Wenckebach periods with repetitive block: evaluation with His bundle recording

Two patients are reported in whom repetitive block of two consecutive P waves occurred during Wenckebach beating induced by atrial pacing. His bundle recordings revealed block proximal to H in the first case, suggesting inhomogeneous conduction in the A-V node. In the second case, long cycle lengths were produced in the His-Purkinje system due to A-V nodal Wenckebach periods. The long cycles prolonged refractory periods in the His Purkinje system so that subsequent beats (short cycles) were blocked distal to H.The repetitive block of consecutive multiple atrial impulses could result in unexpected degrees of ventricular asystole during usually benign Type I second-degree A-V block.     

Concealed intraventricular conduction in the His bundle electrogram.

Multiple areas of concealed intraventricular conduction are deduced on the basis of aftereffects observed in His bundle recordings. Electrocardiograms and His bundle recordings are presented from two patients with unstable bilateral bundle branch block, the instability of which depended on the interval at which ventricular depolarization was initiated by sinus or paced impulses. This circumstance allows postulation of 1) concealed transseptal retrograde penetration of the left bundle branch system; 2) concealed transseptal retrograde penetration of the right bundle branch system; 3) alternate beat Wenckebach phenomenon with two areas of block in the bundle branch system with concealed penetration of the proximal area; 4) concealed re-entry in the right bundle branch system during an H-V Wenckebach cycle with resetting of the sequence of 2:1 H-V block and return of the re-entry wave to the A-V node causing subsequent A-H block; 5) proximal 2:1 block and distal Wenckebach block producing only two consecutively blocked beats; and 6) infrahisian Wenckebach block with changes both in A-V conduction and QRS contour.     

Pseudo A-V block associated with A-H and H-V conduction defects

His bundle electrograms were recorded in a patient with tertiary syphilis whose ECG's showed right bundle branch block, junctional premature systoles, and episodes suggesting both Mobitz Type I and II second degree A-V block. Junctional premature depolarizations were found to cause: (1) ventricular systole, (2) retrograde atrial depolarizations with atrial fusion, and (3) nonconducted P waves of normal contour (pseudo A-V block). Nonconducted nonpremature P waves were also noted to occur secondary to both A-H and H-V forms of second degree A-V block in the absence of junctional premature activity.The presence of an H-V conduction defect may cause antegrade block of junctional premature depolarizations and enhance their expression as pseudo A-V block. This term should, therefore, not be meant to imply A-H and H-V conduction.     

A comparative analysis of antegrade and retrograde conduction patterns in man.

Patterns of antegrade and retrograde conduction and refractory periods were studied using His bundle electrogram recordings, incremental atrial and ventricular pacing and the extrastimulus technique. In 36/50 patients antegrade conduction was "better" than retrograde conduction (group I), as evidenced by a) onset of retrograde atrioventricular (A-V) nodal Wenckebach phenomenon at a slower rate compared to the antegrade counterpart (25 patients: group IA) or b) no ventriculo-atrial conduction at all ventricular paced rates (11 pts: group IB). The site of retrograde block in group IB patients was the A-V node. In eight patients (group II), antegrade and retrograde conduction appeared to be equal up to maximum paced rates of 160 beats/min. In six patients (group III) retrograde conduction was "better" than antegrade conduction, as indicated by onset of antegrade A-V nodal Wenckebach periods at slower rates than retrograde Wenckebach periods. During antegrade refractory period studies the area of maximum refractoriness was the A-V node in 19/40 patients, the His-Purkinje system (HPS) 6/40, and the atrial muscle in 15/40. During retrograde refractory period studies the A-V node was the area of maximum refractoriness in 12/36 pts (4/40 patients had A-V dissociation during ventricular pacing), the HPS in 12/36, and the ventricular muscle in 10/36. In 2/36 patients the site of maximum refractoriness retrogradely could not be determined: The area of maximum refractoriness during both antegrade and retrograde refractory period studies was the same in 11 patients (A-V node in seve and HPS in four), was different (i.e., A-V node or HPS) in 18 patients, and was the artrial or ventricular muscle in six patients. In five patients, including four patients in whom V-A conduction failed to occur, the above comparisons were not made. It is concluded that 1) antegrade conduction is better than retrograde conduction in most patients; 2) it is not always possible to predict area of maximum refractoriness during premature stimulation (both atrium and ventricle) from observations made during incremental pacing; 3) it is equally difficult to extrapolate patterns of retrograde conduction and refractory periods from results of antegrade conduction and refractory period studies.     

His bundle electrocardiography in manifest and concealed right bundle branch extrasystoles.

His bundle electrocardiography was helpful in the diagnosis of impulse formation in the right bundle branch. Ten patients with narrow QRS complexes had ectopic beats with an "incomplete" left bundle branch pattern and almost simultaneous activation of His bundle and ventricles. Both QRS morphology and H- - V intervals depended on the more proximal or distal location of the ectopic focus. In four patients with "complete" right bundle branch block the morphology of ectopic ventricular complexes and H- - V intervals also depeneded on the presence or absence of retrograde block and differential degrees of forward and/or retrograde conduction delays. Nine patients with "complete" right bundle branch block and four with "complete" left bundle branch block had premature beats which could have originated in the proximal right bundle branch, proximal left bundle branch, or distal His bundle. In one patient with "complete" left bundle branch block, "concealed" His bundle depolarizations (probably originating in an ectopic focus located in the right bundle branch) produced pseudo Type II (Mobitz) A-V block. Although lidocaine appeared to have been more effective in patients with bundle branch block than in those with narrow QRS complexes, further studies are necessary to corroborate this impression.     

Electrophysiologic effects of atropine on atrioventricular conduction studied by His bundle electrogram

The electrophysiologic effects of atropine were studied with His bundle recordings in 14 patients. Administration of atropine, 0.5 mg intravenously, produced a moderate degree of sinus acceleration in all patients (average increase 20 percent over control rate). Atrioventricular (A-V) nodal conduction was enhanced during both sinus rhythm and at various paced atrial rates after administration of atropine. The paced atrial rates at which the A-V nodal Wenckebach phenomenon occurred were significantly higher after administration of the drug than before. Similar effects on retrograde conduction were observed during ventricular pacing. Atropine shortened both the functional and effective refractory periods of the A-V node but appeared to have no direct effect on either His-Purkinje conduction time or refractoriness. However, aberrant ventricular conduction and block within the His-Purkinje system increased during premature atrial stimulation after atropine administration. This was the result of shortening of the functional refractory period of the A-V node by atropine, which produced significantly shorter H₁–H₂ intervals. The effect of atropine on the electrophysiologic properties of the A-V conducting system was important in interpreting the conversion of a type I gap in A-V conduction to a type II gap.     

Mobitz type I atrioventricular block in the ventricular specialized conduction system

A patient with a history of multiple syncopal episodes had electrocardiographic findings of Wenckebach type of second degree atrioventricular block and left bundle branch block. He was thought to have intermittent complete heart block. His bundle recordings demonstrated the unusual occurrence of Mobitz type I block localized to the ventricular specialized conduction system. Based on the findings of this case and those of previous case reports, it is recommended that electrophysiologic studies should be performed on all patients with Mobitz type I atrioventricular block who also have bundle branch block.     

Experimental model for study of Mobitz type II and paroxysmal atrioventricular block

In 26 anesthetized dogs ligation of the anterior septal artery in conjunction with rapid atrial pacing resulted in a relatively high frequency (75 percent) of Mobitz type II block and paroxysmal atrioventricular (A-V) block (50 percent). Electrode catheter recordings from the His bundle and bundle branches as well as plunge wire recordings from the His bundle allowed a localization of block within the ischemic HisPurkinje system within 1 to 4 hours after ligation. Intra-His bundle blocks, manifested as first, second or third degree A-V block, alone or in combination, were found in 18 animals (75 percent). Right bundle branch block was found in 15 and left bundle branch block in 8. Bradycardia- and tachycardia-dependent bundle branch block was a common observation. The use of this preparation has provided insights into the nature of Mobitz type II and paroxysmal A-V block as well as other phenomena usually reported only in clinical settings.     

Atrial response during ventricular fibrillation

Electrical activity of the bundle of His and atria were recorded during sinus rhythm and electrically induced ventricular fibrillation in 23 dogs. Multiple bipolar atrial electrograms obtained from several sites within the right and left atria permitted the determination of the frequency, regularity, and sequence of atrial activation (i.e., sinus or retrograde) during ventricular fibrillation. Prior to the induction of ventricular fibrillation, the capacity to retrogradely conduct across the A-V node was tested in each animal by pacing the right ventricle at various cycle lengths. Fourteen animals demonstrated consistent 1:1 retrograde conduction at various paced cycle lengths (Group A); in four animals (Group B) retrograde conduction was intermittent and in three animals (Group C) no retrograde conduction was observed at any paced cycle length. Ventriculo-atrial conduction was also absent in two animals (Group D) with antegrade A-V block within the His-Purkinje system.The most common conduction pattern noted at the onset of ventricular fibrillation was that of rapid, irregular, retrograde activation of both the bundle of His and atria. However, the frequency of retrograde activation of the atria was less than that of the bundle of His indicating that the A-V node was a site of retrograde concealment of impulses. This conduction pattern was noted in all animals of Groups A and B. In all animals of Groups C and D, the atria continued to be activated in a sinus sequence during ventricular fibrillation. In Group C animals, the A-V node was the site of both antegrade and retrograde concealment. In the two animals with A-V block (Group D), the site of retrograde concealment was distal to the site of block.In six studies, retrograde A-V nodal Wenckebach cycles with and without re-entry were observed for varying periods of time.Less often, the irregular atrial responses during ventricular fibrillation were accounted for by short periods of sinus capture interspersed with periods of retrograde capture.During ventricular fibrillation, retrograde conduction across the A-V node could be abolished by vagal stimulation.The results of this study indicate that retrograde concealed conduction within the A-V node is the major determinant of an irregular atrial response during ventricular fibrillation just as antegrade concealed conduction is the major determinant of an irregular ventricular response during atrial fibrillation.     

Wenckebach periods associated with high grade second degree (2 : 1 and 3 : 1) A-V block.

An electrocardiogram (ECG) of bilateral bundle branch block (BBBB) which may be attributable to a mixture of 2 : 1 and 3 : 1 atrioventricular (A-V) block is described. The irregularity of QRS complexes with left bundle branch block (LBBB) pattern during 2 : 1 A-V block may be ascribable to "Wenckebach periods", which might be due either to A-V nodal or His bundle or bundle branch delay. However, it was impossible to distinguish between them precisely because appropriate His bundle studies were not performed during the active arrhythmic phase. Although the exact mechanism involved were not established with certainty, different rates of recovery in conduction in the bundle branches in association with a marked prolongation of the refractoriness would seem to be the unique feature of this complex arrhythmia. An ECG tracing of BBBB indicating high grade second degree (2 : 1 and 3 : 1) A-V block, in which "spontaneous" occurrence of "Wenckebach periods" with 2 consecutive blocked P waves can be observed during 2 : 1 A-V block, has never been reported previously as far as can be ascertained from published records.     

Coexistent Wenckebach phenomenon in the distal branches of the specialized conduction system

A patient in whom Wenckebach phenomenon was observed to coexist in the three distal branches of the specialized ventricular conduction system, with an intermittent trifascicular block producing a second degree A-V block, is described. Surface electrocardiogram demonstrated the presence of this phenomenon in the right bundle branch (RBB) and the anterior division of the left bundle branch (LBB). Evidence of the presence of Wenckebach phenomenon in the remaining fascicle was provided by His bundle recording.     

Alternating Wenckebach periods occurring in the atria, His-Purkinje system, ventricles and kent bundle

Alternating Wenckebach periods were defined as episodes of 2:1 block during which there was a gradual prolongation of the transmission intervals preceding the appearance of 3:1 or 4:1 block. Alternating Wenckebach periods occurring within the His-Purkinje system in symptomatic patients with right bundle branch block could have resulted from involvement of the His bundle only, the left bundle branch only or both structures simultaneously. Alternating Wenckebach patterns presumably occurring in the reentry pathway of ventricular extrasystoles and in the tissues surrounding an ectopic atrial focus or bipolar pacing electrodes were manifested in the coupling intervals of the premature beats; in the P-P intervals of atrial tachycardia with atrioventricular (A-V) block due to digitalis; and in the stimulus (St)-A intervals following electrical stimuli delivered to the atria at fast rates. Alternating Wenckebach periods of St-H and St-delta wave intervals in patients with the Wolff-Parkinson-White syndrome resulted from involvement of the Kent bundle itself, or of the atria as a proximal level common to distal longitudinally dissociated structures (Kent bundle and A-V node).

It is concluded that contrary to what is commonly believed alternating Wenckebach periods may be a tachycardia-dependent phenomenon occurring above, below or outside the A-V node and explaining a variety of spontaneous or electrically induced arrhythmias whose significance depends on the clinical setting in which they occur.     

His bundle electrocardiography in digitalis-induced "atrioventricular junctional" Wenckebach periods with irregular H-H intervals.

His bundle electrograms were recorded during catheter insertion for prophylactic demand pacing in two patients with accelerated or nonaccelerated "atrioventricular (A-V) junctional" rhythms associated with A-V junctional Wenckebach periods. This appears to be the first published report of so-called A-V junctional Wenckebach periods in which the characteristic irregularities of the H-H intervals were recorded. Patient 1 had an additional area of "complete" anterograde A-V nodal (A-H) block. In Patient 2 the rate of impulse formation was consistent with nonparoxysmal A-V junctional tachycardia. The His bundle recordings were obtained in patients with digitalis toxicity and should be interpreted in the context. The integration of clinical and intracardiac findings with extrapolations from microelectrode and pharmacolic studies and with deductions from the clinical electrocardiograms suggests that the conduction disturbances probably occurred within the A-V node itself (in its AN region). This hypothesis implies that automaticity also originated in the A-V node because the site of impulse formation must have been proximal to the site of the Wenckebach periods. However, conclusive proof of of these postulates will require further studies with refined techniques.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Electrophysiologic studies in Mobitz type II second degree heart block

The electrophysiologic basis for Mobitz type II second degree heart block was studied in a patient with documented episodes of complete heart block and Stokes-Adams seizures. Recording of His bundle electrograms demonstrated that all atrial impulses were conducted through the atrioventricular (A-V) node to the bundle of His. Nonconducted P waves were blocked distal to the bundle of His. The frequency of blocked beats increased when the rate was accelerated by atrial pacing. Administration of atropine caused more frequent blocked beats, reaffirming the concept that the block occurred beyond the node. It is concluded that Mobitz type II second degree heart block is a manifestation of bilateral bundle branch block. Testing with atropine in this case was useful in distinguishing block in the bundle branches from that in the A-V node.     

Alternating and intermittent bilateral bundle-branch block in acute myocardial infarct with development of total atrioventricular block]

The development of bilateral bundle branch block of various degree in the course of an acute myocardial infarction was demonstrated in a 74-year-old man during continuous ecg-monitoring. Initially there was a tachycardia- and bradycardia-dependent left bundle branch block, followed by a right bundle branch block with second degree type II AV block (Mobitz), and finally complete bilateral bundle branch block with asystole. Different combinations of incomplete block were shown and the presence of type I and type II second degree block within the bundle branches could be demonstrated; Wenckebach periods became indirectly visualized through changes in the AV conduction. This case illustrates the prognostic importance of progressive intraventricular conduction disturbance and reveals the multiplicity and possible mechanisms of conduction defects within the bundle branches.     

Alternative mechanisms of apparent supernormal atrioventricular conduction

Alternative mechanisms were found to explain several different electrocardiographic examples of apparent supernormal atrioventricular (A-V) conduction in man using programmed premature atrial and ventricular stimulation and His bundle recordings. Sudden shortening of the P-R interval during A-V nodal Wenckebach phenomenon was due to manifest or concealed reentry within the A-V node. Gap phenomena in which late atrial premature depolarizations blocked while earlier atrial premature depolarizations conducted were shown to result from delay of earlier atrial premature depolarizations in the A-V node (type I gap) or in the His-Purkinje system (type II gap). Mechanisms analogous to the latter were found in cases of apparent supernormality of intraventricular conduction: Late atrial premature depolarizations resulted in aberration whereas earlier atrial premature depolarizations conducted normally because of delay within the A-V node or His-Purkinje system. Unexpected normalization of a bundle branch block pattern also resulted from Wenckebach phenomenon in the bundle branches. Atypical Wenckebach phenomenon with the first beat of the period demonstrated that aberration was due to phase 4 depolarization. Preexcitation of the ventricle before the delivery of a previously blocked atrial premature depolarization allowed conduction through the area of block (A-V node) because of earlier depolarization of the latter with earlier recovery. In the His-Purkinje system, 2:1 A-V block was converted to 1:1 conduction when a premature ventricular depolarization shortened the refractoriness of the His-Purkinje system.     

Mobitz II atrioventricular block due to infra-Hisian block and bundle branch extrasystoles.

An asymptomatic elderly male presented with complete right bundle branch block, left anterior fascicular block and Mobitz Type II second degree atrioventricular block. In addition, he was noted to have ventricular premature systoles. Electrophysiologic studies demonstrated two apparently different mechanisms for the second degree A-V block--infra-Hisian block and A-V block due to bundle branch extrasystoles arising in the affected right bundle branch. Concealed conduction of the bundle branch extrasystoles as the proximate cause of infra-Hisian block could not be excluded. However, both forms of A-V block were evidently dependent upon significant distal conduction system disease; this consideration was felt to warrant permanent pacemaker implantation.     

Intermittent pseudocomplete A-V block due to A-V dissociation in presence of 2:1 A-V block.

A false pattern of intermittent complete A-V block was seen in two asymptomatic patients when A-V dissociation was superimposed on a basic 2:1 A-V block. Although the conduction disturbance occurred at the A-V nodal level in both cases, in Case 2 it resembled A-V block due to bilateral or trifascicular disease. This arrhythmia was the end result of Type I (Wenckebach) block and apparently has a better prognosis than those emerging from a Type II (Mobitz) block.     

Patterns of atrioventricular conduction in children.

In this study, intracardiac electrograms were performed in 20 children--ranging in age from eight months to 18 years and without evidence of conduction disturbances on the scalar electrocardiogram--to determine the normal conduction patterns, response to atrial pacing, and values of refractory periods. Atrial pacing--18 cases--induced a prolongation al AH on increasing heart rates in all; 11 developed Wenckebach block proximal to the bundle of His at the mean pacing rate of 224 per minute +/- 45 (1 S.D.). Refractory periods were shorter than in adults. Study of the pattern of A-V conduction revealed three types of response: (1) the atrium was the limiting structure in 11 cases; (2) the delay occurred in the A-V node only in four cases; and (3) the delay occurred both in the A-V node and His-Purkinje system. This response was observed in one case only.