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Right Bundle Branch Block

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Right bundle branch block (RBBB) is a commonly encountered cardiac abnormality on

¬†the electrocardiogram (ECG). As the name suggests, ‚ÄėRight bundle branch block‚Äô (RBBB) occurs when the ¬†transmission of electrical impulses is ¬†either delayed or does not take place at all, along the right side of the heart (Rowlands, 2003). RBBB may at times be seen in perfectly healthy individuals and may not have any medical significance. In these cases it can be treated as a normal variant and safely ignored. However at times, it may be present in patients with underlying heart problems like cardiomyopathy, congestive heat failure etc. Presence of RBBB in association with underlying heart disease has been shown to worsen the prognosis in such patients (Schneider et al, 1980). Prolongation of duration of QRS interval is important for diagnosis of RBBB (Rowlands, 2003). Thus it is important to understand the significance of prolonged duration of QRS interval and functioning of right ventricle in patients with RBBB. I shall be describing these aspects of RBBB in detail in this paper.

Contraction of the heart is essentially due to electrical impulses generated by the

¬†specialized cells in upper part of right atrium called sino-atrial node (SA node) which after causing the contraction of atria travel through another specialized tissue called AV node (atrio-ventricular node), present at the junction of atria and ventricles. From here the electrical impulses move into ‚Äėbundle of his‚Äô which divides to form a right branch (leading into right ventricle) and a left branch (leading into the left ventricle).¬† Left and right bundle branches terminate as ‚Äėpurkinje fibers‚Äô which interlace with cardiac cells and cause their contraction. Synchronized contraction of cardiac muscles then causes both the ventricles to contract together almost simultaneously (Wilcken, 2003).

Figure 1 shows normal conduction of electrical impulses in the heart as described by Wilcken, (2003). ‚ÄėRight bundle branch block‚Äô is a disorder of cardiac conduction and occurs when transmission of the electrical impulses is delayed or not conducted along the right bundle branch. As a result patients with RBBB show significantly longer time for activation of right ventricle. In a study by Fantoni et al (2005), patients with RBBB showed longer times for activation of anterior and lateral regions of right ventricle as compared to patients with left bundle branch block (LBBB).

Thus the right ventricle is not depolarized normally due to failure of passage of normal electrical impulse. Instead, the depolarization of right ventricle occurs by means of cell-to cell conduction which spreads from left ventricle and interventricular septum to right ventricle. (Fantoni et al, 2005). However the function of left bundle branch is not affected in cases of isolated RBBB, with no underlying cardiac pathology. As a result the depolarization of left ventricle and interventricular septum occurs normally but right ventricular contraction occurs later and is slower as compared with left ventricular contraction. These changes in transmission of cardiac impulse through the heart are responsible for producing characteristic changes on ECG.

Figure 1.Diagram of the heart showing the impulse-generating and impulse-conducting system.

Wilcken, D.E.L. (2003). Clinical physiology of normal heart. In D.A.Warrell, T.M. Cox, J.D

Firth & E.J. Benz (EdS.), Oxford Textbook of Medicine: Volume 2 (p. 821). London: Oxford.

RBBB and Prolonged QRS duration

Normal QRS complex of ECG represents the spread of electrical impulses across both the

¬†ventricles. Normal duration of QRS complex varies from 100 to 110ms (milliseconds). Delay in depolarization of the right ventricular free wall results in prolongation of QRS complex to120ms or more, which is a characteristic ECG abnormality seen in RBBB (Rowlands, 2003). In a study by Schneider et al (1980), out of 70 patients who developed RBBB, 59 % of patients had QRS duration of 120 ms, 24% had QRS duration of 130ms and 17% had QRS duration of ‚Č• 140 ms.

¬†Delayed depolarization of right ventricle also results in the development of a secondary positive wave (resulting in rSR’ or rR’ pattern) in precordial leads which further prolongs the total QRS duration. The initial R wave in rSR’ pattern represents activation of inter-ventricular septum, the S wave represents left ventricular activation, and the secondary wave, R’ represents cell-to cell conduction of electrical impulse from the septum and left ventricle to the right ventricle (Rowlands, 2003).

Relationship between Duration of QRS Complex and Underlying Cardiac Disease

In general population, RBBB most commonly develops in persons who either have or are

 at the risk of developing clinically apparent cardiovascular abnormalities in near future. Schneider et al (1980) observed in their study, that among the patients, who developed RBBB, 50% also had an underlying cardiac enlargement and about 67% patients had an underlying coronary heart disease. The study by Schneider et al (1980) suggests that the onset of RBBB in young persons (< 40 years of age) is generally not associated with underlying cardiovascular abnormalities and is usually of no medical significance. RBBB has also been commonly reported to be a secondary manifestation of cardiomyopathy, both ischemic and non ischemic (Silverman et al, 1995).

Longer duration of QRS complex is more commonly seen in those RBBB patients who

¬†have an underlying cardiovascular abnormality in comparison to RBBB patients with no underlying cardiovascular abnormality (Schneider et al, 1980). In the study by Schneider et al (1980), it was seen that patients with RBBB who had no associated cardiovascular abnormalities typically had a QRS interval of 120 ms at the time of onset of RBBB. On the other hand, all the patients with QRS duration ‚Č• 140 milliseconds in ECG were found to be associated with underlying cardiovascular problem like hypertension, congestive heart failure (CHF) etc. More than 33% of patients with RBBB whose ECG showed QRS duration of 120 ms remained free from cardiovascular abnormalities during the entire follow-up period of the study. In contrast to this, only 3% of patients with RBBB whose ECG showed a QRS duration ‚Č• 130 ms were free from cardiovascular abnormalities.

Prognostic significance of prolonged duration of QRS complex depends on the etiology

¬†of underlying heart failure in patients with RBBB. ¬†Silverman et al (1995) in their study demonstrated that prolonged QRS interval in the ECG acted as a prognostic factor, influencing the period of survival only in patients with non-ischemic cardiomyopathy and not in those with ischemic cardiomyopathy. However, in these patients with ischemic cardiomyopathy, SAE (signal averaged ECG- a more detailed type of ECG examination usually performed in individuals with suspected arrhythmias) severed as a prognostic factor. Patients with abnormal SAE’s showed a worse prognosis in comparison to those with normal SAE, independent of whether they had prolonged QRS interval or not. Pundil et al (2000) have observed in their study that prolonged QRS interval (‚Č•130ms) in patients with RBBB with underlying myocardial infraction was associated with poor overall short-term and long-term prognosis.

Measurement of QRS complex

As described before, prolongation of QRS complex is a characteristic feature of RBBB.

Accurate measurement and interpretation of ECG findings is also important for predicting the prognosis of RBBB. However many controversies exist regarding the use of most accurate methodology for measurement of QRS complex in patients with RBBB. Presence of conduction abnormalities like RBBB can reduce the accuracy of ECG interpretations. In a study by Sarubbi, Li & Somerville (2000) the width of the QRS complex in the ECG was not seen to influence the accuracy of the measurements.

However the particular morphology of QRS complex such as presence of notched or slurred waves or terminal slow waves were significantly seen to influence the accuracy of measurement of QRS complex, in this study. Sarubbi et al (2000) in their study also tried to assess the accuracy of manual measurement of the QRS complex in standard 12 lead ECG examinations in patients with RBBB against computerized measurement. They reached a conclusion that, ‚Äėmeasurement of QRS complex is difficult and operator dependent and requires careful attention and correct definition‚Äô. Interestingly, the duration of QRS complex was under-estimated by computerized system of measurement in comparison to manual measurement.

Duration of QRS complex and use of CRT

            There has been a lot of controversy regarding the use of new form of pacing called cardiac resynchronization therapy (CRT) in patients with RBBB. The investigators of MUSTIC (Multisite Stimulation in Cardiomyopathies) study (2001) have recognized the beneficial effect of CRT in patients with RBBB, especially in whom QRS interval is >150ms. Cardiac re-synchronization therapy (CRT) in these patients with RBBB and underlying heat failure helps in improving symptoms of heart failure, quality of life, exercise tolerance and also functional capacity of heart.

Since in patients with RBBB, the conduction time of left ventricles is usually normal, the benefit of CRT has been doubted by many physicians (Madias et al, 2005). However the study by Fantoni et al (2005) emphasizes the usefulness of CRT in these patients since they have shown the total left ventricular delay and activation sequence to be similar in patients with both RBBB and LBBB. The reason for delayed left ventricular activation in patients with RBBB could not be determined for sure in this study. It could be due to the fact that majority of patients with RBBB in this study also had masked LBBB and had a worse haemodynamic profile as compared to patients with LBBB. Madias et al (2005) have suggested repeat assessment of duration of QRS complex in patients with RBBB having an underlying dilated cardiomyopathy or CHF, especially those patients who are being considered for CRT.

.Right ventricular function in the presence of right bundle branch

 Assessment of right ventricular function forms an important parameter in assessment of

 patients with RBBB. Adequate functioning of the right ventricle is important for maintaining an adequate pulmonary perfusion pressure in order to facilitate proper exchange of gases between deoxygenated blood in pulmonary artery and oxygenated blood in pulmonary (Bleeker et al, 2006). Delayed depolarization of right ventricle in patients suffering from RBBB, especially with underlying cardiac pathology is likely to effect the functioning of right ventricle in some ways. RBBB in patients with underlying heart failure or cardiomyopathy is often associated with abnormalities in right ventricular diastolic function which could be related to elevated pulmonary artery systolic pressure or decreased left ventricular ejection fraction (Bleeker et al, 2006). Some effects of RBBB on the functioning of right ventricle in terms of effect on right ventricular size, ventricular wall motion and pulmonary artery systolic pressure are described below in detail. Delayed contraction of right ventricle can have an effect on left ventricular ejection fraction as well. This is also described below in detail.

RBBB and ventricular wall motion abnormalities

In normal subjects, since both the ventricles contract together synchronously, the

ventricular wall motion begins in both the ventricles and ends in either left ventricle or both the ventricles. In patients with RBBB, since the left ventricle gets activated much earlier before the right ventricle, the wall motion begins in the left ventricle and ends in either right ventricle or both ventricles (Rosenbush et al, 1982). In a study conducted by Rosenbush. et al (1982) significant differences in the sequence and timing of right ventricular wall motion in patients with RBBB was found in comparison to control subjects by doing LSPA (least square phase analysis) of radio-nucleide cine-angiograms (RNCAs). In this study Rosenbush et al (1982) found the onset of right ventricular wall motion to be delayed by 28 msec in the right ventricular inflow segment and by 42 seconds in right ventricular outflow segments. Early wall motion of superior lateral segment of left ventricle was also seen in this study. This can be explained by the fact that early endocardial activation of the LV outflow tract occurs in patients with RBBB.

RBBB and pulmonary artery systolic blood pressure

Pulmonary artery systolic pressure is representative of pressure inside the right ventricle.

Normal pulmonary artery pressure at rest varies from 18-25 mm of Hg. Pressure increase in right ventricle is a function of ventricular wall motion. Since in patients with RBBB the wall motion of right ventricle is delayed, pressure rise in right ventricle is delayed too (Rosenbush et al, 1982). In isolated cases of RBBB, pulmonary artery systolic pressure is usually normal; however this pressure may be elevated in patients with RBBB, if left ventricular dysfunction is also present. Dysfunction of left ventricle or atrium can lead to an increased resistance to pulmonary venous or artery drainage due to backward transmission of the elevated left atrial pressure (Bleeker et al, 2006).  Pulmonary artery systolic pressure also depends on degree of dysfunction of right ventricle.

In a study by Schneider et al (1980) there was no statistically significant difference between the cases with RBBB and controls in terms of mean FEV1/FVC ratio, suggesting that pulmonary function tests were essentially within normal limits in these patients. FVC (forced vital capacity) is the amount of air expired by the person after maximum inspiration. FEV1 (forced expiratory volume in one second) is the amount of air which the person can forcibly expire out in one second. Ratio of FEV1 and FVC is considered as a primary indicator of lung function, which can significantly get altered in presence of increased pulmonary artery systolic pressure (Schneider et al 1980). An increase in pulmonary artery systolic pressure to greater than 30 mm of Hg can result in the development of pulmonary hypertension (Bleeker et al, 2006).

RBBB and right ventricular size

In patients with RBBB, underlying pathologies which can lead to right ventricular

 pressure overload can cause right ventricular hypertrophy where as underlying pathologies which result in right ventricular volume overload may lead to right ventricular dilation. (Bleeker et al, 2006). Right ventricular pressure overload could be due to increase in resistance to pulmonary artery or venous drainage due to backward transmission of the elevated left atrial pressure (Bleeker et al, 2006). Contraction of the right ventricle against increased pressure over a period of time can result in right ventricular thickening or hypertrophy. Presence of right ventricle cardiomyopathy along with RBBB may lead to dilatation and dysfunction of right ventricle (Bleeker et al, 2006). Severe RV dilatation or hypertrophy may cause a reduction of RVEF (right ventricular ejection fraction).

RBBB and left ventricular Ejection fraction

Left ventricular ejection fraction can be defined as the fraction of blood pumped out of

 left ventricle with each heart beat (cardiac contraction). In a RBBB, the conduction of impulses takes place normally on the left side, thus left ventricular ejection fraction is usually not affected (Madias et al, 2005). Study by Schneider et al, 1980 has emphasized the association of RBBB with serious underlying cardiovascular diseases, predominantly hypertension, myocardial infraction and CHF. Presence of underlying cardiac abnormality like cardiomyopathy, CHF etc can adversely affect the left ventricular ejection fraction depending on the exact underlying pathology in the heart. Fantoni, et al (2005) in their study observed that patients with RBBB showed delayed activation of left ventricle which was similar to that seen in patients with LBBB. As a result of delayed endocardial activation of left ventricle, left ventricular ejection fraction in these patients with RBBB was significantly reduced in this study.


RBBB can commonly occur in normal, healthy, young individuals and may not be

associated with any medical problems. However RBBB is also commonly present in association with other cardiac abnormalities like CHF, myocardial infraction, cardiomyopathy etc, especially in individuals more than forty years of age (Schneider et al, 1980). Prolongation of QRS complex serves as an important diagnostic as well as prognostic indicator in patients with RBBB (Rowlands, 2003; Silverman, 1995). Duration of QRS complex also helps in deciding whether CRT should be used as a therapeutic option for patients with RBBB or not (MUSTIC study investigators, 2001). Deterioration of right ventricular function in patients with RBBB is more in presence of underlying heart disease (Schneider et al, 1980).

Thus RBBB in association with other cardiac abnormalities especially in presence of abnormally prolonged QRS duration (‚Č• 140 ms) deserves special medical attention. Fantoni et al (2005) have found RBBB to be an important prognostic factor in patients with heart failure. However larger studies in future are required to clarify this. Therefore assessment of right ventricular function is important for determining prognosis of patients with RBBB and heart failure. Thus, until further studies clarify the exact role of RBBB, patients with RBBB, especially those with longer duration of QRS interval must be taken seriously and such patients should be treated with more aggressive form of therapy (Fantoni et al, 2005).


Bleeker, G.B., Steendijk, P., Holman, E.R., Yu, C-M., Breithardt, O.A., Kaandorp, T.A.M., et

  1. (2006). Acquired right ventricular dysfunction. Heart, 92, 14-18.

Fantoni, C., Kawabata, M., Massaro, R., Regoli, F., Raffa, S., Arora, V., et al. (2005). Right and

 left ventricular activation sequence in patients with heart failure and right bundle branch block: A detailed analysis using three-dimensional non-fluoroscopic electroanatomic mapping system. Journal of Cardiovascular Electrophysiology, 16, 112-119.

Madias, J.E., Ashtiani, R., Agarwal, H., Narayan, V.K., Win, M., & Sinha, A. (2005). Stability

of the ECG features of complete right bundle branch block over time: A methodological study for implementation in research and clinical practice. Cardiology, 103, 84-88.

MUSTIC (Multisite Stimulation in Cardiomyopathies) study investigators (2001). Effects of

multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. New England Journal of Medicine, 344, 873-880.

Pudil, R., Feinberg, M.S., Hod, H., Boyko, V., Mandelzweig, L., & Behar, S. (2001). The

 prognostic significance of intermediate QRS prolongation in acute myocardial infarction. International Journal of Cardiology, 78, 233-239.

Rosenbush. S.W., Ruggie, N., Turner, D.A., Von Behren. P.L., Denes, P., Fordham. E.W. et al

 (1982).Sequence and timing of ventricular wall motion in patients with bundle branch block. Assessment by radionuclide cineangiography. Circulation, 66, 1113-1119.

Rowlands, D.J. (2003). Electrocardiography. In D.A.Warrell, T.M. Cox, J.D

Firth & E.J. Benz (EdS.), Oxford Textbook of Medicine: Volume 2 (pp. 859-878). London: Oxford.

Sarubbi, B., Li, W., & Somerville, J. (2000). QRS width in right bundle branch block: Accuracy and reproducibility of manual measurement. International Journal of Cardiology, 75, 71-74.

Schneider, J.R., Thomas, H.E., Kreger, B.E., Mcnamara, P.M., Sorlie, P., & Kannel, W.B.

(1980). Newly Acquired right Bundle-branch Block: The Framingham Study. Annals of Internal Medicine, 92(1), 37-44.

Silverman, M.E., Pressel, M.D., Bracken, J.C., Lauria, S.S., Gold, M.R., & GoItlieb, S.S. (1995).

 Prognostic Value of the Signal-Averaged electrocardiogram and a prolonged QRS in ischaemic and non-ischaemic cardiomyopathy. American Journal of cardiology, 75, 460-464.

Wilcken, D.E.L. (2003). Clinical physiology of normal heart. In D.A.Warrell, T.M. Cox, J.D

Firth & E.J. Benz (EdS.), Oxford Textbook of Medicine: Volume 2 (pp. 820-829). London: Oxford.

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