Paradoxical acceleration of

atrial flutter after “cardioversion”

Leslie J. Shalan, M’.D.* Alan F. Lyon, M.D.**

Bronx, N. I’.

mhe application of a direct-current. IL -- capacitor-stored, synchronized, elec-

tric countershock (hereafter referred to as “cardioversion”) has proved to be a valu- able contribution to the management of certain cardiac arrhythmias. The use of direct rather than alternating current, and the synchronization of the shock to avoid the phase of ventricular vulnera- bility have undoubtedly contributed to the safety and efficacy of the procedure.‘,”

In the clinical application of cardio- version, the synchronization of the shock is such that, although the period of ven- tricular vulnerability is avoided, the dis- charge often occurs during the period of atria1 vulnerability. Therefore, such a shock could conceivably initiate an atria1 arrhythmia potentially more serious than the one for which cardioversion was em- ployed. Moreover, arrhythmias, such as atrial, nodal, and ventricular premature contractions, whose production is not readily explicable on the basis of a dis- charge occurring during the phase of atria1 vulnerability have occurred immediately after cardioversion. To our knowledge, the case reported below is the first occurrence of the unexpected acceleration of the atria1 rate after “cardioversion.”

Ca5e report

A Sl-year-old white man with a past history of two myocardial infarctions was hospitalized be- cause of palpitation and a rapid pulse. The electro- cardiogram revealed an atria1 flutter with 2:l atrio- ventricular block (atria1 rate of 280 per minute and ventricular rate of 140 per minute). The patient was in mild congestive heart failure, and digitaliza- tion with oral digoxin was carried out over the nest 6 days. The patient lost 5 pounds in weight. The electrocardiogram revealed no change in the rhythm. After 10 days of oral anticoagulation at therapeutic levels, two separate attempts to restore normal sinus rhythm with oral quinidine resulted in the production of multiple ventricular premature con- tractions, with no effect on the atria1 flutter rate or ventricular response. Quinidine was discontinued, but digitalization and anticoagulation were main- tained.

Because of progressive heart failure, cardiover- sion was attempted, utilizing a brief high-energy, capacitor-stored, electric shock as described by Lawn and co-workers.* Fig. 1, taken prior to de- livery of the shock, reveals persistence of the atria1 flutter with 2:l atrioventricular block. Fig. 2,d, taken immediately after a discharge of 100 watt- seconds, now reveals a supraventricular tachy- cardia with a ventricular rate of 190 per minute. Carotid compression had no effect on the rate or rhythm. The presence of an apparent initial small R wave and widening of the QRS complex, with loss of the initial Q wave previously present in Lead III (see Fig. 2,B), strongly suggests that this arrhythmia represented an atrial flutter at a rate of 380 per minute with 2 :l atrioventricular block.

Since the tachycardia persisted unchanged for

From the Cardiac Service, Veterans Administration Hospital, Bronx. K. 1’. Received for publication June 18. 1964. *Chief Resident, Cardiac Section. **Chief, Cardiac Section. Address: Veterans Administration Hospital, 130 West Kingsbridge Rd.. Bronx, N. S,, 10468.

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Paradoxical acceleration of atria1 jutter ajter cardioversion 685

Fig. 1. Lead II taken just prior to cardioversion reveals atrial flutter with 2:l atrioventricular block (atrial rate of 280 per minute and ventricular rate of 140 per minute).

Fig. 2. d, Lead III immediately after discharge of 100 watt-seconds reveals atria1 flutter with 2:l atrioventricular block. However, the atria1 rate is now 380 per minute. B, Lead III prior to cardio- version, with atrial flutter rate of 280 per minute. Note initial Q wave not present in A.

Fig. 3. Lead II taken after discharge of 200 watt- seconds reveals sinus tachycardia at 125 per minute.

several minutes, a second discharge of 200 watt- seconds was applied and was promptly followed by restoration of sinus rhythm as noted in Fig. 3 (sinus tachycardia at 125 per minute). The patient was eventually placed on a low maintenance dose of quinidine, and has remained in normal sinus rhythm with no apparent sequelae.

Discussion

With the establishment of sinus rhythm by cardioversion, transient arrhythmias are frequently noted. Lown and his associ- ates” analyzed the occurrence of arrhyth- mias during the initial 30 seconds after cardioversion of 35 episodes of atria1 fibril- lation. Arrhythmias were noted in 16 of the 35 patients, the most common being atrial, nodal, and ventricular premature contractions. In one patient, paroxysms of atria1 tachycardia developed 10 minutes after reversion and continued to recur until full digitalization had been accom- plished.

To our knowledge, this is the first case of acceleration of a pre-existent atria1 flutter after cardioversion. Since the dis- charge was delivered during the phase of atria1 vulnerability, one can speculate that the shock-induced acceleration of the atria1 rate (from 280 to 380 per minute) was prefibrillatory in nature; and had the ar- rhythmia been allowed to persist, atria1 fibrillation might have occurred. It should be added that the atria1 flutter that fol- lowed the initial discharge of 100 watt- seconds was potentially a more serious ar- rhythmia than the one for which cardio- version was employed. Although the ef- fectiveness and safety of cardioversion as a method of terminating certain cardiac arrhythmias has been well documented, the procedure is not without hazard.

REFERENCES

1. Lown, B., Neuman, J., Amarasingham, R., and Berkovits, 8. V.: Comparison of alter- nating current with direct current electroshock across the closed chest, .4m. J. Cardiol. 10:223, 1962.

2. Lown, B., Amarasingham, R., and Neuman, J.: New method for terminating cardiac arrhyth- mias: use of synchronized capacitor discharge, J.A.M.A. 182548, 1962.

3. Lown, B.. Perlroth, M. G., Kaidby, S., ,Abe, T., and Harken, D. E.: “Cardioversion” of atria1 fibrillation, New England J. Med. 269:325, 1963.