Direct current cardioversion

Direct current cardioversion

Appraisal therapy Direct and reappraisal Edited current by Arthur ince its introduction by Lown in 1962, direct current cardioversion has been wi...

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Appraisal therapy

Direct

and reappraisal Edited

current

by Arthur

ince its introduction by Lown in 1962, direct current cardioversion has been widely utilized for the correction of many cardiac arrhythmias. Because of the efficacy of the method, the easeof performance, the rapidity with which results are obtained, and the wide margin of safety associated with the procedure, cardioversion has become the treatment of choice in many instances in which antiarrhythmic drugs were previously employed. and

technique

Cardioversion is the most effective therapy available for the immediate conversion of ventricular tachycardia and in the elective treatment of both acute and chronic atria1 flutter and fibrillation. Its value in the management of atria1 or nodal tachycardia is less evident. Although the many different models of machines, of various manufacture, differ from each other in the waveform and duration of the electrical discharge, the basic methods of use are similar. In general, the patient’s electrocardiogram (ECC;) is displayed on an oscilloscope for continuous monitoring. The ECG is used to activate a synchronizing circuit which causes the actual cardioversion discharge to occur within 20 msec. of the peak of the R wave. By preventing the discharge from falling in the “vulnerable zone” of the T wave in this manner, repetiFrom the Department Received for publication

12x

of Medicine, New York March 26, 1971.

American Heart Journal

and

Julian

Frieden

cardioversion

S

Indications

C. DeGraff

of cardiac

IJniversity

tive ventricular discharge, which might culminate in ventricular tachycardia or fibrillation, is averted. In the emergency treatment of ventricular tachycardia or fibrillation, the synchronizing circuit is not employed and the cardioverting shock may fall at any time. For the treatment of atria1 flutter, a 50 watt-second (w/s) shock is generally used in this laboratory. Smaller shocks, though effective at times, often result in the development of atria1 fibrillation and are not recommended. Atria1 fibrillation is treated with a 200 w/s shock. If this is unsuccessful, 300 and 400 w/s shocks are employed. Ventricular tachycardia or fibrillation is treated in a similar fashion. Whenever possible, the electrodes are placed on the anterior left thorax, over the heart, and directly opposite on the posterior thoracic wall. It has been suggested by several groups that this results in the use of smaller shocks than the conventional method of application. Anesthesia

Since 1966, intravenous diazepam (Valium) has achieved a wide degree of acceptance for use in cardioversion. In our laboratory, diazepam is administered in 5 mg. increments every 4 to 5 minutes up to a maximum of 25 mg. Either somnolence, loss of cutaneous pain sensation, or loss of School

of Medicine,

550 First

July, 1971

Ave.,

New

York,

N. Y. 10016.

Vol. 82, No. 1, pp. 125-130

volume Number

82 1

Direct current cardimersion

coordinated ocular movement is considered an indication that enough diazepam has been administered. With the use of these criteria, the patient will have amnesia for the cardioversion. In general, the effects of diazepam are dissipated within 20 minutes and no postanesthetic complications ensue. It has been our experience that patients who have been receiving large amounts of sedation, tranquilizers, or analgesics prior to cardioversion require the largest amounts of diazepam. Similarly, alcoholic patients have a high requirement to achieve a satisfactory degree of sedation. The policy in our laboratory is that no more than 25 mg. of diazepam is administered. If this is ineffective, small doses of morphine sulfate are administered intravenously. With this method, it has not been necessary to request the services of an anesthesiologist. Indications

and contraindications

The likelihood of conversion to sinus rhythm in instances where atria1 flutter or fibrillation has been present less than one year has been reported to be approximately 90 per cent. In patients who have had the arrhythmia for longer than two years the chance of success decreases to less than 7.5 per cent. Similarly, 2.5 per cent of patients with the shorter duration of fibrillation maintained the sinus rhythm at the end of two years, as opposed to 10 per cent of those with more chronic fibrillation. Accordingly, it is our policy to reserve elective cardioversion for those patients whose arrhythmia is of less than one year’s duration. Other contraindications include a patient’s failure to maintain sinus rhythm after previous conversion, patients who are in the immediate pre- or postoperative (cardiac) state, patients with recent embolization, and those with giant left atria. If cardioversion is to be performed after cardiac surgery, at least three weeks should be allowed to elapse. It is of interest to note that following mitral valve surgery, cardioversion resulted in maintenance of sinus rhythm in only 9 per cent of patients who had atria1 fibrillation preoperatively. By contrast, when atria1 fibrillation appeared initially in the postoperative period, sinus rhythm was maintained in 82 per cent of the patients two years after con-

129

version. Atrioventricular nodal block, manifested by a slow ventricular response without digitalis, is a further contraindication. Antiarrhythmic

drugs

Many investigators have shown that cardioversion of the patient who is receiving digitalis results in a significantly high incidence of serious ventricular arrhythmias. These have ranged from premature ventricular contractions to ventricular tachycardia and fibrillation. It is the policy of the author to discontinue short-acting glycosides three days prior to cardioversion, and longer-acting preparations are discontinued one week in advance. If there is evidence of nodal rhythm manifested by regularization of the ventricular response, group beating, or Wenckebach periods, cardioversion is postponed. Similarly, cardioversion is not attempted when ventricular tachycardia is thought to be secondary to digitalis toxicity. The use of quinidine or procaine amide in the pre- and postconversion management remains a controversial subject. Several authors have described a greater frequency of persistent sinus rhythm in the patient maintained on suppressive therapy,2 while others have been unable to confirm this. In addition, so-called “quinidine syncope,” which is in reality paroxysmal ventricular tachycardia and fibrillation, occurs with a low frequency in patients treated with even relatively small doses of quinidine. Because of the minor degree of improvement in results and the possibility of fatal, toxic reactions, the use of quinidine is not recommended by the author. Anticoagulants Drawing on past experience obtained with quinidine and procaine amide, most groups do not use anticoagulant therapy prior to conversion. However, in a large series from Norway,3 emboli occurred in 11 of 209 (5 per cent) patients not given anticoagulants and in only 2 of 228 patients treated with anticoagulants (1 per cent). It has been our policy that only patients with previous emboli are given anticoagulants, beginning three weeks prior to conversion and maintained indefinitely there-

130

Amer.

Glussman

embolization within after. Furthermore, the previous three months should be considered a contraindication to cardioversion without intervening mitral valve surgery. REFERENCES 1. Lown, B.: Electrical rhythmias, Brit. Heart

reversion J. 29:469,

of cardiac 1967.

ar-

2.

Heart .I. July, 1971

Wagner, G. S., and McIntosh, H. D.: The use of drugs in achieving successful DC cardioversion, Progr. Cardiovasc. Dis. 11:431, 1969. 3. Bjerkelund, C., and Orning, 0.: An evaluation of DC shock treatment of atria1 arrhvthmias, Acta Med. Stand. 184:481, 1968. -