We have used the Leiden anaesthesia simulator, which makes use of a standard anaesthesia machine and monitors, and realistically simulates the anaesthesia work place. After obtaining informed consent, 28 anaesthetists and anaesthesia trainees in one hospital took part in the study. All participants were exposed to a pre-scripted simulated "control" scenario of anaphylactic shock (phase 1). The sessions were videotaped and the performances of individual participants were evaluated using a standardized scoring scheme. During phase 2, the participants were allocated randomly to undergo training in the management of either anaphylactic shock (group A, n = 13) or malignant hyperthermia (group B, n = 15) on the simulator. After 4 months, each participant underwent a blinded evaluation session with a pre-scripted "test" scenario of malignant hyperthermia (phase 3). These sessions were also videotaped and evaluated as for phase 1. The participants in group B responded more quickly, treated better and deviated less from the accepted procedure during phase 3 than those in group A. The total performance of participants in group B during phase 3 was significantly better than those in group A. We conclude that training on an anaesthesia simulator does improve the performance of anaesthetists in dealing with emergencies during anaesthesia.

SummaryA retrospective analysis is presented of all reports of faults, accidents, near accidents and complications associated with anaesthesia in one hospital from 1978 to 1987. 113 074 anaesthetics were administered in that period, of which 97496 were for noncardiac procedures. There were 148 reports; 39 were of dental damage. Peri-operative cardiac arrests during noncardiac surgery were reported 29 times. Sixteen of these were fatal. Anaesthesia was thought to havc played an important role in 13 cardiac arrests ( I per 7500 anaesthetics) and six were not successfully resuscitated ( I per 16 250 anaesthetics). There were 12 reports of postoperative peripheral neuropathies (1 per 9422 anaesthetics). Failure to check, lack of vigilance and inattention or carelessness were the most frequently associated factors with the rest of the reports.

1. Human serum albumin (HSA) concentrations and alpha 1‐acid glycoprotein (AAG) concentrations were measured in 68 subjects, 35 males and 33 females, aged 20‐90 years without evidence of acute or chronic inflammatory disease or malignancy. Subjects were drug free for at least 1 month. HSA and AAG concentrations were measured using rate nephelometry. 2. Age had no effect on alpha 1‐acid glycoprotein concentration, whereas plasma albumin levels decreased as a function of age in both sexes. We observed no differences between males and females in the plasma concentrations of HSA and AAG. 3. These data show that in healthy subjects the HSA concentration decreases with increasing age, whereas age, uncomplicated by disease does not influence AAG concentration.

We describe a prospective analysis, in one hospital, of reported significant observations involving unsafe practices and working conditions during anaesthesia. Of the 549 significant observations reported voluntarily during a period of 18 months, 82% involved occurrences which were considered preventable and 27% could have been fatal if they had not been recognized and corrected. Ninety-three percent of incidents did not lead to a negative outcome. Human error was responsible for 411 (75%) reports. Lack of vigilance and failure to check were the most frequently reported factors associated with human error. Significant observations involving errors in drugs administration were the most frequent. Forty-five percent of all reported significant observations were made during maintenance of anaesthesia.

The effects of midazolam on the EEG were related to plasma midazolam concentrations in 8 healthy male volunteers in order to develop a pharmacokinetic-pharmacodynamic model. The EEG parameters were derived by aperiodic analysis. The EEG was recorded between Fp1-M1 and Fp2-M2. Following a 15-minute baseline EEG registration, midazolam 15 mg was given intravenously over 5 minutes. Venous blood samples were taken until 8 hours after the start of the infusion. Within 2 to 4 minutes of starting the infusion all subjects became asleep, with loss of eyelid reflex. The most obvious EEG changes, in the beta frequency range (12 to 30 Hz), were observed within 2 minutes of the start of drug administration. Seven subjects awoke 60 to 70 minutes after the start of the infusion and 1 awoke after 45 minutes. The EEG parameter that best characterised the effect of midazolam was the total number of waves per second in the frequency range 12 to 30 Hz (TNW12-30). This was used as the effect parameter in the pharmacokinetic-pharmacodynamic modelling. The plasma concentration-time data were characterised by a triexponential function for all subjects. To allow for a possible delay between plasma midazolam concentration and EEG effect, a hypothetical effect compartment was included in the pharmacokinetic-pharmacodynamic model. A sigmoid maximum effect (Emax) model was used to characterise the effect compartment midazolam concentration-TNW12-30 data. The plasma drug concentration corresponding to half the maximum increase in TNW12-30 (EC50) was 290 +/- 98 micrograms/L.(ABSTRACT TRUNCATED AT 250 WORDS)