Intraventricular conduction delay classification: Difference between revisions
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====Phase 4 Block==== | ====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. | 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. Phase 4 aberration would be expected in the setting of bradycardia or enhanced normal automaticity. Phase 4 block results occurs in the following conditions : | ||
* the presence of slow diastolic depolarization, which needs to be enhanced. | |||
* a decrease in excitability (a shift in threshold potential toward zero) so that, in the presence of significant [[bradycardia]], sufficient time elapses before the impulse arrives, thus enabling the bundle branch fibers to reach a potential at which conduction is impaired. | |||
* a deterioration in membrane responsiveness so that significant conduction impairment develops at −75 mV instead of −65 mV; this occurrence would also negate the necessity for such a long cycle before conduction fails. | |||
====Aberration caused by Concealed Transeptal Conduction==== | |||
*Perpetuation of aberrant conduction during tachyarrhythmias : During [[tachyarrythmia|tachyarrythmias]], if PVC's originates from the [[right ventricle]], it can retrogradely activate the right [[bundle of His]] earlier, with retrograde activation of the left bundle later, following transseptal conduction of the [[PVC]]. As a result the left bundle remains refractory because its actual cycle began later than the right bundle. The next impulse traveling down the His bundle encounters an excitable right bundle and a refractory left bundle and conduction subsequently propagates from the right ventricle across the septum to the left ventricle. By this time, the distal left bundle recovers, allowing retrograde penetration of impulses propagates transseptally, thereby rendering the left bundle refractory to each subsequent impulse producing a [[LBBB ]]pattern until another well-timed PVC preexcites the left bundle. | |||
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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. Phase 4 aberration would be expected in the setting of bradycardia or enhanced normal automaticity. Phase 4 block results occurs in the following conditions :
- the presence of slow diastolic depolarization, which needs to be enhanced.
- a decrease in excitability (a shift in threshold potential toward zero) so that, in the presence of significant bradycardia, sufficient time elapses before the impulse arrives, thus enabling the bundle branch fibers to reach a potential at which conduction is impaired.
- a deterioration in membrane responsiveness so that significant conduction impairment develops at −75 mV instead of −65 mV; this occurrence would also negate the necessity for such a long cycle before conduction fails.
Aberration caused by Concealed Transeptal Conduction
- Perpetuation of aberrant conduction during tachyarrhythmias : During tachyarrythmias, if PVC's originates from the right ventricle, it can retrogradely activate the right bundle of His earlier, with retrograde activation of the left bundle later, following transseptal conduction of the PVC. As a result the left bundle remains refractory because its actual cycle began later than the right bundle. The next impulse traveling down the His bundle encounters an excitable right bundle and a refractory left bundle and conduction subsequently propagates from the right ventricle across the septum to the left ventricle. By this time, the distal left bundle recovers, allowing retrograde penetration of impulses propagates transseptally, thereby rendering the left bundle refractory to each subsequent impulse producing a LBBB pattern until another well-timed PVC preexcites the left bundle.