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.     

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.     

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.     

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.     

Aortic blood flow velocity during Wenckebach periods in man

By means of the Doppler ultrasonic flowmeter catheter, phasic aortic blood flow velocity and simultaneous aortic pressure, right atrial pressure, and Lead II of the electrocardiogram were measured in 7 normal subjects and 8 patients with heart disease during right atrial pacing. At pacing rates between 110 and 170 per minute, type I, second-degree atrioventricular block appeared. The increase in peak aortic blood flow velocity was generally proportional to the preceding cycle length and inversely related to the P-R interval. These variations were more pronounced during shorter Wenckebach periods. The first beat of a period always manifested a greater peak flow velocity than did the last beat. Short cycle lengths with less ventricular diastolic filling resulted in diminished aortic systolic flow velocity, with reduction up to 80 per cent. The changes in flow velocity paralleled the changes in aortic pressure.     

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.     

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.     

Echocardiographic features of atrioventricular and ventriculoatrial conduction

The potential application of diagnostic ultrasound to understanding of the hemodynamic effects of various rhythm and conduction disturbances has not been fully explored. To investigate the changes in cardiac function associated with various atrioventricular (A-V) sequencing intervals during cardiac pacing, simultaneous M mode and two dimensional echocardiographic and hemodynamic studies were performed in 23 dogs.One to one A-V and ventriculoatrial (V-A) sequential pacing at cycle lengths of 400 and 300 ms revealed a stepwise reduction in left ventricular pressure and cardiac output as the A-V interval was changed from +100 to —100 ms. These reductions in cardiac hemodynamics were associated with decreases in left ventricular and increases in left atrial dimensions determined with echocardiography. Mitral valve excursion and the duration of valve opening remained constant over the entire range of A-V intervals. There was angiographie evidence of retrograde blood flow from the left atrium into the pulmonary venous system at an A-V interval of —50 and —100 ms, but no evidence of mitral regurgitation.Thus, correlative echocardiographic and hemodynamic studies can suggest multiple pathophysiologic mechanisms contributing to the decrements in cardiac function observed during tachyarrhythmias with intact A-V conduction as well as those occurring consequent to A-V nodal Wenckebach cycles.     

Coexisting intra- and subnodal block: an unusual abnormality of atrioventricular conduction

The presence of A-V block occurring at two levels of the conducting system was demonstrated in an asymptomatic patient by means of the His bundle recordings. During sinus rhythm, first degree A-V block with complete left bundle branch block was noted, suggesting the presence of bilateral bundle branch block. His bundle recordings demonstrated the coexistence of intranodal (Wenckebach periods, Mobitz Type I) and subnodal (Mobitz Type II) block. The evidence of block below the proximal His bundle offered confirmatory evidence of bilateral bundle branch block. In spite of the abnormal antegrade conduction, there was 1:1 V-A conduction during right ventricular pacing at 110 per minute. With more rapid (130 per minute) ventricular pacing, retrograde Wenckebach periods were observed, suggesting that there was, in addition, possible impairment in retrograde conduction. This report serves to demonstrate (1) the limitations of the body surface ECG in the assessment of A-V conduction and (2) that His bundle electrograms make it possible to detect the presence of coincidental lesions at two levels of the A-V conducting system.     

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.     

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.     

Atrial pacing during selective aortocoronary saphenous vein bypass angiography

Selective aortocoronary bypass graft angiography was performed in 30 postoperative subjects. Thirty-one of 39 patent graft injections resulted in cardiac arrhythmias including sinus bradycardia, premature ventricular depolarizations, sinoatrial arrest and atrioventricular (A-V) block. In contrast, only 2 of 39 graft angiograms performed during right atrial pacing produced arrhythmias. We conclude the following: (1) Routine prophylactic right atrial pacing is a valuable method for preventing certain cardiac arrhythmias during aortocoronary graft opacification; and (2) the potential for rapid institution of right ventricular pacing provides safety in the event that angiographically induced A-V block occurs.     

The incidence of typical and atypical A-V Wenckebach periodicity

The classic pattern of the typical WP's consists of (1) progressive lengthening of the P-R intervals with the largest increment occurring in the second conducted beat, (2) progressive decrease in P-R increment which accounts for the progressive shortening of successive R-R intervals, and (3) the pause produced by the nonconducted P-wave is less than two P-P intervals. In 45 patients with atrial pacing-induced Wenckebach periods of A-V conduction, the structure of these was studied with His bundle recordings. Of the 128 periods analyzed exceeding 3:2 A-V conduction ratios, 66 per cent were atypical. In 24 patients with spontaneous WP's of A-V coduction, the electrocardiographic records were studied. Of the 98 periods analyzed exceeding 3:2 A-V conduction ratios, 86 per cent were atypical. WP's with A-V conduction ratios greater than 6:5 were all atypical. Five categories of atypical WP's are described.     

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.     

Atrial tachycardia without P waves masquerading as an A-V junctional tachycardia.

Two patients who presented by scalar ECG with an A-V junctional tachycardia were demonstrated during an electrophysiologic evaluation to have an atrial tachycardia without P waves in the surface ECG. Case 1 had an atrial tachycardia that conducted through the A-V node with a Wenckebach block. Atrial activity was recorded only from the proximal portion of the coronary sinus and from right atrial areas near the tricuspid valve. Case 2 had an atrial tachycardia that abruptly began and terminated following carotid sinus massage. Atrial activity was recorded only in the coronary sinusos, and pacing at that site resulted in atrial capture, with Wenckebach conduction to the ventricles. These observations demonstrate that an atrial tachycardia without P waves can simulate A-V junctional tachycardia with or without Weckebach block. Such findings may have a bearing on some important electrophysiologic concepts such as the origin of A-V junctional rhythms and the need for atrial participation in A-V nodal re-entry.     

The effects of smoking on myocardial conduction in the human heart.

Inhalation of a few puffs on a cigarette increases the velocity of conduction and shortens the effective refractory period of the A-V node. These effects are attributed to adrenergic stimulation produced by minute amounts of nicotine absorbed. Wenckebach block is abolished whether induced by atrial pacing or occurring spontaneously. Conduction velocity in the His-Purkinje system and in the anomalous pathways in the WPW syndrome were not affected. Smoking increases the ventricular rate in atrial fibrillation, and antagonizes the cholinergic effects of digitalis.     

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.     

Doppler measurement of phasic continuous left ventricular blood flow velocity during ventricular arrhythmias

Phasic instantaneous left ventricular blood velocity was continuously measured by means of the Doppler ultrasonic flowmeter catheter radiotelemetry system in 68 patients with ventricular arrhythmias. Ventricular premature depolarizations reduced peak left ventricular blood velocities in relation to their respective coupling intervals, with R-R intervals less than 0.5 second producing the greatest decline. Ventricular tachycardia in 18 subjects produced a 62 per cent mean decrease in left ventricular blood velocity. In a single subject, performance of the Valsalva maneuver effected ventricular tachycardia and a concomitant marked diminution of phasic left ventricular blood velocity. These findings demonstrate the untoward influence of ventricular extrasystoles and tachycardia on left ventricular blood velocity and provide the underlying basis for reductions of blood velocity previously demonstrated in the regional circulations of man during similar arrhythmias.     

Electrophysiologic evidence for selective retrograde utilization of a specialized conducting system in atrioventricular nodal reentrant tachycardia.

In 12 patients with atrioventricular (A-V) nodal reentrant tachycardia, the existence and utilization of retrograde ventriculoatrial bypass tracts in the reentrant process were excluded, and the characteristics of the anterograde and retrograde limbs of the reentrant circuits were studied using His bundle electrograms, incremental atrial and ventricular pacing and atrial and ventricular extrastimulus techniques before and after the administration of 0.01 mg/kg of intravenous ouabain. Similar studies were also performed in five control patients without tachycardia. Paroxysmal supraventricular tachycardia could be induced in all 12 patients during atrial pacing-induced A-V nodal Wenckebach periods or premature atrial stimulation, or both. On the basis of conduction time in the retrograde limb during tachycardia and during retrograde studies, two groups were identified. Group I (seven patients) had (1) short (39 ± 10 msec) and constant conduction time in the retrogarde limb measured from the anterograde His bundle deflection to the retrograde atrial echo response (H-Ae interval), (2) no change in ventriculoatrial conduction time up to maximal ventricular pacing rates, (3) H₂-A₂ intervals during retrograde refractory period studies that were identical to the H-Ae intervals and that did not increase with decreasing V₁-V₂ intervals, and (4) increased conduction time of the anterograde limb (Ae-H intervals) after the administration of ouabain without any effect on retrograde limb conduction (H-Ae and H₂-A₂ intervals) and refractoriness. Group II (five patients) had (1) long and variable H-Ae intervals (60 to 180 msec), (2) a progressive increase in ventriculoatrial intervals during incremental ventricular pacing, (3) an increase in H₂-A₂ intervals in response to decreasing V₁-V₂ intervals, and (4) increased anterograde (Ae-H interval) and retrograde limb (H-Ae and H₂-A₂ intervals) conduction and refractoriness after the administration of ouabain. Changes in the H₂-A₂ interval corresponded to the changes in four of the five control patients. These findings suggest that (1) in group I the anterograde limb was the A-V node, whereas the retrograde limb was an A-V nodal bypass tract or an insulated intranodal tract physiologically unlike the A-V node; and (2) in group II the A-V node comprised both the anterograde and retrograde limbs of the reentrant circuit.