Atrial Ectopic Activity Associatedwith Sinus Bradycardia

By BRIJ G. GOEL, M.D., AND JAOK HAN, M.D., PH.D.

SUMMARYFive cases of atrial ectopic activity associated with sinus bradyeardia are reported.

The ectopic activity was abolished in all cases when the sinus rate was increasedspontaneously or by atropine. The report demonstrated that the incidence of ectopicactivity increases in the atrium at the slower basic rates as it does in the ventricle. Itwas emphasized that atrial ectopic activity associated with sinus bradycardia should betreated by atropine or by rapid pacing of the atrium because atrial premature beats havethe potential of inducing more serious atrial tachyarrhythmias. The possible role of thevagus nerves in facilitating the induction of atrial tachyarrhythmias was discussed, andit was suggested that atropine may have an added benefit of reducing the likelihood ofdevelopment of atrial tachyarrhythmias.

Additional Indexing Words:Atrial tachyarrhythmias Increased vagal a

I T HAS been well established that ectopicbeats occur in the ventricle more

frequently when the basic rate is relativelyslow and that these ectopic beats disappearwhen the basic rate is increased by artificialpacing or by administration of atropine.'-6The efficacy of increased heart rate insupressing ventricular ectopic beats has beenparticularly apparent in patients with acutemyocardial infarction.A6 Han and associates2suggested that the increased incidence ofectopic activity at slow ventricular rates mightbe due to re-entrant activity resulting from anincrease in the asynchrony of repolarizationamong different myocardial fibers. They

From the Department of Medicine (Cardiology),Albany Medical College of Union University and theElectrocardiography Laboratory, Albany MedicalCenter Hospital, Albany, New York.The study was supported by a grant from the Heart

Association of Eastern New York and Grant HE-12498 from the National Institutes of Health,Bethesda, Maryland.

Address for reprints: Jaok Han, M.D., Departmentof Medicine, Albany Medical College, Albany, NewYork 12208.

Received May 25, 1970; revision accepted forpublication July 6, 1970.

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Atropine Pacing of atrium

demonstrated a greater range of refractoryperiods at various points on the ventricularsurface when the basic rate was slow. In thesame study, the range of refractory periodswas also increased in the atrial tissue at slowbasic frequencies. It follows, then, that ectopicactivity should be more frequent in the atriumwhen the basic rate is relatively slow. Thepresent paper describes clinical cases ofincreased atrial ectopic activity associatedwith sinus bradycardia.

Report of Cases

Case 1H. C., a 75-year-old female, developed

weakness, dizziness, nausea, and vomiting 30 minafter receiving meperidine (Demerol), 50 mg,and promethazine (Phenergan), 25 mg, intra-muscularly as preoperative medications forcataract surgery. She had heart disease ofunknown etiology for 15 years, and she wasstarted on digitalis about a year ago for mild heartfailure. Physical examination revealed an irregularpulse of 56/min and blood pressure of 70/10 mmHg. The patient was lethargic but oriented. Therewas cardiomegaly with a left parasternal heaveand a palpable systolic thrill in the fourthintercostal space. A grade III/VI pansystolicmurmur was audible in the same area and at theapex. There were also bilateral basal rales. The

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Case 1. (A) Sinus bradycardiaz and arrhythmia at 50/mm7 wDith freqZuent nlonconducted atrial

premature beats. (B) Less freqBuent atrial premature beats alt a sinus rate of 85/mmn soon after

receiving atropine. (C) No ectopic activity inwute to 105/mim1.

chest x-rays revealed an increase in the cardiacsilhouette with a slight increase in pulmonaryvascular markings. The ECG was consistent withsinus bradyeardia of 50/min with nonphasic sinusarrhythmia, nonconducted premature atrial beatsoccurring at approximately 10/min, and completeright bundle-branch block (fig. IA). Her centralvenous pressure at this time was 17 cm H20.

Because of bradycardia, hypotension, andcongestive failure, the patient was given atropine1 mg intravenously in two divided doses, whichbrought a dramatic increase in the sinus rate to105/mim (fig. lB and C). With the increasedsinus rate, premature atrial beats were completelyabolished, BP rose to 120/70 mm Hg, centralvenous pressure fell to 11 cm H20, and the lungscleared in a short time.

Case 20. B., a 73-year-old male, was first found to

have sinus bradycardia with occasional atrialpremature beats about 20 years ago during a

preoperative ECG for hemiorrhaphy. He ad-mitted to having had some symptoms ofcongestive failure for some years, for which hehas taken digitalis and a diuretic. He was

admitted this time for increasing dyspnea andfrequent anginal attacks. Physical examinationshowed an irregular pulse at 40/min and BP of150/90 mm Hg. There was cardiomegaly up tothe anterior axillary line with a grade II/VIT

the atrium with a further increase in the sinus

systolic ejection murmur, and the third heartsound gallop was audible at the apex. The ECG(fig. 2) revealed a sinus rate of about 40/min, asinus arrhythmia, frequent conducted andnonconducted atrial premature beats occurring inbigeminy, and left bundle-branch block (fig. 2A).After administration of 0.5 mg of atropineintravenously, the sinus rate increased to 80/min,and the ectopic activity disappeared completely(fig. 2C). Since chroinic atropine administrationwas not feasible in this patient, a demandventricular pacemaker was implanted. As shownin figure 2D, the ventricle was depolarized at arate of 75/min by spontaneous sinus beats and thepacemaker stimuli alternately. Significant im-provement of his general condition resulted.

Case 3E. B., a 83-year-old female, was brought to the

emergency room because of sudden onset ofweakness, dyspnea, dizziness, nausea, and re-current vomiting. She denied chest pain or pasthistory of any heart disease, diabetes, andhypertension. On physical examination, BP was90/50 mm Hg, pulse rate was 47/min, andrespiration, 26/min. The patient was oriented andshowed no sign of congestive failure. The ECGshowed sinus bradyeardia at a rate of 50/min withfrequent premature atrial beats and changes ofacute inferior myocardial infarction. Runs of atrialtachycardia were occasionally initiated by atrial

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ATRIAL ECTOPIC ACTIVITY AND BRADYCARDIA

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Figure 2

Case 2. (A) Very frequent conducted and nonconducted premature atrial beats occurring inbigeminy during sinus bradycardia of 40/min. (B) Decreased atrial ectopic activity with anincrease in the sinius rate to 65/min after atropine. (C) Complete disappearance of prematureatrial beats at a sinus rate of 80/min. (D) Functioning QRS-triggered demand pacemaker setat a rate of 75/min.

premature beats (fig. 3A). The patient was givenatropine, 1 mg intraveniously, the sinus rateincreased to 105/min, and premature beatsdisappeared completely (fig. 3B).Cases 4 and 5

J. S., a 79-year-old female, was known to havediabetes and hypeitension, and had been takingdigitalis and chlorothiazide for several years. Shewas admitted this time for fibrosarcoma of leftshoulder. The significant physical findingsincluded a grade II/VI systolic ejection murmurover the precordium and BP of 170/100 mm Hg.The ECG showed sinus bradycardia of 40/minwith frequent premature atrial beats (fig. 4A)and left ventricular enlargement. When the sinusrate was subsequently increased to 70/min,premature atrial activity was not present(fig. 4B).H. F., a 63-year-old male, was admitted for

observation because of anginal pain and dyspnea.The ECG showed no significant changes exceptfor mild sinus arrhythmia. As shown in theCirculation, Volume XLII, November 1970

bottom tracing of figure 4, premature atrial beatsappeared during the phase of slower rhythm atabout 65/mim and disappeared when the sinusrate increased to 70/min.

A

Figure 3

Case 3. Lead V,. (A) Sinus bradycardia at S0/minwith a run of atrial tachycardia. (B) No atrial ectopicactivity during sinus tachycardia of 105/min after ad-ministration of atropine.

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Figure 4

Case 4. (A) Atrial ectopic activity during sinus bradycardia at 40/min. (B) Disappearance ofpremature atrial beats with a spontaneous increase in the sinus rate to 70/min. Case 5 (thebottom tracing). Sinus arrhythmia with atrial ectopic activity during the slow phase.

Discussion

The cases described clearly demonstratethat ectopic activity is increased in the atriumwhen the basic heart rate is slowed just as it isin the ventricle. One of the possiblemechanisms of ectopic impulse formation isfocal re-excitation of already repolarized fibersby the flow of current between theseand neighboring fibers which are stilldepolarized.2 3 When neighboring fibersrepolarize within a few milliseconds of each

other, re-excitation cannot occur, for thedifference in potential between them will notexceed the threshold of already repolarizedfibers, but increased temporal dispersion ofrepolarization would increase the potentialdifference and initiate re-excitation. Han andassociates2 demonstrated that the range ofrefractory periods at various points in theventricular or atrial tissue is increased whenthe basic heart is relatively slow. Accordingly,closely coupled ectopic beats would be more

likely to develop at slow basic frequencies.Sinus bradycardia in some of our cases may be

due to moderate vagal stimulation. Vagalstimulation shortens refractory periods nonuni-formly at various points in the atrium andhence increases the range of refractoryperiods.7 This may further increase theasynchrony of recovery of excitability in theatrium. It is, therefore, suggested that theadministration of atropine would be morebeneficial than the use of artificial pacingwhen they are used to increase the sinus rate.In all of our patients who received atropine,the sinus rate increased significantly, resultingin the disappearance of atrial ectopicactivity.

Atrial ectopic beats are of great significancein patients with acute myocardial infarctionbecause of their potential of initiating atrialtachyarrhythmias and seriously compromisingcardiac output. Supraventricular tachycardia,either atrial or A-V junctional in origin, hasbeen known to be initiated by atrialpremature beats.8"1- The tachycardia mayresult from sustained reciprocation of impulsesbetween the atrium and the nodal tissue (the

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ATRIAL ECTOPIC ACTIVITY AND BRADYCARDIA

sinus or A-V node).8,9,11-13 A prematureimpulse may enter the node slowly andemerge to the surrounding atrial tissue as a re-entrant beat (an echo), and such re-entrantactivity may be sustained to underlie anepisode of tachycardia. The possible increasedvagal activity in some patients with sinusbradycardia may facilitate the induction ofsuch re-entry by slowing conduction in thenodal tissue and by shortening refractoryperiod in the atrium." Atrial flutter may bedue to a circus movement around an obstacle(most probably one of the caval openings) inthe atrium, which can be initiated by apremature atrial response.'4 15 If the prema-ture beat is early enough, it may propagate inonly one direction but be blocked in theopposite direction (unidirectional block)around an obstacle to initiate the circusmovement. Such unidirectional block wouldbe more likely to occur when the asynchronyof recovery of excitation is increased as aresult of nonuniform -vagal effects on theatrial refractory periods.7 Degeneration of atrialflutter into fibrillation would be facilitatedin patients whose sinus bradycardia wasrelated to an increase in vagal activity, since itis believed to set the stage for formation ofirregular independent wavelets of excitationby increasing the nonuniformity of excitabili-ty in the atrial tissue.'6' 17The treatment of sinus bradycardia in

patients with acute myocardial infarctionshould be of great value, for this may not onlyreduce the likelihood of development of atrialpremature beats and the resulting tachyar-rhythmias but may also improve cardiacoutput and symptoms of congestive failure.This can be achieved by rapid atrial pacing oradministration of atropine or catecholamines,but atropine may have an added beneficialeffect in reducing the chance of initiation oftachyarrhythmias when patients are suspectedto have increased vagal activity as a cause ofsinus bradyeardia, as in cases of inferiormyocardial infarction. One of our patients(case 1) had symptoms of low cardiac outputwhich improved rapidly with the accelerationof sinus rate by atropine. Another patientCirculation, Volume XLII, November 1970

(case 3) had episodes of potentially seriousatrial tachycardia during sinus bradycardiawhich completely disappeared when the sinusrate was increased by atropine. In case 5, thesinus rate was critical; an increase in the sinusrate of only 5/min abolished atrial ectopicactivity.

References1. LANGENDORF R, PicK A, WINTERNITZ M:

Mechanisms of intermittent ventricular big-eminy: I. Appearance of ectopic beatsdependent upon length of the ventricular cycle,the "rule of bigeminy." Circulation 11: 422,1955

2. HAN J, MILLET D, CMZZONITTI B, ET AL:Temporal dispersion of recovery of excitabilityin the atrium and ventricle as a function ofheart rate. Amer Heart J 71: 481, 1966

3. HAN J, DETRAGUA J, MILLET D, ET AL:Incidence of ectopic beats as a function ofbasic rate in the ventricle. Amer Heart J 72:632, 1966

4. LowN B, VASSAUX C, HOOD WB, ET AL:Unresolved problems in coronary care. Amer JCardiol 20: 494, 1967

5. HAN J: Mechanisms of ventricular arrhythmiasassociated with myocardial infarction. Amer JCardiol 24: 800, 1969

6. ZIPEs DP: The clinical significance of bradycar-dic rhythms in acute myocardial infarction.Amer J Cardiol 24: 814, 1969

7. ALESSI R, NUSYNOWrTZ M, ABILDSKOV JA, ETAL: Non-uniform distribution of vagal effectson the atrial refractory period. Amer J Physiol194: 406, 1958

8. MOE GK, MENDEZ C, .HAN J: Some features ofdual A-V conduction system. In Mechanismsand Therapy of Cardiac Arrhythmias, editedby LS Dreifus and W Likoff. New York, Grune& Stratton, Inc., 1966, p 361

9. WALLACE AG, DAGGErT WM: Re-excitation ofthe atrium: The echo phenomenon. AmerHeart J 68: 661, 1964

10. BAROLD SS, LINHART JW, SAMET P, ET AL:Supraventricular tachyeardia initiated andterminated by a single electrical stimulus. Amerj Cardiol 24: 37, 1969

11. HAN J: The mechanism of paroxysmal atrialtachycardia. Amer J Cardiol. In press

12. MENDEZ C, MOE GK: Demonstration of a dualA-V nodal conduction system in the isolatedrabbit heart. Circulation Research 19: 378,1966

13. HAN J, MALozzI AM, MOE GK: Sino-atrialreciprocation in the isolated rabbit heart.Circulation Research 22: 355, 1968

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14. LEWVIS T, FEIL HS, STROUD WD: Observationsupon flutter and fibrillation: Part IL. Thenature of auricular flutter. Heart 7: 191,1920

15. ROSENBLUTH A, GARCIA-RAMOS J: Studies onflutter and fibrillation: LI. The influence ofartificial obstacles on experimental auricular

flutter. Amer Heart J 33: 677, 194716. MOE GK, ABILDSKOV JA: Atrial fibrillation as a

self-sustained arrhythmia independent of focaldischarge. Amer Heart J 58: 59, 1959

17. MoE GK: On the multiple wavelet hypothesis ofatrial fibrillation. Arch Internat Pharmacodyn140: 183, 1962

Early Report of Atrial FlutterRecorded Waves from Cervical Veins and Cardiac Apex

Case I. The jugulo-carotid and apical tracings present a series of rhythmic, positivewaves, the rate of which is about 255 per minute. The ventricles contract rhythmically32.2 times per minute.-From: JOLLY WA, RITCHIE WT: Auricular flutter and fibrillation.Heart 2: 177, 1911.

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BRIJ G. GOEL and JAOK HANAtrial Ectopic Activity Associated with Sinus Bradycardia

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1970 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.42.5.853

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