Josephson Clinical Cardiac Electrophysiology

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■ Josephson’s Clinical Cardiac Electrophysiology

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FIGURE 5.5 Multiple levels of concealed conduction during ventricular pacing. The rhythm is sinus, with ventricular pacing at a cycle length of 1,200 msec (S, arrow). Following the first stimulated ventricular complex, the spontaneously occurring sinus impulse is conducted with a long H-V interval and left bundle branch block (LBBB) aberration. This indicates asynchronous concealment into both the left and right bundle branches (long H-V and LBBB morphology). Following the second stimulated complex, the sinus impulse blocks in the atrioventricular (A-V) node, indicating concealed conduction to that structure. Following the third stimulated complex, the sinus impulse blocks below the His bundle, indicating conceal ment into the His-Purkinje system, rendering it totally refractory to the antegrade impulse.

representation on the surface ECG. Incomplete penetration (concealment) of His bundle depolarizations in either direc tion, producing unexpected abnormalities of antegrade or retrograde conduction, may present a particularly difficult di agnostic problem. 9,10 The intracardiac study may be extremely useful in assessing the causes and sites of concealed conduc tion by making all the components of the A-V conduction sys tem available for analysis. Although interference with normal antegrade con duction or with a subsidiary pacemaker by a concealed premature depolarization may be easy to conceptualize, un explained facilitation of conduction requires further expla nation. Most examples of facilitation of conduction (usually in the His-Purkinje system) can be explained by the fol lowing effects of a premature impulse: (a) allowing more time for the structure to recover excitability, which is due to peeling back the refractory period of that tissue, and/or (b) shortening the refractory period of tissues with cycle length-dependent refractoriness (ie, the atria, His-Purkinje system, and ventricles) by decreasing the cycle length pre ceding the subsequent spontaneous impulse ( Figure 5.6 ) or retrograde conduction through a site of antegrade block,

which both shortens the refractory period and allows more time for recovery. Simultaneous shortening of refractoriness and providing more time to recover excitability is the most common mechanism. Abrupt normalization of aberration by a VPC (the finding of which proves retrograde conceal ment as the mechanism for perpetuation of aberration) is based on these principles ( Figures 5.7 and 5.8 ). A-V nodal conduction time and refractoriness may be shortened by VPCs delivered simultaneously with the prior atrial depo larization ( Figure 5.9 ). In an elegant study, Shenasa et al demonstrated that VPCs shorten A-V nodal refractoriness and improve A-V nodal conduction at comparable coupling intervals at both long and short drive cycle lengths. 16 One mechanism for this is summation because VPCs without simultaneous atrial activation prolong refractoriness and slow conduction in the node. Another explanation would be for the VPC to produce earlier activation at the site of A-V nodal conduction delay or block. This allows more time for it to recover when the atrial premature contrac tion (APC) is delivered. These and other mechanisms of facilitation explain some instances of pseudo-supernormal conduction.

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FIGURE 5.6 Facilitation of His-Purkinje conduction by a ventricular premature depolarization (VPD). During atrial pacing at a cycle length of 440 msec, 2:1 block below the His bundle occurs. A VPD (arrow) is introduced just before the fifth atrial paced complex. Following the VPD, the P wave that should block in the 2:1 sequence conducts with the same A-H and H-V intervals as other conducted complexes. Facilitation of His-Purkinje conduction results because the VPD “peeled back” His-Purkinje refractoriness, allowing the atrial impulse to propagate through the previous site of block. See text for discussion. (Reprinted from Gallagher JJ, Damato AN, Varghese PJ, et al. Alternative mechanisms of apparent supernormal atrioventricular conduction. Am J Cardiol . 1973;31:362, with permission from Elsevier.)