body temperature and end-tidal CO2% were controlled. Increasing end-tidal isoflurane concentration from 0.6-2.4% increased BAEP wave I, III and V latencies. The amplitude of wave V decreased with increasing isoflurane concentration. Thus a dose-related change was demonstrated between end-tidal concentration of isoflurane and BAEP latencies.

A case of malignant hyperthermia during isoflurane anaesthesia without the use of muscle relaxants in a healthy 7-year-old girl is presented. In this case only premedication and nitrous oxide were used together with isoflurane. Thus isoflurane by itself can trigger malignant hyperthermia, even in the absence of muscle relaxants.

With atracurium and vecuronium, spontaneous recovery of residual neuromuscular blockade monitored electromyographically during 0.5% isoflurane anaesthesia was studied in 60 patients undergoing plastic surgery. After thiopentone, in random order, either atracurium 0.5 mg kg-1 or vecuronium 0.1 mg kg-1 was administered and isoflurane added to N2O and O2 mixture. Following spontaneous recovery of both the single twitch amplitude (T1) to 75% of the control value and the train-of-four ratio (TOF ratio) to 75%, incremental doses of the relaxant were given to maintain the T1 at less than 10%. Before the end of surgery, the blockade was again permitted to recover spontaneously. During the initial spontaneous recovery, the mean recovery time of T1 from 25% to 75% (the recovery index) with atracurium was longer (P less than 0.001) than that with vecuronium (13.2 min and 10.1 min, respectively) but, during the second recovery, the mean recovery index was shorter (P less than 0.05) with atracurium than with vecuronium (16.1 min and 19.8 min, respectively). The recovery time from T1 75% to TOF ratio 75%, indicating the recovery rate of residual neuromuscular blockade, with atracurium was about 15 min after both the initial and the second recoveries. With vecuronium, the respective recovery times were significantly (P less than 0.001) longer (25.6 min and 38.5 min, respectively). It is concluded that with vecuronium there is slower spontaneous recovery of residual neuromuscular blockade than with atracurium.

To date, only two cases of malignant hyperthermia following isoflurane anaesthesia have been reported, neither of which were fatal. This case describes a very malignant form of hyperthermia after isoflurane, in which the laboratory values were grossly abnormal, and with multi-organ failure and death finally supervening.