Effects of anesthetics on the heart

General anesthetic agents can be divided on the basis of whether or not they "sensitize" the heart to the arrhythmogenic actions of catecholamines. There appear to be two separate means by which the catecholamines cause ventricular arrhythmias during anesthesia: one is related to a reduction in supraventricular driving rate caused both directly by the anesthetic and reflexly in response to the pressor effect of catecholamine injection; the other action (favoring ventricular fibrillation) is caused by direct anesthetic depression of the intraventricular conducting system. Of the anesthetics used today, halothane has the most pronounced cardiac sensitizing action. The same anesthetics can also be divided according to whether or not they stimulate sympathetic nervous system activity. Those that do (e.g., diethyl ether) abolish the barostatic reflexes. Those that do not (e.g. halothane) reset the barostatic reflexes to favor a reduced level of arterial pressure; they also tend to cause a reduction in sympathetic nervous activity efferent to the heart. Parasympathetic nervous actions are relatively insignificant. All general anesthetics cause myocardial depression at all concentrations that are clinically useful. The mechanism appears to involve a reduction in the Ca2+ available to the contractile elements. Exactly how anesthetics do this is unclear, but these drugs appear to decrease both the Ca2+ influx across the plasma membrane and the Ca2+ content of the sarcoplasmic reticulum.