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. 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

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.

Anatomical Classification

Left Bundle Branch Block

Left bundle branch block (LBBB), a conduction delay pattern seen on the surface electrocardiogram (ECG) can result from conduction abnormalities in the main left bundle branch, or in its fascicles, or in the distal conduction system of the left ventricle or less commonly, in the fibers of the bundle of His that become the main left bundle branch. In LBBB myocardial activation changes only affect the left ventricle and thus changes in the morphologic features of local electrograms can be recorded in the left, but not the right. ECG pattern usually shows a wide, entirely negative QS complex (rarely, a wide rS complex) in lead V1 and a wide, tall R wave without a q wave lead V6. LBBB can be classified into

• Complete LBBB : Complete LBBB is a severe form of conduction delay where the activation of the LV originates from the right bundle in a right to left direction, resulting in delayed and abnormal activation and diffuse slowing of conduction throughout the LV. QRS complex is 0.12 sec or wider.
• Incomplete LBBB : Incomplete LBBB is due to mild conduction delay in the left bundle where much of the LV activation occurs via the normal conduction system, although it begins abnormally on the right side of the septum. QRS is between 0.1 and 0.12 sec wide.

Right Bundle Branch Block

Right bundle branch block (RBBB), a conduction delay pattern seen on the surface electrocardiogram (ECG) can result from conduction abnormalities in the main right bundle branch itself, or in the bundle of His, or in the distal right ventricular conduction system. As the right bundle is long and undivided throughout most of its course it is vulnerable to stretch and trauma for two thirds of its course when it travels subendocardially. Development of RBBB alters the activation sequence of the RV but not the LV. Because the LB is not affected, the initial septal activation (r wave in V1 and q wave in V6) which depends on the LB, remains normal, occurring from left to right. ECG pattern usually shows an rSR′ complex with a wide R′ wave in lead V1 and a qRS pattern with a wide S wave in lead V6.

• Complete RBBB : Complete RBBB is a severe form of conduction delay where RV activation spreads slowly by conduction through working muscle fibers rather than the specialized purkinje system. QRS duration is .12 seconds or more
• Incomplete RBBB : An incomplete RBBB can result from lesser degrees of conduction delay in the right bundle. The ECG pattern of incomplete RBBB is similar to that of complete RBBB, except that the QRS duration is between 0.11 and 0.12 seconds.
• Atypical RBBB : Atypical RBBB can be caused by attenuation or loss of posterior deflections in the anteroposterior leads, resulting in an rsR′, qR, or M-shaped QRS pattern in V1.

Fascicular Block

Hemiblock

Fascicular block generally does not substantially prolong QRS duration, but alters only the sequence of LV activation. The primary ECG change is a shift in the frontal plane QRS axis because the conduction disturbance primarily involves the early phases of activation.

• Left anterior fascicular block (LAFB) : In LAFB, the left anterior fascicle that activates the upper part of the septum, the anterolateral LV free wall, and the left anterior papillary muscle early during the QRS complex is activated later than normal, resulting in unbalanced inferior and posterior forces early during ventricular activation initiated by the left posterior fascicle (Initial r waves in inferior leads) and unopposed anterosuperior forces later during the QRS complex (Deep S waves in inferior leads). Mean QRS axis is −45° or more and a QRS width is less than 0.12 sec.
• Left posterior fascicular block (LPFB) : Conduction delay in the left posterior fascicle is considerably less common because of its thicker structure and more protected location near the left ventricular inflow tract. In LPFB, early unopposed activation of the anterosuperior left ventricular free wall, followed by late activation of the inferoposterior aspect of the left ventricle produce rS patterns in leads I and aVL as well as qR complexes in the inferior leads. Mean QRS axis of +120° or more positive, with a QRS width of less than 0.12 sec is seen.
• Left median fascicular block : This uncommon conduction delay is characterized by absence of septal q waves in ECG.

Bifascicular Block

Bifascicular block indicates blockage of any two of the three fascicles.

• RBBB with LAFB : This produces an RBBB pattern with marked left axis deviation.
• RBBB with LPFB : This produces an RBBB pattern with right axis deviation. Other causes of right axis deviation, especially right ventricular hypertrophy and lateral MI need to be excluded before making the diagnosis.
• LAFB with LPFB : This produces a complete LBBB pattern.

Trifascicular Block

The combination of bifascicular block with first-degree AV block on the surface ECG cannot be considered as trifascicular block because the site of AV block can be in the AV node or in the bundle of His. Trifascicular block includes the following :

• RBBB with LAFB and LPFB
• RBBB with LBBB

The resulting electrocardiographic pattern is dependent on the relative degree of delay in the affected structures.

Alternating Bundle Branch Block

Alternating RBBB and LBBB is manifested by QRS complexes with LBBB morphology coexisting with complexes with RBBB morphology. When this is associated with a change in the PR interval, it represents an ominous sign for progression to complete AV block. This phenomenon implies a diffuse instability of the His-Purkinje system.

Peri-Infarction Block

It refers to conduction delay in the region of a myocardial infarction. In the leads with pathologic Q waves the terminal portion of the QRS complex is wide and directed opposite to the Q wave, such as a QR complex in leads III and aVF. A related abnormality is peri-ischemic block, manifested by a reversible widening of the QRS complex in electrocardiographic leads with ST-segment elevation caused by acute injury.

Notching

In known coronary artery disease patients multiple deflections within the QRS complex (e.g., rSr, Rsr′, rSR′ or multiple r′ patterns) or the presence of high-frequency notches within the R and S wave without overall prolongation of the QRS complex may is seen indicating some form of intraventricular conduction delay.