Upsala J Med Sci 80: 113-117, 1975 Mode of Spontaneous Onset and Termination of Supra- ventricular Tachyarrhythmias B E N G T FURBERG and L A R S N O R D G R E N From the D e p a r t m e n t of Clinical Physiology, University H o s p i t a l , U p p s a l a , S w e d e n ABSTRACT the present study, a recording technique which ECG tracings from 16 patients with spontaneous Onset gives a high r e s o h t i o n of t h e atrial waves has been and/or termination of supraventricular tachyarrhythmias used, thereby offering better possibilities for pre- (SVTA) were studied. Of these recordings, 13 were made cise assessment of p wave aberration and p-p in- with a special technique which gives a high resolution of the t e r v a l s . atrial waves. At the onset of SVTA, the first atrial wave invariably had an aberrant configuration. The coupling index (coupling interval (P-'P) preceding cycle length) was 0.50 or less in 9 of 15 cases but more than 0.60 in 4 cases. In the 5 cases of onset of atrial fibrillation, the intervals M A T E R I A L A N D M E T H O D S The study was performed on ECG tracings from 16 pa- between the first few atrial waves corresponded to a fre- tients (9 men and 7 women, with ages between 19 and 7 2 ) quency of 300-350 per minute. Acceleration of the atrial activity occurred within the first 30 seconds. At the ter- mination of SVTA, no successive modification of the atrial activity was found. The termination often did not occur a t or shortly after a QRS complex. It is concluded that a premature atrial beat-even a single one-with a short coupling interval may well initiate a circus-movement SVTA, while an ectopic atrial beat with a long coupling interval apparently must be followed by repeated rapid discharges from the ectopic focus in order for SVTA to ensue. The functional conditions of the atria may then determine which kind of SVTA eventually results. I N T R O D U C T I O N T h e mechanisms responsible for the initiation, maintenance and termination of supraventricular tachyarrhythmias (SVTA), have been the subject of continuing controversy and investigation. Experi- ments with electrical o r chemical stimulation of t h e with spontaneous onset and/or termination of SVTA. I n tracings with more than one bout of SVTA a representa- tive one was selected for the s t u d y . The change from sinus rhythm to atrial fibrillation was studied in 5 tracings, to atrial flutter in 8 and to atrial tachycardia in 2. The rever- sion to sinus rhythm from atrial fibrillation was studied in 2 tracings, from atrial flutter in 6 and from atrial tachy- cardia in 2 . I n 3 patients the ECG was recorded with conventional amplification ( 1 mV=lO mm), lead V , and at least 3 other leads being recorded. I n 13 patients a special recording technique was used (7), using three bipolar leads. The common reference electrode was placed at the midline of the angle of sternum and the three different electrodes were placed at the highest attainable point of the armpit in the left mid-axillary line (S 1 ) . at the caudal end of the sternal body (S2) and at a point over the vertebral column at the transthoracic level of the sternal angle (S3). The three bipolar leads were recorded with conventional amplification, as well as with a tenfold grea- ter amplification (0.1 m V = l O mrn), using a 3-channel dif- ferential preamplifier and a Mingograph 81 (Siemens- atrium, while yielding important information con- cerning the electro-physiological characteristics of S V T A , have not solved t h e Problems of onset and Elema L t d . , For measurements, the system illustrated in Fig. I was used, The SVTA type was defined according to t h e main atrial wave frequency. An atrial wave frequency of termination of spontaneous S V T A . Since the first electrocardiogram showing t h e onset of atrial fibrillation was presented in 1918 150-210/min was judged as supraventricular tachycardia (SVT), of 220-340 as atrial flutter (AFu) and of 350 or more as atrial (AFi), (lo), numerous tracings of S V T A onset and termi- nation have been published. Most of these tracings were made with a conventional recording techni- que, which is not sufficiently sensitive to clearly (exhibit changes in the atrial wave configuration. In R E S U L T S T h e tracings of S V T A with the special recording technique permitted analysis of the atrial wave con- 8-752858 Upsala J Med Sci 80 114 B . Furberg cind L . Nordgrrn F i g . I . Onset and termination of atrial flutter (patient no. 9). The nomenclature of the atrial waves is shown. The three special leads S I-S 3 are recorded with conventional and tenfold amplification. F i g . 2. Short episode of atrial flutter (patient no. 12). Note the long coupling interval. Upsala J Med Sci 80 Onset rind terminrrtion of tcichyrirrhythmiris 1 15 Fig. 3. Onset of atrial fibrillation (patient no. 4). The premature atrial beat is followed by a rapid atrial tachy- cardia and within 2 s by atrial fibrillation. figuration and intervals; this had been difficult t o obtain with the conventional recording technique. Examples of these new recordings a r e shown in Figs. 1-3. At the onset of S V T A , the first atrial wave ('P) invariably had an aberrant configuration in com- parison t o the ordinary P wave. T h e following atrial waves ( W " P ) of the S V T A had the same configura- tion a s 'P in the 2 S V T cases and in 6 of t h e 8 AFu cases. In the 5 AFi cases the configuration changed. In 9 of the I5 cases, t h e 'coupling index' (the ratio of coupling interval (P-'P) t o preceding cycle length (P-P)) was 0.50 o r less, while it was more than 0.60 in 1 AFi case, in 2 A F u cases and in 1 S V T case. Acceleration of the atrial activity after *P was seen in t h e 5 AFi cases, in 3 of the AFu cases and in none of t h e S V T cases. T h e final atrial wave frequency was always obtained within 30 s. T h e termination of S V T A occurred in 5 of t h e 10 cases studied within 30 cs from the beginning of a Q R S complex. T h e point of termination was de- ' fined as the start of the P' wave plus t h e Pz-P1 interval. There was no deceleration of the last few atrial impulses before t h e termination and t h e form of t h e atrial waves did not change. The first atrial wave after termination of S V T A exhibited a n ordi- nary configuration in all but o n e case. DISCUSSION When dealing with the mechanism of S V T A onset and maintenance, some authors have concluded that a t least S V T and A F u , and possibly AFi, are evoked b y a n ectopic atrial focus with a high impulse-formation rate. Other authors have con- cluded that S V T A depends o n the establishment of a n atrial circus movement with o r without engage- ment of the atrio-ventricular node. From experi- mental studies there is evidence that S V T A can result from either of these mechanisms. T h e argu- ments in favour of both hypotheses have been re- viewed by Hecht e t al. 1953 (4), Scherf, Schaffer & Blumenfeld 1953 ( 1 I ) , Katz & Pick 1960 (9, Rytand 1966 (8) and Guiney & Lown 1972 (3). Studies of the Upsala J Med Sci 80 116 B . Furherg find L . N o r d g r e n Table I . O n s e t of suprciventricular t ~ i ~ i i y ~ i r r i i y t i i m i ~ i Final atrial Constant Patient Ordinary P-'P 'P-*P zP-3P 3P-4P frequency p-'p configuration no. P-P, cs (cs) (cs) (cs) (cs) (waveslmin) P-P of lP-"P Sinus rhythm to atrial fibrillation, n = 5 1 186 38 20 2 83 40 17 3 65 43 19 4 110 26 26 5 80 28 19 Sinus rhythm to citrialflutter, n =8 6 126 38 22 7 84 46 30 8 108 54 27 9 80 35 26 10 80 40 28 1 1 81 52 28 12 84 1 9 29 13 216 112 28 Sinus rhythm t o atrial tachycardia, n =2 14 I 0 49 38 15 98 40 39 17 18 17 26 18 20 20 25 26 19 21 26 22 36 40 16 17 16 19 19 20 20 25 26 20 19 27 21 3 1 41 400 390 410 430 360 340 330 230 280 280 330 23 0 270 160 150 0.20 0.48 0.66 0.24 0.35 0.30 0.55 0.50 0.44 0.50 0.64 0.94 0.52 0.70 0.41 + + spontaneous onset and termination of S V T A may have some bearing on this problem. Killip & Gault (6) studied changes from sinus rhythm to AFi in 14 patients. An atrial premature discharge preceded the onset of AFi in all 14 episodes. I n 10 of these t h e premature P wave was immediately followed by AFi. I n the o t h e r 4 cases t h e premature P wave appeared t o initiate a brief run of S V T (less than 6 beats) which accelerated to AFi. T h e relative pre- maturity of ectopic atrial beats was expressed by calculating the coupling index. T h e coupling index was less than 0.50 in 9 of t h e 14 patients. Killip & Gault t h u s concluded that a spontaneously occur- ring atrial premature impulse may initiate AFi. When the coupling index is less than 0.50, the chance of ensuing AFi is high; when it i s greater than 0.60, t h e chance of ensuing AFi is small. Bennett & Pentecost ( 1 ) studied t h e onset of AFi in 8 patients with acute myocardial infarction. One intra-atrial and o n e surface lead were registered. A Table 11. T e r m i n a t i o n of s u p r a v e n t r i c u l a r tachyarrizythmia Termination within Patient Ordinary P4-P3 P3-PZ PZ-PL P '-P p'-p 30 cs from no. P-P, cs (cs) (CS) (cs) (cs) P-P beginning of QRS Atrial fibrillation to sinus rhythm, n =2 5 80 19 20 22 83 1.04 + 16 69 17 16 16 52 0.75 + Atrialgutter to sinus rhythm, n = 6 6 126 18 18 16 27 0.21 - 8 1 08 27 25 25 86 0.80 + 9 80 21 22 20 104 1.30 - 1 1 81 20 20 22 96 1.19 12 84 29 26 27 96 1.14 + 13 216 22 22 22 132 0.61 + Attriaf tachycardia to sinus rhythm, n = 2 1.09 - 14 70 36 37 36 76 15 98 39 40 41 1 02 1.04 - - Vpsala J Med Sci 80 Onset crnd termincition of tcrchycirrliytlimitrs 1 17 total of 32 episodes were studied, and o n each occa- sion the arrhythmia was preceded by a premature atrial beat. T h e premature atrial beat was always followed by a rapid regular atrial tachycardia of variable duration with a rate of approximately 340 beats/min; on some occasions the tachycardia lasted as little as 1 o r 2 s, but at other times the duration was up t o 30 s. Bigger & Goldreyer ( 2 ) studied the repeated onset of paroxysmal S V T in 5 patients. T h e S V T always began with a n atrial premature depolarization (APD). Spontaneous episodes of S V T were in- itiated only by APDs occurring in the relative A-V refractory period, while electrical stimuli during the atrial vulnerable period did not elicit S V T . From these and other findings Bigger & Goldryer con- cluded that paroxysmal S V T is most often d u e to reentry utilizing t h e A-V conduction system. T h e results of the present study in general cor- respond well with t h e results of the earlier reports. T h e first premature atrial wave was shown to b e aberrant in all cases studied and the coupling inter- val was in most cases short. The coupling index, however, was more than 0.60 in 4 of our cases (Fig. 2 shows o n e of these cases). In these cases t h e first premature atrial wave could scarcely have occurred during the vulnerable period of t h e atria o r t h e rela- tive refractory period of the A-V conduction system. In these cases, therefore, the onset of S V T A probably depended o n a rapidly firing ectopic focus rather than o n circus movement. O u r study of t h e termination phase indicates that there is not a successive modification of atrial activ- ity during the last seconds of a SVTA: the S V T A always ended abruptly in o u r cases. Rytand (9) re- ported similarly for 3 cases of A F u , while Bennett & Pentecost ( l ) , in their study of AFi in patients with acute myocardial infarction, found that a change of atrial wave form in the intra-atrial lead preceded t h e cessation of AFi o n all 28 occasions observed. Several explanations f o r the interruption of S V T A have been offered, for example, exit block from a rapidly firing ectopic focus o r interruption of a circus movement with o r without engagement of the atrio-ventricular node. One possible cause of such interruption could b e retrograde depolariza- tion of the atrio-ventricular node. In t h e latter case, the S V T A should b e expected to terminate a t o r shortly after a Q R S complex. This was observed in only 5 of our cases of AFi or A F u , so that this explanation is probably not t h e only one. Our results t h u s indicate that the theory of circus movement does not explain the mode of spontane- ous onset o r termination of S V T A in all cases. Onset and maintenance of S V T A in some cases may perhaps be governed b y different mechanisms, the onset being initiated from an atrial ectopic focus and a circus movement being responsible for the maintenance. The importance of the vulnerable period of the atria could b e that o n e single ectopic and premature atrial impulse occurring during the vulnerable period of t h e atria may initiate a circus movement S V T A , while an ectopic atrial beat with a long coupling interval must be followed by re- peated rapid discharges from the ectopic focus in order for S V T A to ensue. The functional conditions of the atria may then determine which kind of S V T A eventually results. REFERENCES 1. 2. 3. 4. 5 . 6. 7. 8. 9. 10. 11. Bennett, M. & Pentecost, B.: The pattern of onset and spontaneous cessation of atrial fibrillation in man. Circulation4/:981, 1970. Bigger, T. & Goldreyer, B.: The mechanism of supraventricular tachycardia. Circulation 42: 673, I 970. Guiney, T. & Lown, B.: Electrical conversion of atrial flutter to atrial fibrillation. Brit Heart 5 3 4 : 1215, 1972. Hecht, H . , Katz, L., Pick, A . , Prinzmetaf, M. & Rosenblueth, A.: The nature of auricular fibrillation and flutter. A symposium. Circulation 7: 591, 1953. Katz, L. & Pick, A.: Current status of theories of mechanisms of atrial tachycardias, flutter and fibrilla- tion. Progr Cardiov Dis 2: 650, 1960. Killip, T. & Gault, J . : Mode of onset of atrial fibrilla- tion in man. Am Heart J 70: 172, 1965. Nordgren, L.: A new method to study atrial activi- ty-intended for clinical use. Acta SOC Med Upsal 74: 186, 1969. Rytand, D.: The circus movement (entrapped circuit wave) hypothesis and atrial flutter. Ann Int Med 65: 125, 1966. Rytand, D.: Electrocardiographic patterns at the termination ofatrjal flutter. Am Heart 574: 741, 1967. Semerau, M . : Uber Riickbildung der Arrhythmia Perpetua. Arch Klin Med 126: 161, 1918. Scherf, D., SchafTer, A . I . & Blumenfeld, S . : Mechanism of flutter and fibrillation. Arch Intern Med 91: 333, 1953. Received November 28, 1974 Address for reprints: Bengt Furberg, M.D. Department of Clinical Physiology Central Hospital S-800 07 Gavle Sweden Upsola J Med Sci 80