Automatic Rhythms Produced by Ectopic. Agustin CASTELLANOS, Jr., M.D. and Worawit WONGTHONGSRI, M.D.

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1 Automatic Rhythms Produced by Ectopic Ventricular Contractions Agustin CASTELLANOS, Jr., M.D. and Worawit WONGTHONGSRI, M.D. There is no uniform agreement between pertinent authorities as to whether ventricular extrasystoles in man are produced by a disturbance in impulse formation or by a disturbance in impulse conduction (re-entry theory). Several selected cases are presented which illustrate automatic impulse formation induced by true, coupled, extrasystoles. We believe that the term facilitation best described this phenomenon. Another interesting feature was the fact that rhythmicity was elicited by impulse formation coming from the ventricles, rather than those following an orthograde direction. It seems probable that extrasystolic and automatic beats are produced by a disturbance in rhythmicity, and that the difference in their mode of appearance depends on whether the affected cell (or cells) are able to manifest their activity at any moment; or only during the periods of lowered threshold produced by a previous contraction. UTOMATIC impulse formation in the A-V node is a common finding in clinical electrocardiography.19) Basically, the initiation of such rhythms follows the accepted rules of ectopic impulse formation.7) Rare cases have been reported in which nodal beats have been precipitated by impulses arising in another (ectopic) pacemaker. 1)-6),8),10),19)-23),26),27) Moreover, in some occasions A-V nodal rhythms have been preferentially induced by activation coming from one direction only.2),8),19),22),17) Such examples of active rhythms are to be interpreted in a different sense to what sometimes occurs after atrial or ventricular extrasystoles are conducted retrogradely to the sinus node. Whenever the latter center is sufficiently depressed, an escape beat (passive rhythm) will ensue.9) Even though the escape can originate in any region of the heart, it is generally accepted that if an A-V nodal escape occurs in man, the beats will be of the type showing simultaneous activation of atria and ventricles.22) Active nodal impulse formation induced by premature ventricular contractions can be seen in Fig. 1 to 3 and its significance shall be discussed subsequently. All the patients were old, with atherosclerotic heart disease and the From the Section of Cardiology, Department of Medicine, University of Miami School of Medicine and the Department of Electrophysiology, Jackson Memorial Hospital, Miami, Florida, U.S.A. Aided in part by a Grant from the Heart Association of Greater Miami. 144

2 Vol. 6 No. 2 AUTOMATIC RHYTHM 145 first had received no digitalis previously. The term gextrasystole h will be used throughout this communication to designate those ectopic contractions coupled to preceding QRS complex.21) On the other hand gautomatic h beats will be considered to be those which are not systematically dependent on an initiating beat.21) It is the purpose of this paper to bring out clearly that there exists an inter-relationship between both types of beats. Fig. 1. gfacilitation h of an A-V beat by a premature ventricular contraction with retrograde conduction to the atria. Fig. 1 initially shows sinus rhythm (first 3 complexes). The fourth ventricular complex is a premature contraction showing retrograde conduction to the atria. The QRS measured 0.12 sec. in leads I and avf (not shown). It fulfills the criteria for a ventricular extrasystole, although its exact site of origin (whether ventricular or low nodal with aberration) is irrelevant for the interpretation of the curious events to which it led. The extrasystole is paradoxically followed by a nodal beat with preceding stimulation of the atria (facilitation), instead of the expected gmiddle h ectopic contraction. The post-extrasystolic pause being shorter than compensatory suggested that the A-V rhythm was gactive h (not a true escape) thereby probably induced by the premature contraction. It is interesting to note that in this patient nodal activity was never stimulated by sinus impulses, but only by impulses coming from the ventricles. Fig. 2. gfacilitation h of an intermittent A-V nodal parasystole by premature ventricular contractions with retrograde conduction to the atria. Fig. 2 shows the precipitation of an gupper h A-V nodal rhythm by a premature ventricular contraction with retrograde conduction to the atria. The former appears after a shorter than compensatory pause indicating active impulse formation. In addition, the nodal pacemaker develops intermittent, self-sustained activity, its inter-ectopic intervals and couplings measuring

3 146 CASTELLANOS AND WONGTHONGSRI Jap. Heart J. M arch, ; 1.52; 1.52 and 0.70; 0.83; 0.53 and 0.58 respectively. Towards the end of the strip the ectopic pacemaker fails to discharge at the expected time (vertical broken lines). The last QRS in a ventricular extrasystole, which re-initiated the sequence of events. Always in each series the first QRS complex of nodal origin showed a fixed coupling. Spontaneous activity was limited to 4 automatic contractions. In this case, the repetition of the ectopic impulses, the varying couplings, the fixed coupling of the first one in each series, suggests intermittent parasystole.11) This electrocardiogram was taken from a 72-year-old patient with mild congestive heart failure which was on maintenance doses of digitalis. Fig. 3. gfacilitation h of gupper h A-V nodal tachycardia by a rapid ectopic ventricular pacemaker. The 2 strips in Fig. 3 are continuous. The first 5 complexes are of sinus origin (rate 108/min.). The sixth QRS beat is a fusion beat resulting from the simultaneous depolarization of the ventricles by the oncoming supraventricular (sinus) impulse and by an ectopic ventricular pacemaker. The latter subsequently discharges at a rate of 108/min. (ventricular tachycardia). In addition, after 3 ventricular beats have occurred, there is a change in the pacemaker in atria. A predominantly negative P wave is seen, persisting until the end of the ventricular paroxysm. The rate of the ectopic supraventricular rhythm was also 111, therefore, it can be considered a tachycardia slightly faster than the sinus one. In this patient who was considered to be intoxicated with digitalis, the same change in A-V rhythm was invariably seen whenever ventricular tachycardia ensued. In consequence, it is suggested that the retrograde conduction of the ventricular beats, ascending into the A-V junction, stimulated (facilitated) rapid impulse formation in these regions (nodal tachycardia). The multiphasic P wave can be explained on the basis of intra-atrial conduction disturbance. Automatic impulse formation occurring after true, coupled, extrasystoles but not after A-V nodal or supraventricular beats is presented in Fig. 4. These electrocardiograms were recorded from a 73-year-old patient with atherosclerotic heart disease, congestive heart failure, and chronic atrial fibrillation. The

4 Vol. 6 No. 2 AUTOMATIC RHYTHM 147 Fig. 4. Atrial fibrillation and A-V nodal rhythm with coupled (bigeminated) extrasystoles. Automatic beats (A) are seen to occur only after extrasystoles, but never following A-V nodal beats. electrocardiograms were recorded after increasing the maintenance digitalis, this provoking clinical and electrocardiographic manifestations of toxicity. The tracings show atrial fibrillation with apparently complete heart block and a fairly regular nodal pacemaker. The exact rate of the latter is difficult to ascertain for there are bigeminated and occasionally multifocal ventricular extrasystoles, which are transmitted retrogradely to the A-V node. The interesting finding in this case is the fact that there is a certain type of automatic ventricular beat (marked with an A) which occurs only after the bigeminated extrasystole and not following a nodal beat. It can be seen that the distance between the last nodal impulse and the first automatic beat is shorter than that between 2 (regular) nodal contractions, thereby suggesting that the beat marked with an A is automatic. Other tracings of this patient (not shown) displayed intermittent ventricular bigeminy and occasional disappearance of the complete A-V block. Yet, in no instance were automatic beats seen to appear after QRS complexes of supraventricular contour. Hence, this case constitutes an example of an automatic rhythm elicited by impulses coming from the ventricles themselves rather than by those coming from the high septal (A-V nodal) regions. DISCUSSION There have been several reports of cases in which extrasystoles have been seen to induce runs of A-V nodal tachycardia.1),2),4)-6),10),19),20),26) Some of them have been interpreted by supposing that the extrasystole was conducted to the distal chamber and then back to the chamber of origin, or that is, by assuming the occurrence of a reciprocating tachycardia.4),10) However, Scherf and Cohen,19) and Scherf et al.,20) made the keen observation that

5 148 CASTELLANOS AND WONGTHONGSRI Jap. Heart J. M arch, 1965 whenever some extrasystoles occurred during the paroxysm, they were followed by compensatory pauses. This would mean that the extrasystoles did not disturb the A-V nodal center which continued to form impulses rhythmically. The most likely explanation for the initiation of the arrhythmia would be that the extrasystoles arrived to the A-V node during the vulnerable period of the latter, hence provoking multiple responses. As the origin of flutter and fibrillation by vulnerability is well accepted, Scherf and co-workers estimated that such hypothesis could also be applied to the genesis of paroxysmal tachycardia.19),20) In some reports from the literature facilitation of impulse formation has been seen to occur preferentially by activation coming from the ventricles, rather than by impulses propagating from the supra nodal area. For instance, Castellanos Jr. et al. (Ref. 2, Fig. 10) described a case of A-V nodal tachycardia triggered by ventricular extrasystoles, which were assumed to be conducted retrogradely to the A-V node. Sinus or atrial beats never exalted rhythmicity in the A-V junctional tissue. A similar arrhythmia was reported by Scherf et al. (Ref. 20, Fig. 4). The cases described by Schott22) are similar to our Fig. 1, in the sense that ventricular extrasystoles with retrograde conduction to the atria elicited g upper h A-V nodal beats. Wenckebach and Winterberg (Ref. 27, Fig. 185) reported a ventricular tachycardia always initiated by a ventricular complex of completely different form. Kato et al.8) studied 2 cases of complex interference dissociation. Their Figs. 2 and 3, obtained from a patient with 2 pacemakers located within the A-V conducting system, shows that high A-V beats were exclusively after impulses spreading from the atria and never after those coming from the ventricles. Schott and Scherf23) refer to 3 patients with ectopic ventricular arrhythmias in which coupled extrasystoles were precipitated exclusively or preferentially by automatic ventricular beats. The 4 cases presented in this communication are examples of the same phenomenon, that is, automatic impulse formation elicited by extrasystoles. The most interesting fact about this arrhythmia is that the nodal beats as well as the automatic ventricular beats were initiated by impulses coming only from the ventricles and not by those propagating in the normal A-V fashion. According to Schott and Scherf,23) this phenomenon is in a way due to the existence of directional element not necessarily related to the old concept of a wall of refractory tissue surrounding an ectopic center. It was estimated that the uni-directional block (and block in general) could well be related to the

6 Vol. 6 No. 2 AUTOMATIC RHYTHM 149 ratio, strength of impulse-to-excitability. In favor of this assumption are the experiences of Rosenblueth and Rubie17) stressing the fact that the differences in speed of conduction through the A-V conducting system is due mainly to the relationship between the action potential and the threshold of a given segment. Their theory was originally elaborated in the squid axon16) and later translated into the mammalian heart so as to explain the difference in A-V and V-A conduction times with increasing rates of stimulation.17) Also, they found that in the dogs in which the sinus node was clamped off and the adrenals ligated, A-V rhythm would ensue. Thereafter induced ventricular systoles (traveling in A-V direction) produced automatic nodal discharges while those produced in the atria (traveling in A-V direction) failed to do so.15) According to Lloyd,14) the term gfacilitation h means that because of some antecedent or concomitant event the job is more easily done or a bigger job can be done. The term was originally introduced by Skramlik,24) in experiences carried out in the frog's heart. This author found that if cardiac standstill occurred after the application of Stannius first ligature and if retrograde V-A conduction was absent, the latter could be initiated by the stimulation of the ventricles after stimulating the atria several times. In other words A-V propagation facilitated the production of V-A conduction. On the contrary, the appearance of antegrade conduction only after V-A propagation was frequently seen in the fish's heart.25) Evidently, gfacilitation h can be also used in different sense, that is, in relation, not to impulse conduction, but to impulse formation.3) From this point of view it can be said that A-V nodal rhythms were induced (facilitated) by the retrograde conduction of premature ventricular contractions. It is not unusual for a given electophysiological term to be applied in 2 different senses. For instance, the well known important phenomenon gconcealed conduction h has been used by Langendorf and Pick,12) in a dual sense so as to describe the effects of block impulse on conduction, as well as on formation of subsequent impulses. We have presented several examples of automatic beats elicited by extrasystoles. This is not a recently described phenomenon, for as way back as 1912 Lewis observed that the first P wave after an atrial extrasystole occasionally showed the same morphology as the ectopic contraction.13) In 1929, Scherf went one step further when he first noted that the events described by Lewis might not end after the gescaped h beat, but that on the contrary, the ectopic center could develop gparasystolic h properties (intermittent parasystole).18) In general, there seems to be a definite relation between extrasystolic and automatic impulse formation. More evidence seems to have accumulated in

7 150 CASTELLANOS AND WONGTHONGSRI Jap. Heart J. M arch, 1965 the recent years in favor of the unitary nature of extrasystoles which believes that they are due to an abnormality in rhythmicity rather than to a disturbance of impulse conduction (re-entry theory).19) According to Scherf and Schott the affected cell or group of cells will discharge on its own whenever the corresponding prepotential attains threshold values. On the other hand if the discharge occurs only during periods of reduced threshold which are known to follow a conducted beat, then a coupled beat will occur.19) SUMMARY Facilitation of A-V nodal and automatic ventricular rhythms by ectopic ventricular contractions was described. In one case only A-V nodal beats were induced, but in the other three, the self-sustained rhythms presented themselves as intermittent parasystole, nodal tachycardia, and automatic ventricular beats. The elicited automatic rhythms were never seen after impulses traveling in an orthograde fashion. The term gfacilitation h was employed here in reference to disturbances in impulse formation, contrasting with its previous use in connection chiefly to impulse conduction. The examples presented represent another instance in which an automatic rhythm was precipitated by a coupled (true) extrasystole, thereby emphasizing the relationship between both types of ectopic beats. REFERENCES 1. Braun Menendez, E. and Mora, B.: Rev. Arg. Cardiol. 4: 329, Castellanos, A. Jr., Cano, L. A., Calvino, J. M., and Taquechel, N.: Rev. Cubana Cardiol. 16: 419, Castellanos, A., Jr., Meyer, J. W., and Lemberg, L.: Acta Cardiol. 17: 49, Dreifus, L. S. and Siegel, P. D.: Dis. Chest 36: 676, Gallavardin, L.: Arch. Mal. Coeur. 151, Gallavardin, L. and Froment, R.: J. Medec. Lyon 11: 517, Hoffman, B. F. and Cranefield, P. F.: Electrophysiology of the Heart, McGraw-Hill, New York, Kato, K., Shimomura, K., Matsuyama, K., Iizuka, M., Muras, S., and Ueda, H.: Jap. Heart J. 3: 204, Katz, L. N. and Pick, A.: Clinical Electrocardiography. Part I. The arrhythmias, Grune and Stratton, Philadelphia, Kistin, A. D.: Am. J. Cardiol. 3: 365, Langendorf, R. and Pick, A.: Circulation 11: 431, Langendorf, R. and Pick, A.: Circulation 13: 381, Lewis, T.: Heart 3: 279, Lloyd, D.P.C.: Principles of Nervous Activity. In Fulton, Textbook of Physiology, 16th Ed., Saunders, Philadelphia, Rosenblueth, A.: Arch. Inst. Cardiol. Mex. 25: 171, 1955.

8 Vol. 6 AUTOMATIC RHYTHM 151 No Rosenblueth, A., Alanis, J., and Mandoki, J.: J. Cell. Comp. Physiol. 33: 405, Rosenblueth, A. and Rubio, R.: Arch Inst. Cardiol. Mex. 25: 535, Scherf, D.: Z. ges. exp. med. 51: 816, Schef, D. and Cohen, J.: The atrioventricular node and selected cardiac arrhythmias, Grune and Stratton, New York, Scher, D., Cohen, J., Parangi, A., and Yeldiz, M.: Am. J. Cardiol. 11: 757, Scherf, D. and Schott, A.: Extrasystoles and Allied Arrhythmias, Grune and Stratton, New York, Schott, A. and Scherf D.: Brit. Heart J. 17: 247, Schott, A. and Scherf, D.: Brit. Heart J. 21: 177, Skramlik, E.: Pflug. Arch ges. Physiol. 180: 30, Skramlik, E.: Z. Vergl. Physiol. 6: 53, Wedd, A. M.: Arch. Int. Med. 27: 571, Wenckebach, K. F. and Winterberg, H.: Die Unregelmaessige Herztaetigkeit, W. Englemann, Leipzig, 1927.