Figure 166

Conduction disorders due to reentry as might occur in the ischemic or postinfarcted myocardium. See Fig. 16.5 for a description of the format. As in the previous figure, antegrade conduction occurs in a normal manner over the proximal Purkinje system (P1) and in the distal Purkinje network on the left of the diagram. However, the Purkinje network on the right (P2) has been subjected to injury. The intracellular recordings from the respective electrodes indicate that the resting membrane potential from P2 is decreased due to the presence of injury at this site. Therefore, the impulse conducts slowly and decrementally, and finally is blocked in the area of injury (unidirectional block). The ventricular myocardium, however, has been depolarized from normally conducting Purkinje fibers at remote insertion sites. The excitatory impulses traversing within the ventricular myocardium will reenter the distal portion of the Purkinje network (right side of diagram) and conduct slowly in the retrograde direction through the area of unidirectional block. The appropriate conditions are established by the conduction velocities and refractory periods in the respective tissues. The retrograde impulse can reenter the proximal Purkinje system and initiate reexcitation of the proximal and distal Purkinje network as well as the ventricular myocardium if each of these sites has recovered its excitability from the previous depolarization. The reentry impulse may give rise to a premature coupled ventricular complex in which the normally conducted impulse (V1) is followed with precise timing by a reentry ventricular complex (V2). The reentry impulses could occur more frequently so that the cardiac rhythm becomes dominated by the activity in the reentry pathway, thus leading to a rapid, repetitive series of ventricular complexes (ventricular tachycardia) in which the ventricular rate becomes rapid (>100 beats min) and may degenerate into ventricular fibrillation. The object of antiarrhythmic drug therapy is to reduce the frequency of hemodynamically disturbing premature ventricular impulses and to prevent the establishment of a sustained and rapidly conducting reentrant rhythm capable of becoming lethal.

In the undamaged myocardium, cardiac impulses travel rapidly antegrade through the Purkinje fibers to deliver the excitatory electrical impulse to the ventricular myocardium. During the normal activation sequence, retrograde conduction from ventricular myocardium to the conducting fibers is prevented by the longer duration of the membrane action potential and thus the refractory period in the Purkinje fibers.

In the presence of myocardial ischemia, propagation of cardiac impulses may be interfered with and a functional unidirectional block may occur. Impulses may fail to conduct longer in the anterograde direction to excite the more distal ventricular myocardium. Thus, the terminal segments of the Purkinje fibers within the affected region may be activated by impulses passing from the ventricular myocardium to conduct in a retrograde direction (impulse 1, Fig. 16.6), albeit at a slower rate of conduction. In some situations, the retrograde impulse will enter an area of normal myocardium sufficiently repolarized that it is no longer refractory, and a propagated action potential will result. The generation of an action potential may produce an increased rate of ventricular activation and may become self-sustaining. The latter phenomenon is known as a reentrant, or circus, rhythm. If propagation is too rapid through the region of myocardial damage, the retrograde impulse will attempt to reenter the normal region while the tissue is refractory. This will give rise to bidirectional block, terminating the reentrant wave front. Therefore, for reentry to occur, there must be a region of unidirectional block and slow conduction. The delay in conduction permits the tissue ahead of the advancing wave front to regain its excitability, sustaining the reentry circuit. As shown in Figure 16.6, the reentrant wave front gives rise to a second depolarizing impulse (2) in the ventricular myocardium and in each of the branches of the Purkinje network (P1 and P2). The net result of the reentrant wave is depicted in the electrocardiogram (ECG), in which coupled ventricular premature complexes (V2) follow each normal (V1) complex.

It is estimated that 80 to 90% of clinical arrhythmias have a reentry mechanism. One explanation of how an antiarrhythmic agent may abolish reentry is by converting unidirectional block to bidirectional block. A second mechanism to explain the action of antiarrhythmic drugs is that they can prevent reentry by increasing the ERP of the cardiac fibers within or surrounding the region of the reentrant circuit.

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