A remarkable feature of healthy ventricular myocardium, exposed by electrical stimulation and high-resolution mapping, is that, despite its gross nonuniformities and structural discontinuities on the submillimeter scale, it behaves electrically so much like a continuous uniformly anisotropic excitable medium. Such media are susceptible to a self-sustaining high-frequency periodic mode of activity in the form of freely movable paired vortices in two dimensions or vortex filaments in three dimensions. These can be evoked by a timely stimulus of the right size, for example, in myocardium by an electrical stimulus during the vulnerable period. Such stimuli may occur at random within complex patterns of stimulation and activation, even in healthy uniform tissue. Discontinuities and heterogeneity apparently make diseased tissue more vulnerable. Such vortices may underlie common reentrant tachycardias that degenerate into ventricular fibrillation, the commonest cause of sudden cardiac death. If the normal mechanism here reviewed also plays a role in diseased tissue, then it provides a quantitative basis for design of improved procedures for management of reentrant ventricular tachycardias that threaten to degrade to fibrillation.