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CHEST, VOL. 63, NO. 6, JUNE, 1973 995

CRITICAL REVIEWRapid Atrial Stimulationin the Treatment ofSupraventricularTachycardiaJohn W. Lister, M.D., F.C.C.P.;#{176}Arthur I. Gosselin, M.D., F.C.C.P.;**David A. Nathan, M.D., F.C.C.P.;* and S. Serge Barold, M.R.A.C.P.f

Rapid atrial stimulation (RAS) has been found to be therapeutically useful in thetreatment of selected cases of supraventricular tachycardias (SVT). RAS may(1) immediately revert the SVT to normal sinus rhythm, (2) transiently convertthe rhythm to atrial fibrillation which after a variable period usually convertsspontaneously to normal sinus rhythm, (3) permanent conversion of the rhythmto atrial fibrillation with the immediate slowing of the ventricular rate, or (4)in cases in which the tachycardia cannot be terminated and atrial fibrillationcannot be initiated, the ventricular rate may be slowed by increasing the atrialrate until second degree heart block occurs. To date, there have been remarkablyfew deleterious side effects with RAS. Previous digitalis administration is not acontraindication to the procedure. Although RAS has been successfully used toterminate SVTs in the WPW syndrome, under most circumstances the procedureis contraindicated in patients with anomalous atriovenfricular connections.

During recent years, various modes of atrial pac-ing have been used to terminate or prevent

supraventricular tachyarrhythmias. Among these,rapid atrial stimulation (RAS) has been used suc-cessfully to terminate all types of tachycardia,2except atrial fibrillation in which it is ineffectual.The purpose of this communication is to clarify thepresent clinical indications for this procedure.

RAS comprises the application of pacemakerimpulses to the atria at a rate faster (usually from150 to over 600/mm) than the tachycardia beingtreated. Atrial capture need not necessarily occurwith each stimulus to produce the desired effect;indeed, the refractory period of the atrium limitsthe maximal rate of atrial capture to about 350-450/ mm.

#{176}Attendingphysician, Department of Medicine, MiamiHeart Institute, MiamniBeach, Fla.

*#{176}Director,Cardiopulmonary Laboratory, Miami Heart Insti-tute, Miami Beach, Fla.

Chief of Cardiology, The Genesee Hospital, and AssistantProfessor of Medicine, University of Rochester School ofMedicine and Dentistry, Rochester, N.Y.

Reprint requests: Dr. Lirter, Miami Heart Institute, 4701Meridian Avenue, Miami Beach 33140

Under fluoroscopy, a bipolar electrode catheter ispositioned in the high right atrium. The initialpacing rate should be slow while using the maximaloutput of the pacemaker to detect the absence ofinadvertent ventricular pacing.422 During RAS,atrial capture may be inferred when the ventricularrate is decreased or the rhythm is altered. If initiallyunsuccessful, RAS should then be tried from severalother atrial sites, because the physiologic effect ofpacing may vary according to the area stimu-lated,23 and, in some cases, may be of criticalimportance for cardioversion. Like others,9 wehave observed that ineffectual RAS may sometimesbecome successful when combined with carotidsinus pressure, presumably because the lattershortens the refractory period of the atrium.2422Although the literature suggests that the use ofrather complicated stimulators is necessary for thisprocedure, an ordinary external fixed rate pulsegenerator can be modified easily by the manufac-turers to increase its maximal rate. Alternatively,several external pacemakers may be connected inseries.26

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FIGuRE 1. Intracardiac electrograms clearly depict mechanism by which atrial fibrillation usuallyterminates, Ic, by variable period of sinoatrial standstill. This record was obtained three minutesafter discontinuation of rapid atrial stimulation and rhythm had been converted from atrialtachycardia to atrial fibrillation. SAN = sinoatrial node; HRA = high right atrium; LRA = lowright atrium; A-A = conduction time from HRA - LRA; A-H = conduction time from LRAto BH (A-V nodal conduction time); BH = His bundle; H-V = conduction time from BH toseptal myocardium of ventricles; V = ventricles; I = ECG lead I; II = ECG lead II.

996 LISTER ET AL

CHEST, VOL. 63, NO. 6, JUNE, 1973

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RAS may cause: (1) immediate termination ofsupraventricular tachycardia by interrupting a re-entry circus movement due to atrial paced beats oroverdrive suppression of an ectopic pacemakerfocus; (2) transient conversion of the rhythm toatrial fibrillation, which after a variable time (up to48 hours) usually converts spontaneously to normalsinus rhythm because in essentially normal atria,atrial fibrillation is a self-limiting dysrhythmia (Fig1); (3) permanent conversion of the rhythm toatrial fibrillation with immediate slowing of theventricular rate; in cases of long standing heart dis-ease associated with dilatation of the atria sinusrhythm may no longer be sustained; and (4) incases in which the tachycardia cannot be terminatedand atrial fibrillation cannot be initiated, the ven-tricular rate may be slowed by increasing the atrialrate by pacing until second degree heart blockoccurs.

In the usual clinical setting the preferred treat-ment of supraventricular tachycardia includes thestandard pharmacologic agents and/or DC cardio-version. Current indications for using RAS are: (1)cases with possible digitalis intoxication accom-panied by clinical deterioration;236 (2) patientswith recurrent supraventricular tachycardia inwhom the tachyarrhythmias occur at relativelyshort intervals and in whom there is also associatedclinical deterioration;23 (3) after open heart sur-

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gery; (4) during cardiac catheterization;2 and (5)for the treatment of chronically recurring drug-resistant supraventricular tachycardias.4Supraventricular Tachycardia with Suspected Dig-italis Toxicity

In this instance, there is a relative contraindica-tion for cardioversion because of the danger ofinducing ventricular tachycardia or fibrillation.273#{176}RAS is used after treatment with appropriatepharmacologic agents (other than digitalis) hasbeen unsuccessful, the clinical situation is deterio-rating, and it is urgent that the tachycardia beterminated or the ventricular rate slowed. Thus far,there have been no complications reported withRAS in patients who may have been receivingexcessive doses of digitalis.Episodes of Supraventrwular Tachycardia Recur-ring at Short Intervals

These patients have usually had a recent myocar-dial infarction and the customary recurrent tachyar-rhythmia is atrial flutter or tachycardia. HAS isindicated under such circumstances, provided thetachyarrhythmia is accompanied by significant clin-ical deterioration and the episodes cannot be sup-pressed by pharmacologic agents. In these cases,HAS is preferable to DC countershock, because itrequires no anesthesia and causes no discomfort to


TREATMENTOF SUPRAVENTRICULARTACHYCARDIA 997


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FIGURE 2. Conversion of atrial flutter to normal sinus rhythm by RAS. Records obtained frompatient in whom 14 episodes of atrial flutter were converted by RAS (see text). (A) and (B)lead II ECG. (C) atrial unipolar intracardiac electrogram (AUE). A = atrial flutter withaberrant ventricular activation and/or ventricular beats; B = RAS (500 pacemaker inpulses/mm) terminates atrial flutter. On discontinuation of RAS there is A-V dissociation. Apparentvariability of configuration of QRS complexes is due to superimposition of P-waves. C = AUErecorded several minutes after (B) reveals that rhythm has stabilized in normal sinus.

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the patient.233 Recently we terminated 14 epi-sodes of supraventricular tachycardia during a 48-hour period using RAS in a patient who hadsustained myocardial infarction three days previous-ly (Fig2).

After Open Heart SurgeryAfter open heart surgery, atrial and ventricular

pacemaker wires are left hi place routinely by thesurgeons. Therefore, we treat all such patients whodevelop supraventricular tachycardia with RAS aswell as with the appropriate pharmacologic agents.Figure 3 shows a record from a patienttwo hoursafter surgery. This patient had atrial tachycardiawith a heart rate of 160/mm, hypotension, andanuria. Atrial pacing at 200/mm reduced the ven-tricular rate to slightly below 100/mm. Immediatelyafter reduction of the ventricular rate, the arterialpressure reverted to normal and shortly thereafterthe patient began to urinate. It was not possible toproduce atrial fibrillation in this patient, and, whenpacing was discontinued, there was a reversion tothe original tachyarrhythmia with its associatedhypotension. Because the patient could not tolerate

his tachycardia, continuous atrial pacing at 200/mmfor two hours and 15 minutes was carried out.During this period, 1.25 mg of digoxmn was admin-istered intravenously in divided doses. Then, whenthe pacing was discontinued, the patient was foundto be in sinus rhythm. The remainder of the clinicalcourse was uncomplicated.

In many cases of rheumatic heart disease, atrialfibrillation has existed for a considerable time priorto surgery. If supraventricular tachycardia developspostoperatively, RAS results in atrial fibrillationrather than normal sinus rhythm. Usually on con-version, the ventricular rate slows significant-ly.2343 However, in many cases, even afterinduction of atnal fibrillation, the ventricular ratemay be excessive. When this occurs, the ventricu-lar rate can usually be controlled adequately bysupplementary administration of digitalis.

During Cardiac CatheterizationWhen supraventricular tachycardia occurs during

cardiac catheterization, since an electrode catheteris already in the right heart, the simplicity of theprocedure makes HAS the treatment of choice.


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FIGURE 3. Records obtained from patient treated with RAS and digoxin two hours after cardiacsurgery (see text). A = simultaneous EGG and AUE. There is atrial tachycardia at rate of156/mm with 1: 1 atrioventricular response; B = (A) pacing atria at 200/mm resulted invariable A-V block and slowing of ventricular rate to approximately 100/mm. (B) immediatelyon cessation of RAS, heart rate is approximately 150/mm. (C) AUE obtained about one minuteafter (B) shows that rhythm was converted to sinus tachycardia.

998 LISTER ET AL


Drug Resistant Supraventricular TachycardiasThe use of atrial pacing by means of an im-

planted radiofrequency pacing system for thetreatment of refractory repetitive supraventriculartachycardia has been described recently.4 Accord-ing to this report, the induction of atrial fibrillationduring the first few days after operation caused asignificant slowing of the ventricular rate. Afterdigitalization, rapid atrial pacing during supraven-tricular tachycardia no longer precipitated atrialfibrillation but induced a greater degree of func-tional A-V block resulting in a significant slowing ofthe ventricular rate and associated improvement.This approach holds promise for the managementof chronically recurring disabling supraventriculartacliycardias.

Most reports indicate that RAS is effective in

about 70 percent of cases.231267 Patientselection may account for some of the recordeddiscrepancies. Atrial size, duration of the arrhyth-mia, and differences in pharmacologic therapy un-doubtedly determine the ease of conversion. Thus,the success rate of RAS would tend to be high insupraventricular tachycardia of short duration oc-curring in relatively small atria unable to self-perpetuate atrial fibrillation induced by atrial pac-ing. In one series,20 the failure of RAS in atrialflutter may be explained partly in terms of adifferent patient population and partly becausestandard DC cardioversion was performed if sinusrhythm had not returned in one hour. We feel thata certain number of these patients might haveresponded spontaneously with sinus rhythm severalhours after HAS.


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TREATMENT OF SUPRAVENTRICULARTACHYCARDIA 999


To date, there have been remarkably few dele-terious side effects reported with HAS. Although ithas been used successfully to terminate supraven-tricular tachycardias hi the Wolff-Parkinson-Whitesyndrome, under most circumstances the procedure

is contraindicated in patients with anomalous A-Vconduction (WPW syndrome and James fiber by-pass tracts). The initiation of atrial fibrillation inthese patients may result in ventricular rates greaterthan 300/mm. We had one such case (James fiber

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VR.250/MINFscunz 4. Records obtained from 41-year-old patient with Ebsteins anomaly and James fiberbypass tract of A-V node, whose chief complaint was recurrent incapacitating palpitations.During normal sinus rhythm A-H time was at lower limits of normal, 65 msec. (A) Atrialtachycardia at rate of 200/mm with aberrant ventricular activation and 1: 1 atrioventricularresponse. During tachycardia A-H time was increased by 55 mnsec to 120 msec. A-H interval isshort for this heart rate because of James fiber bypass tract. (B) Rapid atrial stimulationconverted rhythm to atrial fibrillation, with aberrant ventricular activation and further increasein heart rate. This rapid ventricular response in atrial fibrillation is only observed in cases withanomalous A-V connections. Brachial artery pressure shows that most ventricular contractionsare ineffectual. This rhythm was tenninated uneventfully by D-C countershock. B-A = brachialartery pressure; ABE = atrial bipolar electrogram.


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