Alternating Wenckebach periodicity: A common electrophysiologic response.

Alternating Wenckebach periods are defined as episodes of 2:1 atrioventricular (A-V) block in which conducted P-R intervals progressively prolong, terminating in two or three blocked P waves. In this study, His bundle recordings were obtained in 13 patients with pacing-induced alternating Wenckebach periods. Three patterns were noted: Pattern 1 (one patient with a narrow QRS complex) was characterized by 2:1 block distal to the H deflection (block in the His bundle) and Wenckebach periods proximal to the H deflection, terminating with two blocked P waves. Pattern 2 (four patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with three blocked P waves. Pattern 3 (eight patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with two blocked P waves. Alternating Wenckebach periods are best explained by postulating two levels of block. When alternating Wenckebach periods are terminated by three blocked P waves (pattern 2), the condition may be explained by postulating 2:1 block (proximal level) and type I block (distal level). When alternating Wenckebach periods are terminated by two blocked P waves (patterns 1 and 3), the condition may be explained by postulating type I block (proximal level) and 2:1 block (distal level). Pattern 1 reflects block at two levels, the A-V node and His bundle. Patterns 2 and 3 most likely reflect horizontal dissociation within the A-V node.     

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.     

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.     

Atrial tachycardia, 2:1 alternate Wenckebach periodicity, and atrial standstill

A case of atrial tachycardia, 2:1 alternate Wenckebach periodicity and atrial standstill is reported in an 80-year-old woman who complained of exertional dyspnea and occasional syncope for two years. Two blocked P' waves appeared after each Wenckebach period suggesting type B alternating Wenckebach phenomenon (Mobitz type II 2:1 A-V block distal, and Wenckebach conduction proximal).     

Atrioventricular alternating Wenckebach periodicity: conduction patterns in multilevel block

Atrioventricular (A-V) conduction patterns were analyzed in three patients with atrial pacing-induced alternating Wenckebach periodicity. These cases were unique because in each (1) separate levels of block responsible for the conduction disturbance were located above and below the His bundle recording site, and (2) there were several departures from the simple alternating Wenckebach pattern. Apparent supernormal conduction, temporary 1:1 conduction and a specific form of gap in A-V conduction resulted from the interplay of many factors including a simple mathematic relation of the blocking ratio at the two levels, the characteristics of the Wenckebach cycles, and the cycle length-dependent features of refractory periods at the different sites. The findings indicate that (1) delay in proximal impulse transmission is usually the critical factor in overcoming prolonged distal refractoriness and producing variable conduction patterns during the course of alternating Wenckebach periodicity; (2) many irregularities in alternating Wenckebach periodicity can be explained by known electrophysiologic mechanisms; and (3) simple mathematic equations alone are too rigid to reflect properly the dynamic process underlying this conduction disturbance.     

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.     

Exposure of concealed right bundle branch block in Wolff-Parkinson-White type B by pacing from the vicinity of the A-V node.

In two infants with Wolff-Parkinson-White type B, right bundle branch block was concealed during sinus rhythm and pacing from close to the atrial entrance of the right-sided accessory pathway. However, pacing from the vicinity of the A-V node, the A-V node itself, and the His bundle exposed the right bundle branch block by producing exclusive ventricular activation through the normal, A-V nodal His-Purkinje pathway. In addition, pacing from close to the A-V node also resulted in fusion beats characterized by absence of delta waves with (pseudo) normal QRS complexes and short H-V intervals. False patterns of tachycardia-dependent and bradycardia-dependent block in the accessory pathway also occurred. These dynamic phenomena were attributed to the (peri-A-V nodal) pacing-related, relatively early arrival of excitation at the ventricles through the normal pathways coexisting with delayed arrival of excitation via the accessory pathway. The latter in turn was due to the longer intra-atrial conduction time from paced (peri-A-V nodal) site to atrial entrance of the accessory pathway.     

Electrophysiologic studies on atrioventricular nodal Wenckebach cycles

Wenckebach cycles with a 4:3 ratio, produced by rapid atrial pacing, were studied in 27 anesthetized denervated dogs using programmed stimulation. A test stimulus (S') could be inserted after any preselected beat of the Wenckebach cycle. An on-line computer measured the atrial (A) to His bundle (H) intervals. In all dogs a progressive increase in atrioventricular (A-V) nodal refractoriness was seen in the effective refractory period for each beat and a rightward shift of the A'-H' relative to the A-A' refractory curves. Atypical Wenckebach cycles could be produced by small changes in the basic cycle length. No evidence for reentry was found from the refractory curves of Wenckebach cycles and by interruption of stimulation after the third stimulus of a 4:3 Wenckebach cycle. Analysis of the A'-H' relative to the H-A' refractory curves did not confirm a positive feedback mechanism. In order to mimic a Wenckebach cycle, a blocked premature beat was inserted during stressed 1:1 conduction. The changes in the refractory curves for successive beats after the premature beat were rate-dependent and similar to those in Wenckebach cycles but smaller in magnitude. In Wenckebach cycles there is a progressive increase in refractoriness, caused by cumulative effect similar to that seen after a blocked beat during stressed 1:1 conduction, until block occurs and the cycle resets.     

Pathophysiology of second degree atrioventricular block: A unified hypothesis

An in vivo and in vitro correlative study of second degree atrioventricular (A-V) block in the canine proximal His-Purkinje system after ligation of the anterior septal artery is reported. Evidence is presented to suggest that Mobitz type II and the Wenckebach type of conduction represent different degrees of the same disorder rather than two distinct electrophysiologic processes. The in vivo study showed that an increment of conduction delay almost always preceded the blocked impulse in second degree A-V block. The increment, as small as 1 or 2 msec at the early stage of block, often increased gradually up to 180 msec. The in vitro study consistently showed an increment of conduction delay preceding the blocked impulse. The same experiments revealed a greater increment in conduction delay early after excision that, on recovery during superfusion, gradually decreased to a few milliseconds (the reverse order of the in vivo observation). Characteristic changes in duration and configuration of action potentials in the ischemic proximal His-Purkinje system were observed depending on the state of transmission and the temporal relation of the impaled cell to areas of slow propagation and block. The study revealed a remarkable similarity between characteristics of conduction in the ischemic His-Purkinje system and conduction in both the normal A-V node and Purkinje fibers subjected to various pathophysiologic interventions.It is suggested that in the pathologic situation—exemplified in this study by acute myocardial ischemia—the normal His-Purkinje system may gradually lose the characteristics of the fast response and start showing properties of the slow response. At an early stage of departure from normal, the proximal His-Purkinje system may show second degree A-V block with no perceptible to a few milliseconds' increment of conduction delay (the equivalent of Mobitz type II block). On further departure from normal, the His-Purkinje system resembles the A-V node in showing a significant increment of conduction delay prior to the blocked impulse (the equivalent of Wenckebach periodicity). Both the in vivo and in vitro observations demonstrated a clear propensity of the ischemic proximal His-Purkinje system to develop paroxysmal A-V block during the stage of second degree A-V block when there is no perceptible to a few milliseconds′ increment of conduction delay. A new classification of second degree A-V block is presented based on the suggested electrophysiologic mechanism.     

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.     

Atypical Wenckebach periodicity simulating Mobitz II AV block.

Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a ''classical'' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised.     

Electrophysiologic observations in a patient with bradycardia-dependent atrioventricular block

In a patient with atrioventricular (A-V) block distal to the His bundle (H), 1:1 A-V conduction with right bundle branch block and an H-V interval of 70 msec was established with atrial pacing at rates of 120 to 150/min, suggesting that the A-V block was bradycardia-dependent. Advanced second degree A-V block distal to the H deflection occurred with atrial pacing at 160/min after completion of A-V nodal Wenckebach periodicity proximal to the H deflection because of the long H-H encompassing the blocked P wave. Atrial extrastimulus testing coupled with sinus rhythm (with A-V block) demonstrated that critical H₁-H₂ intervals of less than 545 msec allowed conduction to the ventricles. The H₂-V₂ interval shortened progressively from 290 to 70 msec with shortening of these critical H₁-H₂ intervals. Atrial extrastimulus testing coupled with an atrial driven cycle length of 500 msec (with intact A-V conduction) revealed block of the H₂ deflection with an H₁-H₂ interval longer than 540 msec.In conclusion, at critical diastolic intervals, impulses were blocked, creating a state of decreased responsiveness. If a cycle length of subsequent impulses was shorter than the critical diastolic blocking interval, membrane responsiveness gradually improved and conduction resumed. If a cycle length of subsequent impulses was longer than the critical blocking diastolic interval, A-V block was sustained. Blocked impulses continually penetrated to the site of block and reset the state of membrane responsiveness.     

Electrophysiologic effects of tolamolol on atrioventricular conduction in man

The electrophysiologic effects of tolamolol (UK-6558-01), a beta-adrenergic blocking agent, were studied in 13 patients by means of intracardiac electrograms and the extrastimulus method. Tolamolol (4 to 30 mg. intravenously) resulted in : (1) prolongation of sinus cycle length (SCL) in all patients (p less than 0.01); (2) prolongation of sinus escape time (SET) in 11 of 13 patients (p less than 0.001); (3) prolongation of A-V nodal conduction time during sinus rhythm in 1i of 13 patients (p less than 0.001); (4) onset of A-V nodal Wenckebach block at longer paced cycle lengths in 10 of 11 patients (p less than 0.001); (5) prolongation of the functional refractory period (FRP) of the A-V node in 11 of 11 patients (p less than 0.001); and (6) prolongation of the effective refractory period (ERP) of the A-V node in 10 of 10 patients (P less than 0.001). Tolamolol had no effect on His-Purkinje system (HPS) conduction time in any patient, including 3 patients with abnormal H-V intervals. Because of the marked increase in A-V nodal conduction time encountered by premature atrial depolarizations, the relative and effective refractory periods of the HPS could not be determined in any patient after tolamolol. Atropine (0.5 or 1.0 mg. intravenously) significantly reversed the effects of tolamolol on: sinus cycle length (4 of 5 patients); sinus escape time (3 of 3 patients); A-V nodal conduction time (4 of 5 patients); and A-V nodal refractioriness (5 of 5 patients).     

Influence of pacemaker-induced tachycardia with A-V block on left ventricular blood velocity in man.

Phasic instantaneous left ventricular blood velocity was measured by radiotelemetry in 28 subjects with a Doppler ultrasonic flowmeter catheter during atrial pacing and induced A-V block Type I Wenckebach A-V block with conduction ratios of 9:8 or lower generally produced a stepwise reduction of peak left ventricular blood velocity in relation to shortened R-R intervals. Longer Wenckebach periods resulted in little or no blood velocity alteration during 1:1 A-V conduction. Those beats following a blocked atrial depolarization were associated with augmented blood velocities. In three subjects, bigeminal periods of 3:2 A-V block resulted in larger left ventricular blood velocities when compared with 2:1 A-V block, despite identical R-R intervals following the blocked P wave. This latter phenomenon was attributed to diastolic augmentation of left ventricular contraction following the second and hemodynamically ineffective beat during 3:2 A-V block. Three patients manifested true blood velocity alternation during second-degree A-V block and changing R-R intervals. The variations in peak left ventricular blood velocity observed during atrial pacing and A-V block are related to changing inotropic state and cycle length dependent alterations of left ventricular diastolic filling.     

Observations during clinical 2:1 and 3:1 A-V block below the A-V node. Evidence of partial penetration of atrial impulses into the His bundle

A clinical His bundle recording during 2:1 A-V block below the A-V node displayed RBBB, a prolonged H-V interval, and alternating amplitude and duration of the His potentials. The reduced amplitude of the non-conducted His potential suggests a lesser depth of penetration into the His tissue with subsequent block. The reduced His potential amplitude may be due to decremental conduction within the His bundle and/or prolonged refractoriness of the His tissue following atrioventricular conduction of the preceding atrial impulse.During 3:1 A-V block progressively deeper penetration of the atrial impulses into the His-Purkinje system occurred. Progressive penetration into the more proximal His-Purkinje system may have permitted recovery of a more distal area of refractoriness with subsequent atrioventricular conduction. This mechanisms appears similar to one of the mechanisms of 3:1 A-V block demonstrated experimentally, except that in this clinical record the major site of impaired conduction and progressive penetration is within the His-Purkinje system rather than within the A-V node.     

Type A alternating Wenckebach periodicity in the re-entrant path of ventricular extrasystoles

A patient with ventricular extrasystoles is reported in whom Type A alternating Wenckebach periodicity in the re-entrant path of the extrasystoles is suggested for the first time. Namely, it appears that 2:1 exit block occurs at a proximal level in the re-entrant path and block of the Wenckebach form occurs at a distal level in the path. The presence of three-level block in the re-entrant path is also suggested in this patient.     

Effects of lidocaine on impulse formation and conduction defects in man.

The acute electrophysiologic effects of a bolus injection of 100 mg. of lidocaine were investigated in 39 patients with impulse formation and conduction defects by means of His-bundle recording and were correlated with plasma lidocaine levels. The effects of therapeutic plasma levels on conduction intervals and refractory periods were subsequently studied during sinus rhythm and atrial pacing. The sinus-node function was studied by measurement of the sino-atrial recovery time. Seventeen patients had conduction defects in or distal to the His bundle, six exclusively proximal to the His bundle, and nine at both levels. Nine patients had pre-existent sinus-node malfunction. Ten out of 39 patients suffered from acute myocardial infarction. Two patients were studied twice because of changed A-V conduction. Intravenous injection of 100 mg. of lidocaine within 20 seconds produced peak arterial plasma levels (mean 26.6 mug per milliliter) 60 seconds after the beginning of the injection. Seven out of 26 patients showed transient progression of their pre-existent infra-His conduction impairment, coincident with peak plasma levels, apparently due to drug toxicity. Even at therapeutic plasma levels, five out of 26 patients showed decremental intraventricular conduction during atrial pacing when compared to control tracings. His-Purkinje refractoriness was not shortened in these patients and increased in two. Lidocaine had no effect on ventricular automaticity in three patients with complete heart block. Lidocaine had no consistent effects on sinus rate, SART, atrial refractoriness, or A-V nodal conduction as measured by pooled AH intervals and the Wenckebach point, and on A-V nodal refractoriness. It is concluded that lidocaine is safe in patients with high degrees of A-V nodal block and in patients with impulse formation disturbances. However, patients with intraventricular conduction defects are prone to deterioration of their conduction disturbance due to drug toxicity. The drug should be given to such patients preferably if monitoring and pacemaker facilities are available and by the intramuscular route to avoid peak plasma levels.     

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.     

Two-to-one A-V block with four-to-three A-V nodal wenckebach, a form of spontaneous multilevel block

Electrophysiologic studies in one patient with spontaneous 2:1 atrioventricular block and variable PR intervals revealed two sites of conduction block. Typical 4:3 A-V nodal Wenckebach was present in addition to Mobitz type II infra-His block. The HV of conducted complexes was 120 msec and the shortest recorded AH interval was 250 msec. When 2:1 A-V block with fixed PR interval was present, only 2:1 Mobitz type II infra His-block was present. The mechanism of this example of spontaneous multilevel A-V block is discussed and compared to other previously reported cases.     

Type A alternating Wenckebach periodicity in the reentrant pathway of interpolated ventricular extrasystoles

A 67-year-old man with interpolated ventricular extrasystoles is reported in whom alternate sinus QRS complexes were followed by interpolated ventricular extrasystoles with progressively lengthening coupling intervals until one of these alternate sinus complexes failed to be followed by an extrasystole. This is the first report to suggest the presence of type A alternating Wenckebach periodicity in the reentrant pathway of interpolated ventricular extrasystoles. It is suggested that 2:1 block occurred at a proximal level in the reentrant pathway, while Wenckebach block occurred at a distal level in the pathway.