A 72-year-old woman was admitted because of a near-syncopal episode. Her ECG showed a normal sinus rhythm at a rate of 65 bpm, and her PR interval was prolonged (240 ms). The ECG also showed a pattern of right bundle branch block and left posterior hemiblock. The morphology of the QRS complex was identical to that of QRS complexes 3 and 5 on the ECG. Her heart rhythm became irregular, and an ECG was recorded (Figure⇓).
The rhythm was sinus (rate, 65 bpm) with 2:1 and Wenckebach-type atrioventricular conduction. Of interest is the changing QRS morphology. QRS complexes 1, 2, 4, and 6 are conducted with a right bundle branch block/left anterior hemiblock pattern; thus, ventricular activation occurs via the left posterior fascicle. However, this QRS pattern occurs only after a long R-R interval, which is due to atrioventricular block. Thus, block in the left anterior fascicle is bradycardia-dependent. When the QRS is conducted with a short R-R interval, the left anterior fascicle conducts before (ahead of) the left posterior fascicle, thus resulting in a left posterior hemiblock pattern. Slow, rather than blocked, conduction in the left posterior fascicle explains its ability to conduct during bradycardia-dependent left anterior hemiblock, thus resulting in a wider QRS complex. This is best seen when comparing QRS complexes 4 and 5 in lead V1.
Bradycardia-dependent block implies a diseased conduction system and can occur in various disease states such as ischemia or hypertrophy. The mechanism is that of enhanced diastolic depolarization (phase 4 depolarization),1 which renders the tissue refractory to activation at slow heart rates.
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
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