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 physiology 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. 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 conduction delay mechanism always results in RBBB at a normal heart rate whereas in faster hearts it mostly results in LBBB.
• Ashman phenomenon : 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 : This conduction delay mechanism results in LBBB at lower heart rates and RBBB at faster heart 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. This type of aberration is sometimes referred to as bradycardia-dependent BBB and always manifests an LBBB pattern because the left ventricular (LV) conduction system is more susceptible to ischemic damage and has a higher rate of spontaneous phase 4 depolarization than the right ventricle.

Aberration by Concealed Transeptal Conduction

This conduction delay mechanism is due retrograde activation of bundle branches, where one bundle is activated earlier than the other following transseptal conduction, making it refractory for the next following impulse. This can result in either RBBB or LBBB depending upon side of origin of the retrograde impulses.

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) : 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. 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 fascicles or its combination with bundle branch block.

• 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.
• LAFB with LPFB : This produces a complete LBBB pattern.

Trifascicular Block

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. 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.

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.