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.     

Gap in A-V conduction in man; types I and II

The mechanism of the “gap” phenomenon in A-V conduction was studied in man during premature atrial stimulation studies using His bundle recordings. Previous reports have demonstrated that while relatively late premature atrial impulses are blocked within the His-Purkinje system, earlier premature atrial impulses may successfully propagate to the ventricle if they encounter sufficient A-V nodal delay to allow recovery of the distal area of refractoriness (Type I “gap”). In the present report, an analogous mechanism of the “gap” is described which is due to delay within the His-Purkinje system (Type II “gap”). Relatively late premature atrial impulses were noted to block within the His-Purkinje system, similar to the findings in Type I. Conduction resumed in Type II, however, when earlier premature atrial impulses encountered delay in a relatively proximal area of the His-Purkinje system, allowing more complete recovery of the distal area of refractoriness. Both types of gap phenomena represent examples of apparent supernormal conduction.     

Effects of digoxin on atrioventricular conduction patterns in man

Digoxin was acutely administered to 17 patients, and its effects on atrioventricular (A-V) conduction were assessed. In the control state, before administration of digoxin, progressively premature atrial depolarization showed conduction delay and block confined solely to the A-V node in eight patients and to both the A-V node and the more distal His-Purkinje tissue in nine patients. His-Purkinje conduction delay was manifested on the surface electrocardiogram by ventricular aberration. After administration of digoxin, an early atrial premature impulse either was blocked in the A-V node or reached the distal intraventricular conduction system so late that block or conduction delay below the His bundle was reduced or no longer occurred. Ventricular aberration on the surface electrocardiogram was thus reduced or eliminated. These effects of digoxin on A-V conduction were due to its effect on the A-V node of slowing conduction of a premature impulse. Such action on the A-V node may abolish aberrant ventricular conduction in atrial fibrillation.     

Observations on the mechanism of one type of so-called supernormal A-V conduction

The mechanism of one type of so-called supernormal A-V conduction was elucidated in 11 subjects during premature atrial stimulation studies using His bundle electrogram recordings. At relatively long R-P intervals atrial impulses failed to conduct to the ventricles and were blocked distal to the bundle of His. At shorter R-P intervals A-V conduction resumed. The more premature atrial impulses encountered greater A-V nodal delay (longer A-H interval) and arrived within the His-Purkinje system after the latter was more completely repolarized. The electrophysiological mechanism for this type of so-called supernormal A-V conduction is based on the relationship between the state of refractoriness of the A-V nodal and His-Purkinje conduction systems.     

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.     

Electrophysiologic properties of procainamide in man

The electrophysiologic properties of procainamide were studied in 16 patients and correlated with plasma levels. Procainamide caused a minimal prolongation of atrioventricular (A-V) nodal conduction in 11 of 16 patients during sinus rhythm, but His-Purkinje conduction time was significantly prolonged in 15 of 16 patients. The effective refractory period of the atrium was prolonged by procainamide in 14 of 16 patients. The effective refractory period of the A-V node decreased in 8 of 9 patients. This may have been due to (1) anticholinergic properties of procainamide, (2) production of an A-V nodal “gap” by procainamide, or (3) an apparent A-V nodal block that actually represented decremental conduction in the His bundle; procainamide then caused delay in the A-V node allowing improved intra-His conduction and ventricular depolarization. The relative refractory period of the His-Purkinje system was prolonged in 10 of 11 patients. The effective refractory period was prolonged in one patient, unchanged in a second and apparently shortened in a third. In this third patient, procainamide produced a marked delay in proximal His-Purkinje conduction allowing a distal area of refractoriness to recover, thus causing apparent shortening of the effective refractory period. Plasma levels averaged 7.1 mg/ liter at the end of the study; no toxicity was noted.     

The mechanism of A-V conduction delay in A-V nodal gap

Initial block in the His-Purkinje system was demonstrated in 17 of 71 patients during atrial extrastimulus testing. Of the 17 patients who demonstrated initial block in the His-Purkinje system, ten patients had A-V nodal gap (a type 1 gap). Of these ten patients, progressive increase in A-V nodal conduction was responsible for a resumption of A-V conduction in six patients, dual pathways within the A-V node was responsible in three patients, and the presence of an extra nodal pathway of the A-V node was responsible in one patient.     

Determination of His-Purkinje refractoriness in man with His bundle pacing.

Consistent His bundle pacing was accomplished in one of 60 consecutive patients. Intracardiac electrophysiologic studies in this patient revealed rapid atrioventricular nodal conduction (AH = 55 msec). While the relative refractory period of the His-Purkinje system as a whole determined by His bundle pacing (using the extrastimulus technique) was identical to that determined by atrial pacing, changes in right bundle branch refractoriness differed. An atrial extrasystolic interval of 370 msec resulted in right bundle branch block, whereas direct His pacing at a shorter extrasystolic interval (360 msec) failed to produce a bundle branch block pattern. The effective refractory period of the His-Purkinje system could not be determined by atrial pacing because of atrial refractoriness, but was obtained by His bundle pacing. Theoretically, direct His bundle pacing may be of value in determining His-Purkinje system refractoriness when this parameter is unobtainable due to either atrial or atrioventricular nodal refractoriness. This technique appears to have limited clinical usefulness, however, because of the very small success rates. Finally, His-Purkinje system refractoriness may differ, depending on site of stimulation, presumably due to differing inputs into the His-Purkinje system.     

Exercise-induced distal atrioventricular block

Three patients with 1:1 atrioventricular (AV) conduction at rest developed fixed 2:1 or 3:1 AV block during treadmill exercise testing. Electrophysiologic study documented block distal to the AV node in all three patients, and suggested that the exercise-induced block occurred because of increased atrial rate and abnormal refractoriness of the His-Purkinje conduction system. The findings in these three patients suggest that high grade AV block appearing during exercise reflects conduction disease of the His-Purkinje system rather than of the AV node, even in the absence of bundle branch block. Patients with this diagnosis should be considered for permanent cardiac pacing.     

Improved intraventricular conduction of premature beats after diphenylhydantoin

To determine the effect of diphenylhydantoin on intraventricular conduction in man, we utilized His bundle recordings and coupled atrial pacing to record the relative refractory period of the His-Purkinje system and the functional refractory period of the atrioventricular (A-V) node in 14 patients before and after administration of diphenylhydantoin at a rate of 50 mg/min. Before infusion of diphenylhydantoin (5 mg/kg at a rate of 50 mg/min) His-Purkinje conduction delay occurred with right bundle branch block in nine patients and with left bundle branch block in five patients. After infusion of diphenylhydantoin the onset or degree of His-Purkinje delay was altered in all patients. In nine patients diphenylhydantoin reduced the relative refractory period of the His-Purkinje system to a value less than that of the functional refractory period of the A-V node so that His-Purkinje conduction delay could not be demonstrated after diphenylhydantoin. In five patients, diphenylhydantoin reduced the relative refractory period of the His-Purkinje system or altered the degree of aberrant conduction, or both. Diphenylhydantoin reduced the minimal H₁–H₂ interval achieved before the onset of His-Purkinje block from 421 ± 27 (standard deviation) to 384 ± 34 msec (P <0.01). The functional refractory period of the A-V node was decreased from a control value of 389 ± 39 to 374 ± 26 msec after administration of diphenylhydantoin, but the effect was not statistically significant (P > 0.1). These results establish that diphenylhydantoin has a significant effect on intraventricular conduction in man.     

A demonstration of differential refractoriness within a single fascicle of the human ventricular specialized conduction system

In 15 patients with left bundle branch block (LBBB), atrial (A), His bundle (H), and ventricular (V) electrograms were recorded. Successively more premature atrial depolarizations were introduced via a catheter in the right atrium. In eight patients, the ventricular specialized conducting system (VSCS) was the most refractory portion of the entire atrioventricular conducting system (AVCS) and A-V conduction, which had been occurring via the right bundle branch (RBB), failed below the His bundle as the effective refractory period (ERP) of the VSCS was reached. In two of these eight patients, after the ERP of the VSCS was exceeded, further shortening of the H₁-H₂ interval (by 40 to 50 msec.) resulted in an unexpected resumption of A-V conduction, but with markedly prolonged H-V intervals (160 to 230 msec.). This demonstrates that differential refractoriness exists within the RBB of these patients. A zone of maximal refractoriness was initially encountered within the RBB when the premature impulse first blocked below the His bundle. In relative terms, this zone was distal to a more proximal area of the RBB where, with further shortening of the H₁-H₂ interval, sufficient conduction delay occurred to permit recovery of excitability distally and the resumption of A-V conduction.     

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.     

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.     

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.     

Combined intra-Hisian block and A-V nodal bypass

A patient with first and second degree atrio-ventricular (A-V) block and left bundle branch block was shown on electrophysiological study to have an intra and infra-His bundle branch block. In addition, this patient also had an A-V nodal bypass tract. The intra-Hisian block was concealed on the resting His bundle electrogram and became evident only during atrial pacing. The A-V nodal bypass was masked on the surface electrocardiogram (ECG) by the associated A-V conduction defect. The clinical significance of A-V bypass and combined block below the A-V node is discussed. The diagnostic value of His bundle electrocardiography in a patient with complex electrophysiological abnormalities is stressed.     

A-V conduction disturbances in Reiter's syndrome

High grade atrioventricular (A-V) block is a rarely described complication of Reiter's syndrome. This 65 year old man had recurrent episodes of arthritis, conjunctivitis and urethritis beginning at age 16. A prolonged P-R interval was first noted at age 32. The conduction disturbance progressed to intermittent episodes of high grade and complete heart block by age 65. His bundle electrograms located the site of block above the level of the bundle of His. Atrial pacing to rates of 150/min produced 5:1 A-V block, whereas exercise and atropine administration resulted in 1:1 A-V conduction. In view of these results, artificial pacemaker therapy is not indicated. The association of conduction disorders and Reiter's syndrome is reviewed.     

The electrophysiological effects of intramuscular guinidine on the atrioventricular conducting system in man

The electrophysiological effects of intramuscular quinidine were evaluated using His bundle electrograms and the extrastimulus method. The mean mid-study plasma quinidine level was 4.6 mg. per liter. Our results show that quinidine tends to shorten A-V nodal conduction time while it routinely prolongs His-Purkinje and intraventricular conduction time. The refractory periods of the atrium and His-Purkinje system were prolonged by quinidine while the effective refractory period of the A-V node was consistently shortened. Those patients with evidence of infra-His conduction disturbances manifested no difference in their response to quinidine from the group as a whole. These studies suggest quinidine has antivagal properties which are of clinical significance. In addition, the effects of quinidine on His-Purkinje conduction and refractoriness may lead to the ventricular tachyarrhythmias implicated in “quinidine syncope” by a re-entrant mechanism.     

Electrophysiologic effects of pindolol on atrioventricular conduction in canine heart.

The effects of intravenous pindolol on the electrophysiologic properties of the atrioventricular conduction system was studied in intact dog, using His bundle electrogram and the extrastimulus method. Pindolol was administered intravenously in a dose range of 4 to 40 micrograms/Kg. The latter dosage of pindolol is above those used clinically. Significant effects of intravenous pindolol were observed on sinus cycle length, the A-V nodal conduction time, the ERP of the atrium, the ERP and FRP of the A-V node, and the ERP of the ventricle. Sinus cycle length was prolonged during sinus rhythm. Intraatrial conduction time was not altered by pindolol, while the ERP of the atrium was slightly increased. The A-H interval was generally prolonged by pindolol without Wenckebach type A-V block, but the H-V interval was unchanged. Both ERP and FRP of the A-V node was prolonged. The ERP and RRP of the His-Purkinje system were not statistically evaluated, because no block within the His-Purkinje system were not statistically evaluated, because no block with the His-Purkinje system or prolongation of H-V interval was produced and only a few QRS complexes by extrastimulus showed aberrant configration in the intact canine heart. In addition, pindolol prolonged the ERP of the ventricle.     

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.     

Intermittent atrio-ventricular block induced by exertion. Description of 3 cases

Three patients with 1:1 atrio-ventricular conduction at rest developed fixed 2nd or 3rd degree atrio-ventricular block during exercise testing. In all patients electrophysiologic study documented block distal to the atrioventricular node. The exercise induced block probably occurred because of increased atrial rate and abnormal refractoriness of the His-Purkinje conduction system. These findings suggest that high degree atrioventricular block appearing during exercise reflects conduction disease of the His-Purkinje system rather than of the atrio-ventricular node, even in absence of bundle branch block. These patients should be considered for permanent cardiac pacing.