The scarcity of available literature and the absence of standardized diagnostic criteria have contributed to the limited recognition and comprehension of right fascicular blocks (RFB), also referred to as right distal or peripheral blocks. This lack of clarity has led to an increased misdiagnosis rate, with these blocks frequently being mistaken for left fascicular blocks (LFB), right bundle branch blocks (RBBB), pseudo-infarctions, right ventricular enlargement (RVE), and Brugada patterns. Furthermore, the clinical significance of right fascicular blocks remains ambiguous.

In 1960, Uhley and Rivkin conducted an anatomical examination of the intraventricular conduction system in canine models, leading to the conclusion that the right bundle branch (RBB) subdivides into an anterior, a middle or lateral, and a posterior fascicle, each accompanied by its respective Purkinje network [1]. Subsequently, in 1961, they executed an experimental study inducing localized subendocardial lesions in the hearts of living dogs, enabling the electrocardiographic characterization of the RFB. This trunk-level interruption primarily manifests as an augmentation in the QRS complex duration, while fascicular-level interruption does not alter the duration but exhibits an increase in terminal forces. [2].

In 1975, Medrano and De Micheli acquired electrocardiographic and vectocardiographic records from canine hearts subjected to interruptions of the anterior and posterior right fascicles. Their observations indicated that these disorders manifest as an R-wave notch in right leads and a delay in the R-peak time (RPT). Moreover, anterior interruption deviated the axis leftward, while posterior interruption deviated it rightward [3]. By 1980, the authors compiled data from patients with chronic pulmonary hypertension and isolated atrial septal defects, providing the first description of diagnosis in humans [[4], [5], [6]].1.

Until now, only a limited number of authors have delineated diagnostic criteria for RBBB and RFB, including Medrano and De Micheli [3,6], Ortega [7], the Brazilian Society of Cardiology [8], and Obregón et al. [9] [Table 1].

Building upon these foundational investigations, there is a compelling need to investigate the incidence and prevalence of RFB, establish robust diagnostic criteria for their precise identification, and, when feasible, elucidate clinically significant associations.

The origin of the RBB becomes evident in proximity to the septal leaflet of the tricuspid valve. It follows a descending trajectory, progressively dividing into three distinct fascicles upon reaching the anterior papillary muscle. The anterior fascicle ascends along the free wall of the right ventricle towards the pulmonary artery infundibulum, the middle fascicle takes a lateral course towards the free ventricular wall and the anteroinferior septal area, and the posterior fascicle directs itself towards the posterior papillary muscle and the posterolateral free ventricular wall [Fig. 1] [1,3].

Under normal circumstances, the first septal vector (V1) arises as a consequence of the temporal differences in the initial activation of the right and left septal surfaces at the mid-septal region. The second vector (V2) corresponds to the activation of the ventricular free walls, with predominance on the left side due to the significant muscle mass of the homolateral ventricle. Lastly, the third vector (V3), or basal vector, results from the electromotive forces generated by the activation of the basal portions of the ventricular free walls [10] [Fig. 2].

From an electrophysiological perspective, the RBB displays two areas of distribution: one situated in the superoanterior region and the other in the posteroinferior region. Under normal circumstances, both areas undergo simultaneous activation, thereby generating an overall 3R vector directed upwards and to the right [11] [Fig. 2].

The activation stimulus of the ventricles can be delayed or halted under different circumstances before reaching the division of the RBB [12]. The first scenario is known as incomplete right bundle branch block (IRBBB) [Fig. 3], while the second is referred to as complete right bundle branch block (CRBBB) [Fig. 4]. Although different literature establishes a duration between 110 and 120 ms for the first scenario and > 120 ms for the second, there are those who argue that it is not possible to establish a clear cutoff point for complete blocks based solely on surface electrocardiograms [10,13]. Whatever the case, as long as the stimulus cannot be conducted through the right system, a vector 3 must leap the septal electrical barrier to achieve depolarization of the right ventricle, thus giving rise to a V4 in the basal region [Fig. 5]. This abnormal activation process leads to the presence of broad and slurred complexes in right-sided leads, along with T-wave inversion and a rightward deviation of the cardiac axis.

In the presence of a right anterior fascicular block (RAFB), terminal forces oriented upwards are initiated, giving rise to an electrocardiographic pattern characterized by an S wave in leads DII, DIII, and aVF, a terminal R wave in aVR, and a terminal S wave in V6, occasionally extending to lead DI. Given the parallel orientation of these terminal forces to lead DII, SII surpasses SIII, enabling differentiation from a left anterior fascicular block (LAFB) [Fig. 2, Fig. 5] [11]. In the case of RAFB, the cardiac axis shifts from +60° to −180° [9].

Conversely, a right posterior fascicular block (RPFB) generates terminal forces directed inferiorly, resulting in the presence of an R wave in leads DII, DIII, and aVF, along with a terminal R wave in aVR and an S wave in lead DI and V6. These downward-oriented terminal forces, parallel to lead DII, lead to a greater or equal R wave amplitude in lead DII when compared to lead DIII [Fig. 2, Fig. 6] [11]. In such instances, the cardiac axis shifts from +60° to +180° [9].