Right bundle branch block

INTRODUCTION — Right bundle branch block (RBBB), a pattern seen on the surface electrocardiogram (ECG), results when normal electrical activity in the His-Purkinje system is interrupted (figure 1). The normal sequence of activation is altered dramatically in RBBB, with a resultant characteristic appearance on the ECG manifest by a widened QRS complex and changes in the directional vectors of the R and S waves (waveform 1). (See 'ECG findings and diagnosis' below.)

The anatomy, clinical manifestations, differential diagnosis, prognostic implications, and treatment of RBBB will be reviewed here. Additional details regarding the ECG manifestations of RBBB are discussed separately. (See "ECG tutorial: Intraventricular block", section on 'Right bundle branch block'.)

ANATOMY AND ELECTROPHYSIOLOGY

Anatomy — The bundle of His divides at the juncture of the fibrous and muscular boundaries of the intraventricular septum into the left and right bundle branches (figure 1). The right bundle branch is a long, thin, discrete structure that consists of fast response Purkinje fibers. The right bundle branch courses down the right side of interventricular septum near the endocardium in its upper third, deeper in the muscular portion of the septum in the middle third, and then again near the endocardium in its lower third. The right bundle branch does not divide throughout most of its course, but begins to ramify as it approaches the base of the right anterior papillary muscle with fascicles going to the septal and free walls of the right ventricle.

Blood supply — The right bundle branch receives most of its blood supply from septal branches of the left anterior descending coronary artery, particularly in its initial course. In most patients, it also receives some collateral supply from either the right or circumflex coronary systems depending upon the dominance of the coronary system (figure 2).

Electrophysiology — The right bundle branch consists of a bundle of Purkinje cells covered by a dense sheath of connective tissue. Purkinje cells are specialized to conduct rapidly at 1 to 3 m/sec, as phase 0 is dependent on the rapid inward sodium current (figure 3). Initial activation occurs near the apex of the right ventricular endocardium, subsequently spreading to the septum and the free wall of the right ventricle, then moving much more slowly through the myocardial cells. (See "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs".)

Intraoperative studies in humans have shown that RBBB can occur at three discrete levels [1,2]:

●The proximal right bundle, which is the most common site of RBBB.

●The distal right bundle, which is unusual unless there has been transection of the moderator band during surgery.

●The terminal right bundle, which may be produced by ventriculotomy or transatrial resection.

In addition, RBBB may be induced by disease in the His bundle, resulting in activation that is asynchronous from that in the rest of the infranodal conducting system, possibly resulting in a bundle branch or fascicular block [3-5].

EPIDEMIOLOGY — The prevalence of RBBB increases with age. In one prospective study of 855 males followed for 30 years, the prevalence was 0.8 percent in subjects at age 50 and 11.3 percent by age 80 (figure 4) [6]. There was no significant association with risk factors for, or the presence of, ischemic heart disease, myocardial infarction, or cardiovascular deaths, suggesting that RBBB is usually a marker of a slowly progressive degenerative disease that also affects the myocardium. Similar observations apply to left bundle branch block [6]. (See "Left bundle branch block".)

RBBB can rarely occur in an otherwise normal heart, with a prevalence estimated between 0.2 and 2.3 percent, as illustrated by the following observations [7-11]:

●In a study of 237,000 airmen under age 30; there were 394 cases of complete RBBB, representing a prevalence of 0.2 percent [8].

●Among 66,450 participants in the Women's Health Initiative trial, 832 had RBBB at study entry, representing a prevalence of 1.3 percent [9].

●Among 8527 participants in the NHANES study (mean age 61 years, 87 percent were White Americans, 53 percent female, 16 percent with coronary heart disease at baseline), RBBB was present at baseline in 192 people (2.3 percent) [10].

Incomplete RBBB (QRS duration between 100 and 119 ms) can also be seen in apparently healthy persons, and in contrast to complete RBBB, it appears to be less common with advancing age. In a study of 43,401 Swiss military conscripts (mean age 19.1 years), incomplete RBBB was the most common ECG abnormality, seen in 13.5 percent of the cohort, while among 18,441 participants (mean age 50.1 years) in the Copenhagen City Heart Study, 3.4 percent had an incomplete RBBB [12,13].

ETIOLOGY — The right bundle branch is vulnerable to stretch and trauma for two-thirds of its course when it is near the subendocardial surface (figure 1). Conduction in the right bundle can be compromised by both structural and functional factors.

Structural heart disease — Cardiac conditions that can cause RBBB include the following:

●Chronically increased right ventricular pressure, as in cor pulmonale, which may also be associated with electrocardiographic findings of right ventricular hypertrophy (waveform 2). (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Epidemiology, pathogenesis, and diagnostic evaluation in adults", section on 'Diagnosis'.)

●A sudden increase in right ventricular pressure with stretch, as in pulmonary embolism. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Electrocardiography'.)

●Myocardial ischemia, infarction, or inflammation (as in myocarditis). (See "Conduction abnormalities after myocardial infarction" and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Electrocardiogram'.)

Other less common causes of RBBB include hypertension, cardiomyopathies, and congenital heart disease. RBBB can also result from idiopathic progressive cardiac conduction disease (also called Lenegre's disease or Lev's disease) [8,14,15]. (See "Etiology of atrioventricular block", section on 'Idiopathic'.)

Iatrogenic RBBB — RBBB can also be caused by procedures and interventions:

●Right heart catheter insertion results in transient RBBB in approximately 5 percent of cases. In this setting, RBBB is related to minor catheter trauma to the conduction system, which is usually transient and relieved by removal of the catheter. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults", section on 'Insertion'.)

●Nonsurgical septal reduction therapy with ethanol ablation, used in patients with hypertrophic cardiomyopathy and left ventricular outflow tract obstruction, results in RBBB in approximately 50 percent of cases. (See "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Septal reduction therapy'.)

Functional RBBB — RBBB may be functional, as a result of a long preceding R-R interval following by a short cycle ("rate-related bundle branch block"). Functional RBBB may be sustained if, after the initial aberration, the impulse down the left bundle reenters the right bundle branch rendering it again refractory, and this pattern repeats for several cycles.

Ventricular tachycardia may mimic RBBB, as in idiopathic left ventricular tachycardia with RBBB morphology and left axis deviation (Belhassen type) or in bundle branch reentrant ventricular tachycardia. (See "Ventricular tachycardia in the absence of apparent structural heart disease" and "Bundle branch reentrant ventricular tachycardia".)

Hyperkalemia can depress conduction in the His-Purkinje system and rarely causes RBBB [16,17]. (See "ECG tutorial: Miscellaneous diagnoses", section on 'Hyperkalemia'.)

Pseudo RBBB pattern — Some patients with uncommon primary ventricular arrhythmia syndromes (ie, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy) have ECG patterns similar to RBBB. However, these patients have distinct types of right ventricular myocardial disease that produce an ECG pattern similar to RBBB and should not be considered to have true RBBB. (See 'Differential diagnosis' below and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation" and "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis".)

ECG FINDINGS AND DIAGNOSIS — To best understand the electrocardiographic (ECG) findings in RBBB, one should have a basic understanding of the vectors involved in electrocardiography as well as the basic conventions of nomenclature used in electrocardiography. This information is presented elsewhere. (See "ECG tutorial: Intraventricular block", section on 'Right bundle branch block'.)

Most of the ECG findings with RBBB are related to the QRS complex. However, some accompanying changes may also be seen in the ST segment and T wave.

QRS complex — A task force from the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society has defined the electrocardiographic features of RBBB [18]. These criteria incorporate the activation forces described above and include:

●QRS duration greater than or equal to 120 ms in adults.

●Rsr', rsR', or rSR' in leads V1 or V2. The R' or r' deflection is usually wider than the initial R wave. In a minority of patients, a wide and often notched R-wave pattern may be seen in lead V1 and/or V2.

●S wave of greater duration than R wave or greater than 40 ms in leads I and V6 in adults.

●Normal R peak time in leads V5 and V6 but greater than 50 ms in lead V1 (associated with the R' wave).

The QRS morphology in patients with RBBB will vary depending on the position on the heart within the thorax as well as with other cardiac conditions that alter conduction (eg, prior anterior myocardial infarction).

ST segment and T waves — Accompanying ST-segment and T-wave changes are due to an altered sequence of repolarization. The ST-segment change is usually small, but, when present, it is discordant (ie, has an axis in the opposite direction) to the terminal mean QRS spatial vector. The T wave also tends to be discordant to the terminal conduction disturbance, resulting in inverted T waves in the right precordial leads (where there is a terminal R' wave) and upright T waves in the left precordial leads (where there is a terminal S wave).

Other diagnostic considerations — There are several other diagnostic considerations in the ECG interpretation of RBBB:

●RBBB does not interfere with the diagnosis of coexistent myocardial infarction on the basis of the usual Q- and R-wave criteria, since the vectorial forces of the initial 30 to 40 ms are essentially normal [19].

●Increased right ventricular pressures may cause the initial vector to swing superiorly and posteriorly, which may produce Q waves in the inferior and right precordial leads. This can occasionally simulate the changes seen with inferior and anterior myocardial infarction.

●There is a low sensitivity in the voltage criteria for left ventricular enlargement due to the late anterior forces and due to the reduction of amplitude of the S wave in the right precordial leads [20,21].

DIFFERENTIAL DIAGNOSIS — While RBBB has a fairly characteristic appearance on ECG, there are other conditions in which the ECG may have a similar appearance that need to be excluded prior to the diagnosis of RBBB.

Incomplete RBBB — Delay in the right bundle conduction ranges from trivial to severe, producing a similar spectrum displacement and duration of the rightward terminal conduction disturbance. RBBB is arbitrarily said to be "complete" when the QRS duration is 120 ms or more, and "incomplete" when it is between 100 and 119 ms. A RBBB pattern with a QRS duration less than 100 ms may be a normal variant, presumably reflecting a slight delay in the terminal posterobasal forces in some individuals.

Ventricular tachycardia and accelerated idioventricular rhythm — If the dominant ventricular rhythm originates from a pacemaker in the ventricle, the QRS will be widened and can have the appearance of a RBBB. However, both ventricular tachycardia (heart rate greater than 100 beats per minute) (waveform 3) and accelerated idioventricular rhythm (heart rate between 60 and 100 beats per minute) (waveform 4) are associated with atrioventricular (AV) dissociation, which should distinguish the rhythm from a supraventricular rhythm with aberrant conduction seen with RBBB. (See "Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation" and "ECG tutorial: Ventricular arrhythmias", section on 'Accelerated idioventricular rhythm'.)

Ventricular pacing — Ventricular pacing from the right ventricular apex typically results in a QRS complex resembling that seen with left bundle branch block (LBBB) on the surface ECG. However, the QRS complex resulting from biventricular pacing is more complicated and may sometimes give the appearance of a RBBB (waveform 5). When a paced QRS complex has a RBBB morphology in the absence of an LV lead, the possibility of RV lead perforation or inadvertent LV lead placement must be considered. In nearly all patients, however, the presence of pacemaker spikes preceding the QRS complex differentiates a paced complex from a RBBB.

Brugada syndrome — The Brugada syndrome is associated with particular ECG changes and an increased risk of sudden death. The ECG pattern of Brugada syndrome occurs in less than 0.2 percent of individuals overall but in as many as 3 to 24 percent of those presenting with idiopathic ventricular fibrillation. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

The ECG in Brugada syndrome consists of a pseudo-RBBB pattern and ST-segment elevation in leads V1 to V3 (waveform 6) [22-24]. The ST-segment elevation usually slopes downward, and the T wave is inverted. The widened S wave in left lateral leads that is characteristic of typical RBBB is absent in most patients with Brugada syndrome. This observation suggests that there is a high takeoff of the ST segment in the right precordium (ie, a "J" wave) rather than a true RBBB [23].

In some patients, the ST-segment abnormalities are transient but can be exposed by a sodium channel blocker, such as flecainide, ajmaline, or procainamide [25,26].

PROGNOSIS — The prognosis in patients with RBBB is related largely to the presence, type, and severity of underlying heart disease or associated conduction abnormalities:

●In patients with known or suspected cardiovascular disease (CVD), RBBB is an independent predictor of all-cause mortality. Several large cohort studies have shown an increase in mortality among patients with CVD and complete RBBB [9,27-29]. As an example, among 12,346 females with CVD (excluding those with LBBB) who participated in the Women's Health Initiative trial, there was a significantly greater risk of death from coronary heart disease (adjusted hazard ratio [HR] 1.62, 95% CI 1.08-2.43) but not overall mortality (adjusted HR 1.10, 95% CI 0.84-1.44) among females with RBBB compared with no BBB [9]. The presence of RBBB after a myocardial infarction is also associated with an increase in mortality. (See "Conduction abnormalities after myocardial infarction", section on 'Bundle branch block'.)

●The presence of a RBBB in the setting of an acute myocardial infarction is associated with a significant increase in mortality, even when thrombolytic therapy has been administered. This issue is discussed separately. (See "Conduction abnormalities after myocardial infarction".)

●In patients with heart failure (HF), there is an association between RBBB and higher mortality compared with those without a bundle branch block. In one study of 1888 patients with a recent HF hospitalization, RBBB was associated with worse long-term outcomes over a follow-up of four years [30]. This was also seen in 2907 consecutive patients admitted to an intensive care unit with decompensated HF [31].

●Patients who also have type II second-degree atrioventricular (AV) block or multi-fascicular block generally have more significant myocardial disease and a guarded prognosis. (See "Second-degree atrioventricular block: Mobitz type II" and "Chronic bifascicular blocks".)

Long-term outcomes are generally excellent in patients with RBBB and without apparent heart disease, although some reports have suggested an increase in all-cause and cardiac mortality in persons with a RBBB [8,11,32-39].

●In a primary prevention study from Sweden in which 7392 middle-aged males were followed for 28 years, males with RBBB had a nonsignificant increase in progression to high-degree AV block and no increase in myocardial infarction (MI) or coronary or all-cause mortality compared with males without bundle branch block [32]. Similarly, among 53,197 females free of CVD (excluding those with LBBB) upon entry into the Women's Health Initiative trial, there was no significant increase in either death from coronary heart disease (adjusted HR 1.31, 95% CI 0.77-2.23) or death from any cause (adjusted HR 0.89, 95% CI 0.67-1.19) [9].

●In contrast, among 18,441 participants in the Copenhagen City Heart Study without a prior MI, HF, or LBBB who were followed for over 20 years, persons with RBBB had significantly greater all-cause and cardiovascular mortality compared with those without RBBB (adjusted HR 1.31, 95% CI 1.11-1.54 for all-cause mortality and 1.87, 95% CI 1.48-2.36 for cardiovascular mortality, respectively) [13]. Similarly, among 8527 participants in the NHANES study (87 percent White Americans, 53 percent female, 16 percent with coronary heart disease at baseline), cardiovascular mortality was significantly higher in those with RBBB at baseline (adjusted HR 1.9 compared with those without BBB, 95% CI 1.2-3.0) [10].

●A study evaluated 22,806 patients without known cardiovascular disease undergoing exercise stress testing. In that study, RBBB was associated with increased risk of all-cause mortality after adjusting for clinical risk factors [39]. There was also an association between RBBB and presence of hypertension and decreased exercise capacity.

●In a 2015 systematic review and meta-analysis, which included six cohorts free of known CVD (1019 patients with RBBB and 95,079 without RBBB), RBBB with associated with greater all-cause mortality (HR 1.17, 95% CI 1.03-1.33), although there was a moderate amount of heterogeneity identified between the studies [40].

●In the largest single study evaluating 202,268 subjects >40 years of age in a primary care population in Copenhagen, the presence of RBBB was associated with increased risk of pacemaker requirement in both males and females over a mean follow up of 7.8 years. In addition, RBBB was associated with an increased risk of HF in both males and females. In this study, RBBB was associated with cardiovascular mortality in males but not females (HR 1.22, 95% CI 1.07-1.39) [11].

EVALUATION AND TREATMENT — Patients with isolated chronic RBBB (complete or incomplete) are generally asymptomatic and do not require further diagnostic evaluation for RBBB or placement of a pacemaker or any other specific therapy. However, a pacemaker may be needed if syncope occurs, particularly if other conduction disturbances are present, such as third-degree or type II second-degree AV block. In a patient with a new RBBB, a careful history should be taken focused on potential causes of RV stretch/strain (eg, pulmonary hypertension, obstructive sleep apnea, pulmonary embolism); if there is suspicion of pulmonary disease potentially impacting the RV, an echocardiogram should be obtained for further evaluation.

CRT is indicated in selected patients with RBBB and HF, although the evidence for such therapy is more limited than that for patients with LBBB and HF [41-43]. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system" and "Cardiac resynchronization therapy in heart failure: Indications and choice of system", section on 'Rationale for CRT'.)

Patients with pre-existing left bundle branch block who require right heart catheter placement are at risk for complete heart block if RBBB develops. Although the risk is low and complete heart block is usually transient, catheter insertion should not be undertaken in patients with LBBB without the ability to institute immediate transcutaneous or transvenous cardiac pacing. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults", section on 'Insertion'.)

SUMMARY AND RECOMMENDATIONS

●Anatomy and electrophysiology – Right bundle branch block (RBBB) results when normal electrical activity in the His-Purkinje system is interrupted, thereby altering the normal sequence of activation, resulting in the characteristic ECG appearance of a widened QRS complex and changes in the directional vectors of the R and S waves (waveform 1). (See 'Anatomy and electrophysiology' above and 'ECG findings and diagnosis' above.)

The bundle of His divides at the juncture of the fibrous and muscular boundaries of the intraventricular septum into the left and right bundle branches (figure 1). The right bundle branch is a long, thin, discrete structure that courses down the right side of interventricular septum, receiving most of its blood supply from the left anterior descending coronary artery, although in most patients, it also receives some collateral supply from either the right or circumflex coronary systems. (See 'Anatomy and electrophysiology' above.)

●Epidemiology – The prevalence of RBBB, which appears to increase with age, has been estimated between 0.2 to 0.8 percent of the general population. (See 'Epidemiology' above.)

●Causes – Various clinical conditions are associated with the development of RBBB or other electrocardiographic findings similar to RBBB (see 'Etiology' above):

•RBBB is associated with several types of structural heart disease including cor pulmonale, pulmonary embolism, myocardial ischemia/infarction, myocarditis, hypertension, and congenital heart disease. (See 'Structural heart disease' above.)

•RBBB can develop iatrogenically in patients undergoing right heart catheterization or ethanol ablation of the basal ventricular septum. (See 'Iatrogenic RBBB' above.)

●Diagnostic features – The electrocardiographic features of the QRS complex which define RBBB in adults include QRS duration greater than or equal to 120 ms, rsr', rsR', or rSR' in leads V1 or V2, S wave of greater duration than R wave or greater than 40 ms in leads I and V6, and normal R peak time in leads V5 and V6 but greater than 50 ms in lead V1. Accompanying ST-segment and T-wave changes are due to an altered sequence of repolarization. (See 'ECG findings and diagnosis' above.)

●Differential diagnosis – Ventricular rhythms, ventricular pacing, and the Brugada syndrome, conditions in which the QRS complex has a similar morphology to RBBB, need to be excluded prior to making the diagnosis of RBBB. (See 'Differential diagnosis' above.)

●Impact on diagnosis of myocardial infarction – The presence of RBBB does not interfere with the diagnosis of coexistent myocardial infarction on the basis of the usual Q- and R-wave criteria, since the vectorial forces of the initial 30 to 40 ms are essentially normal. (See 'Other diagnostic considerations' above.)

●Prognosis – The prognosis in patients with RBBB is related largely to the type and severity of any concurrent underlying heart disease and to the possible presence of other conduction disturbances. Long-term outcomes are generally excellent in patients without apparent heart disease, while those with RBBB in the setting of underlying cardiac disease generally have worse outcomes than those without bundle branch block. (See 'Prognosis' above.)

●Management – For asymptomatic patients with an isolated RBBB (complete or incomplete) and no other evidence of cardiac disease, no further diagnostic evaluation or specific therapy is required. However, permanent pacemaker insertion is indicated for patients with RBBB who develop symptomatic conduction system disturbances, such as third-degree or type II second-degree AV block that is not associated with a reversible or transient condition. (See 'Evaluation and treatment' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.