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.
3. In all subjects the ventilatorv C(2 sensitivities obtained with the rebreathing method (Sr) were appreciably larger than the steady-state CO2 sensitivities (S). The ratio Sr/Ss ranged from t 40 to 2 59 with a mean value of tP85.4. We argue that these results can be explained by considering the effect of changes in cerebral blood flow upon increasing the arterial CO2 tension during rebreathing and the steady state.5. AVe conclude that in general the CO2 sensitivity obtained with Read's rebreathing method does not represent the steady-state CO2 sensitivity.
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.
Patients with heart failure have a diminished cardiac reserve capacity that may be further compromised by anesthesia. In addition to depression of sympathetic activity, most anaesthetics interfere with cardiovascular performance, either by a direct myocardial depression or by modifying cardiovascular control mechanisms. Etomidate causes the least cardiovascular depression. It is popular for induction of anesthesia in cardiac-compromised patients; however, it is not suitable for maintenance of anesthesia because it depresses adrenocortical function. Ketamine has a favorable cardiovascular profile related to central sympathetic stimulation and inhibition of neuronal catecholamine uptake. These counteract its direct negative inotropic effect. In patients with a failing myocardium, however, the negative inotropic effects may be unmasked, resulting in deterioration in cardiac performance and cardiovascular instability. Propofol is the most popular intravenous anesthetic for maintenance of anesthesia. It does have a negative inotropic effect, but the net effect on myocardial contractility is insignificant at clinical concentrations, probably because of a simultaneous increase in the sensitivity of the myofilaments to Ca2+. Propofol protects the myocardium against ischemia-reperfusion injury, an action derived from its antioxidant and free-radical-scavenging properties as well as the related inhibition of the mitochondrial permeability transition pore. For intravenous anesthesia, propofol is always combined with an opioid. Opioids have relatively few cardiovascular side effects and, in particular, do not cause myocardial depression. Indeed, they are cardioprotective, with antiarrhythmic activity, and induce pharmacologic preconditioning of the myocardium by a mechanism similar to the inhalational anesthetics.
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