Basic approach to delayed intraventricular conduction

INTRODUCTION — Delayed intraventricular conduction is a common clinical abnormality detected on the electrocardiogram (ECG). This topic will review the basic aspects of this problem [1,2]. More complete discussions of left and right bundle branch block are presented elsewhere. (See "Left bundle branch block" and "Right bundle branch block" and "ECG tutorial: Intraventricular block".)

Normal ventricular depolarization occurs after an impulse traverses the atrioventricular (AV) node and the bundle of His. This bundle of specialized conducting tissue splits into two main branches, the right and the left bundles, that rapidly transmit depolarization impulses to the right and left ventricular myocardium, respectively, via the Purkinje fibers. The main left bundle bifurcates into two primary subdivisions: a left anterior fascicle and a left posterior fascicle. Some patients have a third subdivision, a median fascicle. The depolarization wavefronts spread through the ventricular wall, from endocardium (inner layer) to epicardium (outer layer), triggering intracellular calcium release and myofilament contraction (electromechanical coupling).

RIGHT AND LEFT BUNDLE BRANCH BLOCKS — Right and left bundle branch blocks usually reflect intrinsic impairment of conduction in either the right or left bundle system, respectively (intraventricular conduction disturbances). Bundle branch block can be chronic or intermittent. As an example, transient rate-related bundle branch blocks commonly occur when the heart rate exceeds some critical value (tachycardia- or acceleration-dependent). Bradycardia or deceleration-dependent bundle branch blocks, in which conduction delay occurs when the rate falls below a certain level, are relatively rare.

Electrocardiographic changes — Bundle branch block leads to prolongation of the QRS interval and sometimes to alterations in the QRS vector (see "Basic principles of electrocardiographic interpretation"). The degree of prolongation of the QRS interval depends upon the severity of the impairment. With complete bundle branch blocks, the QRS interval is classically stated to be greater than or equal to 120 ms (0.12 s) in duration (three small [40 ms] box widths on standard ECG displays); with incomplete blocks, the QRS interval is defined between 100 (or 110 by computer) and 120 ms (0.10 [or 0.11 by computer] to 0.12 s).

The QRS vector in bundle branch block is generally oriented in the direction of the myocardial region in which depolarization is delayed. The major late QRS vector is normally directed to the left and posteriorly due to depolarization of the left ventricle. However, right bundle branch block (RBBB) delays activation of the right ventricle to the late phase of depolarization. As a result, the terminal QRS vector is oriented anteriorly and to the right. This vector points toward the positive axis of the anterior-posterior lead V1 and away from the positive axis of left-right lead V6. Therefore, these changes are represented on the ECG by a late positive wave (rSRʹ) in V1 and a late negative wave (qRS) in V6 (waveform 1 and table 1).

Left bundle branch block (LBBB) is different in that it alters both early and late phases of ventricular depolarization. The late QRS vector is still directed to the left and posteriorly, since depolarization is delayed in the left ventricle. However, the normal early left-to-right pattern of septal activation is disrupted so that septal depolarization proceeds from right-to-left as well. As a result, LBBB generates wide, predominantly negative (QS) complexes in lead V1 and entirely positive (wide R wave) complexes in lead V6 (waveform 2 and table 2). A pattern identical to that of LBBB, preceded by a sharp spike, is seen in most cases of electronic right ventricular pacing because of the relative delay in left ventricular activation.

ST-T abnormalities — Bundle branch blocks and pacemaker patterns are characteristically associated with secondary repolarization (ST-T) abnormalities. The T wave is typically opposite in polarity to the last deflection of the QRS, a discordance due solely to the altered sequence of repolarization that occurs secondary to altered depolarization. This relationship is different from that seen with primary repolarization abnormalities induced by ischemia, electrolyte disorders, and drugs such as digitalis. The ST-T changes in this setting are independent of changes in the QRS, being induced by alterations in the electrical properties of the myocardial fibers (resting membrane potential or action potential duration), not just by changes in the sequence of repolarization.

Primary and secondary T wave changes can coexist. As examples, ST depression or T wave inversion in the right precordial leads with LBBB or in the left precordial leads with RBBB may be important markers of underlying ischemia.

T wave inversions in normally conducted beats following intermittent LBBB or intermittent right ventricular electronic pacing (so-called “memory T waves”) are discussed separately. These repolarization findings are important because they may mimic myocardial ischemia. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Differential diagnosis of ECG abnormalities'.)

Impact on the QT interval — The impact of bundle branch block on the QT interval is discussed separately. (See "ECG tutorial: Basic principles of ECG analysis", section on 'QT interval'.)

Major causes — Bundle branch blocks can occur in a variety of conditions. Right bundle branch block (RBBB) is more commonly seen in subjects without structural heart disease than LBBB. RBBB also occurs with congenital (eg, atrial septal defect) and acquired (eg, valvular, ischemic) heart disease. In comparison, LBBB is often a marker of one of four underlying conditions: advanced coronary heart disease, long-standing hypertension, aortic valve disease, or cardiomyopathy. LBBB, especially with left atrial abnormality, is a highly specific, though not sensitive, sign of underlying left ventricular hypertrophy.

FASCICULAR BLOCKS — Partial (fascicular) blocks (also called hemiblocks) in the left bundle system affect the left anterior, posterior, or median fascicle, singly or in combination. They generally do not substantially prolong QRS duration, as the primary ECG change is a shift in the frontal plane QRS axis.

●Left anterior fascicular (hemi-) block leads to a QRS axis that is usually between -45° and -90° and is probably the most common cause of marked left axis deviation. (See "Left anterior fascicular block".)

●Left posterior fascicular (hemi-) block is typically associated with a QRS axis of about +120°; it is a relatively rare cause of right axis deviation, especially in younger adults. The diagnosis of left posterior fascicular block cannot be made without first excluding other causes of right axis deviation such as normal variants, acute or chronic right ventricular overload (eg, due to pulmonary embolism or chronic obstructive pulmonary disease), lateral wall myocardial infarction, and dextrocardia (table 3) (see "Left posterior fascicular block"). Artifactual right axis deviation, induced by reversal of the right and left electrodes, also must be excluded.

●Some individuals are thought to have a third fascicle originating from the left bundle, the left septal (median) fascicle. Paradoxically, ECG findings simulating septal or posterior wall myocardial infarction have both been attributed to block of this fascicle (see "Left septal fascicular block"). However, clinical readings that cite "median or septal fascicular blocks" are vanishingly rare in clinical practice. For this reason, they are not employed by the author of this topic review.

●A commonly posed clinical question is whether a sustained new or an intermittent left bundle branch block (LBBB) "causes" a leftward shift in axis in the wide-complex beats. LBBB with left axis deviation is usually associated with underlying severe organic heart disease (eg, advanced coronary, cardiomyopathic, hypertensive, valvular in origin). LBBB with right axis deviation is extremely rare and usually the subject of case reports. This combination in adults (excluding lead misplacement or dextrocardia) appears to be most commonly associated with cardiomyopathy and may reflect biventricular enlargement or relatively greater slowing of conduction in the left posterior fascicle.

Bifascicular and trifascicular block — More complex combinations of fascicular and bundle branch blocks can occur with involvement of both the left and right bundle system. Examples of bifascicular block include right bundle branch block (RBBB) and left posterior fascicular block, RBBB with left anterior fascicular block, and complete LBBB (waveform 3). Chronic bifascicular block in an asymptomatic individual is associated with a relatively low risk of progression to high-degree AV heart block. In contrast, a new bifascicular block with acute anterior myocardial infarction carries a much greater risk of complete heart block. (See "Conduction abnormalities after myocardial infarction".)

Alternating right and left bundle branch block is interpreted as a sign of trifascicular block. In contrast, first degree AV block plus bifascicular block does not necessarily indicate trifascicular involvement, since this combination can reflect slow conduction in the AV node with concomitant bifascicular block.

DIFFERENTIAL DIAGNOSIS OF WIDE QRS COMPLEX — Prolongation of QRS duration can be induced by intrinsic conduction disease (eg, right bundle branch block, left bundle branch block [LBBB], or other "nonspecific" intraventricular conduction delays), by extrinsic ("toxic") factors (especially hyperkalemia and certain drugs), by ventricular beats (eg, premature, paced or as an escape complex), or by preexcitation of the ventricles via a bypass tract as in the Wolff-Parkinson-White (WPW) pattern and its variants (table 4). The diagnostic triad of the WPW pattern consists of a wide QRS complex, a relatively short PR interval, and slurring of the initial part of the QRS complex (delta wave) due to aberrant activation of ventricular myocardium (waveform 4). The presence of a bypass tract predisposes to reentrant supraventricular tachyarrhythmias (see "Wide QRS complex tachycardias: Approach to the diagnosis" and "Wide QRS complex tachycardias: Approach to management"). In cases of partial preexcitation and certain preexcitation variants, the classic triad may not be as apparent, leading to diagnostic confusion. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome" and "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis" and "ECG tutorial: Preexcitation syndromes".)

A common oversight in general clinical reading of pacemaker ECGs is not addressing the atrial mechanism. Clinicians should also be aware that in some cases of ventricular pacing (right, biventricular, His bundle, or left bundle branch (see "Permanent cardiac pacing: Overview of devices and indications", section on 'Types of permanent pacemaker systems')), the initiating electronic pacemaker spikes may be of sufficiently low amplitude that they are overlooked. Examining the ECG at magnified gain may be helpful. In addition, in cases of right ventricular pacing with underlying atrial fibrillation, the ventricular response will usually be regularized, with a LBBB QRS morphology (waveform 5). Special care must be taken not to overlook the atrial fibrillatory waves in such cases. A major clue from the ECG alone is regularization of the QRS with a left bundle branch morphology at a rate of about 70 beats/min without discrete P waves.

CONDUCTION ABNORMALITIES AND DYSSYNCHRONY — There is a growing appreciation for the clinical significance of dyssynchronous ventricular contraction. Normal, rapid conduction of the depolarizing wavefront results in synchronous (near simultaneous) contraction of the left- and right-sided ventricular myocardium, which optimizes mechanical pump function. Delayed activation, particularly of the lateral wall of the left ventricle, can produce dyssynchronous contraction, which impairs ventricular pump efficacy.

Mechanical dyssynchrony is usually associated with abnormalities of intraventricular conduction, particularly left bundle branch block (LBBB). This correlation is imperfect; not all patients with conduction abnormalities have mechanical dyssynchrony, and mechanical dyssynchrony has been documented in some patients without QRS prolongation. Mechanical dyssynchrony can also be caused by right ventricular pacing. (See "Cardiac resynchronization therapy and conduction system pacing in heart failure: System implantation and programming".)

Cardiac resynchronization therapy (using biventricular pacing, His bundle pacing, or left bundle pacing) is increasingly employed to help restore ventricular synchrony and improve ventricular function, especially in cases of cardiomyopathy with left ventricular conduction delays. In patients with reduced left ventricular function, mechanical dyssynchrony, and heart failure, cardiac resynchronization with biventricular pacing can improve ventricular function, symptoms, and survival, as discussed separately. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system" and "Cardiac resynchronization therapy in atrial fibrillation" and "Cardiac resynchronization therapy and conduction system pacing in heart failure: System implantation and programming".)

IVCD — The acronym IVCD is used for "intraventricular conduction delay (or defect/disturbance)" in different contexts, creating potential confusion among clinicians.

●General term – IVCD refers to abnormalities in the intraventricular propagation of supraventricular impulses that give rise to changes in the shape and/or duration of the QRS complex [3]. As such, this term includes classic left and right bundle branch block patterns and their variants, as well as left anterior and left posterior fascicular blocks (hemiblocks).

As defined above, this term can also be used to include Wolff-Parkinson-White (WPW) preexcitation patterns [3]. However, as indicated by the term "preexcitation," WPW patterns are initiated by early (not delayed) ventricular depolarization. Thus, WPW patterns and their variants are not usually considered as IVCDs. To avoid confusion, the authors favor considering WPW patterns as separate from the category of IVCD, but as qualifying as types of anomalous or aberrant ventricular activation.

●Nonspecific IVCD – Nonspecific IVCD is a subset of IVCD. Nonspecific IVCD refers to QRS complexes that are wide (usually with duration of 0.11 to 0.12 s [110 to 120 ms] or greater in adults), but do not have a classical left or right bundle morphology; in some cases, the complexes may exhibit a combination of features of both of these morphologies. Use of the term "IVCD" as a synonym for nonspecific IVCD is discouraged, as this can cause confusion.

SUMMARY

●A variety of disturbances of the His-Purkinje/ventricular conduction system can affect the electrocardiogram (ECG) in distinctive ways and lead to a wide QRS complex and/or axis deviation.

●Left and right bundle branch block are examples of intraventricular conduction delays. (See 'Right and left bundle branch blocks' above.)

●Partial blocks in the left bundle system may affect the left anterior, posterior, or median fascicle, singly or in combination. They generally do not substantially prolong QRS duration, but the former two (sometimes called hemiblocks) change the frontal plane QRS axis. (See 'Fascicular blocks' above.)

●With complete bundle branch blocks, the QRS interval is greater than or equal to 120 ms (0.12 s) in duration (three small [40 ms] box widths on standard ECG paper); with incomplete blocks, the QRS interval is defined between 100 and 120 ms (0.10 to 0.12 s). (See 'Electrocardiographic changes' above.)

●Prolongation of QRS duration can be caused by structural heart disease or factors extrinsic to the conduction system (such as hyperkalemia or certain drugs), a ventricular-originating beat (premature or escape), or preexcitation of the ventricles via a bypass tract as in the Wolff-Parkinson-White pattern and its variants. (See 'Major causes' above.)