Reflected reentry in nonhomogeneous ventricular muscle as a mechanism of cardiac arrhythmias.

Arrhythmogenesis in ventricular muscle exhibiting nonhomogeneous excitability was studied in isolated tissues from feline and canine hearts. Longitudinal bundles were mounted in a three-chambered bath and simultaneous transmembrane recordings were obtained from fibers in each chamber. Nonhomogeneous excitability was established by depressing only the central segment (1 to 2 mm wide) with high-K+ Tyrode's solution, which induced discontinuity of propagation associated with step delays mediated by electrotonic current flowing through the depressed zone. When transmission delays were long, activity distal to the site of block returned to proximal tissue as one of two forms of reflected reentry, each elicited by a different mechanism. Type I reflection, occurring with antegrade delays of 30 to 60 msec, was characterized by an early secondary depolarization due to electrotonic spread of currents from delayed responses in the depressed segment. Type II reflection evolved with delays greater than 90 msec and was manifest as a closely coupled regenerative action potential that developed independently of a pacemaker mechanism and of slow but continuous conduction. We conclude that delayed activation of excitable elements, which occurs when propagation is discontinuous, may lead to rhythm disturbances of focal origin that are mediated by electrotonic interactions across a zone of depressed tissue.