Josephson Clinical Cardiac Electrophysiology

172

■ Josephson’s Clinical Cardiac Electrophysiology

2

V1

A

V

A

V

V

V

A V

A V H

A V H

H

HBE

V

V

V

V

V

V

V

RVA

A

A

A

A

A

A

V

V

V

V

V

V

V

CS

V

V

V

V

V

V

V

LV p

V

V

V

LV d

V

V

V

V

T

FIGURE 6.24 Accelerated idioventricular rhythm. Leads 2 and V1 are shown with a His bundle electrogram (HBE) and electrograms from the right ventricular apex (RVA), coronary sinus (CS), and at the left ventricular apex from proximal (LVp) and distal (LVd) pairs of electrodes. After one sinus complex, four complexes of an accelerated ventricular rhythm with slightly irregular cycle length begin. No His bundle deflections are observed during the tachycardia, but they are clearly observed immediately before initiation and after termination. HBE, His bundle electrogram; T, time line.

associated with the supraventricular complex immediately preceding or following the ventricular rhythm, it can be in ferred that the catheter was placed correctly. Occasionally, His bundle spikes may be observed at the terminal portion of a premature ventricular complex. The relationship of ventric ular activation to retrograde His bundle activation depends on the prematurity of the ventricular impulse (see Chap ter 1). The earlier the VPD, the longer the retrograde His Purkinje conduction time. 23,57 In the presence of coronary artery disease with prior infarction, VPDs usually originate in areas of infarction characterized by abnormal fragmented

electrograms (see Chapter 10; Figure 6.25 ). Such VPDs may have a retrograde His deflection before the QRS (see Chap ter 10). Fragmented electrograms appear to be markers of a pathologic substrate that is potentially arrhythmogenic. Sus tained ventricular arrhythmias can occur because of reperfu sion, and in my experience, they signify successful reperfusion and have no negative clinical implications . The appearance of premature depolarizations from mul tiple sites in the heart simultaneously is one of the signs of advanced digitalis intoxication ( Figure 6.26 ), which requires appropriate therapy.

1

aVF V1

LV11

UNI

B1

5 mm

LV11

10 mm

B1

LV11 T

Copyright © 2023 Wolters Kluwer, Inc. Unauthorized reproduction of the content is prohibited.

FIGURE 6.25 Premature ventricular complexes in a patient with prior infarction. Leads 1, aVF, and V1 are shown with electrograms from left ventricle site 11 (LV11) (see Figure 1.46). The top tracing is the unipolar (UNI) tracing, and the bottom two are bipolar (BI) with 5- and 10-mm interelectrode distances, respectively. During sinus rhythm, an anteroseptal infarction can be recognized. At the recording site, a split potential—the second component, inscribed well after the termination of the QRS—is observed (see Chapters 1 and 10). This electrogram denotes marked abnormalities of conduction associated with infarction. Two premature ventricular complexes are then observed originating from this site, with activity preceding the QRS by 90 msec. Note that during the premature complexes, the electrogram is also split into two components The close relationship of abnormalities of activation during sinus rhythm and sites of origin of ventricular complexes is discussed in Chapter 10. T, time line.