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Ventricular Conduction Disturbances: Bundle Branch Blocks and Related Abnormalities


Recall that in the normal process of ventricular activation the electrical stimulus (signal) reaches the ventricles from the atria by way of the atrioventricular (AV) node and His–Purkinje system ( 1, 5 ). The first part of the ventricles to be stimulated (depolarized) is the left side of the ventricular septum. Soon after, the depolarization spreads simultaneously to the main mass of the left and right ventricles by way of the left and right bundle branches. Normally the entire process of ventricular depolarization in adults is completed within approximately 100 to 110 msec (less than three small box widths on electrocardiogram [ECG]). Any perturbation that interferes with the physiologic, near simultaneous stimulation of the ventricles through the His–Purkinje system may prolong the QRS width (i.e., a longer total depolarization time) or change the QRS axis. This chapter primarily focuses on a major topic: the effects of blocks or delays within the bundle branch system on the QRS complex and ST-T waves. We also briefly describe the clinical implications of these findings.

ECG in Ventricular Conduction Disturbances: General Principles

A unifying principle in predicting what the ECG will show with a bundle branch or fascicular block is that the last (and usually dominant) component of the QRS vector will shift in the direction of the last part of the ventricles to be depolarized. In other words, the major QRS vector (arrow) shifts toward the regions of the heart that are most delayed in being stimulated ( Box 8.1 ).

Box 8.1
QRS Vector Shifts in Bundle Branch and Fascicular Blocks

  • Right bundle branch block (RBBB): late QRS forces point toward the right ventricle (positive in V 1 and negative in V 6 ).

  • Left bundle branch block (LBBB): late QRS forces point toward the left ventricle (negative in V 1 and positive in V 6 ).

  • Left anterior fascicular block (LAFB): late QRS forces point in a leftward and superior direction (negative in leads II, III, and aVF, and positive in I and aVL).

  • Left posterior fascicular block (LPFB): late QRS forces point in an inferior and rightward direction (negative in lead I and positive in II and III).

Right Bundle Branch Block

Consider the effect of cutting the right bundle branch, or slowing conduction in this structure relative to the left bundle. Right ventricular stimulation will be delayed and the QRS complex will be widened. The actual shape of the QRS with a right bundle branch block (RBBB) can be anticipated based on familiar vector principles.

Normally, the first part of the ventricles to be depolarized is the left side of the interventricular septum (see Fig. 5.6A ). On the normal ECG, this septal depolarization produces a small septal r wave in lead V 1 and a small septal q wave in lead V 6 ( Fig. 8.1A ). Because the left side of the septum is stimulated by a branch of the left bundle, RBBB should not affect septal depolarization.

Fig. 8.1, Step-by-step sequence of ventricular depolarization in right bundle branch block (see text).

The second phase of ventricular stimulation is the simultaneous depolarization of the left and right ventricles (see Fig. 6.6B ). RBBB should not affect this phase much either because the left ventricle is normally electrically predominant, producing deep S waves in the right chest leads and tall R waves in the left chest leads (see Fig. 8.1B ). The key change in the QRS complex produced by RBBB is a result of the delay in the total time needed for stimulation of the right ventricle. This means that after the left ventricle has completely depolarized, the right ventricle continues to depolarize (through the right bundle branch [RBB] and/or cell-to-cell depolarization from the left ventricle).

This delayed right ventricular depolarization produces a third phase of ventricular stimulation. The electrical voltages in the third phase are directed anteriorly and to the right, reflecting the delayed depolarization and slow spread of the depolarization wave outward through the right ventricle. Therefore a lead placed over the right side of the chest (e.g., lead V 1 ) records this phase of ventricular stimulation as a positive wide deflection (R’ wave). The rightward spread of the delayed and slow right ventricular depolarization voltages produces a wide negative (S wave) deflection in the left chest leads (e.g., lead V 6 ) (see Fig. 8.1C ).

Understanding this step-by-step process allows you to deduce the patterns seen in the chest leads with RBBB. With RBBB, lead V 1 typically shows an rSR′ complex with a broad R′ wave. Lead V 6 , in contrast, shows a qRS-type complex with a broad S wave. The wide, tall R′ wave in the right chest leads and the deep terminal S wave in the left chest leads represent the same event viewed from opposite sides of the chest, namely the relatively slow spread of delayed depolarization voltages through the right ventricle.

To make the initial diagnosis of RBBB, look at leads V 1 and V 6 in particular. The characteristic appearance of QRS complexes in these leads makes the diagnosis simple. ( Fig. 8.1 shows how the delay in ventricular depolarization with RBBB produces the characteristic ECG patterns.)

In summary, the ventricular stimulation process in RBBB can be divided into three phases. The first two phases are normal septal and left ventricular depolarization. The third phase is delayed stimulation of the right ventricle. These three phases of ventricular stimulation with RBBB are represented on the ECG by the triphasic complexes seen in the chest leads:

  • Lead V 1 shows an rSR′ complex with a wide R′ wave.

  • Lead V 6 shows a qRS pattern with a wide S wave.

As noted, with typical RBBB patterns, the QRS complex in lead V 1 generally shows an rSR′ pattern ( Fig. 8.2 ). Occasionally, however, the S wave does not make its way below the baseline. Consequently, the complex in lead V 1 has the appearance of a wide, notched R wave with largest amplitude at the end of the complex ( Fig. 8.3 ). Another variant of RBBB is the presence of a multiphasic rSR’S’ in lead V1. However nonspecific, this multiphasic pattern may be seen with right ventricular overload syndromes, such as atrial septal defect ( Fig. 8.4 ).

Fig. 8.2, Notice the wide rSR′ complex in lead V 1 and the qRS complex in lead V 6 . Inverted T waves in the right precordial leads (in this case V 1 to V 3 ) are common with RBBB and are called secondary T wave inversions. Note also the left atrial abnormality pattern (biphasic P in V 1 with prominent negative component) and prominent R waves in V 5 , consistent with underlying left ventricular hypertrophy.

Fig. 8.3, Instead of the classic rSR′ pattern with RBBB, the right precordial leads sometimes show a wide notched R wave (seen here in leads V 1 to V 3 ). Notice the secondary T wave inversions in leads V 1 to V 2 .

Fig. 8.4, ECG for the secundum (common)-type atrial septal defect typically shows a right ventricular conduction delay, often with a vertical to rightward QRS axis (not present here). Note the multiphasic rSR′S′ variant of RBBB (arrow in V 1 ), which may be associated with right ventricular overload states. Notching of the R wave peak in one or more of the inferior leads (“crochetage sign”) is also often present (see lead aVF here; region within oval). ST-T abnormalities in the right to mid precordial leads may be related to the right-sided conduction delay as well as to right ventricular overload. Tall P waves resulting from right atrial abnormality may be seen (not present here). Atrial septal defects are among the most common types of congenital heart disease that may escape recognition until adulthood.

Figs. 8.2 and 8.3 show examples of RBBB. Do you notice anything abnormal about the ST-T complexes in these tracings? If you look carefully, you can see that the T waves in the right chest leads are inverted (negative). T wave inversions in the right chest leads are a characteristic finding with RBBB. Slight-moderate ST depressions also may be seen, sometimes simulating ischemia. These alterations are referred to as secondary changes because they just reflect the delay in ventricular stimulation. By contrast, primary ST-T wave abnormalities reflect alterations in repolarization, independent of any QRS change. Examples of primary T wave abnormalities include T wave inversions resulting from ischemia/infarction ( 9, 10 ), select electrolyte abnormalities (e.g., hypokalemia, hyperkalemia) ( Chapter 11 ), and drugs (e.g., digoxin) ( Chapter 20 ).

Of note, some ECGs show both primary and secondary ST-T changes. In Fig. 8.3 the T wave inversions in leads V 1 to V 3 and leads II, III, and aVF can be explained solely on the basis of the RBBB because the negative T waves occur in leads with an rSR′-type complex. However, any T wave inversions or ST segment depressions in leads with a qRS pattern, not seen in these examples, would represent a primary change, perhaps resulting from ischemia or a drug effect.

Complete and Incomplete RBBB

RBBB is traditionally subdivided into complete and incomplete forms, depending on the width of the QRS complex. Complete RBBB in adults is defined by a QRS that is 120 msec or more in duration with an rSR′ in lead V 1 and a qRS in lead V 6 . Incomplete RBBB shows the same QRS patterns but with a waveform duration between 110 and 120 msec (0.11 and 0.12 sec). Note: An isolated rSr′ pattern with a narrow QRS duration (110 msec or less in adults) and a very small (≤2 mm) terminal r′ wave in V 1 or V 1 –V 2 is a common normal variant and should not be overread as an RBBB variant.

Clinical Significance

RBBB may be caused by a number of factors. First, some individuals have RBBB as an incidental finding without any identifiable underlying heart disorder. Therefore RBBB itself, as an isolated ECG abnormality, does not indicate underlying heart disease. Second, even under pathologic conditions, RBBB is nonspecific as it may be associated with many types of organic heart disease. It may occur with virtually any condition that affects the right side of the heart, including atrial septal defect with left-to-right shunting of blood (see Fig. 8.4 ), chronic pulmonary disease with pulmonary hypertension, and valvular lesions such as pulmonary stenosis, as well as cardiomyopathies and coronary disease. In some people (particularly older individuals), RBBB is sometimes related to chronic degenerative changes in the conduction system. RBBB may also occur transiently or permanently after cardiac surgery or cardiac contusion.

Acute pulmonary embolism, which produces acute right-sided heart overload, may cause a right ventricular conduction delay, usually associated with sinus tachycardia (see Chapter 11 ).

By itself, RBBB does not require any specific treatment. RBBB may be permanent or transient. Sometimes it appears only when the heart rate exceeds a certain critical value (rate-related RBBB), a nondiagnostic finding. However, as noted later, in patients with acute ST segment elevation anterior myocardial infarction (MI), a new RBBB is of major importance because it indicates an increased risk of complete heart block, particularly when the RBBB is associated with left anterior or posterior fascicular block and a prolonged PR interval. A new RBBB in that setting is also a marker of more extensive myocardial damage, often associated with heart failure or even cardiogenic shock (see Fig. 9.20 ).

RBBB is a characteristic feature in some infectious diseases (i.e., Chagas disease) and hereditary neurolomuscular conditions (including myotonic dystrophy type 1 and Kearns-Sayre disease; see also Chapter 12 ).

A pattern resembling RBBB (sometimes called a pseudo-RBBB ) is characteristic of the Brugada pattern, which is important because it may be associated with increased risk of ventricular tachyarrhythmias (see Fig. 21.9 and 21.10 ).

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