Multiple atrial arrhythmias in intra-atrial and inter-atrial block

J. ELECTROCARDIOLOGY, 5 (3) 281-288, 1972

Case Reports Multiple Atrial Arrhythmias in Intra-Atrial and Inter-Atrial Block BY MOHAMED K.A. DAYEM, M.R.C.P., M.R.C.P.E., PH.D., NESET AYTAN, M.D., AND BEATRICE J. ARGANO, M.D.

vomiting, but subsequently the attacks ceased to respond. She had b e e n p r e v i o u s l y hospitalized several times for the same condition, and had been followed in the Cardiac Clinic since 1958 while being treated with digitalis preparations.

SUMMARY T h e c a s e o f an e l d e r l y p a t i e n t w i t h repeated e p i s o d e s o f atrial fibrillation, atrial flutter, and supraventricular tachycardia With spontaneous reversion to sinus r h y t h m is p r e s e n t e d . D u r i n g a p e r i o d

of sinus rhythm, atrial flutter involving only a small p a r t of the a t r i a l walls (atrial dissociation) also a p p e a r e d . Some electrophysiologic c o n s i d e r a t i o n s as to the underlying m e c h a n i s m and etiology of these a r r h y t h m i a s are presented.

Physical examination. Elderly, obese woman in no distress. Pulse 130/min, blood pressure 130/82. The jugular veins were slightly distended and there was +1 ankle edema; multiple varicosities were noted in the legs. The apex b e a t was not palpable. A u s c u l t a t i o n revealed normal first and second heart sounds, a fourth sound at the apex, and no murmurs. The chest and abdomen showed no abnormal findings. Blood glucose was 120 mg %. Serum enzymes and all other laboratory tests were within normal limits. The chest x-ray was i n t e r p r e t e d as s h o w i n g left v e n t r i c u l a r enlargement.

Evidence has accumulated 1-4demonstrating that the spread of the excitation wave from the sino-atrial node follows the anatomic pathw a y s f o r m e d by c o n d u c t i n g b u n d l e s , as d e s c r i b e d by T h o r e l 5, W e n c k e b a c h e, and BachmanL The anterior, middle, and posterior internodal tracts carry impulses from the S-A node to the A-V node while the inter-atrial tract of Bachman carries the impulses from the right to the left atrium. These specialized conduction pathways in the atrial walls are as vulnerable to disease as those existing in the ventricles. The syndromes resulting from various inter-atrial and intra-atrial conduct i o n d e f e c t s a r e j u s t b e g i n n i n g to be appreciated. The purpose of the present report is to describe a case of gradually developing intra-atrial block with multiple complicating arrhythmias including atrial dissociation.

Electrocardiogram. Careful analysis of serial

CASE REPORT A 72-year-old female was admitted to the Hospital following an episode of palpitation and dyspnea. She gave a history of recurrent attacks of rapid heart rate increasing both in frequency and duration for about 25 years. At first she could terminate the attacks by performing certain maneuvers, like induction of

From the Division of Cardiology, The Mount Sinai Hospital Medical Center and The Chicago Medical School, University of Health Sciences. 281

electrocardiograms recorded since 1958 was made (Table 1 summarizes the sequence of observed arrhythmias). The QRS configuration remained the same in all tracings indicating incomplet e right bundle branch block and a frontal axis of 0 to +20 ~ The ST segment and T waves were normal except for T wave i n v e r s i o n o v e r t h e left p r e c o r d i a l leads, recorded in two consecutive tracings in 1961. The sinus rate was initially normal but sinus bradycardia and arrhythmia gradually developed. The heart rate varied between 45 and 55/rain since 1962. A tracing recorded in 1961 (Fig. 1) showed broadened (0.21 sec) and slightly notched P waves. The Paxis was +35 ~ in the frontal plane and +25 ~ in the horizontal plane. The direction of vectors of the initial and terminal parts of the P wave was the same. Subsequent tracings showed variations in the shape and duration of the P waves, which frequently became normal, with disappearance of the notching and broadening. On 12/17162, r e c u r r e n t a t t a c k s of s u p r a v e n t r i c u l a r tachycardia with a rate of 160/rain were first

282

DAYEM ET AL

Table 1 Sequence of Observed Arrhythmias Date

Duration (Days)

12/17/62

?

6/26/69

--

1/11/71

Digoxin mg. Junctional tachycardia --

Normal sinus r h y t h m with Grade 1 A-V block

2

.25

Atrial flutter with 2:1 block

1/13/71

1

.25

Inter-atrial block with partial atrial flutter in presence of sinus bradycardia

1/14/71

< 1

.25

Atrial fibrillation

1/18/71

2

.25

Atrial fibrillation

1/22/71

2

.125

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1/28/71

2

.125

Atrial fibrillation

1/31/71

< 1

.125

Junctional tachycardia

2/4/71

< 1

.25

Sinus arrhythmia, sinus arrest with junctional escapes

2/8/71

< 1

None

Junctional tachycardia

2/10/71

< 1

None

Atrial fibrillation

2/11/71

1

None

Inter-atrial block with partial atrial flutter in the presence of sinus bradycardia

2/12/71

2

None

Atrial fibrillation

2/21/71

< 1

None

Junctional r h y t h m

2/25/71

2

None

Atrial fibrillation

2/27/71

1

None

Junctional tachycardia Sinus bradycardia with Grade I A-V block

3/1/71

1

None

Atrial fibrillation

3/4/71

2

None

Atrial fibrillation

3/6/71

1

None

Junctional tachycardia

3/7/71

--

None

Atrial fibrillation

The rhythm at all other times from the last admission (1/11/71) up to discharge (3/8/71) was sinus bradycardia with Grade I A-V block and occasional atrial ectopic beats. documented (Fig. 2). The P-R interval between attacks varied but was always prolonged (0.22 0.24 sec). A routine tracing of 6/26/69 showed normal P waves (Fig. 3). On the present hospitalization, in January, 1971, the QRS configuration was unchanged, t h e ST s e g m e n t and T waves were normal (Fig. 4). The P waves became markedly broadened (0.24 sec). The initial part of P was a positive deflection in -

all leads except AVR. The terminal portion of P was negative in leads II, HI, and V1 V4. It was isoelectric or positive in leads I, AVL, AVF, Vs and Ve. T h e P-R interval was 0.24 sec. T h e r e were frequent atrial, and occasional ventricular ectopic beats. During her h o s p i t a l s t a y , t h e p a t i e n t d e v e l o p e d 11 episodes of atrial fibrillation, 3 episodes of atrial flutter, and 5 episodes of supravenJ. ELECTROCARDIOLOGY, VOL 5, NO. 3, 1972

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tricular tachycardia. The P-R interval remained prolonged, and varied between 0.24 and 0.32 sec. Sinus b r a d y c a r d i a w i t h r a t e s between 44 and 60 also occurred. In an attempt to o v e r d r i v e the a t r i u m and t h u s suppress ectopic discharge, the patient was first given large doses of atropine, and subsequently isoproterenol by intravenous infusion at a r a t e of 1-2 gm/min. I. T h e r e was minimal response the infusions with only a slight increase of J. ELECTROCARDIOLOGY, VOL. 5, NO. 3, 1972

t h e r a t e to 72/rain. T h e frequency of a t r i a l arrhythmias was unaffected. Fig. 5 is a series of V1 strips recorded in double voltage documenting the complexity of this patient's arrhythmias. Strip A shows the extreme variations in rate with a basic sinus mechanism. Strip B shows varying degrees of A V dissociation. Strip C shows temporary conversion to sinus rhythm during an episode of supraventricular tachycardia.

284

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in t h e Clinic. She still shows episodes of The sawtooth pattern of the baseline in both strips A and D suggests the possibility of coex- a r r h y t h m i a , s i m i l a r to t h o s e p r e v i o u s l y described. i s t i n g a b n o r m a l a t r i a l a c t i v i t y and sinus r h y t h m . Such a possibility was c o n f i r m e d w h e n an episode of atrial dissociation was DISCUSSION detected (Fig. 6, bottom strip) 2 days after an The tracings of this patient showed broad episode of atrial flutter with 2:1 block (Fig. bifid P waves since 1961. A diagnosis of left 6, top strip). During the entire recording, the basic atrial enlargement, secondary to left ventricular failure, was made at first. However, rhythm w a s regular sinus rhythm. Immediately after the 5th P wave (Fig. 6, bot- t h e w i d e n i n g and notching of t h e P w a v e s tom strip)regular flutterwaves with sawtooth varied from day to day and occasionally disappeared. Moreover, widening of the P waves pattern at a rate of 310-320/rain appeared, increased at times, in spite of improvement superimposed on the basic rhythm. Although of left ventricular function, as judged by cliniitis generally feltthat this type of arrhythmia is mostly observed in critically ill patients a cal and radiologic criteria. O n her second admission, further widening few hours before death 9, our patient was discharged from the hospital and is being followed of P waves was observed. The initial vector J. ELECTROCARDIOLOG'Y.VOL. 5, NO. 3, 1972

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VOL

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ARRHYTHMIAS IN ATRIAL BLOCK

287

r h y t h m r e t u r n e d spontaneously each time. of P was directed inferiorly, anteriorly, and to the left, and was the same as her original She had 3 episodes of a t r i a l f l u t t e r and 5 P vector. The terminal vector was directed episodes of supraventricular tachycardia during the same period. Again the heart reverted superiorly, posteriorly, and to the left. This spontaneously to sinus rhythm. There was no suggested late activation of the left atrium, precipitating cause for any of these attacks. probably secondary to a lesion of the bundle For the past 25 years the patient had experiof Bachmann. Similar findings were described enced recurrent attacks of paroxysmal supby Eiselberg et al s in a case which presented, at autopsy, localized fibrosis of the bundle of raventricular tachycardia. The attacks gradually i n c r e a s e d in f r e q u e n c y and duration. Bachmann and severe coronary arterioTheir progression to recurrent atrial flutter sclerosis. and atrial fibrillation lends support to the One episode of atrial dissociation was noted u n i t a r i a n t h e o r y of a t r i a l a r r h y t h m i a s of in the tracings of the present case with an Prinzmetal et a117. ectopic rhythm (atrial flutter). As the sinus The cause of the inter-atrial block, of the node was still responsible for the activation recurrent arrhythmias, and of the prolongaof the ventricles and most of the atrial walls, the a u t h o r s believe t h a t t h e ectopic focus tion of the PR interval can only be speculated upon. Deviation of the P-Q segment which, depolarized only a small part of the atrial wall according to Liu et aP s, is the major criterion causing a very rapid discharge of impulses. This focus should be.considered as caused by for diagnosis of atrial infarction, could not be demonstrated. Owing to the slow progressive disease of the atrial wall rather than of the nature of the condition, it may be related to bundle of Bachmann. This view is based on m i c r o a n g i o p a t h y and c o r o n a r y s c l e r o s i s t h e fact t h a t t h e s h a p e of t h e P w a v e s secondary to diabetes mellitus. Atrial dissociar e m a i n e d t h e same, and t h e i r a m p l i t u d e d e c r e a s e d only slightly a f t e r the onset of tion due to coronary sclerosis was described by Scherf and Cohen TM and Eiselberg et al s dissociation. Atrial dissociation with the ectopic focus in several cases, and this case may well fall into this category. The persistance of the varydepolarizing only small part of the atrial wall was described in animals by Lewis l~ Tait 1~, ing arrhythmias, even 33 days after digitalis was withheld, suggests that the drug probably and Sharma 12, and in humans by Cohen and did not play a major role in the genesis of the Scherf ~3,~4. It is conceivable that a small area of atrial musculature may be effectively con- observed arrhythmias. trolled by an ectopic pacemaker and physiologically separated from the rest of the atrial wall REFERENCES by the simultaneous presence of an entrance 1. James, T.N.: The connecting pathways between and exit block xs. The entrance block can be the sinus node and AV node and between the right and the left atrium in the human heart. explained by physiologic refractory state, due Am. Heart J. 66: 498, 1963. to the high rate of ectopic discharge, and the 2.Sherf, L., and James, T.N.: A new electrocardioexit block must have its origin in myocardial graphic concept -- Synchronized sinoventricular disease. Anatomic localization of the site of conduction. Dis. Chest 55: 127, 1969. the ectopic focus is impossible because the P 3. Marriott, H.J.L.: Ways and means of conduction. vector, as calculated from scalar leads, has (Editorial) Chest 55: 93, 1969. been shown to be an unreliable guide le. 4. Bellet, S., and Jedlicka, J.: Sinoventricular conduction and its relation to sinoatrial conduction. In addition there was evidence of disease Am. J. Cardiol. 24: 831, 1969. of the sinus node itself, as revealed by persis5.Thorel, C.: Uber den Aufbau den inus Kotens, tent sinus bradycardia and repetitive short seine Verbindung mit der Cava Superior und periods of sinus arrest. Large doses of atropine, den Wenckebachen Bundeln. Mfinch. Med. sufficient to inhibit vagal impulses, did not Wschr. 57: 183, 1910. increase the heart rate, indicating that the 6. Wenckebach, K.F.: Beitrage zur Kenntnis des menschlichen Herztiitigkeit. Arch. Anat. bradycardia was due to disease of the SA node Physiol. 1-2: 1, 1907. and not to vagal stimulation. Intravenous iso7. Bachmann, G.: The inter-auricular time interproterenol infusion also resulted in modest val. Am. J. Physiol. 41: 309, 1916. increase of the sinus rate. 8. Eiselberg, K., Zischka-Konorsa, W., and Busch, The patient had 11 episodes of atrial fibrillaW.: Eine inter-atriale Reizleitungstorung and tion during her last hospitalization lasting ihr pathologisch-anatomisches Substrat. Ztschr. from a few hours to t h r e e days, and sinus Kreislaufforseh. 53: 89, 1964. J ELECTROCARDIOLOGY, VOL. 5, NO. 3. 1972

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9. Chung, E.K.: A reappraisal of atrial dissociation. Am. J. Cardiol. 28: 111, 1971. 10. Lewis, T.: The Mechanism and Graphic Registration of the Heart Beat. Shaw & Sons, London, 1925. 11. Tait, J.: The action of yohimbine on the heart with special reference to toxic h e a r t block. Quart. J. Exp. Physiol. 3: 185, 1910. 12. Sharma, P.L.: Effects of adrenaline and noradr e n a l i n e on a t r i a l f i b r i l l a t i o n produced by acetylcholine: With observations on the mechanism of fibrillation. Quart. J. Exp. Physiol. 49: 134, 1964. 13. Cohen, J., and Scherf, D.: Complete inter-atrial and intra-atrial block (atrial dissociation). Am. Heart J. 70: 23, 1965.

14. Scherf, D., and Cohen, J.: The atrioventricular Node and Selected Cardiac Arrhythmias. Grune & Stratton, New York, 1964. 15. Deitz, G.W., HI, Marriott, H.J.L., Fletcher, E., and Bellet, S.: Atrial dissociation and unilateral atrial fibrillation. Circulation 15: 883, 1957. 16. Frankl, W.S. and Soloff, L.A.: Left atrial rhythm analysis by intra-atrial electrocardiogram and vectorcardiogram. Am. J. Cardiol. 22: 645, 1968. 17. Prinzmetal, M., Corday, E., Brill, C., Oblath, R.W. a n d K r u g e r , H : E . : T h e A u r i c u l a r Arrhythmias. C.C. Thomas Co., Springfield, Ill., 1952. 18. Liu, C.K., Greenspan, G. and Piccirillo, R.T.: Atrial infarction of the heart. Circulation 23: 331, 1961.

J. ELECTROCARDIOLOGY.VOL 5, NO. 3, 1972