Alfred Pick

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.

The supernormal phase of atrioventricular conduction. I. Fundamental mechanisms.

THE TERM supernormal phase designates a short, early, and linmited period of the cardiac cycle during which a stimulus elicits either a totally unexpected response or one that is less abnormal than expected considering the state of recovery from the preceding impulse. Such enhancement of responsiveness, first demonstrated experimnentally in isolated nerve preparations, may involve two of the basic properties of cardiac tissue, excitability or conductivity.2 3 Supernormal excitability has been observed experimentally in cold-blooded animal and mammalian hearts4-7 and invoked as the cause of coupled premature ectopic beats (extrasystoles),8-11 but it has not yet been conclusively demonstrated in normal or diseased human hearts. Supernormal states of impulse conduction, on the other hand, sporadically implied in the interpretation of unusual clinical electrocardiograms of atrioventricular or intraventricular blocks, have been shown to occur in isolated compressed cardiac tissue12 and, recently, as a transient manifestation of hyperkalemia in the intact heart of the dog.3 Clinical electrocardiograms that lend themselves to a satisfactory and complete analysis by invoking a supernormal phase of atrioventricular conduction are not so rare as would perhaps appear, considering the relativelv small number of published cases (see table 2) In the past 5 years, since our attention was focused on the subject, we were able to collect 18 such cases in addition to those published previously from this department.14-17 All were

Ventricular Tachycardia with Narrow QRS Complexes (Left Posterior Fascicular Tachycardia)

Ectopic atrial, A-V junctional, and ventricular tachycardias in man have been associated with digitalis medication. Recently it has become possible to distinguish various locations of pacemakers within the specialized conduction system of the ventricles on the basis of the form of the QRS complexes in the standard electrocardiogram. Tachycardias originating in the left bundle branch and documented by right, left, and His bundle recordings have been produced in animals given excessive digitalis. We have noted a similar tachycardia in a patient with ischemic heart disease receiving digitalis during hypokalemia. The QRS complexes were 0.10 sec in duration and by contour suggested an ectopic focus located in the posterior fascicle of the left bundle; His bundle recordings were consistent with this diagnosis. As the ectopic rhythm became synchronized with a slightly irregular sinus rhythm, bidirectional depolarization of the His bundle with fusion His potentials could be demonstrated.

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.

ANOMALOUS ATRIOVENTRICULAR EXCITATION: PANEL DISCUSSION

H. H. HECHT (University of Utah, Salt Lake City, Utah) : Although we are not primarily concerned with the clinical and physiological aspects of abnormal ventricular excitation, it would seem beneficial to follow the searching analysis of the normal propagation of depolarization presented on the preceding pages with an account of a peculiar syndrome that may occur in otherwise normal individuals-a syndrome characterized by an unusual deformation of the early portion of the QRS complex. Detailed electrocardiographic analyses have led to certain inevitable conclusions that presented the anatomist and the histologist with pointed questions. FIGURE 1 illustrates the general configuration of the entity, a short PR interval with a wide QRS complex in a subject who a t other times displayed an entirely normal atrioventricular (AV) and intraventricular conduction, and who, in the sequence from which the illustration was taken, alternated between normal and abnormal complexes. When the two types of complexes are superimposed (FIGURE 2) it is clear that a relationship exists between the normal and the abnormal complex: the QRS deformation involves only the early portion of QRS, and ventricular depolarization obviously begins earlier in the abnormal complex, encroaching upon the normal PR interval. PR is, therefore, short, while PS and the interval from the beginning of P to the summit of R are identical with those of the normal complexes. Because of its shape, the abnormal early portion of QRS has been termed the “delta wave.”’ If the disorder is due to some unusual spread of excitation over ventricular musculature, the spread of recovery will be altered correspondingly and, therefore, T will change in size and direction (FIGURES 1 and 2). The basic myocardial function will remain unchanged and the total area of QRS and T, the ventricular gradient, will therefore remain unaltered. Some frontal plane measurements for normal and abnormal complexes are listed in TABLE 1. I t is generally referred to as the Wolff-Parkinson-White (WPW) syndrome according to the authors of the first definite account: although isolated cases were reported before, the first by Wilson in 1915.3 The more descriptive term “anomalous atrioventricular excitation,” coined in 194S14 implies no more than the existence of an unusual excitatory sequence, the presence of which cannot be denied. We have made this term the title for the panel. Prinzmetal has demonstrated that experimental procedures involving the atrioventricular junction may result in similar electrocardiographic complexes, and he has proposed the concept of “accelerated conduction.llS Others have demonstrated that complexes of this type may occur as a consequence of damage to certain portions of the ventricular musculature, including the septum.6

Mahaim and James fibers as a basis for a unique variety of ventricular preexcitation

This report concerns pathologic findings in a 54 year old woman with intermittent preexcitation who died of carcinoma of the breast. Electrocardiograms revealed predominantly normal sinus rhythm with a normal P-R interval and narrow QRS complex. Episodes of sinus rhythm, short P-R interval and QRS widening (with delta wave) were also recorded. During preexcitation QS complexes were noted in leads II, III, aVF, V1 and V4 to V6. Delta waves were negative in leads II, III, aVF and V1 isoelectric in leads V4 to V6 and positive only in leads I, aVL, V2 and V3. This case thus defies classification into any known variety of preexcitation. Complete serial sections, cut through the entire conduction system and both atrioventricular (A-V) rims, totaled 18,600 sections. These revealed no bundle of Kent. Instead, Mahaim fibers histologically identified as His bundle tissue gave off from the A-V bundle to both the right and the left sides of the septum associated with the normal fibers of James. This case reveals that (1) fibers of James can bypass the A-V node, (2) fibers of Mahaim can conduct, and (3) there are types of preexcitation in addition to types A and B.

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).

The nature and type of arrhythmias in acute experimental hyperkalemia in the intact dog

Abstract Progressive A-V block was produced in the intact dog by rapid intravenous infusion of isotonic potassium chloride (KCl) solution. The site of the conduction disturbance was determined with electrode catheter recordings from the atria and region of the His bundle, and a simultaneous conventional ECG. First-degree and seconddegree A-V block and then complete A-V dissociation were produced, with the block above the bundle of His, the ventricles following a pacemaker originating in the bundle of His. During A-V dissociation, atrial potentials maintained their control rate. “Sinoventricular” conduction could not be produced under the conditions of the experiments. Further infusion of KCl produced conduction defects below the bundle of His with an irregular ventricular action. Unexpectedly, with the most rapid infusions of KCl, the experimental animals developed complete block below the site of the His bundle recording at a time when conduction above the junctional pacemaker was only partially blocked. Ventricular arrhythmias, including terminal tachycardias, are probably the consequence of depressed or failing propagation of the cardiac impulse.

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.