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 'Electrocardiographic findings' 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 "Myocardial action potential and action of antiarrhythmic drugs".)