Role of calcium in arrhythmogenesis.

Cardiac arrhythmias are generated as the result of disorders of automaticity or impulse conduction. Regardless of the mechanism, however, calcium is likely to be involved. The rate of Ca2+ flux across the membrane of automatic cells alters their firing rate. Myocardial cells that do not ordinarily initiate action potentials can do so when they are partially depolarized. Low extracellular Ca2+ concentrations or Ca2+ channel-blocking drugs can reduce or abolish such ectopic firing. Early afterdepolarizations are also induced in cardiac cells by partial depolarization, whereas delayed afterdepolarizations are induced by Ca2+ overloading. Early afterdepolarizations and delayed afterdepolarizations can both be suppressed by low external Ca2+ concentrations or by Ca2+ channel blockers. With respect to arrhythmias ascribable to disorders of conduction, Ca2+ channel blockers can aggravate conduction disturbances in the sinoatrial node or atrioventricular junction. Furthermore, these drugs can abolish those reentrant arrhythmias in which a cardiac impulse rotates around a loop in which nodal tissue is an integral element. Ca2+ channel blockers can also reduce the susceptibility for ventricular fibrillation to supervene in ischemic hearts, especially when the sympathetic nervous system is overactive.