This session will describe briefly the models driving the simulation, provide and overview of some of the current simulation programs available for medical education, and demonstrate how these programs can be used by an instructor or by individual users. It depends on sympathetic tone, parasympathetic tone, and drug levels. When the heart is not in sinus rhythm, certain conduction times may still be based on the underlying sympathetic and parasympathetic influences, but the initial depolarization rate is not based on the sinus rhythm. The rhythm is ordinarily normal sinus rhythm with ectopy. All three of these occur randomly, but the probabilities of each rhythm disturbance is markedly dependent on the physiologic state of the patient.
Antiarrhythmic drugs act via changes to the transition probabilities.
Cardiac timing depends on which rhythm is currently active. Depending on which chamber initiates the signal, the activation is propagated from chamber to chamber, and this depends on the conduction velocity in whichever part of the system is active. These are produced by time scaling exemplar waveforms that were recorded from actual patients. However, results are plausible and tightly coupled to the mechanical simulation. In a mechanical sense, all of these models function together to predict elastance as a function of time for each of the four cardiac chambers.