Anthony R. Caracta

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.

Electrophysiologic properties of procainamide in man

Abstract 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.

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.

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

Abstract 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 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.

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.

Functional 2:1 A-V Block within the His-Purkinje System Simulation of Type II Second-Degree A-V Block

In eight subjects in whom the effective refractory period of the His-Purkinje system was determined to be longer than that of the A-V node or atrium, abrupt acceleration of the atrial rate resulted in either 2:1 block within the His-Purkinje system or 1:1 A-V conduction. The former conduction pattern simulated a type II second-degree A-V block. The occurrence of either 2:1 block within the His-Purkinje system or 1:1 A-V conduction was determined primarily by (1) an effective refractory period of the His-Purkinje system which exceeded that of the A-V node, (2) the coupling interval of the first atrial capture beat and its effect or lack thereof on the refractory period of His-Purkinje system as it relates to changes in ventricular cycle length, and (3) the relative speed of A-V nodal conduction time. The distinction between this functional 2:1 block within the His-Purkinje system and a true type II second-degree block is discussed from both the clinical and electrophysiologic points of view. Functional 2:1 block within the His-Purkinje can also result when sudden acceleration of atrial rate occurs spontaneously such as in atrial flutter or A-V nodal reentrant atrial tachycardias.

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.