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Source: Used with permission from Castellanos and Myerburg.15

Table 11-3: Criteria for Diagnosis of Pure Left Anterior Fascicular Block

1. Abnormal left-axis deviation (usually between -45 and -60°)

2. rS complexes in leads II, III, and aVp and qR complexes in leads I and aVp

3. Delayed intrinsicoid deflection in leads I and aVp

4. Peak of r wave in lead III occurring earlier than peak of r wave in lead II

5. Peak of R wave in lead aVp occurring earlier than peak of R wave in aVR

Source: From Castellanos et al.61 and Milliken,64 with permission.

Left Anterior Fascicular Block Coexisting with MI

The ECG changes imposed by MIs of different locations on the LAFB are shown in Fig. 11-15. An inferior wall MI can be masked by a LAFB if the infarction does not involve the areas first depolarized by the impulse emergency from the unaffected fascicle.8 In these cases, an r (slurred or not) can be seen in leads III and aVF. It also has been stated that the change in left septal activation produced by the fascicular block may produce small r waves in V1, V2, and V3 capable of modifying the characteristics QS complexes produced by anteroseptal MI in these leads.8

Coronary Artery And Locations

Figure 11-15: Diagnosis of LAFB associated with MI. Diagnostic feature given in parentheses. A. LAFB and anteroseptal MI (QR or QS complex in right chest leads). B. LAFB and anterolateral MI (abnormal Q wave in leads I and V6). C. LAFB and anterolateral MI with electrical axis in the right superior quadrant (Q wave in leads I and V6). D. LAFB and inferior wall MI (QR or QS complexes and elevation of J point and ST segments in leads II and III).

Figure 11-15: Diagnosis of LAFB associated with MI. Diagnostic feature given in parentheses. A. LAFB and anteroseptal MI (QR or QS complex in right chest leads). B. LAFB and anterolateral MI (abnormal Q wave in leads I and V6). C. LAFB and anterolateral MI with electrical axis in the right superior quadrant (Q wave in leads I and V6). D. LAFB and inferior wall MI (QR or QS complexes and elevation of J point and ST segments in leads II and III).

Nonspecific Intraventricular Conduction Delays

Several names have been applied to the conduction disturbances occurring in the left-sided Purkinje-myocardial junctions, left septal surface, or free wall of the left ventricle: arborization block, diffuse (nonspecific) intraventricular block, peri-infarction block, parietal block, focal block,, etc.8'66-75 These conduction disturbances have different electrogenetic mechanisms. Thus the cellular "affectation" due to acute injury resulting from coronary artery disease, hyperkalemia, drugs, and intracoronary injections of contrast material occurs within (inside) the affected regions.5,15,75 Blocks occurring in subacute or chronic MI after the appearance of abnormal Q waves (peri-infarction block) (B+sHi Fig. 11-16), as well as those occurring in the presence of diffuse myocardial fibrosis Fig. 11-17), are due to the circuitous and irregular activation of living cells surrounding areas of fibrotic tissue.68-75

Left Posterior Fascicular Block

In pure left posterior fascicular block (LPFB), the impulse emerges from the unblocked anterosuperior division, thus producing small q waves in leads II, III, and aVF.815 Thereafter, the impulse moves through the electrically predominant left ventricle in an inferior and rightward direction, thus explaining the S waves in leads I and aVL as well as the R waves in leads II, III, and aVF.815 Radiologic studies of the human heart in situ have shown that the paraseptal regions of the posteroinferior (diaphragmatic) surface of the anatomic left ventricle are spatially located more to the right than certain (anterior) portions of the anatomic right ventricle.15 Since the portions of the left ventricle that are spatially located to the right are less than those located superiorly, the degree of right-axis deviation produced by pure LPFB is of lesser magnitude than that of left-axis deviation produced by LAFB.15 The hallmark of LPFB, therefore, is an "inferior" axis shift as much as "right" axis deviation (Figs. 11-18 to 11-20). Because a similar sequence of ventricular activation also can occur in right ventricular hypertrophy, pleuropulmonary disease (acute or chronic), and extremely vertical anatomic heart positions due to a slender body build or chest wall deformities, it is evident that the diagnosis of "pure" LPFB cannot be made from the ECG alone. Additional clinical, radiologic, or pathologic information is required for this purpose.8'15'61'66 The changes imposed in LPFB by MIs of different locations are depicted in Figs. 11-18 to 11-20.

Figure 11-18: Premature atrial beats showing increasing degrees of (incomplete and complete) LPFB aberration. The first beats in all panels are escape beats with the same morphology as that of sinus beats. The second, aberrantly induced ventricular complexes show different degrees of right-axis shift with an increase in size of the R waves in leads II and III. Note that the fundamental characteristic of LPFB was not right-axis deviation (beyond +90°) but an inferior-axis shift. (From Castellanos A, Myerburg RJ. The Hemiblocks in Myocardial Infarction. New York: Appleton-Century-Crofts; 1976. Reproduced with permission from the publisher and authors.)

Figure 11-18: Premature atrial beats showing increasing degrees of (incomplete and complete) LPFB aberration. The first beats in all panels are escape beats with the same morphology as that of sinus beats. The second, aberrantly induced ventricular complexes show different degrees of right-axis shift with an increase in size of the R waves in leads II and III. Note that the fundamental characteristic of LPFB was not right-axis deviation (beyond +90°) but an inferior-axis shift. (From Castellanos A, Myerburg RJ. The Hemiblocks in Myocardial Infarction. New York: Appleton-Century-Crofts; 1976. Reproduced with permission from the publisher and authors.)

Left Fascicular Blocks Produced by Intra-His Bundle Lesions

Rosenbaum et al.8 attributed surgically induced LAFB (coexisting with RBBB) to a lesion of the "pseudobifurcating" part of the His bundle. The production of LBBB and LPFB by catheters located in the right-sided cavities, however, cannot be explained by assuming direct affectation of these left-sided structures.7677 Nevertheless, they have been reported and attributed to the His bundle trauma produced by Swan-Ganz catheters.76,77 In fact, certain clinical and experimental studies have shown that some bundle branch block patterns could be normalized by distal His bundle pacing.78 Longitudinal dissociation of conduction within a usually diseased His bundle should be present for this to occur. There is, however, disagreement as to the mechanism involved, especially in regard to the predestination of fibers (within the His bundle) to specific right- or left-sided structures and to the role played by the transverse fibers connecting the various longitudinal strands.77-80

Left-Middle (Septal) Fascicular Blocks

This disorder has been demonstrated anatomically and is associated with ischemic heart disease and fibrosis of the middle (septal) fascicle of the left branch.81,82 While some authors consider that the right precordial leads show prominent R waves (similar to those found in true posterior, basal, myocardial infarction), others have described Q waves in leads V1, V2, and V3.8182 It also has been considered that left-middle (septal) fascicular blocks are manifested by the absence of the expected q waves in leads V5 and V6 in ECG intermediate or horizontal hearts. Such a diversity of diagnostic criteria shows that there are marked discrepancies regarding the ECG characteristics of this conduction disturbance. Recently, Dhala et al.83 described what they considered as the unmasking of the trifascicular conduction system by catheter ablation of the right bundle branch with a diseased left intraventricular conduction system. In these cases, ablation-

induced damage to "predestined" fibers in a diseased His bundle cannot be totally excluded.

Complete RBBB

A "complete" RBBB pattern (with QRS duration of >0.12 s) does not necessarily reflect the existence of a total conduction block in the right branch. This pattern only indicates that the entire or major parts of both ventricles are activated by the impulse emerging from the left branch.15-84'85 Thus a significant degree of conduction delay ("high grade" or "incomplete" RBBB) can produce a similar pattern. In pure complete RBBB, the EA should not be deviated abnormally either to the left or to the right. These axis deviations reflect coexisting fascicular block (see Figs. 11-14 and 11-19) or right ventricular hypertrophy.

Incomplete RBBB Pattern

For many years what has been proven with endocardial (catheter) and epicardial mapping has been recognized-namely, that incomplete RBBB "patterns" can be produced by various mechanisms84-90: (1) different degrees of conduction delays through the main trunk of the right bundle branch, (2) an increased conduction time through an elongated right bundle branch that is stretched because of a concomitant enlargement of the right septal surface, (3) a diffused Purkinje-myocardial delay due to right ventricular (RV) stretch or dilatation, (4) surgical trauma or disease-related interruption of the major ramifications of the right branch ("distal" RBBB), or (5) congenital variations of the distribution of the major distal ramifications resulting in a slight delay in activation of the crista supraventricularis.6 In arrhythmogenic RV dysplasia, the S wave in V1 is followed by a sharp, wide, positive deflection (epsilon wave; Fig. 11-5.B) attributed to delayed ventricular activation (postexcitation) in some RV myocardial fibers.30 Wide QRS complexes in this lead (wider than in other precordial leads) were attributed to a "parietal" block superimposed on a RBBB.35

Concealed RBBB

A minor conduction delay in the main trunk of the right bundle branch or in its major ramifications may be "concealed" (not manifested in the surface ECG) when there are coexisting (and of greater degree) conduction disturbances in the main left bundle branch, the anterosuperior division of the left bundle branch, and/or the free LV wall.8,15 An RBBB also can be concealed in some patients with Wolff-Parkinson-White syndrome if the ventricular insertion of the accessory pathway causes preexcitation of the RV regions that would be activated late because of the RBBB.0!

Complete LBBB

This conduction disturbance is characterized by wide (>0.11 s) QRS complexes. The diagnostic criteria consist of prolongation of the QRS complexes (>0.11 s) with neither a q nor an S wave in leads I, aVL, and a properlyplaced V6. A wide R wave with a notch on its top ("plateau") is seen in these leads. Apparently, the EAs of most uncomplicated complete LBBBs usually are not located beyond 300.81516 Complete LBBB with abnormal left-axis deviation indicates a great degree of left Purkinje and myocardial disease.

Complete LBBB with Acute MI

The classic pattern of LBBB may not be modified by a small area of myocardial necrosis. This explains why thrombolytics may be given if clinical findings characteristic of MI occur in patients with a LBBB pattern. Recent studies, however, have shown that occlusions of a coronary artery by either an angioplasty balloon or (a presumably large) MI can produce ST-segment changes as in the absence of a conduction disturbance.112 Recently, Sgarbossa02 has suggested that ST-segment elevation of 1 mm or more concordant with QRS polarity has a high specificity and sensitivity. ST-segment elevation of 5 mm or more discordant with QRS polarity, ST-segment depression of 1 mm or more in V1, V2, and V3, and (sudden) positive T waves in V4 and V5 have a high specificity but a low sensitivity. The latter can occur transiently during acute ischemia (pseudonormalization) without myocardial necrosis or be persistently present in cases where its significance is unclear. Examples of LBBB complicated by acute anterior and inferior MI are shown in Figs. 11-21 and 11-22. The above-mentioned criteria also can be applied to diagnose acute MI in patients with pacemakers.92,93

Complete LBBB with Old MI

Normally, in complete LBBB, the impulse emerges from the right bundle branch and propagates inferiorly, to the left, and slightly anteriorly. This orientation of the initial forces tends to abolish previously present inferiorly and laterally located abnormal Q waves characteristic of inferior and lateral wall MIs.15-93'94 If the infarction is anteroseptal, however, the impulse cannot propagate toward the left. Instead, the initial vectors point toward the free wall of the right ventricle because now the RV free-wall forces are not neutralized by the normally preponderant septal and/or initial LV free-wall forces.15 Thus a small q wave will be recorded in leads I, V5, and V6, where it is not normally present in complete LBBB Fig. 11-

23A). For a recent review of this subject, see Ref. 92. Similar findings can be seen in paced beats when in lead I the spike is followed by a well-defined q wave (see Fi». 11-23/J). Several studies reported that Q waves in lead I or in two or more lateral leads (I, aVL or V5 and V6) have high specificity but moderate sensitivity.92 The sign of Cabrera and Friedland (late notching of S waves in V3 through V5) has been found to have higher to moderate specificity and moderate to low sensitivity.94 Notching of the upstroke of the R wave in leads I, aVL, V5, and V6 (sign of Chapman) has a sensitivity of 21 percent and a specificity of 82 percent.94

Complete LBBB with LV Hypertrophy

This is discussed under "LV Hypertrophy," below.

Incomplete LBBB Pattern

An incomplete LBBB pattern can be diagnosed if leads I and an appropriately placed V6 show an R wave not preceded by a q wave.6 Lead V1 shows rS or QS complexes, and lead V2 shows rS complexes. Although QRS duration usualy ranges between 0.08 and 0.11 s, this pattern can be observed with QRS durations of 0.12 and 0.13 s.

Wide QRS Complexes in Patients with Manifest Preexcitation Syndromes

The characteristic pattern of manifest Wolff-Parkinson-White syndrome during sinus rhythm is well known.95-103 The ventricular complex is a fusion beat resulting from ventricular activation by two wave fronts.116-126 The degree of preexcitation (amount of muscle activated through the accessory pathway) is variable and depends on many factors. Foremost among these are the distance between the sinus node and atrial insertion of the accessory pathway and, more important, the differences in refractory period duration and in conduction time through the normal pathway and the accessory pathway. Other things being equal, a patient with rapid (enhanced) AV nodal conduction will have a smaller delta wave than a patient with slow conduction through the AV node. Moreover, if there is total block at the AV node or His-Purkinje system, the impulse will be conducted exclusively via the accessory pathway bundle.96,99-101 Consequently, the QRS complexes are different from fusion beats, although the direction of the delta wave remains the same. Moreover, the QRS complexes are as wide as (and really simulating) those produced by artificial or spontaneous beats arising in the vicinity of the ventricular end of the accessory pathway.96,99-101 The original ECG classification of manifest Wolff-Parkinson-White syndrome proposed by Rosenbaum et al.97 is now of historical interest only. Nevertheless, initial noninvasive determination of the anatomic position of the accessory pathway is of great clinical importance because of the introduction of surgical and catheter ablative techniques for symptomatic cases of preexcitation.

Toward the end of the millennium, Basiouny et al.104 reported that there were 41 publications dealing with methods for localizing the accessory pathways of patients with preexcitation syndrome. Of these, they analyzed what they considered the most important algorithms available for this purpose. The interested reader can consult this article.104 For the purposes of this chapter and due to space limitations, we will refer to the pioneer study of Milstein et al.,102 who analyzed the direction of the delta wave and divided the mitral and tricuspid ring areas where the pathways are located into various segments. These investigators considered that only four segments were necessary. This appeared logical, for at the time that this method was proposed, most ablations were performed surgically.102'103 Left free-wall accessory pathways are characterized by isoelectric and even positive delta waves in leads I, aVL, V5, or V6. Lead V1 shows R or Rs complexes (G-hH; Fig. 11-24). During sinus rhythm, the electrical axis may be normal, but when atrial fibrillation develops and exclusive accessory pathway conduction occurs, the EA is deviated to the right and inferiorly (see Fig. 11-24). Posteroseptal accessory pathways show negative delta waves in leads III and aVF and R waves in V2. An Rs (or RS) wave in V1 suggests a left posteroseptal pathway; a QS complex in the same lead may correspond to a right posteroseptal pathway Fig. 11-25). Right free wall accessory pathways display an LBBB pattern defined, for purposes of accessory pathway localization, by an R wave greater than 0.09 s in lead I and rS complexes in leads V1 and V2 with an electrical axis ranging between +30 and -60° Fig. 11-26).

Right anteroseptal accessory pathways show an LBBB pattern (as defined) with an electrical axis ranging between +30 and +120° Fig. 11-27). A q wave may be present in lead aV| but not in leads I and V6.

Mixed patterns resulted from the existence of two separate accessory pathways.

Since accessory pathways can traverse almost any part of the atrioventricular annulus, this classification is obviously insufficient when catheter ablation is contemplated. As mentioned earlier, multiple algorithms have been proposed. Since the most useful are complex, electrocardiographers find them difficult to memorize. They are also not completely satisfactory, since smaller degrees of preexcitation seem to limit diagnostic accuracy, and the polarity of delta waves [positive, biphasic (+ or -), negative, and isoelectric] has to be properly categorized. Figure 11-28 illustrates a useful algorithm to predict accessory pathway location from the 12-lead ECG.105

Left Posterolateral Accessory Pathway
Figure 11-28: Useful algorithm to predict accessory pathway location from the 12-lead ECG. Step 1:

Analysis of R/S ratio in V2. Step 2: Existence of positive (+) delta wave in lead III (initial 40 ms). Step 3: Existence of positive or negative (-) delta wave in V1 (initial 60 ms). Step 4: Delta-wave polarity in aVF (initial 40 ms) or analysis of R/S ratio in V1 (± = biphasic or isoelectric). The accuracy of the algorithm for each location in 187 prospective patients is also shown at the bottom. LAL, left anterolateral; LL, left lateral; LP, left posterior; LPL, left posterolateral; LPS, left posteroseptal; MS, midseptal; RA, right anterior; RAL, right anterolateral; RAS, right anteroseptal; RL, right lateral; RP, right posterior; RPL, right posterolateral; RPS, right posteroseptal. (From Chiang et al.165 Reproduced with permission from the publisher and authors.)

Wide QRS Complexes Produced by Ventricular Pacing from Different Sites

In determining the location of the stimulating electrodes, one should take special care not to consider that the distortion produced by large unipolar spikes constitutes parts of the pacing-induced QRS complexes. It is best not to describe the electrically produced ventricular beats as having an RBBB or LBBB morphology, since what is relevant is the polarity of the properly positioned V1 and V2 electrodes and the direction of the EA106'107 (Fig. 11-29). For example, endocardial or epicardial stimulation of the anteriorly located right ventricle at any site [apical (inferior), or mid/outflow tract (superior)] yields predominantly negative deflections in the right chest leads due to the posterior spread of activation (first and second vertical rows in Fig. 11-29). The reverse (positive deflections in V1 and V2) occurs when the epicardial stimulation of the superior and lateral portions of the posterior left ventricle by catheter electrodes in the distal coronary sinus or great and middle cardiac veins (or by implanted electrodes in the nearby muscle) results in anteriorly oriented forces (third and fourth vertical rows in Fig. 11-29). Right ventricular apical pacing may produce positive deflections in V1 if this lead is (mis)placed above its usual level. On the other hand, superior deviation of the electrical axis only indicates that a spatial inferior ventricular site has been stimulated, regardless of whether this site is the apical portion of the right ventricle or the inferior part of the left ventricle, the latter being paced through the middle cardiac vein (first and fourth vertical rows in Fig. 1129). Conversely, an inferior vertical axis is simply a consequence of pacing from a superior site, which can be the endocardium of the RV outflow tract or the epicardium of the posterosuperior and lateral portions of the left ventricle (second and third vertical rows in Fig. 11-29). The changes produced on the basic ECG patterns of paced beats produced by MI were briefly discussed in the section of LBBB and MI. The method discussed above to locate the site of impulse initiation during pacing is simpler than the more complicated ones used to determine the ventricular sites of exit from accessory pathways (crossing the AV junction), which require the use of right anterior oblique and, specially, left anterior oblique projections. The currently used nomenclature for accessory pathway location was discussed recently and challenged by a group of notable experts in the field of preexcitation.168

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