John J. Gallagher

The electrophysiologic demonstration of atrial ectopic tachycardia in man

Abstract Three patients with almost continuous atrial tachycardia were studied in an attempt to delineate the mechanism responsible for their cardiac arrhythmia. During cardiac catheterization intracardiac electrograms and specific atrial stimulation sequences revealed: (1) episodes of tachycardia were initiated by atrial premature depolarizations (APDs) which exhibited no increased delay in AV nodal conduction, (2) during tachycardia atrial cycle length was not a direct function of AV nodal conduction, (3) initial cycles of tachycardia showed progressive shortening in cycle length, (4) APDs introduced during tachycardia resulted in resetting of the atrial cycle, and (5) single APDs and atrial overdrive during tachycardia failed to interrupt it. The electrophysiologic behavior of the arrhythmia was consistent with the hypothesis that it was initiated and was sustained by an ectopic rapidly firing automatic atrial pacemaker.

Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex☆

Eighteen subjects with a short P-R interval (<0.12 second) and normal QRS complex were studied by means of His bundle recordings and programmed atrial premature depolarizations. Eight subjects had a history of supraventricular tachycardia. During sinus rhythm, the A-H interval was less than or at the lower limits of normal values (45 to 80 msec), and the H-V interval was normal (30 to 50 msec). Atrial pacing at rates of up to 160/min produced 3 types of responses. Thirteen subjects showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. Three subjects showed an initial increase at low pacing rates, followed by a plateau response and further increase at higher rates. Two subjects showed no significant increase in the A-H interval. In 6 of 8 subjects with supraventricular tachycardia, atrial premature depolarizations produced atrial echo beats and sustained supraventricular tachycardia in 4, indicating atrioventricular (A-V) nodal reentry as the mechanism for the supraventricular tachycardia. In 10 subjects, refractory periods of the various components of the A-V conducting system were found to be similar to those of subjects with a normal P-R interval. The data suggest the following possible explanations for the short P-R interval: (1) total or partial bypass of the A-V node; (2) an anatomically small A-V node; (3) a short or rapidly conducting intranodal pathway; or (4) isorhythmic A-V dissociation.

Effects of lidocaine on refractory periods in man

Abstract The effect of lidocaine on the refractory periods of the atrium, A-V node, and His-Purkinje system were studied using His bundle recordings and the extrastimulus method. This method provides a safe and systematic approach to the evaluation of electrophysiological properties of drugs in man. In usual therapeutic doses, the present study demonstrated no consistent effect of lidocaine on the ERP of the atrium or the A-V node. However, in these doses it shortened the ERP and the RRP of the His-Purkinje system. These results explain the effectiveness of lidocaine in the management of ventricular arrhythmias and its inconsistency in the treatment of supraventricular rhythm disturbances. The potential for lidocaine toxicity in the presence of heart failure and/or liver disease is noted.

Electrophysiologic studies during accelerated idioventricular rhythms.

Accelerated idioventricular rhythms (AIVR) are ectopic ventricular rhythms with rates intermediate between idioventricular escape rhythms (30 to 40/min) and ventricular tachycardia (120 to 180/min). Differentiation of AIVR from supraventricular arrhythmias rests primarily on demonstration of their ventricular origin. His bundle electrograms (HBE) were recorded in four patients during AIVR. HBE verified the idioventricular nature of the ectopic rhythm and excluded supraventricular rhythm with aberration as a cause. In addition, they permitted the recognition of normally conducted sinus beats, fusion beats, and idioventricular beats. The pacemaker site for the AIVR was below the bundle of His. AIVR became manifest when the heart rate was slowed by increasing vagal tone, premature atrial stimulation, and high degree atrioventricular (A-V) block. AIVR could be suppressed and 1:1 A-V conduction established by increasing the atrial rate with atropine or by atrial pacing.

Electrophysiologic Properties of Diphenylhydantoin

The electrophysiologic properties of diphenylhydantoin (DPH) (5-10 mg/kg) intravenously was studied in 14 subjects using His bundle recordings and correlated with blood levels. Conduction through the A-V conducting system (AVCS) was studied at various paced atrial rates and refractory periods determined using programmed atrial premature depolarization within 10 min of drug administration. In 11 of 14 subjects the sinus cycle length was shortened by an average of 110 msec, lengthened in three (average 116 msec). Conduction through the A-V node (AVN) was shortened in seven subjects (average 10 msec), lengthened in one (5 msec), and unchanged in the remaining six. Conductinged by 5 msec). Prior to DPH, the longest mained constant in all but two subjects (proloengthened in four, and was unchanged in the re-refractory period of the AVCS was in the AVN in nine subjects, the atrium in four and the HPS in one. After DPH, the following effects were noted: (1) the effective refractory period (ERP) of the atria shortened in four subjects, lengthened in four, and was unchanged in the remaining six; (2) the ERP of the AVN shortened in 6/9 subjects, lengthened in 3/9; (3) functional refractory period of AVN shortened in six, prolonged in three subjects, and remained unchanged in five subjects; (4) the relative refractory period (RRP) of the HPS shortened in 7/7 subjects; (5) ERP of HPS in 1/1 subject shortened. Thus, DPH showed varied effects on A-V nodal conduction, inconsistent effect in the atrium, and consistent shortening of the refractory period of the HPS. The data suggest DPH differs from other antiarrhythmic drugs such as quinidine and procaine amide.

Gap in A-V conduction in man: Types I and II☆

Abstract 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.

Alternative mechanisms of apparent supernormal atrioventricular conduction

Abstract 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.

Manifest and Concealed Reentry: A MECHANISM OF AV NODAL WENCKEBACH PHENOMENON

The mechanism of the AV nodal Wenckebach phenomenon was studied in 25 dogs by multiple atrial and His bundle electrogram (HBE) recordings. During ventricular stimulation with 1:1 retrograde conduction, the interval from the stimulus artifact to the retrograde His deflection (S-H) interval) remained constant. Decreasing the cycle length of stimulation (CLS) resulted in retrograde AV nodal Wenckebeach cycles. When retrograde AV nodal delay reached a critical value, the Wenckebach cycles were terminated by a reciprocal beat (manifest reentry). The His bundle and ventricles were antegradely depolarized by the reentrant impulse. A further decrease in CLS produced what electrocardiographically looked like ordinary Wenckebach cycles. However, the HBE tracing revealed that reentry was occurring but was concealed by the CLS. This was confirmed by noting that the His deflection of the last ventricular paced beat of the Wenckebach cycle was antegradely depolarized and had a shorter S-H interval then all other beats of that cycle. The reentrant and retrograde impulses collided in the bundle-branch system. Further decreases in CLS masked the reentrant phenomenon on both standard ECG and HBE tracings. The S-H interval remained constant for all ventricular paced beats of the Wenckebach cycle. Under these circumstances, reentry could still be uncovered by turning off the stimulator at an appropriate time during the Wenckebach cycle. This maneuver exposed the reciprocal beat. Thus collision of the reentrant and retrograde impulses occurred within the AV node. These findings provide a satisfactory explanation for why the last beat of the Wenckebach cycle is not conducted retrogradely to the atria.

Site of conduction disturbances in a family with myotonic dystrophy

Myotonic dystrophy has a high incidence of electrocardiographic abnormalities in the absence of clinical heart disease; the most common are atrioventricular and intraventricular conduction defects. The few pathologic studies of hearts from patients with myotonic dystrophy have not been helpful in determining the site of conduction delay. A father and son with myotonic dystrophy and conduction defects were studied with the use of His bundle electrocardiograms to determine the physiologic site of these disturbances. The father demonstrated H-V prolongation, Wenckebach phenomenon in the left bundle branch and spontaneous as well as pacing-induced type II (Mobitz II) A-V block, all of which signify marked impairment of His-Purkinje conduction. In the son, A-V nodal, intra-His bundle and infra-His bundle conduction delays were manifested by prolonged A-H and H-V intervals and a broad His deflection. This study confirms the usefulness of His bundle electrocardiograms in determining the site of conduction disturbances.

Manifest and Concealed Reentry A Mechanism of A-V Nodal Wenckebach in Man

In five patients, bundle of His electrograms were recorded during right ventricular pacing at various cycle lengths. In all patients, as the cycle length of stimulation was decreased, the pattern of retrograde conduction proceeded from 1:1 retrograde conduction to retrograde Wenckebach with or without manifest reentry, to retrograde Wenckebach cycles with concealed reentry. The requisite condition for reentry was a critical retrograde A-V nodal delay. During retrograde Wenckebach cycles, reentry could be either concealed or manifest. Concealed reentry resulted in typical or ordinary Wenckebach cycles on the surface electrocardiogram and manifest reentry resulted in ventricular echo beats. Depending upon the cycle length of stimulation, reentry could be concealed on the surface electrocardiogram but manifest on the His bundle electrogram recording. Concealed reentry could be manifest by turning off the stimulator at the appropriate time in the cardiac cycle while manifest reentry could be concealed by changing the cycle length of stimulation. Reentry with collision of wavefronts within the A-V node or proximal His-Purkinje conduction system explains why the last ventricular impulse is not conducted to the atria during ordinary Wenckebach cycles.