Intraventricular conduction delay classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]

Overview

Intraventricular conduction delay can be caused by structural abnormalities in the bundle of His or purkinje system or ventricular myocardium, functional refractoriness in a portion of the conduction system (i.e., aberrant ventricular conduction), or ventricular preexcitation over a bypass tract. Intraventricular conduction disturbances can be broadly classified based upon the underlying physiological abnormality or based upon the site of block (anatomical classification). However, the anatomic description of conduction abnormalities are not intended to localize sites of impaired function precisely because the electrocardiographic changes may be caused by abnormalities in various sites within the ventricles.

Classification

Physiological Classification

Phase 3 Block

Phase 3 block (tachycardia-dependent block), occurs when an impulse arrives at tissues that are still refractory caused by incomplete repolarization. Functional phase 3 block can occurs if the impulse is sufficiently premature to encroach on the physiological refractory period of the preceding beat, when the membrane potential is still reduced. Phase 3 block can also occur pathologically if electrical systole and the refractory period are abnormally prolonged with refractoriness extending beyond the action potential duration or the QT interval and the involved fibre is stimulated at a relatively rapid rate. Manifestations of phase 3 block include mostly RBBB and fascicular block and less commonly LBBB. Phase 3 block is the underlying physiology for the following phenomenons of conduction delay :

• Aberration caused by premature excitation : This causes intraventicular conduction block by impulses encroaching on the refractory period of the bundle branch prior to full recovery of the action potential, namely during so-called voltage-dependent refractoriness. At normal heart rate it always results in RBBB whereas in faster hearts it mostly results in LBBB.
• Ashman phenomenon : Normally, the refractory period of the His-purkinje system lengthens as the heart rate slows and shortens as the heart rate increases, even when heart rate changes are abrupt. Ashman phenomenon results when a short cycle follows a long R-R interval i.e the QRS complex that ends the long pause is conducted normally but creates a prolonged effective refractory period of the bundle branches, whereby the next QRS complex that occurs after a short coupling interval is conducted aberrantly because one of the bundles is still refractory as a result of a lengthening of the refractory period. RBBB aberration is more common than LBBB because the right bundle has a longer effective refractory period than the left. The Ashman phenomenon can occur during second-degree AV block, but it is most common during atrial fibrillation (AF).
• Acceleration-dependent aberration : Acceleration-dependent blocks is a result of failure of the action potential of the bundle branches to shorten or paradoxical lengthening of action potential lengthens in response to acceleration of the heart rate. The effective refractory period of the right bundle normally shortens at faster heart rates more than the left bundle which explains the more frequent LBBB at faster rates.

Phase 4 Block

Phase 4 block occurs when conduction of an impulse is blocked in tissues well after their normal refractory periods have ended. The membrane depolarization in phase 4 block is different from that in phase 3 block. Enhanced automaticity or partial depolarization of injured myocardial tissue, or both cause an enhanced phase 4 depolarization within the bundle branches. As the maximum diastolic potential immediately follows repolarization, from which point the membrane potential is steadily reduced (by the pacemaker current), it results in inactivation of some Na+ channels. Thus, an action potential initiated early in the cycle (immediately after repolarization) would have a steeper and higher phase 0 and consequently better conduction than would an action potential initiated later in the cycle when the membrane potential at the time of the stimulus is reduced, with resulting reductions in the velocity and height of phase 0 and slower conduction.