In the presence of a right bundle-branch block (RBBB), septal depolarization occurs in a normal left-to-right pattern (orange arrow) but for a longer duration than normal. The initial deflection is therefore positive in right-sided leads (V1) and negative in left-sided leads (V6).

The left ventricle is activated first in a right-to-left pattern (blue arrow) via the functional left bundle branch and distal Purkinje fibers. This major leftward force accounts for the negative deflection sometimes present in V1 and the positive deflection in V6.

The right ventricle is activated last by myocardial spread (dotted red arrow) from the left ventricle. This delayed activation is no longer opposed by left ventricular depolarization forces and accounts for the R′ wave in V1 and a terminal wide S wave in V6 (Fig. 3.1A-C).

1. QRS > 120 msec in adults

2. Right lead morphology: rSR′, rsR′, RR′; notched single R in V1 or V2

3. Left lead morphology: Terminal S wave in V6 and I; S wave of greater duration than R wave

4. R peak time greater than 50 msec in V1 and normal in leads V5 and V6

The ST segments and T waves in RBBB are discordant with (in the opposite direction of) the terminal portion of the QRS complex. These changes represent repolarization abnormalities secondary to abnormal depolarization (Fig. 3.3).

Suspect abnormal pathology (i.e., ischemia) if ST segments and T waves are concordant with the terminal portion of the QRS complex.

Delay rather than complete block. QRS < 120 msec (Fig. 3.4).

RBBB can be a normal finding in healthy people. Pathologic causes to consider include severe pulmonary hypertension and pulmonary embolism. Other causes include acute myocardial ischemia, infiltrative diseases, valve disorders, and iatrogenesis (right heart catheterization, septal ablation).

The septum is depolarized abnormally from right to left and is delayed. The initial deflection is thus positive in lead V6 and negative in lead V1. This eliminates the normal septal q waves in left-sided leads.

Ventricular depolarization also proceeds in a right-to-left direction. The combination of right-to-left septal and ventricular depolarization creates wide monophasic complexes (QS in V1 and R wave in V6, I, and aVL) (Fig. 3.7A-C).

1. QRS > 120 msec in adults

2. Right-sided morphology: QS or rS in V1, V2

3. Left-sided morphology: monophasic, slurred, or notched R wave in V5, V6, and I, aVL

4. Absent septal q wave in left precordial leads (Fig. 3.8)

LBBB can result from proximal block in the left bundle before it divides into fascicles (pre-divisional) or from simultaneous conduction block in the left anterior and posterior fascicles (post-divisional).

The ST segments and T waves in LBBB are discordant with (in the opposite direction of) the terminal portion of the QRS complex. These changes represent repolarization abnormalities secondary to abnormal depolarization and are more pronounced than in RBBB (Fig. 3.9).

Delay rather than complete block. QRS < 120 msec (Fig. 3.10).

While LBBB can rarely occur in asymptomatic individuals free of cardiovascular disease, this block usually indicates underlying cardiac pathology. Common causes include degenerative disease of the conduction system, hypertension, coronary artery disease, aortic stenosis, myocarditis, and cardiomyopathy.³

LBBB can result in varying degrees of intraventricular and interventricular dysynchrony and wall motion abnormalities. These wall motion abnormalities interfere with interpretation of echo stress test results. Sequential rather than simultaneous activation of the ventricles from LBBB can compromise effective contraction. Cardiac contractility becomes more compromised with greater delays in left ventricular conduction (i.e., wider QRS complexes).

Patients with symptomatic heart failure and BBB may benefit from cardiac resynchronization therapy (CRT). CRT entails placement of a biventricular pacemaker that stimulates the right and left ventricles simultaneously.