A Mechanism for Reentry in Canine Ventricular Tissue

Abstract

In isolated canine papillary muscle-false tendon preparations it was possible by selecting the pattern of stimulation to obtain conduction block within the peripheral distribution of the Purkinje network. Action potentials recorded just proximal to the site of block were always extremely brief in duration; refractory periods were abbreviated accordingly. When propagation from specialized fibers to muscle fibers was made very critical, conduction block occurred at some Purkinje-muscle junctions while propagation continued through others. Under these conditions very early reentrant activity could be obtained in terminal Purkinje fibers. With proper timing, the impulse propagated back to the false tendon and emerged as a closely coupled extrasystole. Occasionally, the activity returned again to muscle and resulted in a double reentry. Electrotonic shortening of action potentials of Purkinje fibers at relatively long distances upstream from a site of block facilitated the reentry of proximal elements. Partial reentry of the Purkinje system created conditions favoring fractionation of the reentrant wave front-KEY WORDS unidirectional conduction block refractory period of Purkinje fibers Purkinje-muscle junctions repetitive activity in ventricular tissue abbreviation of action potentials electronus in heart muscle cardiac arrhythmias• The concept of reentry as a mechanism for initiating ectopic activity dates back to the early experiments of Schmitt and Erlanger (1). There is now general agreement among investigators that the necessary conditions for reentry include: (1) unidirectional block of an impulse in one or more regions of the heart; (2) slow passage of the impulse over an alternative route; (3) delayed excitation of the tissue just distal to the blocked site; and (4) reexcitation of the tissue proximal to the site of block. This last event can take place only if the conduction time over the alterna- This work was supported in part by a grant from the American Heart Association, and it was done during Dr. Sasyniuk's tenure of a Post-doctoral Fellowship from the Medical Research Council of Canada.Dr. Sasyniuk's present address is Department of Pharmacology, Mayo Clinic, Rochester, Minnesota 55901.Received August 26, 1970. Accepted for publication November 3,1970. tive route exceeds the refractory period of the path to be reentered. The difficulty in this hypothesis is that the refractory period of cardiac tissue, particularly in the ventricles, is so long. All the above requirements can be met with relative ease in the mammalian A-V node where conduction velocities of about 0.02 m/sec have been demonstrated. However, it is questionable whether propagation over an alternative route in the ventricles could be slow enough to permit reexcitation of elements with such a long refractory period. Wallace and Mignone (2) were able to produce reentrant extrasystoles in the ventricles only by cooling a discrete area of the left ventricle sufficiently to produce unidirectional block at the junction of the warm a...

Overdrive suppression of conduction at the canine Purkinje-muscle junction.

“…Since conduction block at Purkinje-muscle junctions frequently is unidirectional,9' 11, 13, 14 postoverdrive Purkinje-muscle conduction block could be conducive to the development of reentry. 26 Limitations. Since the passive membrane properties of cells at the Purkinje-muscle junction are unknown, it is not possible to calculate the charge required for activation of junctional cells.…”

Dynamics of Intramural and Transmural Reentry During Ventricular Fibrillation in Isolated Swine Ventricles

“…A propensity for unidirectional conduction block at the PVJs has been well described in pacing studies. 18,19,35 This block sets the stage for Purkinjemuscle reentrant excitation, 36 which has been recently implicated as a mechanism of polymorphic ventricular arrhythmias in simulation studies. 37 Our data suggest that both conduction block (leading to wave splitting) and reentry at the PM root could have had the participation of PVJ, further confirming the relevance of the Purkinje system during VF.…”

Toward an Integrated Understanding of the Purkinje Fibers in the Heart: The Functional and Morphological Interconnection between the Purkinje Fibers and Ventricular Muscle

“…Conduction disturbance at P-V junctions can occur under various pathological states, especially under ischemic conditions, e.g., hypoxia, hyperkalemia, and acidosis [12]. Impairment of electrical coupling at the P-V junction provides an opportunity to create a reentrant circuit of excitation, an important substrate for the development of ventricular tachyarrhythmias [21,34,39]. Microelectrode recording also suggested that ventricular arrhythmias in acute ischemia arise from ectopic focal excitation within the Purkinje-fiber network of the peri-infarct zone [17].…”