Richard Langendorf

Ventricular Response in Atrial Fibrillation Role of Concealed Conduction in the AV Junction

The ventricular response in atrial fibrillation is determined by the long refractory period of the AV junction. Since an atrial impulse is always available for transmission to the ventricles, a regular ventricular rhythm would be expected, the rate of which would reflect the duration of a stable junctional refractory phase. The irregularity of the ventricular action associated with atrial fibrillation, therefore, indicates changes of refractoriness of the AV junctional tissues from cycle to cycle. This can best be attributed to varying degrees of penetration of “blocked” atrial impulses into parts of the AV junction, and to the effect of such concealed conduction on the propagation of subsequent impulses.The following facts are pointed out and illustrated as evidence of concealed AV and VA conduction during atrial fibrillation: (a) Occurrence of a “compensatory pause” following a ventricular premature systole. (b) Failure of an AV nodal escape to appear at the expected time due to concealed discharge of a subsidiary AV nodal pacemaker by a penetrating atrial impulse. (c) Acceleration of the ventricular rate when atrial fibrillation changes to flutter (elimination of concealed conduction with slowing of the atria). (d) A tendency for two or more long cycles to occur in succession (each containing one or more concealed responses).The reasons for the variations of the refractory period at different levels of the AV junction as a result of concealed conduction are analyzed. Their complex interplay may readily account for the over-all irregularity of the ventricular response associated with atrial fibrillation.

Intermittent Parasystole—Mechanism of Protection

Analysis of ten cases of intermittent ventricular parasystole suggested temporary loss of protection of the parasystolic focus resulting in discharge and “resetting” of the parasystole by sinus or other supraventricular beats. Parasystolic centers appear to be protected from supraventricular and other ventricular ectopic impulses early in their cycle by their refractory periods, and late in the cycle by diastolic depolarization. Between these two areas of protection is a period of “susceptibility” during which supraventricular beats can discharge the parasystolic focus. This phenomenon accounted for fixed coupling of the first parasystolic beat of a series to a preceding sinus beat. Under certain conditions all parasystolic beats may have such fixed coupling, a new and previously unconsidered mechanism for parasystole with fixed coupling.In one case of intermittent ventricular parasystole, the parasystole was shown to originate in the posterior fascicle of the left bundle branch on the basis of the shape of the standard electrocardiogram and by His bundle recordings. These parasystolic impulses produced a compensatory pause regardless of whether their discharge was manifest or concealed, and thus imitated a second degree (Type II) atrioventricular (A-V) block. This represents the first description of completely blocked atrial impulses resulting from concealed parasystolic beats arising within the ventricular conduction system.

Experimental Demonstration of Concealed AV Conduction in the Human Heart

Artificial pacing of patients with Stokes-Adams disease provided an opportunity to study experimentally the ways of operation of concealed antegrade or retrograde conduction, or both, in the AV junction.With a catheter electrode in the right atrium the classical experiment of Lewis and Master was repeated, revealing, during a 2:1 ventricular response to an atrial tachycardia, the delaying effect of seemingly blocked atrial impulses on subsequent AV conduction.Shifting the position of a single premature atrial impulse within a constant driving cycle of the atria produced graded effects of “blocked” atrial impulses on AV junctional refractoriness, permitting an estimation of the duration of the “phase of concealed AV conduction.”Interpolation of such premature atrial impulses into successive driving cycles resulted in “repetitive concealed conduction.”In an artificially produced atrial parasystole there was observed “concealed discharge” of a subsidiary (escaping) AV junctional pacemaker by an apparently nonconducted atrial impulse.With a catheter electrode in the right ventricle in a case of advanced AV block, concealed retrograde conduction of pacer stimuli disturbed the rhythmicity of a spontaneous AV junctional pacemaker.In a case of advanced AV block with preservedretrograde conduction (unidirectional block), evidence of penetration of the upper AV junction by the “blocked” antegrade impulse was found.With electrodes implanted in the left ventricle in a case of advanced AV block, concealed retrograde conduction of the artificial pacemaker stimuli enhanced antegrade conduction by transiently changing an area of unidirectional block to one of supernormal conduction.Thus, all known manifestations of concealed atrioventricular and ventriculo-atrial conduction, occurring spontaneously in clinical records or induced in animal experiments, were artificially reproduced in the human heart.

Elective Countershock in Unanesthetized Patients with Use of an Esophageal Electrode

A new electrode arrangement for the administration of elective direct-current countershock was studied, in which one electrode was placed in the esophagus, adjacent to the heart, and the other on the precordium.Thirteen patients with chronic atrial fibrillation were converted to sinus rhythm by the esophageal technic. Though the majority were, on clinical grounds, difficult cases for conversion, 11 were converted with shocks of 40 watt-seconds or less, and two with 60, after 40 failed. Five patients were defibrillated by both the esophageal and the conventional, anteroposterior chest technics; the energy requirement with the esophageal method averaged less than one third of that with the conventional one. Four patients received 40, and one 30 watt-second shocks without anesthesia; all five tolerated the shocks well, and three of four who had had countershock previously under anesthesia, expressed preference for the esophageal technic without anesthesia in the future. All patients were observed carefully for any symptoms suggestive of esophageal injury or dysfunction. None such occurred, either immediately or within 4 months.We conclude that this technic may have a place in elective countershock in that it may allow cardioversion to be undertaken in many patients who would otherwise require anesthesia.

Observations on second degree atrioventricular block, including new criteria for the differential diagnosis between type I and type II block☆

Abstract Since type I atrioventricular (A-V) block tends to be temporary and does not give rise to prolonged asystole, and type II A-V block tends to be progressive, ultimately leading to complete block and Adams-Stokes attacks, it is important to identify the type in each patient with acute or chronic second degree A-V block. The usual definition of these 2 types needs expansion. This new definition is given and new criteria are presented to permit differentiation of the 2 types of A-V block even in the presence of (1) incomplete A-V dissociation with single ventricular captures and (2) persistent 2:1 A-V block. The different roles and sites of concealed conduction in the 2 types of A-V block are defined. In type I, concealed conduction occurs within the region of block and depresses subsequent conduction, occasionally leading to blockage of consecutive atrial impulses. In type II, concealed conduction occurs down to the region of block, discharging subsidiary junctional pacemakers and thus preventing their escape. The frequent association of type II A-V block with bundle branch block and ventricular escapes with normal retrograde conduction (unidirectional block) is emphasized. Concealed retrograde conduction across the region of unidirectional block facilitates antegrade A-V transmission (early ventricular captures, supernormal phase of A-V conduction). The evidence is reviewed for placing the lesion causing type II A-V block below the A-V node; this is based on correlation of electrocardiographic findings, including His bundle recordings and anatomic data. Exceptions to the rule occur occasionally but should not lead to abandonment of the electrocardiographic classification of second degree A-V block into type I and type II because the distinction has proved of great value for clinical orientation.

Artificial pacing of the human heart: its contribution to the understanding of the arrhythmias.

Abstract Nineteen different disturbances of impulse formation or impulse conduction, or both, are pointed out; they were elucidated by artificial pacing, some in conjunction with the recording of His bundle electrograms. The following 8 are discussed in some detail and illustrated by representative electrocardiograms: (1) depression of impulse formation and conduction after premature stimulation; (2) complete atrioventricular (A-V) dissociation during partial (first or second degree) A-V block; (3) and (4) concealed conduction in the A-V bundle and in the bundle branch system (its different role in type I and type II block); (5) unidirectional A-V block (dependence of its manifestation oh the rate relationship of the atria and ventricles); (6) supernormal phase of conduction in type II A-V block (enhancing effect of concealed retrograde [V-A] conduction on antegrade [A-V] conduction); (7) parasystole (fixed coupling as a result of “reversed” coupling); and (8) reciprocating tachycardia (point of reflection of the retrograde impulse below the atria).

Response of Resistant Ventricular Tachycardia to Bretylium: Relation to Site of Ectopic Focus and Location of Myocardial Disease

Ventricular tachycardias were determined to be of either right-or left-sided origin in 25 patients whose arrhythmias were life-threatening and resistant to lidocaine and other antiarrhythmic drugs. All five patients with right ventricular tachycardia responded well to bretylium and survived. Eleven of 20 patients with left ventricular tachycardia did not do well. Four did not respond to bretylium but survived, five had no response and died, and two responded but died when hypotension prevented continued treatment. Eight of these 11 had acute anterior myocardial infarction or ischemia. Of nine patients with left ventricular tachycardia who responded well to bretylium and survived, only two had anterior infarction, and none had anterior ischemia. Because bretylium was efficacious in all patients with right ventricular tachycardia or inferior myocardial infarction in this study, it seems warranted to investigate further the relationship between drug responsiveness and the site of ectopic impulse formation and the location of myocardial disease.

Tachycardia and bradycardia-dependent bundle branch block alternans: clinical observations.

Eleven patients with tachycardia-dependent, bradycardia dependent, or “pseudobradyeardia-dependent” bundle branch block (BBB) alternans were studied. This classification is based on the following criteria: 1) When alternans is initiated by a sudden acceleration in ventricular rate, or it appears with aberration of the second beat after a pause, the alternans is tachycardia-dependent and results from a 2: 1 bidirectional block in the affected bundle branch. 2) When alternans begins with the aberrant complex terminating a pause it is bradycardia-dependent; such an alternans results from alternating bundle branch cycle lengths and refractoriness, possibly produced by alternating transseptal retrograde penetration of the affected bundle branch. 3) In cases referred to as “pseudobradycardia dependent BBB” alternans, a change from alternans to persistent BBB occurs as the cycle lengthens; however, the disappearance of BBB with further increase of the cycle length proves the tachycardia-dependence of the conduction defect.

The dual function of the A-V junction

Abstract The various electrocardiographic syndromes that develop as a consequence of abnormal dissociation of the two functions of the A-V junction can be summarized as follows (Table II): Acceleration of impulse formation in one or two pacemakers without any block in the A-V junction leads either to junctional rhythm with retrograde activation of the atria, or to isorhythmic A-V dissociation; when associated with retrograde block, the dissociation is incomplete with ventricular captures; when first- or second-degree antegrade block develops in addition, the captures tend to disappear and the A-V dissociation to become complete. An exit block of the junctional impulses may slow the manifest ventricular rate during the dissociation, and finally, an additional protective entrance block around the junctional pacemaker results in junctional parasystole. On the other hand, depression of junctional impulse formation without A-V block is one of the mechanisms responsible for the tachycardia-bradycardia syndrome. The basis of such a functional separation of the two properties of A-V junctional tissues appears to be a difference in structure and electrophysiologic behavior of cell elements that constitute the A-V junction.