Bundle branch block on alternate beats: by what mechanism?

In a patient with right bundle branch block occurring on alternate beats during regular sinus rhythm, the conduction disturbance disappeared during hyperventilation induced increase in heart rate, and reappeared with slight slowing of the sinus rate due to carotid sinus massage. The following mechanisms are potentially involved in the electrogenesis of bundle branch block alternans with regular RR intervals: a) phase-3 2:1 bidirectional block; b) phase-3 antegrade block with retrograde concealed activation of the involved bundle branch and subsequent "supernormal" conduction; and c) phase-4 antegrade block with transseptal retrograde concealed invasion of the affected bundle branch by impulses traversing the unimpaired bundle branch. Analysis of the tracing excluded both mechanisms a and b and favored bradycardia-dependent right bundle branch block as a key to explain the alternate pattern of intraventricular conduction.     

Supernormal Conduction in the Left Bundle Branch

Supernormal Conduction. This report describes a patient with tachycardia-dependent left bundle branch block (LBBB) and atrial extrasystoles, some of which were followed by an unexpectedly narrow QRS complex. His-bundle recordings and premature atrial stimulation were performed to analyze the mechanism underlying the normalized intraventricular conduction of some of the early atrial impulses. The results suggested the presence of supernormal conduction in the left bundle branch (LBB), because(1) the HV interval was identical in LBBB complexes and in early narrow QRS complexes; (2) during single lest stimulation using different paced atrial cycle lengths, there was a well-defined range of H₁, H₂, intervals resulting in normalization of intraventricular conduction; and (3) atrial pacing with a cycle length of 500 msec resulted in alternation between wide and narrow QRS complexes. These findings rule out alternative mechanisms that could explain the unexpectedly normal intraventricular conduction of early impulses.     

Tachycardia and bradycardia-dependent bundle branch block alternans: clinical observations.

Eleven patients with tachycardia-dependent, bradycardia-dependent, or "pseudobradycardia-dependent" bundle branch block (BBB) alternans were studied. This classification is based on the following criteria: 1) When alternans is initiated by a sudden acceleration in ventricular rate, or it appears with aberration of the second beat after a pause, the alternans is tachycardia-dependent and results from a 2:1 bidirectional block in the affected bundle branch. 2) When alternans begins with the aberrant complex terminating a pause it is bradycardia-dependent; such an alternans results from alternating bundle branch cycle lengths and refractoriness, possibly produced by alternating transseptal retrograde penetration of the affected bundle branch. 3) In cases referred to as "pseudobradycardia-dependent BBB" alternans, a change from alternans to persiscardia-dependent BBB" alternans, a change from alternans to persistent BBB occurs as the cycle lengthens; however, the disappearance of BBB with further increase of the cycle length proves the tachycardia-dependence of the conduction defect.     

Tachycardia-dependent right bundle-branch block with supernormal conduction

This paper reports the case of a 76-year-old man in whom atrial flutter with varying atrioventricular block and intermittent right bundle-branch block was found. This is the first report on tachycardia-dependent right bundle-branch block associated with supernormal conduction in a case of atrial flutter. When an impulse is conducted to the ventricles beyond 0.72 s after a QRS complex of right bundle-branch block configuration, the impulse falls after the abnormally long effective refractor period of the right bundle branch and passes through the right bundle branch. When the conducted impulse occurs within 0.72 s after a QRS complex of right bundle-branch block configuration, the impulse usually falls in the refractory period and is blocked in the right bundle branch; however, only when the impulse occurs 0.48 or 0.49 s after that does it fall in the supernormal period and passes through the right bundle branch. The findings in the present report strengthen our previous suggestion that the presence of supernormal conduction plays an important role in the initiation of reentrant ventricular tachycardia.     

Bundle branch block in alternate beats during 2:1 atrial flutter

This presentation deals with a case of atrial flutter. During 2:1 A/V conduction, the QRS complexes showed a regular alternation of narrow beats and wide beats with a typical configuration of left bundle branch block. In contrast, pauses resulting from 4:1 A/V conduction ratio always resulted in narrow beats. Disappearance of left bundle branch block with long R-R intervals demonstrated that the block was tachycardia-dependent or phase 3. Analysis of the tracing suggested that narrowing of QRS complexes in alternate beats was due to supernormal left bundle branch conduction associated with retrograde concealed conduction into the anterogradely blocked bundle branch.     

Right Bundle Branch Block on Alternate Beats during Acute Pulmonary Embolism

The electrocardiogram of a patient with acute pulmonary embolism showed right bundle branch block (RBBB) on alternate beats; following thrombolysis, the pattern evolved to persistent RBBB and eventually to normal conduction. Analysis of serial tracings suggested that the mechanism of RBBB alternans was tachycardia‐dependent bidirectional bundle branch block, caused by prolongation of both anterograde and retrograde refractory periods (RPs) of the right bundle branch (RBB). The sinus impulse found the RBB refractory, and was conducted over the left bundle branch only, depolarizing the left ventricle and then attempting to penetrate retrogradely the RBB; at that time, however, the RBB was still refractory. When a QRS complex had a RBBB configuration, therefore, the RBB was not depolarized; the ensuing sinus impulse found the RBB fully responsive as a consequence of the long period intervening between two successive depolarizations, and resulted in normal intraventricular conduction. With right ventricular afterload decrease, the recovery of RBB anterograde and retrograde excitability was asynchronous, since the retrograde RP became normal earlier than the anterograde one. In accordance with the relatively short retrograde RP, the RBB was retrogradely invaded by the transseptal impulse coming from the left ventricle; this “shifted to the right” the anterograde RP of the RBB. The RBB, thus, was still refractory to the next sinus impulse, and RBBB again occurred; the RBB, thus, was once more depolarized retrogradely, and this led to perpetuation of RBBB. Finally, intraventricular conduction became normal owing to full normalization of RBB anterograde and retrograde refractoriness. Ann Noninvasive Electrocardiol 2011;16(3):311–314     

Effects of stable and changing rates and premature ventricular beats on transient tachycardia-, pseudobradycardia-, and bradycardia-dependent bundle branch block alternans.

New circumstances under which bundle block (BBB) alternans may appear or disappear are described. 1) Tachycardia-dependent as well as bradycardia-dependent BBB alternans may begin after constant BBB is interrupted by a premature ventricular beat. Tachycardia- and bradycardia- dependence may be differentiated by the shape of the first beat after the pause. 2) When BBB alternans disappears during a constant ventricular rate, tachycardia-dependent BBB alternans changes to persistent normal or more normal intraventricular conduction, whereas bradycardia-dependent BBB alternans changes to a persistently greater degree of BBB. 3) BBB alternans appears to be tachycardia- or pseudobradycardia-dependent in relation to the cycle length and antegrade and retrograde refractory periods in the involved bundle branch. 4) BBB alternans may be recognized during persistent irregular ventricular action in atrial fibrillation. Here the recognition of BBB alternans depends upon the sequence of contours as well as upon the cycle lengths.     

John B. Barlow: master clinician and compleat cardiologist

This paper reports the case of a 76‐year‐old man in whom atrial flutter with varying atrioventricular block and intermittent right bundle‐branch block was found. This is the first report on tachycardia‐dependent right bundle‐branch block associated with supernormal conduction in a case of atrial flutter. When an impulse is conducted to the ventricles beyond 0.72 s after a QRS complex of right bundle‐branch block configuration, the impulse falls after the abnormally long effective refractory period of the right bundle branch and passes through the right bundle branch. When the conducted impulse occurs within 0.72 s after a QRS complex of right bundle‐branch block configuration, the impulse usually falls in the refractory period and is blocked in the right bundle branch; however, only when the impulse occurs 0.48 or 0.49 s after that does it fall in the supernormal period and passes through the right bundle branch. The findings in the present report strengthen our previous suggestion that the presence of supernormal conduction plays an important role in the initiation of reentrant ventricular tachycardia.     

The linking phenomenon in tachycardia-dependent intraventricular block

Seven cases of tachycardia-dependent, or phase-3, intraventricular block have been examined. Analysis revealed a constant overlap between the range of the R-R intervals ending in normal conduction and the range of the R-R intervals where the second beat is associated with intraventricular block. The block, indeed, may occur at the end of relatively long R-R intervals, whereas R-R intervals which are shorter (up to 0.11 sec) can unexpectedly result in normal intraventricular conduction. A relatively late QRS complex, however, can reflect an intraventricular block only when the preceding complex also manifests the block. This phenomenon has been interpreted as due to the so called "linking", namely the retrograde concealed penetration of an anterogradely blocked bundle branch by the impulse traversing the controlateral bundle branch. This delays the activation of the affected bundle branch, whose refractory period is, accordingly, "shifted to the right" within the cardiac cycle. A relatively late sinus impulse, thus, can result in intraventricular block since the refractory period of the affected bundle branch ends later, with respect to the beginning of the QRS complex, than it does after a normally conducted sinus impulse.     

Gap in bundle-branch conduction elicited by programmed His bundle stimulation

The gap phenomenon in right bundle-branch conduction was elicited during programmed stimulation of the His bundle. Premature beats with short and long coupling intervals showed undisturbed intraventricular conduction, while the premature beat with intermediate coupling interval blocked within the right bundle branch. The electrophysiologic mechanism of "supernormal" conduction of the earliest beats was conduction delay at a proximal site within the His bundle which allowed recovery of the right bundle branch. This study shows that programmed His bundle stimulation is a valuable method in analyzing conduction characteristics of the distal atrioventricular conduction system in cases where atrioventricular nodal refractoriness would preclude this by atrial stimulation.     

Ischemia-associated intraventricular conduction disturbances during exercise testing as a predictor of proximal left anterior descending coronary artery disease

To determine the incidence and significance of transient intraventricular conduction abnormalities occurring in association with myocardial ischemia during exercise testing, the recordings of 2,200 consecutive exercise tests were reviewed. Ten patients (0.45%) were identified as having both ischemia and intraventricular conduction abnormalities that developed transiently during the exercise test. In all 10 patients both typical angina and electrocardiographic evidence of ischemia developed during exercise. Among the 10 patients, left anterior hemiblock developed in 4, left posterior hemiblock in 2, right bundle branch block (RBBB) in 2, RBBB with left axis deviation in 1, and left anterior hemiblock progressing to complete left bundle branch block (LBBB) in 1. All 10 patients had cardiac catheterization showing significant obstruction of the left anterior descending (LAD) coronary artery at or before the origin of the first septal branch. Eight patients were treated surgically and 2 medically, all with relief of ischemic symptoms. Nine of the 10 had repeat exercise stress testing without angina or electrocardiographic evidence of ischemia and without recurrence of the transient intraventricular conduction disturbance.It is concluded that the development of transient intraventricular conduction abnormalities associated with myocardial ischemia during exercise testing is an uncommon occurrence (0.45%). When such conduction disturbances do develop, the existence of significant disease in the proximal portion of the LAD coronary artery is strongly suggested. With control of myocardial ischemia, the transient conduction disturbances during exercise are ameliorated.     

Apparent bradycardia-dependent right bundle branch block associated with atypical atrioventricular Wenckebach periodicity as a possible mechanism

The Holter monitor electrocardiogram was taken from a 15-year-old male athlete. Intermittent right bundle branch block frequently occurred at rest. When sinus cycles gradually lengthened, sinus impulses were conducted to the ventricles with right bundle branch block (RBBB) in succession. When, thereafter, sinus cycles gradually shortened, sinus impulses were conducted without RBBB. However, it seems that these findings do not show true bradycardia-dependent RBBB. Atypical atrioventricular Wenckebach periodicity was occasionally found in which sudden shift from the period of comparatively short PR intervals to the period of long PR intervals occurred. In the Wenckebach periodicity, when a QRS complex occurs after a much longer pause, RBBB was not found, while when it occurs after a much shorter period, RBBB was found. This suggests that this case may be apparent bradycardia-dependent RBBB, namely, a form of tachycardia-dependent RBBB. This is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles, as a possible mechanism.     

QRS Alternans with 2:1 Atrioventricular Conduction Block: What Is the Mechanism?

An 81‐year‐old woman was admitted for symptomatic bradycardia. On admission, the ECG exhibited QRS alternans, narrow QRS complex and left bundle branch block with 2:1 AV block. The patient soon had complete AV block and underwent a pacemaker implantation. An appropriate mechanism for explaining those ECG findings might be 4:1 conduction over the left bundle branch and 2:1 conduction over the right bundle branch. An ECG pattern exhibiting QRS alternans with a narrow QRS complex and bundle branch block with 2:1 AV block may suggest the coexistence of both bundle branch blocks and a high risk of complete AV block.     

Trifascicular block with asynchronous intraventricular recovery and "supernormal" AV conduction

The authors present a case of trifascicular block: complete right bundle branch block, tachycardia-dependent left anterior hemiblock, and bradycardia-dependent left posterior hemiblock. There is, in addition, a complicating independent AV junctional rhythm that is in most instances not affected by the conducted sinus impulses. Occasionally, however, this focus is discharged by very early sinus impulses that are unexpectedly conducted to the ventricles (a manifestation of "supernormal" conduction). A complex electrocardiographic pattern results from the interplay of the aforementioned mechanisms.     

Gap, phase III and IV block and supernormal conduction of the right bundle branch

A recent review of the literature corroborated that several factors explained why supraventricular impulses falling gradually earlier in the cycle could traverse the His-Purkinje system while other impulses occurring later could fail to do so. The present report deals with the coexistence (in the same patient) of three distinct mechanisms whereby progressively more premature impulses could be "unexpectedly" conducted. Phase III left bundle branch block coexisted with the following conduction disturbances in the right bundle branch; late "pseudosupernormal" conduction sandwiched in between periods of phase III and phase IV block; intermediate "pseudosupernormal" conduction resulting from the so-called type 2 gap, during which propagation occurred, but with H-V intervals longer than later in the cycle; early "true" supernormal conduction (related temporarily to the end of the T wave) exposed when a premature ventricular beat reached the affected zone in a concealed retrograde fashion. These findings show how, with block late in the cycle, conduction in earlier part of the cycle was not always due to "true" supernormal conduction.     

Tachycardia-dependent and bradycardia-dependent intraventricular conduction defects in acute myocardial infarction: Electrocardiographic,electrophysiologic, and clinical correlates

Presence of rate-dependent (RD) intraventricular conduction defects (IVCD) was documented by inducing variations in heart rate in 30 acute myocardial infarction (AMI) patients (10 right bundle branch block, six left bundle branch block, 13 left anterior hemiblocks, and two left posterior hemiblocks). Five IVCDs were tachycardia-dependent (TD), 20 were bradycardia-dependent (BD), and six were both TD and BD. In TD blocks shortest cycles showing normal intraventricular conduction ranged from 410 to 1330 msec (697 ± 84 SE); in BD blocks longest cycles with normal intraventricular conduction ranged from 450 to 1450 msec (962 ± 52). In 60% of cases intermittent incomplete RD blocks were also present. In one patient RD-IVCD intermittency remained until discharge; in the others it lasted from 4 minutes to 10 days. Afterwards 19 RD-IVCDs disappeared and four became stable; six patients died during RD-IVCD intermittency period. Disappearance of RD block was preceded by gradual reduction in cycle length showing TD block and lengthening of cycles stopped beats with BD block. Serial observation of RD-IVCDs provides information about sequence of electophysiologic effects on the intraventricular conduction system in clinical AMI.     

Exercise testing and thallium-201 emission computed tomography in patients with intraventricular conduction disturbances.

The specificity of exercise thallium-201 emission computed tomography for coronary artery disease was assessed in patients with intraventricular conduction disturbances. Eighty-seven patients were studied: 33 with right bundle branch block (RBBB), 11 with RBBB and left-axis deviation, 11 with left (L)BBB, 12 on right ventricular pacing, and 20 with Wolff-Parkinson-White (WPW) syndrome. A control group of 349 consecutive patients with normal intraventricular conduction was also examined. The specificity of diagnosis of coronary artery disease in patients with LBBB (30%), right ventricular pacing (44%) or RBBB plus left-axis deviation (50%) was significantly lower than in patients with normal intraventricular conduction (94%; p less than 0.01). In contrast, there was no significant difference between specificity in patients with RBBB (86%) or WPW syndrome (90%) and patients with normal intraventricular conduction. Perfusion defects were found in the anterior, septal and inferior segments in patients with LBBB, and in the septal and inferior segments in patients with RBBB plus left-axis deviation despite the absence of coronary stenosis. Furthermore, diffuse slow washout was seen more often in patients with WPW syndrome (35%) than in controls who had normal intraventricular conduction (11%; p less than 0.05), despite a good exercise performance in the former group. This study suggests that there is an increased incidence of abnormal perfusion and clearance during exercise thallium-201 emission computed tomography in patients with intraventricular conduction disturbances.     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

Contrasting effects of verapamil and procainamide on rate-dependent bundle branch block: pharmacologic evidence for the role of depressed sodium channel responses

The mechanisms responsible for intermittent bundle branch block are still under debate. The role of the time-dependent behavior of the slow calcium channel has recently been emphasized. To test this hypothesis and ascertain the possible involvement of the fast sodium channel, the effects of the slow calcium channel blocker verapamil and the fast sodium channel blocker procainamide were compared in 10 patients with intermittent bundle branch block. All 10 patients showed bundle branch block during spontaneous sinus rhythm. Maneuvers to slow cardiac rate (that is, carotid sinus massage, Valsalva maneuver) were performed to identify normal conduction as well as phase 4 bundle branch block. Thus, the ranges of diastolic intervals (RR) resulting in phase 3 (tachycardia-dependent) bundle branch block, phase 4 (bradycardia-dependent) bundle branch block and normal conduction were measured in two control studies performed before intravenous administration of verapamil (control 1) and procainamide (control 2) and at the peak effect of both drugs. In the control studies, all 10 patients showed phase 3 bundle branch block, whereas phase 4 bundle branch block occurred in only 4 patients. The ranges of phase 3 bundle branch block, phase 4 bundle branch block and normal conduction were very similar in control studies 1 and 2. The phase 3 bundle branch block range was slightly shortened by verapamil (983 +/- 83.5 ms in control 1; 930 +/- 69.4 ms at the peak effect of verapamil), whereas phase 4 bundle branch block remained unchanged. In contrast, conduction was systematically worsened by procainamide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Asynchronous intraventricular recovery as a basis for apparent 'supernormality'

Various mechanisms have been postulated for the supernormal phase of intraventricular conduction where relatively early impulses are conducted with normal intraventricular conduction and relatively late impulses with abnormal intraventricular conduction. The cases presented here illustrate how asynchronous recovery of conducting tissue may result in fortuitous momentary synchrony early on in the recovery phase with asynchronous conduction properties in the later phases of recovery. This will facilitate potential synchronous conduction early on in the cycle which would result in a normal QRS complex, and potential asynchronous conduction in the later phases which would manifest with a bundle branch block QRS complex.