[Intermittent bundle branch block: a clinical model for the study of electrophysiological phenomena]
Insights
Intermittent bundle branch blocks can be rate-dependent, indicating true pathology like phase 3 (tachycardia-dependent) or phase 4 (bradycardia-dependent) block. These blocks offer insights into cardiac memory and drug effects.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Conduction System
Context:
- Intraventricular conduction disorders, such as bundle branch block and hemiblock, are typically stable.
- However, their presentation can be influenced by heart rate and cardiac cycle duration.
- Intermittent blocks may indicate underlying bundle branch pathology rather than physiological aberrant conduction.
Purpose:
- To differentiate between physiological rate-related aberrant conduction and pathological bundle branch block.
- To explain the mechanisms of tachycardia-dependent (phase 3) and bradycardia-dependent (phase 4) blocks.
- To highlight the diagnostic and research utility of intermittent bundle branch block.
Summary:
- Bundle branch blocks can be intermittent and rate-dependent, classified as phase 3 (tachycardia-dependent) or phase 4 (bradycardia-dependent) blocks.
- Phase 3 block relates to prolonged recovery periods, while phase 4 block involves enhanced early depolarization.
- Intermittent blocks can exhibit phenomena like supernormal conduction and are models for studying cardiac memory and antiarrhythmic drugs.
Impact:
- Provides a clearer understanding of the pathophysiology of intermittent bundle branch blocks.
- Establishes intermittent bundle branch block as a valuable model for in vivo research.
- Clarifies the interpretation of ECG findings, distinguishing cardiac memory from ischemia.
Abstract:
Disorders of intraventricular conduction (bundle branch block and hemiblock) are usually stable and remain unchanged irrespective of heart rate. Not infrequently, however, their appearance is related to the duration of the cardiac cycle, so that they appear and disappear with changes in heart rate. This may not even represent a pathological phenomenon, since sudden and consistent changes in cardiac cycle can result, even physiologically, in aberrant conduction. However, when a bundle branch block appears intermittently for simple and progressive increments, or even deceleration, of the sinus rate, this is related to a true bundle branch pathology, i.e. tachycardia-dependent (or phase 3) block or bradycardia-dependent (or phase 4) block, respectively. Phase 3 block is believed to express a pathological increase in the duration of the recovery period of the bundle branch. Phase 4 block was best explained on the basis of enhanced phase 4 depolarization of the bundle branch system, with inability of excitation if the cardiac cycle is particularly prolonged. The two types of block, phase 3 and phase 4, often coexist. An intraventricular conduction disturbance that appears during increasing heart rate for a phase 3 block is maintained, if frequency slows down, even for cycles greater than those that brought about its appearance. This is due to retrograde activation of the bundle branch blocked in the antegrade direction, with delay of its action potential inscription. Sometimes, in the presence of phase 3 bundle branch block, very early atrial ectopic beats are paradoxically conducted in the normal way (supernormal conduction). Perhaps, this phenomenon is related to a possible "climb over" of the injured zone of the bundle branch by the blocked impulses that arise beyond the injured area as subliminal impulses, exciting the healthy tissues if catches them during their phase of supernormal excitability. In the presence of intermittent bundle branch block, it is not uncommon to observe long periods of sinus rhythm with regular PP interval, conducted with alternating (2:1) bundle branch block. Intermittent left bundle branch block is a clinical model of cardiac memory: in these cases, negative T waves in the antero-septal leads during normal conduction are often evident. This negativity is an expression of cardiac memory, and not of ischemia as initially interpreted. Intermittent bundle branch block is an excellent model to study in vivo the effects of antiarrhythmic drugs on the pathological bundle branches. Narrowing of the QRS complex in the presence of bundle branch block is not always an expression of intermittent aberrancy: beware of late ectopic beats originating from the ipsilateral ventricle to the blocked branch, that merging with the antegrade beat conducted with bundle branch block, restrict the QRS, simulating intermittent aberrancy.
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