This experimental model demonstrates that mechanical injury to ventricular fascicles can produce both phase 3 and phase 4 bundle branch block, linked to hypopolarization and prolonged refractoriness.
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Hypothesis-generating for rate-dependent conduction mechanisms; leaves open translation to human bundle branch block.
The main ventricular conducting fascicles were slightly injured in anesthetized dogs by gently scratching them with a blunt needle introduced through the ventricular wall. Initially the bundle branch block that resulted was rate independent (stage 1). When conduction returned to normal, both premature atrial and vagal stimulation reproduced the bundle branch block (stage 2). During stage 2 (5-15 minutes), three conduction ranges were documented: an early (phase 3) block range, a late (phase 4) block range, and an intermediate normal conduction range. The normal conduction range was narrow at the beginning but widened progressively, mostly at the expense of the phase 4 block range. Another period during which only phase 4 bundle branch block occurred (stage 3) preceded total normalization (stage 4). The escape beats that arose from the injured fascicle were most abundant and had the shortest coupling during stage 1, they were less common and their coupling became longer during stages 2 and 3, and they disappeared in stage 4. The tachycardia-dependent or phase 3 bundle branch block was related to a prolongation of refractoriness; the bradycardia-dependent or phase 4 bundle branch block was attributed to slight hypopolarization, enhanced spontaneous diastolic depolarization, and a shift in the threshold potential toward zero. These abnormalities were assumed to be secondary to the hypopolarization, which was probably the basic derangement. This hypothesis satisfactorily accounts for the observation that phase 3 and phase 4 bundle branch block commonly coexist in the same injured fascicle.
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Elizari et al. (1974) studied this question.
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