Refractoriness of cardiac muscle as affected by intercalated disks: a model study implications for fibrillation and defibrillation.
It is generally agreed that inhomogeneities of the recovery process in cardiac tissue play an important role in the genesis of reentrant arrhythmias. Regarding cardiac muscle as an assembly of discrete cells connected by gap junctions, differences in recovery may result from a nonuniformity of membrane or cable properties. In this study, a computer model of a one-dimensional cardiac muscle fiber including a periodic intercalated disk structure is used to study the influence of disk resistance (Rj) and stimulus strength (J) on refractoriness. Stimulating currents are applied externally in a bipolar arrangement. The basic effect of a current pulse is local de- and hyperpolarizations at the ends of an individual cell. Polarization develops very rapidly and increases with increasing values of Rj or J so that an interaction with membrane current kinetics becomes possible. When a premature stimulus is applied during repolarization of a conditioning action potential, multiple Na currents can occur, either caused by depolarization of the cathodal end of a cell or in the form of anode break excitation at the hyperpolarized end. Those currents affect the response of a fiber such that, at a given value of J, the refractory period is shortened by an increase in Rj. In a ring fiber model with different Rj values in the two halves of ring an extrastimulus timed between the refractory periods of the two branches results in a sustained circus movement. Varying stimulus strength yields an upper limit of vulnerability characterized by a "synchronized extrasystole". The ring model also implies the suppression of circus movement by an external shock. The minimal shock strength required for suppression is close to the upper limit of vulnerability. The simulations suggest that discrete effects of junctional resistance may be involved in fibrillation and defibrillation.
Haas
H G
HG
Department of Physiology, University of Bonn, Bonn, Germany.
Solchenbach
K
K
D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology* / Q000628:therapy*; D003198:Computer Simulation; D004554:Electric Countershock / Q000379:methods*; D004558:Electric Stimulation; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D008959:Models, Neurological; D032342:Muscle Cells / Q000502:physiology; D009415:Nerve Net / Q000503:physiopathology; D012032:Refractory Period, Electrophysiological; D009435:Synaptic Transmission