Definition of terms

Historically (Sodi et al. 1964; Cooksey et al. 1977; Laham 1980; Alboni 1981; Macfarlane and Veitch Lawrie 1989), it was thought that an electrical impulse was usually blocked in the trunk of the right or the left bundle branch, respectively, producing ECG patterns of right bundle branch block (RBBB) or left bundle branch block (LBBB). However, it was also known that ECG morphologies similar to right or left bundle branch block patterns may be produced not only by trunk injuries, but also by injuries located more proximal to the bundle of His of right or left branches, or distal to the trunk in the periphery (parietal) (Narula 1977; Sung et al. 1976; Horowitz et al. 1980).

While the concepts of superoanterior division block and inferoposterior division block of the left bundle branch (hemiblocks) have already been defined (Rosenbaum et al. 1968), it is currently under debate whether a pattern expressing surely blockage of the middle fibers of the left bundle branch exists (Bayés de Luna et al. 2012). An additional ECG pattern for the diagnosis of right zonal blocks has also been described (Bayés de Luna et al. 1982).

Finally, there are cases with mild increase of QRS duration (≥110 ms) due to non‐specific diffuse conduction delay but without any typical pattern of right or left bundle branch block.

Anatomic considerations (see also Chapter 4)

The ventricular conduction system is formed by the right and left bundle branches, their respective divisions and their interconnected Purkinje networks (Figure 11.1).

There are three distinct terminal fascicles within the ventricular conduction system: the right bundle branch, the superoanterior division of the left bundle branch, and the inferoposterior division of the left bundle branch. They form the basis of the three‐fascicular concept of the intraventricular conduction system (Rosenbaum et al. 1968). The middle fibers of the left bundle might be considered another terminal area, although very often they are not fascicles but instead show a fan‐shaped morphology, potentially forming the fourth input of ventricular activation (Uhley and Rivkin 1964; Durrer et al. 1970).

The right bundle branch is at first subendocardial; later, it penetrates the septal myocardium before reaching the moderator band. Anatomically speaking, the divisions are not well‐defined, but are considered to consist of approximately two that encompass a unique Purkinje network. From an electrophysiological point of view, the network may act as two separate areas and produce zonal blocks.

The left bundle branch has two anatomically well‐defined divisions: the superoanterior division, which is longer and narrower, and the inferoposterior division. The midseptal fibers are distributed between them with an inconsistent presentation and variable morphology (Figure 11.2). The electrophysiological significance of these fibers is still not completely understood, but as previously mentioned, it appears that a block in this area may induce a particular ECG pattern (see later).

Electrophysiological considerations

From an electrophysiological point of view, blocks at a ventricular level, as with the other types of heart block (see Chapter 11), may be first degree or partial ventricular. In this case, the stimulus may always cross the fascicle, or area in question, but it is delayed. In third‐degree block or advanced ventricular, the stimulus cannot activate the blocked area through the normal pathway. In second‐degree ventricular block, the presence of the block is intermittent.

Impulse conduction may be delayed on either the right or left side at a proximal or peripheral level. Proximal blocks are the most frequent, with the zone involved usually located in the proximal part of the left or right bundle branch trunks, or in the proximal portion of the superoanterior or inferoposterior divisions. Proximal blocks include the infrequent cases in which a block is the result of the involvement of the corresponding His fibers (see Figure 11.1). In right peripheral block, the lesion is located in the distal part of the branch or in the corresponding Purkinje network. Left peripheral block, if global, involves the entire left Purkinje network; if partial (superoanterior or inferoposterior division), only the corresponding Purkinje network is involved.

From an electrocardiographic point of view, the pattern of RBBB and LBBB, including the patterns of superoanterior and inferoposterior hemiblocks, are well‐defined (Tables 11.1–11.6). We will look at them first individually, then as a simultaneous block of two or three of these structures. In each case, we will briefly mention the clinical and prognostic implications of these types of blocks. We will refer to the combined blocks as “bifascicular” or “trifascicular” because it is helpful to think of these four structures (right bundle branch, left bundle branch trunk and superoanterior and inferoposterior divisions of the left bundle branch) as being equivalent to fascicles (Figure 11.2). We will also describe the possible ECG expression of the middle block fibers (Chapter 5) (Figure 11.3) (see later anteroseptal middle fibers block).

The ECG morphologies of different degrees of right or left bundle branch block are the result of abnormal activation of right and left ventricle due to the presence of the block (Wilson 1941; Grant and Dodge 1956; Sodi et al. 1964; Strauss and Selvester 2009; Strauss et al. 2011) (Tables 11.1–11.4).

The ECG morphology on the RBBB is similar irrespective of the origin of the block, whether it is located in the trunk (e.g. bundle branch block) in the hisian fibers (Aguilar et al. 1977; Narula 1977; Sobrino et al. 1978; Castellanos et al. 1981) or is caused by an extensive peripheral block. However, some cases of peripheral block present with special morphological characteristics (i.e. Ebstein’s disease, arrhythmogenic right ventricular dysplasia). In all of these cases, there is an abnormal and delayed right ventricular depolarization with the different degrees of conduction delay.

The ECG morphology of the LBBB is also similar at all levels, except in some cases of LBBB at a peripheral level that may have more slurrings and wider QRS than when the block is in the proximal part of the left bundle. In the case of hemiblocks, the morphology when the block is peripheral and predominantly affects the area of the Purkinje network dependent on the corresponding fascicle may be similar to the typical ECG pattern seen in cases of superoanterior or inferoposterior block at a proximal level of the fascicle.

Abnormal and delayed activation (the activation phenomenon encompasses depolarization + repolarization) of part of a ventricle (divisional or zonal block) or the entire ventricle (right or left bundle branch block) produces vectors directed toward the blocked zone that are more important in a third‐degree block than in a first‐degree block. For example, the right ventricle in third‐degree RBBB is the last part of the heart to depolarize and it produces vectors directed from left to right and from the posterior to the anterior. This aspect is very important for understanding how changes in depolarization produced by ventricular blocks modify the vectorcardiographic loop and consequently the electrocardiographic morphology of different types of block in the corresponding leads.

ECG diagnosis of advanced (third‐degree) RBBB and LBBB patterns offers the following features:

• The diagnosis is performed mainly in the horizontal plane leads (V1 and V6).
  
• The QRS should measure 0.12 sec or more (see Table 11.5for LBBB) and the slurrings should be in the direction opposite to the T wave.
  
• Depolarization of the ventricle corresponding to the blocked area is effected transseptally from the contralateral ventricle (Sodi et al. 1964; Van Dam and Janse 1974; Windham et al. 1978), which modifies and delays the sequence of ventricular activation. The variations in the activation sequence and cardiac contraction occasioned by this anomalous activation can be confirmed by echocardiography or other imaging techniques (Frais et al. 1982; Strasberg 1982).
  
• Septal repolarization dominates over that of the free left ventricular wall and is responsible for the ST–T changes seen in advanced bundle branch block.

Third‐degree right and left bundle branch blocks are better termed “advanced” than “complete.” This is because if there were no transseptal depolarization from the opposite ventricle to the blocked zone, the right ventricle could theoretically still be depolarized by the impulse that slowly advances through the normal route.

Patients with advanced bundle branch block, especially on the left side, often present with an enlarged homolateral ventricle. It seems clear that a certain degree of conduction block in the area of the homolateral ventricle plays an important role in the electrogenesis of ventricular enlargement morphologies (Piccolo et al. 1979) (see Chapter 10). In addition, the partial bundle branch block patterns (right and left) have ECG patterns that are often similar to patterns found in the respective ventricular enlargements. In fact, atrial blocks also have ECG patterns that are often similar to atrial enlargement (see Chapter 9).

In general, the anatomic substrate is more diffuse than its ECG expression (Lenegre 1964). Frequently, when the ECG morphology reflects isolated advanced right or left bundle branch block, the entire ventricular conduction system is involved to some degree.

Right bundle branch block (Table 11.1)

This type of block produces a somewhat important global delay in right ventricular activation. We will first examine the different aspects of RBBB according to whether the resulting morphology corresponds to third‐degree, or advanced, RBBB (QRS ≥0.12 sec and rsR′ in V1); second‐degree, or intermittent, RBBB; or first‐degree, or partial, RBBB (QRS < 0.12 sec and rsr′ or rsR′ in V1). We will then discuss zonal right ventricular block (RVB).

Third‐degree (advanced) right bundle branch block

The blockade site of advanced RBBB can be proximal or peripheral. Proximal block includes those cases caused by involvement of the His fibers corresponding to the right bundle branch, but this block is more often located in the proximal part of the right bundle. In peripheral block, the conduction delay is located either in the distal part of the right bundle branch (moderator band) or in the terminal ramifications of the branch (Purkinje network). The most frequent blocks are located in the proximal part of the right bundle. In both cases, proximal or peripheral origin, we use the same terminology because all have the same ECG pattern (RBBB).

Activation (Figures 11.4, 11.5, and 11.7)

Advanced RBBB of proximal origin

In proximal RBBB

In proximal RBBB, the impulse is blocked in most cases in the proximal area of the right bundle, and consequently the ventricular depolarization starts normally, with the impulse descending by the left bundle branch, but it does not descend by the right branch, or it does so with a delay of 60 ms or more. This is sufficient time for transseptal depolarization of the entire septum, originating from the left ventricle. Recently, studies performed with three‐dimensional endocardial mapping (Auricchio et al. 2004) have demonstrated that all patients with RBBB pattern have a single right ventricular septal break with a mean transseptal activation time of ≈60 ms. The QRS loop is modified by the left–right direction of transseptal depolarization and predominates over that of the free left ventricular wall, generated important vectors directed forward, to the right and somewhat upward (Sodi et al. 1964). The projection of this loop on the frontal and horizontal planes accounts for the different lead morphologies according to the loop–hemifield concept (see Chapters 1 and 6).

The horizontal loop, which shows the most important changes for the diagnosis of this type of block, rotates counterclockwise and is directed somewhat more forward than normal. Afterward, it moves forward and to the right with a delay (slurrings). The changes of the loop configuration in this plane are the key to understanding V1 and V6 morphologies in advanced RBBB. In the frontal plane, the last part of the loop also presents with slurrings with an upward and unusually rightward direction (Figures 11.4–11.6). Peñaloza et al. (1961) reproduced each of these changes in humans through progressive RBBB induction by pressuring the right bundle during heart catheterization (Figure 11.6).

To comprehend these variations, we can imagine ventricular depolarization in advanced RBBB to be represented by four vectors (Figures 11.4 and 11.5). Since depolarization initiates normally, Vector 1 does not vary due to RBBB. Vector 2 is somewhat diminished in voltage and slightly anterior, influenced by the anterior and right forces of powerful Vector 3, which begins at this moment and moves in the opposite direction. Vector 3 represents transseptal depolarization and is very important. Although the depolarization is of a relatively small ventricular mass, this process is slow due to the scarce number of Purkinje fibers in the septum. In the field of electrocardiography, the vectors that take longer to form are the most prominent. Vector 4, which is directed forward, to the right and upward, accounts for the late depolarization of the superior portion of the septum and part of the right ventricular wall.

The ventricular repolarization does not depend on the free left ventricular wall as is the norm, but rather on the septum. Septal depolarization predominates over that of the free left ventricular wall. Consequently, repolarization begins on the left side of the septum, where depolarization starts (Figure 11.7B), before depolarization of the right side of the septum is complete. For this reason, from its onset, repolarization (ST) is opposed to depolarization (end of R) and usually draws the final part of the R wave in V1 somewhat below the isoelectric line (Figure 11.7B,C). In the surface ECG, this is not visible in the leads that face the left ventricle, where the ST segment is normally isoelectric. Finally, when depolarization is complete, a single repolarization vector is formed, directed from right to left, a little downward and backward (Figure 11.7C). The T loop is therefore situated to the left and somewhat downward and backward, opposite to the slurrings formed by Vectors 3 and 4.

These alterations in the QRS and T loops are responsible for the changes observed in ECG patterns and loops in advanced RBBB described below (Figure 11.8).

In peripheral RBBB

In peripheral RBBB, right ventricular activation is also delayed, but the activation sequence is different because the transseptal component is missing.

It has been demonstrated (Horowitz et al. 1980) that the activation time in the right ventricular apex, the area where right ventricular depolarization commences, is normal or almost normal when the block results from a lesion of the moderator band or Purkinje network. This is the key to distinguishing between proximal and peripheral RBBB (Figure 11.9).

The impulse in peripheral RBBB is detained at the peripheral level, and there is no transseptal activation of the right ventricle, as in the case of proximal RBBB, but it represents the same delay of activation of this ventricle. This explains why the ECG pattern is similar to that of proximal RBBB.

In Ebstein’s disease (Figure 11.10), activation is delayed in the atrialized zone of the right ventricle (Bialostosky et al. 1972).

Epicardial mapping of patients with arrhythmogenic right ventricular dysplasia has shown that right activation delay is caused by a peripheral block (Fontaine et al. 1987) (Figure 11.11).

There are also frequent RBBBs of peripheral origin after certain types of surgery for congenital heart diseases (Fallot’s tetralogy) (Figure 11.12).

A delay of conduction in the basal part of RV related to RV dilation may explain the presence of final wide R in aVR in cases of patients with heart failure and LBBB more than an associated partial true RBBB (see Figure 11.30) (Van Bommel et al. 2011).

ECG changes (Figures 11.8, 11.10–11.12)

QRS duration

In a proximal block due to the transseptal activation of the right ventricle described above, the duration of the QRS complex is longer than normal, 0.12 sec or more. In a peripheral block, it is ≥0.12 sec, often ≥0.14 sec, and even ≥0.16 sec, particularly when right ventricular enlargement coexists.

ÂQRS in the frontal plane

In a proximal block, the axis is not usually deviated with respect to its anterior direction, except for terminal slurrings directed upward and to the right (see Figures 11.4 and 11.5). Extreme deviation to the left or right is observed in bifascicular block, advanced RBBB + superoanterior hemiblock‐left deviation or inferoposterior hemiblock‐right deviation (see later).

The association of RBBB with right ventricular enlargement produces a right‐deviated ÂQRS that has to be differentiated from advanced RBBB with inferoposterior hemiblock. Aside from the clinical manifestations, the following suggests advanced RBBB with right ventricular enlargement: (i) ECG signs of right atrial enlargement and (ii) a shallow Q in II, III, and aVF (see Chapter 10).

In a peripheral block, if right ventricular enlargement coexists, the axis is also usually deviated to the right (see Figures 11.10–11.12). In the post‐operative RBBB that occurs after surgery for congenital heart disease, an ÂQRS hyperdeviated to the left practically ensures the proximal origin of the block (Sung et al. 1976).

ECG diagnostic criteria (Table 11.2)

Proximal block (Figure 11.8)

• QRS complex in the frontal plane: The delayed final forces directed upward and to the right (Vectors 3 and 4) produce the following constant alterations in I, aVL, and aVR: wide “S” in I and aVL and terminal wide “R” in aVR. In the other leads, the morphology is more variable and is affected by the orientation and magnitude of the slurred forces. In an intermediate‐positioned heart, S is slurred in II and aVF and the final forces are isodiphasic or slightly positive in III.
  
• QRS complex in the horizontal plane: The initial loop forces are deviated slightly forward and the final forces are directed forward and to the right, generating the typical rsR′ morphology in V1, with a negative asymmetric T in V1 and V2 (r = Vector 1, s = Vector 2, R″ = Vectors 3 + 4). V5 and V6 have a qRs morphology with a wide “s” (q = Vector 1, R = Vector 2, s = Vectors 3 + 4). In V3–V4 intermediate leads, we find variable morphologies, most of which are the type shown in Figure 11.5.
  
• ST segment and T wave: As mentioned above, the T wave moves in the direction opposite to the slurrings and therefore is negative in V1, V2, and aVR, and positive in I, aVL, V5, and V6. In the intermediate precordial leads, the T wave varies, although it is more often positive or flat than negative (see Figure 11.5). The ST segment is slightly depressed in V1–V2 and isoelectric in the rest of the leads.

Peripheral block

• In general, the ECG morphologies of global advanced peripheral RBBB are indistinguishable from those of proximal RBBB. However, in some situations (such as Ebstein’s disease), a peculiar rsr′s′ morphology can be seen in V1–V2, with final slurrings (see Figure 11.10) that are different from those of classic RBBB. An atypical RBBB pattern may also be seen in arrhythmogenic right ventricular dysplasia (see Figure 11.11).

Association with other processes (Figure 11.13)

Diagnosis of associated right ventricular enlargement

The following criteria can suggest right ventricular enlargement (RVE) (see also Chapter 10):

QRS ≥0.12 sec V1 rsR′ with slurring in R′ V6 qRs with slurring in S VR qRs with slurring in R

• A qR morphology in V1 in the absence of septal infarction. This morphology (Chapter 9) is very suggestive of right atrial enlargement, which is often associated with RVE.
  
• A rsR′ morphology extended beyond V2. This is especially seen in cases of right ventricular dilation (i.e. atrial septal defect).
  
• A high‐voltage R′. As R′ increases in height, so does the likelihood of associated RVE. However, there are instances of tall R′ without RVE, and vice versa.
  
• A solitary R in V1 with QRS ≥0.12 sec. This results from the anterior orientation of the whole loop. This solitary R can be low‐voltage in emphysematous subjects (Figure 11.13A). It is frequently attended by the absence of “q” in V6.
  
• An “rS” morphology in lead I and “qR” in lead III. In this case, the possibility of inferoposterior division hemiblock in addition to advanced RBBB must be considered.

Diagnosis of associated left ventricular enlargement (Figure 11.13B)

In an echocardiographic correlation study (Vanderburg et al. 1985), the most sensitive and specific criteria for diagnosing left ventricular enlargement in the presence of advanced RBBB were described. They are:

• Tall R in V6 >20 mm.
  
• Deep S in V1, and
  
• qR in lead I and rS in lead III.

Biventricular enlargement

Biventricular enlargement may be diagnosed when in the presence of ECG criteria of RBBB, we see a tall R′ in V1 and V2 and sometimes V3–V4 with a qRs morphology in V5–V6 with high R voltage. (>20 mm) (see Figure 11.13C).

Ischemic heart disease

The association of RBBB with chronic Q wave myocardial infarction and also the ECG changes in this pattern due to acute ischemia are described extensively in Chapter 13.

Pre‐excitation

This association is infrequent and the diagnosis difficult. We briefly discuss it in Chapter 12.

Differential diagnosis

The differential diagnosis of all ECG patterns with dominant R morphology in V1 or rSr′ is described in Chapter 10 (see Table 10.3).

Clinical implications

Advanced RBBB morphology appears in 0.3–0.4% of the normal population (Barret et al. 1981). If heart disease is present, the prognosis will be determined by the type of associated disease. In isolated advanced RBBB, the prognosis is good (Rotman and Frietwaser 1975) with no tendency to develop complete atrioventricular (AV) block or elevated incidence of coronary heart disease. Some epidemiological studies (Schneider et al. 1980) indicate that the mortality in patients with advanced RBBB initiated in adulthood is greater than that of a control population group. However, when Kulbertus et al. (1980) studied a series of patients with virtually no heart disease, the prognosis was not worse than that of a control group.

Patients with proximal RBBB secondary to surgery for Fallot’s tetralogy are more likely to develop AV block (Horowitz et al. 1980). It has been demonstrated (Sung 1979) that the advanced RBBB that appears after corrective surgery for Fallot’s Tetralogy is usually peripheral (normal V–RVA time) when it presents alone, and is generally proximal (lengthened V–RVA) when associated with superoanterior hemiblock. Most of the chronic advanced RBBBs unrelated to cardiac surgery have been considered proximal. However, other authors (Dancy et al. 1982) consider that peripheral advanced RBBB is also common.

Pre‐existing RBBB was observed in 13% of patients that underwent TAVR increases risk for overall mortality after TAVR with a balloon‐expandable valve (Watanabe et al. 2016).

Peripheral block appearing in adulthood has a poor prognosis that is related to a greater number of clinical complications/syncope and presyncope (Dancy et al. 1982). The appearance of wide final R in aVR in patients with LBBB and heart failure suggest associated delay of basal part of the right ventricle (Van Bommel et al. 2011).

Thirty percent of cases of advanced RBBB with normal PR have a lengthened HV interval (Narula 1979). If HV >100 ms, especially in the presence of symptoms (syncope), pacemaker implantation is indicated.

In the presence of advanced RBBB morphology, measurement of the HV interval and V–RV apex (distance from the onset of ventricular activation on the left side to the arrival of the impulse at the apex of the right ventricle) helps to locate the blockade site (see Figure 11.9). The block is truncal when HV is normal and the V–RVA is lengthened. It is peripheral when both HV and RVA are normal. However, in practice we usually do not perform that, because as we have said the prognosis is related to associated disease.

An advanced RBBB pattern which appears during pulmonary embolism usually indicates that the pulmonary embolism is massive (see Figure 10.16).

In patients with acute infarction, RBBB usually occurs in cases of anterior infarction due to occlusion of proximal LAD because the right bundle is perfused by the first septal branch. Thus, it is accompanied by prolonged V–RVA (Mayorga‐Costes et al. 1979).

First‐degree (partial) right bundle branch block (Figures 11.14–11.17)

Activation

The location of the block can also be proximal or peripheral. If proximal, the impulse is delayed in the right bundle branch trunk, or, much less often, through the right side of the bundle of His. The delay is less than 0.06 sec. Two consequences ensue: (i) part of the right septum depolarizes transseptally, and (ii) the rest of the right septum and right ventricle depolarize normally, although late, and are the last parts of the heart to depolarize. The longer the delay, the more septum is depolarized transseptally and the larger the portion of right ventricle to depolarize last (Figure 11.14). In the last part of the QRS loop, the slurrings are directed right and forward. The shorter the delay, the less marked the slurrings. This is because the transseptal depolarization vector and the delayed final depolarization vector are directed forward, upward, and to the right. The duration of the QRS complex is always less than 0.12 sec.

If the site of partial RBBB is peripheral, right ventricular activation is also slowed. A delayed right ventricular depolarization that is probably not transseptal presents with less delay than in the case of advanced peripheral block (see before). The morphology observed in atrial septal defect (ASD) and in some cases of cor pulmonale (rsR′ with QRS < 0.12 sec) is mixed, partly due to RVE and partly due to the accompanying global non‐advanced probably peripheral RBBB (De Micheli et al. 1983).

Ventricular repolarization is less opposed to QRS in proportion to the lesser degree of delayed right ventricular depolarization seen.

ECG changes

The loop–hemifield correlation accounts for the morphologies seen in either proximal or peripheral partial RBBB (Figures 11.15 and 11.16): I and V6 (narrow S), aVR (final R) and V1 (rsr′) with greater r′ height in proportion with the degree of delay, resulting in more septum depolarizing abnormally and more free right ventricular wall depolarizing late, but always with a QRS narrower than 0.12 sec.

The induction of progressive RBBB morphologies (Figures 11.6 and 11.16) (Peñaloza et al. 1961; Piccolo 1981) demonstrates that before the r′ morphology appears in V1, a globally more anterior QRS loop without final forces directed to the right and forward is usually seen in the horizontal plane (counterclockwise rotation). In this case, the QRS complex in V1 progresses from rS to Rs with slurring or RS, and finally to rsr′. As a result, partial RBBB can exist without r′ in V1 (Figures 11.6 and 11.16). To avoid overdiagnosing partial RBBB, we continue to use r′ morphology in V1 as a diagnostic criterion (see block of middle fibers).

Differential diagnosis and clinical implications

Generally speaking, the rsR′ morphology with QRS <0.12 sec results more from RVE with some degree of RBBB than from isolated partial RBBB. It is often a more severe disorder due to associated RVE (chronic obstructive pulmonary disease (COPD) or other) with a worse prognosis than the pattern of isolated RBBB with QRS ≥ 0.12 sec morphology.

The rSr′ morphology may also be due to a highly misplaced V1 electrode (Figure 11.17), thoracic malformation (pectus excavatum), or sport. In these cases, the rSr′ pattern has no clinical significance. However, this ECG pattern has to be differentiated from the ECG pattern with r′ in V1 corresponding to type II Brugada pattern. In Chapters 7 and 22, we describe the differential ECG patterns between pectus excavatum, athletes, and type II Brugada pattern (see Figure 7.16). Other explanations for prominent R or rSr′ in V1 are shown in Table 10.3.

	The conduction delay zone can be situated at different levels of the His–Purkinje system (see text). The classical form is in the trunk of the left bundle
Global	The ECG morphology depends especially on the grade of the block, not on its location (see VR1, V1, and V6). Some types of peripheral block present slightly different ECG characteristics (see text): Third‐degree (advanced)—corresponds to type III of the Mexican School. First‐degree (partial)—corresponds to types I and II of the Mexican School. Second‐degree—corresponds to a special type of ventricular aberration
Zonal or divisional	The block is located in the divisions of the left bundle branch. Superoanterior and inferoposterior hemiblocks (Rosenbaum et al. 1968) Possible block of middle fibers (see text)

It is important to remember (see Chapter 9) that the P terminal in force V1 (PtfV1) may be considered abnormal a risk marker of AF, and even stroke. However, if the ±pattern presents as a consequence of bad placement of electrodes of V1 in a higher position, then the pattern ± is not considered abnormal.

Second‐degree right bundle branch block (Figure 11.18)

This type of block usually located in the proximal right bundle branch trunk is responsible for the intermittent appearance of advanced or partial RBBB morphology (Figure 11.14). This relatively infrequent phenomenon can appear without changes in heart rate or without being conditioned by variations in heart rate (phase 3 achycardia‐dependent block and phase 4 bradycardia‐dependent block) (see Chapter 14). Its presentation can be either sudden (Mobitz type II block: abrupt appearance of advanced or partial RBBB morphology) or progressive (Mobitz type I block, a Wenckebach‐type that is much more rare). In the latter, the RBBB pattern progressively appears in successive complexes of advanced degree. Second‐degree block corresponds to a type of ventricular aberrancy (see Chapter 14).

Left bundle branch block (Tables 11.3 and 11.4)

This block produces a somewhat marked global delay in left ventricular activation. Like RBBB, the morphology depends more on the degree of block than on its location (proximal or peripheral). Classically, it was considered that third-degree (or advanced) LBBB occurred when the QRS ≥0.12 sec with slurring in the plateau of the R wave; first-degree LBBB when the QRS <0.12 sec with solitary R in V6; and second-degree LBBB when the pattern is intermittent. However, these values may be currently a little different (Strauss et al. 2011) (see later) (see Table 11.4). Later, we will explain zonal or divisional left ventricular blocks, which include hemiblocks and the controversial block of the middle fibers.

Third‐degree (advanced) LBBB

This can be produced by proximal block of the trunk or, rarely, the left hisian area, or peripheral block (Table 11.2). Peripheral block is caused by involvement of the entire left Purkinje network and produces ECG morphologies similar to those of proximal blocks, with some increase in the slurrings and usually a wider QRS (see later). Distal or proximal blocks of the two divisions of the left bundle can also produce a third-degree LBBB pattern, although they really are a type of bifascicular block (see Figure 11.3). However, the activation wave in this case could hypothetically reach the left ventricle via the middle fibers (Medrano et al. 1970).

Activation (Figures 11.22–11.24) (Wilson 1941; Grant and Dodge 1956; Sodi et al. 1964; Strauss et al. 2011)

Advanced LBBB of proximal origin

This is the most frequent LBBB. The depolarization process starts with the impulse descending through the right bundle branch normally, but not descending though the left bundle branch, or descending with a delay of 0.06 sec or more. This delay lasts long enough for the whole septum to be depolarized transseptally from the right ventricle (Figures 11.22 and 11.23). This produces a prolongation of HV and QRS (Cannom et al. 1980).

QRS ≥120 ms. Recent studies suggest ≥130 ms per women and 140 ms for men (Strauss et al. 2011) V1 QS or rS with tiny r. Positive asymmetric T wave V6 R exclusive with usually negative asymmetric T wave In all the leads, the ST is opposed to the polarity of QRS and is quickly followed by asymmetric T wave Presence of mid‐QRS notching or slurring in ≥2 of leads V1, V2, V5, V6, I, and aVL

The QRS loop undergoes alterations as a consequence of the change in cardiac depolarization from the onset of QRS occasioned by advanced LBBB. Activation commences at the base of the anterior papillary muscle of the right ventricle, then transseptally depolarizes the septum anteriorly to posteriorly before depolarizing the free left ventricular wall (Figure 11.22). This type of depolarization is completely abnormal, with a slow impulse conduction, and produces slurring of the QRS loop and QRS complex, especially in the middle part of QRS (median slurrings). Projection of this loop on the frontal and horizontal planes accounts for the different lead morphologies according to the loop–hemifield correlation theory (Figure 11.22).

Projection of the loop in the horizontal plane shows the most important changes for the diagnosis of advanced LBBB. The loop is first directed to the left and forward, followed by a backward counterclockwise rotation and finally a forward clockwise rotation (Figure 11.22). In the frontal plane, the loop

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