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Simulation has gained an important role in medical education and continuing education in the field of anaesthesia and emergency medicine. This article gives background information on how full-scale simulators are applied in medical education as well as in continuing education for advanced anesthesia and scientific applications. Acceptance of training seems enhanced by inclusion of the human factor aspect, since this has proven to be a major source for the development of critical situations in our specialty. Furthermore, drawbacks of the simulators available and the current training availability in Germany is described.

The loss of pipeline pressure in a central gas supply system is a rare but potentially hazardous complication in anaesthesia and critical care. In an anaesthesia simulator study, reactions of 20 anaesthetists to this simulated critical incident were monitored and evaluated. A comparison between novice (n = 10) and experienced anaesthesia residents/consultants (n = 10) determined a significantly quicker and more on-target reaction by the experienced anaesthetists. Unlike older cycle system anaesthesia machines, update anaesthesia ventilators (CICERO EM, Dräger, Lübeck) do not permit manual ventilation of a patient in a "closed-system" once pipeline pressure drops to zero. In this highly hazardous event, the patient has to be ventilated by reservoir bag until a sufficient back-up system delivering high inspiratory oxygen concentrations can be installed, because he is otherwise prone to diffusion hypoxia. Installation of mandatory (anaesthesia-machine integrated) back-up systems for respirators without cycle systems would therefore increase patient safety. A general algorithm for loss of pipeline pressure can be described only after a back-up system has been installed.

In a porcine CPR-model, we investigated the pharmacokinetics and pharmacodynamics of norepinephrine (NE) after intravenous (10 g/kg, n = 10, group A) and endobronchial (e.b., 100 micrograms/kg, n = 10, group B) administration. After 3 min of cardiac arrest induced by electroshock, restitution of spontaneous circulation (ROSC) was achieved in 8 animals in group A after 3.3 +/- 1.6 min, and in group B in 6 animals after 2.5 +/- 0.6 min. Haemodynamics during CPR were not significantly different, but during the first hour after ROSC e.b. NE showed a depot effect. Maximum venous (642 +/- 182 ng/ml after 3.5 +/- 0.3 min) and arterial (147 +/- 21 ng/ml after 4.2 +/- 0.4 min) NE concentrations in group A were significantly higher compared with values in group B (77 +/- 18 ng/ml after 5.5 +/- 0.5 min venous, 46 +/- 11 ng/ml after 6.0 +/- 0.7 min arterial). The area under the curve (AUC) in group A was calculated to be 55 +/- 12 ng/ml min (venous) and 35 +/- 7 ng/ml min (arterial) representing a pulmonary first-pass effect of 40%. In group B, the dose-adjusted AUC (39 +/- 13 ng/ml min venous, 30 +/- 10 ng/ml min arterial) represented a pulmonary first-pass effect of only 25%. Despite this lower pulmonary first pass, however, it is concluded that after e.b. administration of NE absorption is too much delayed and peak concentrations are too low. Therefore, NE should not be given via this route during CPR.

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