Josephson Clinical Cardiac Electrophysiology

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Chapter 5: Miscellaneous Phenomena Related to Atrioventricular Conduction ■

CONTROL

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QUINIDINE

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FIGURE 5.12 Type III gap in atrioventricular (A-V) conduction induced by quinidine. The basic atrial drive rate (A1-A1) in both panels is constant at 850 msec. A premature atrial stimulus (A2) introduced at a coupling interval (A1-A2) of 380 msec during the control period (top panel) results in an H1-H2 interval of 410 msec and block of the impulse in the HPS. One hour after the administration of quinidine gluconate, 800 mg intra muscularly (bottom panel), an identical H1-H2 interval (410 msec) A2 results in an intra-His delay (H2-H ′ ) sufficient to allow the distal HPS to recover and conduct the beat to the ventricles. Note the right bundle branch block (RBBB) aberration in this conducted beat.

premature depolarization (VPD) from the “blocked” ventricle. This pattern, however, is rarely repetitive and/or reproducible. Although equal and sudden simultaneous delay in the oppo site bundle branch could theoretically normalize the QRS, it would be associated with a prolonged H-V (and P-R) interval (see Figure 5.16 ). Furthermore, further premature complexes would unlikely conduct with a normal QRS because it would require continuous equal slowing in both bundle branches. Another form of pseudo-supernormal conduction is fa cilitation of A-V nodal conduction by a VPD ( Figure 5.19 ). Because A-V nodal refractoriness is inversely proportional to cycle length, facilitation of A-V nodal conduction by a VPD cannot implicitly be explained by alterations in refractoriness either directly or by peeling back. Such facilitation, which has been shown to require simultaneous atrial activation, 16 more likely results from summation, as suggested by Zipes et al 6 Another cause of pseudo-supernormal conduction is bradycardia-dependent bundle branch block with normalization

of the QRS complexes at shorter cycle lengths or with APCs ( Figure 5.20 ). The physiologic explanation for Phase 4 block is enhanced automaticity and/or partial depolarization of injured myocardial tissue. Propagation of supraventricular impulses is more difficult late in diastole because the impulses encounter partially depolarized tissue through which voltage-dependent conduction is not possible (see Chapter 4). Dual A-V nodal pathways can be manifested by intermit tent long or short P-R intervals, depending on which pathway is used for antegrade conduction. Perpetuation of one pattern of antegrade conduction by retrograde concealment over the other pathway has been demonstrated by Wu et al 28 Apparent supernormal conduction of an APD that is due to a shift from slow to fast conduction has been demonstrated by Denes et al 29 We have seen spontaneous examples of junctional prema ture complexes and VPC shift fast to slow pathways and vice versa. The methods of evaluating dual A-V nodal pathways are described in Chapter 7.

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