Josephson Clinical Cardiac Electrophysiology

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■ Josephson’s Clinical Cardiac Electrophysiology

1 3 V1

A1

A1

A2

900

505

HRA

V1

V1

S

S

S

H1

H2

H1

A1

A2

A1

HBE

H1-H2 525

70

90

70

V1-V2 525

45

45

45

T

A

1

3 V1

A1

A2

470

HRA

900

V1

S

S

S

H1 V1

H1

H2

A1

A1

H1-H2 490

A2

HBE

90

T

B

1 3

V1

A1

A1

A2

HRA

900

400

V2

S

S

S

H1 V1

H1 V1

A2

H2

A1

A1

H1-H2 430

HBE

100

V1-V2 520

135

T

C

FIGURE 5.11 Type II gap in atrioventricular (A-V) conduction. The basic atrial drive rate (A1-A1) is 900 msec. Progressively premature atrial extra stimuli (A2) are introduced. A. A-V conduction is intact. B. A2 is blocked below the His bundle as the H1-H2 interval of 490 msec is shorter than the effective refractory period (ERP) of some portion of the His-Purkinje system (HPS). C. Conduction resumes despite a still shorter A1-A2 (400 msec) and a shorter H1-H2 (430 msec). This resumption is postulated to be due to a delay in the proximal HPS, resulting in an H2-V2 interval of 135 msec, sufficient to allow the most refractory region (the “gate area”) of the distal HPS to recover.

in proximal His-Purkinje conduction allows an initial area of distal His-Purkinje block to recover excitability and resume conduction is shown in Figure 5.15 . Normalization of aber rant conduction with progressively atrial premature depolar izations (APDs) is associated with progressive intra-His delay ( Figure 5.16 ) or proximal His-Purkinje delay ( Figure 5.17 ), allowing recovery of the right bundle branch (RBB) and left anterior division of the left bundle branch (LBB). Alternatively, Figure 5.17 may represent slowing of conduction in both the RBB and the left anterior fascicle in panel A; subsequently, fur ther delay in the posterior fascicle, or more likely, the proximal LBB, produces an equal delay in both the RBB and the LBB so

that the QRS “normalizes.” As noted in Chapter 1, His-Purkinje refractoriness is cycle length dependent, and therefore, aberra tion may not be manifested at identical coupling intervals if the preceding cycle length is shortened (see Figure 1.63 ). Type I (Wenckebach) second-degree block in the bundle branch system may result in either a progressive or a sudden normalization of aberration, with progressive delay being con cealed in the surface ECG and with only the recovered cycle manifesting normal conduction ( Figure 5.18 ). Theoretically, any mechanism that removes retrograde invasion will nor malize A-V conduction (see Figure 5.7 ). Another cause of normalization of aberration is the appearance of a ventricular

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