Josephson Clinical Cardiac Electrophysiology

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Chapter 6: Ectopic Rhythms and Premature Depolarizations ■

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FIGURE 6.12 Pseudo-Mobitz Type II atrioventricular (A-V) block produced by concealed His bundle depolarizations. Surface leads 1, 2, and V1 demonstrate Mobitz Type II A-V block in the presence of RBBB with LAH. Intracardiac recordings from the high right atrium (HRA), left atrium (LA), and His bundle region (HBE) demonstrate that a concealed premature His bundle (H) depolarization is responsible for failure of the second sinus impulse to conduct to the ventricles. See text for discussion. LAH, left anterior hemiblock; RBBB, right bundle branch block; T, time lines.

with a narrow QRS complex. These forms of “pseudo-block” should not necessarily be treated with a pacemaker; if treatment for hemodynamic stability is required, antiarrhythmic drugs can be used. A dramatic example of pseudo-block that was success fully treated with quinidine is shown in Figure 6.12 . This patient (described in Chapter 3), who had a right bundle branch (RBB) block and left anterior hemiblock morphology, had experienced dizzy spells and had been referred for permanent implanta tion of a pacemaker. The electrophysiologic study revealed pseudo-block that was due to concealed His bundle depolariza tions, a finding that was crucial to the appropriate management of the patient's condition. Nevertheless, His bundle extrasystoles often exist with impaired excitability in the His bundle. Thus, in many of such cases, drugs plus a pacemaker are needed. His bundle depolarizations can also be manifested as blocked APDs ( Figure 6.13 ). 38 Moreover, the presence of such extrasystoles can lead to block in the His bundle (above or below the recording site) during refractory period determinations. Finally, His bundle depolarizations may be truly concealed and have no representation, direct or indirect, on the surface ECG. In this instance, intracardiac recordings demonstrate

The response of the junctional pacemaker to atropine and/or isoproterenol may help localize the site within the A-V junction from which the automatic focus arises. 32 A rapid response sug gests a pacemaker in the proximal His bundle, N-H region of the node, or the node itself, whereas a sluggish response suggests a more distal (or an impaired proximal) focus. The use of cal cium blockers, beta blockers, or adenosine may also be of value. A marked depression of automaticity suggests a nodal origin because it is the site most sensitive to these agents. 33 Lidocaine could suppress impulse formation in sodium-dependent tissue (ie, the His bundle) but should have no effect on A-V nodal im pulse formation. Finally, the response to APDs can differenti ate if the impulse originates in the node or His bundle; slowing or transiently suppressing the rhythm without depolarizing the His bundle points to the A-V node as the source of impulse for mation as suggested by Hariman. 1 His bundle depolarizations may also manifest themselves only by concealed conduction (see Chapter 5), which may lead to sudden changes in the P-R interval or even to second-degree A-V block. 34-37 His bundle depolarizations should always be considered a possibility with the sudden appearance of Mobitz Type II A-V block in a patient

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FIGURE 6.13 Premature His bundle depolarization mani fested as a blocked atrial premature depolarization (APD). In this patient, who has marked infranodal conduction de lay (H-V = 330 msec), a premature His bundle depolariza tion blocks below the recorded His bundle deflection but is able to conduct retrogradely to the atrium, appearing as a blocked APD on the surface electrocardiogram (ECG) (arrow). HBE, His bundle electrogram; HRA, high right atrium; RV, right ventricle; T, time line.

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