CRITICAL REVIEW

Rapid Atrial Stimulationin the Treatment of

SupraventricularTachycardia
John 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 the
treatment of selected cases of supraventricular tachycardias (SVT). RAS may
(1) immediately revert the SVT to normal sinus rhythm, (2) transiently convert
the rhythm to atrial fibrillation which after a variable period usually converts
spontaneously to normal sinus rhythm, (3) permanent conversion of the rhythm
to atrial fibrillation with the immediate slowing of the ventricular rate, or (4)
in cases in which the tachycardia cannot be terminated and atrial fibrillation
cannot be initiated, the ventricular rate may be slowed by increasing the atrial
rate until second degree heart block occurs. To date, there have been remarkably
few deleterious side effects with RAS. Previous digitalis administration is not a
contraindication to the procedure. Although RAS has been successfully used to
terminate SVTs in the WPW syndrome, under most circumstances the procedure
is contraindicated in patients with anomalous atriovenfricular connections.

D ing have

uring recent years, various modes of atrial pac-

been used to terminate or prevent

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

for this procedure.

RAS comprises the application of pacemaker

impulses to the atria at a rate faster (usually from
150 to over 600/mm) than the tachycardia being
treated. Atrial capture need not necessarily occur
with each stimulus to produce the desired effect;
indeed, the refractory period of the atrium limits
the maximal rate of atrial capture to about 350450/ mm.
#{176}Attending
physician, Department of Medicine, Miami
Heart Institute, MiamniBeach,
Fla.
Laboratory, Miami Heart Institute, Miami Beach, Fla.
Chief of Cardiology, The Genesee Hospital, and Assistant

*#{176}Director,
Cardiopulmonary

Professor of Medicine, University of Rochester School of

Medicine and Dentistry, Rochester, N.Y.
Reprint requests: Dr. Lirter, Miami Heart Institute, 4701
Meridian Avenue, Miami Beach 33140

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Under fluoroscopy, a bipolar electrode catheter is

positioned in the high right atrium. The initial
pacing rate should be slow while using the maximal
output of the pacemaker to detect the absence of
inadvertent ventricular pacing.422 During RAS,
atrial capture may be inferred when the ventricular

rate is decreased or the rhythm is altered. If initially

unsuccessful, RAS should then be tried from several
other atrial sites, because the physiologic effect of
pacing may vary according to the area stimulated,23 and, in some cases, may be of critical
importance for cardioversion. Like others,9 we
have observed that ineffectual RAS may sometimes
become successful when combined with carotid
sinus pressure, presumably because the latter
shortens the refractory period of the atrium.2422
Although the literature suggests that the use of
rather complicated stimulators is necessary for this
procedure, an ordinary external fixed rate pulse
generator can be modified easily by the manufacturers to increase its maximal rate. Alternatively,
several external pacemakers may be connected in
series.26

995

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LISTER ET AL

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

RAS may cause: (1) immediate

supraventricular

tachycardia

termination of
by interrupting
a re-

entry circus movement due to atrial paced beats or

overdrive suppression of an ectopic pacemaker
focus; (2) transient conversion of the rhythm to
atrial fibrillation, which after a variable time (up to
48 hours) usually converts spontaneously to normal
sinus rhythm because in essentially normal atria,

atrial fibrillation is a self-limiting dysrhythmia (Fig

1); (3) permanent conversion of the rhythm to
atrial fibrillation with immediate slowing of the
ventricular rate; in cases of long standing heart disease associated with dilatation of the atria sinus
rhythm may no longer be sustained; and (4) in
cases in which the tachycardia cannot be terminated
and atrial fibrillation cannot be initiated, the ventricular rate may be slowed by increasing the atrial
rate by pacing until second degree heart block
occurs.
In the usual clinical setting the preferred treatment of supraventricular tachycardia includes the
standard pharmacologic agents and/or DC cardioversion. Current indications for using RAS are: (1)
cases with possible digitalis intoxication accompanied by clinical deterioration;236 (2) patients
with recurrent supraventricular
tachycardia in
whom the tachyarrhythmias occur at relatively
short intervals and in whom there is also associated
clinical deterioration;23 (3) after open heart sur-

gery; (4) during cardiac catheterization;2

and (5)
for the treatment of chronically recurring drugresistant supraventricular tachycardias.4
Supraventricular Tachycardia with Suspected Digitalis Toxicity
In this instance, there is a relative contraindication for cardioversion because of the danger of
inducing ventricular tachycardia or fibrillation.273#{176}
RAS is used after treatment with appropriate
pharmacologic

agents

(other

than

digitalis)

has

been unsuccessful, the clinical situation is deteriorating, and it is urgent that the tachycardia be
terminated or the ventricular rate slowed. Thus far,
there have been no complications reported with
RAS in patients who may have been receiving
excessive doses of digitalis.
Episodes of Supraventrwular Tachycardia Recurring at Short Intervals
These patients have usually had a recent myocardial infarction and the customary recurrent tachyarrhythmia is atrial flutter or tachycardia. HAS is
indicated under such circumstances, provided the
tachyarrhythmia
is accompanied by significant clinical deterioration
and the episodes cannot be suppressed by pharmacologic
agents. In these cases,
HAS is preferable to DC countershock, because it

requires no anesthesia and causes no discomfort to

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TREATMENT OF SUPRAVENTRICULARTACHYCARDIA

997

C
V

a
a....
FIGURE 2. Conversion of atrial flutter to normal sinus rhythm by RAS. Records obtained from
patient 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 with

aberrant ventricular activation and/or ventricular beats; B = RAS (500 pacemaker inpulses/
mm) terminates atrial flutter. On discontinuation of RAS there is A-V dissociation. Apparent
variability of configuration of QRS complexes is due to superimposition of P-waves. C = AUE
recorded several minutes after (B) reveals that rhythm has stabilized in normal sinus.

the patient.233 Recently we terminated 14 episodes of supraventricular

tachycardia during a 48hour period using RAS in a patient who had
sustained myocardial infarction three days previously (Fig2).

his tachycardia, continuous atrial pacing at 200/mm

for two hours and 15 minutes was carried out.
During this period, 1.25 mg of digoxmn was administered intravenously in divided doses. Then, when
the pacing was discontinued, the patient was found
to be in sinus rhythm. The remainder of the clinical

After Open Heart Surgery

course was uncomplicated.

After open heart surgery, atrial and ventricular

pacemaker wires are left hi place routinely by the

In many cases of rheumatic heart disease, atrial

fibrillation has existed for a considerable time prior
to surgery. If supraventricular
tachycardia develops
postoperatively, RAS results in atrial fibrillation
rather than normal sinus rhythm. Usually on conversion, the ventricular rate slows significant-

surgeons. Therefore, we treat all such patients who

develop

supraventricular

tachycardia

with RAS as

well as with the appropriate pharmacologic agents.

Figure 3 shows a record from a patienttwo hours
after surgery.
This patient had atrial tachycardia
with a heart rate of 160/mm, hypotension, and
anuria. Atrial pacing at 200/mm reduced the ventricular rate to slightly below 100/mm. Immediately
after reduction of the ventricular rate, the arterial
pressure reverted to normal and shortly thereafter
the patient began to urinate. It was not possible to
produce atrial fibrillation in this patient, and, when
pacing was discontinued, there was a reversion to
the original tachyarrhythmia with its associated
hypotension.

Because the patient could not tolerate

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ly.2343 However,

in many

cases,

even

after

induction of atnal fibrillation, the ventricular rate

may be excessive. When this occurs, the ventricular rate can usually be controlled adequately by
supplementary administration of digitalis.
During Cardiac Catheterization
When supraventricular tachycardia occurs during
cardiac catheterization,
since an electrode catheter

is already in the right heart, the simplicity of the

procedure makes HAS the treatment of choice.

LISTER ET AL

998

I.

AVE
A

II

3. Records obtained from patient treated with RAS and digoxin two hours after cardiac
(see text). A = simultaneous EGG and AUE. There is atrial tachycardia at rate of
156/mm with 1: 1 atrioventricular response; B = (A) pacing atria at 200/mm resulted in
variable A-V block and slowing of ventricular rate to approximately 100/mm. (B) immediately
FIGURE

surgery

on cessation of RAS, heart rate is approximately 150/mm. (C) AUE obtained

after (B) shows that rhythm was converted to sinus tachycardia.

Drug Resistant Supraventricular Tachycardias

The use of atrial pacing by means of an implanted radiofrequency pacing system for the
treatment of refractory repetitive supraventricular
tachycardia has been described recently.4 According to this report, the induction of atrial fibrillation
during the first few days after operation caused a
significant slowing of the ventricular rate. After
digitalization, rapid atrial pacing during supraventricular tachycardia no longer precipitated atrial
fibrillation but induced a greater degree of functional A-V block resulting in a significant slowing of
the ventricular rate and associated improvement.
This approach

holds promise

for the management

of chronically recurring disabling supraventricular

tacliycardias.
Most reports indicate that RAS is effective in

about one minute

about 70 percent of cases.231267 Patient

selection may account for some of the recorded
discrepancies. Atrial size, duration of the arrhythmia, and differences in pharmacologic therapy undoubtedly determine the ease of conversion. Thus,
the success rate of RAS would tend to be high in
supraventricular tachycardia of short duration occurring in relatively small atria unable to selfperpetuate atrial fibrillation induced by atrial pacing. In one series,20 the failure of RAS in atrial
flutter may be explained partly in terms of a
different patient population and partly because
standard DC cardioversion was performed if sinus
rhythm had not returned in one hour. We feel that
a certain number of these patients might have
responded spontaneously with sinus rhythm several
hours after HAS.

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TREATMENT OF SUPRAVENTRICULARTACHYCARDIA
To date, there have been remarkably few deleterious side effects reported with HAS. Although it
has been used successfully to terminate supraventricular tachycardias hi the Wolff-Parkinson-White
syndrome,

under most circumstances

the procedure

999

is contraindicated in patients with anomalous A-V

conduction (WPW syndrome and James fiber bypass tracts). The initiation of atrial fibrillation in
these patients may result in ventricular rates greater
than 300/mm. We had one such case (James fiber

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Fscunz 4. Records obtained from 41-year-old patient with Ebsteins anomaly and James fiber
bypass 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) Atrial
tachycardia at rate of 200/mm with aberrant ventricular activation and 1: 1 atrioventricular
response. During tachycardia A-H time was increased by 55 mnsec to 120 msec. A-H interval is
short for this heart rate because of James fiber bypass tract. (B) Rapid atrial stimulation
converted rhythm to atrial fibrillation, with aberrant ventricular activation and further increase
in heart rate. This rapid ventricular response in atrial fibrillation is only observed in cases with
anomalous A-V connections. Brachial artery pressure shows that most ventricular contractions
are ineffectual. This rhythm was tenninated uneventfully by D-C countershock. B-A = brachial
artery pressure;

ABE = atrial bipolar electrogram.

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