Ventricular arrhythmias after precordial electric shock

doi:10.1016/0002-8703(67)90169-X

American Heart Journal

Volume 73, Issue 5, May 1967, Pages 595-601

https://doi.org/10.1016/0002-8703(67)90169-X Get rights and content

Abstract

New cardiac arrhythmias occurred 43 times in 50 patients who underwent 55 elective precordial applications of synchronized D.C. shock for the control of cardiac arrhythmias. Ventricular arrhythmias were seen after 27 procedures. There were unifocal ventricular premature systoles in 11, multifocal ventricular premature systoles in 15, and ventricular bigeminy in 17. Three of these patients developed runs of ventricular tachycardia, and 2 developed ventricular fibrillation. One patient with ventricular fibrillation received additional D.C. shock to control this arrhythmia. Except for this one patient, all arrhythmias were transient and self-limited. All patients survived the procedure, and there were no complications due to the new arrhythmias.

Although there were only 7 patients who were not receiving digitalis, 3 of these 7 patients developed new ventricular arrhythmias (bigeminy, unifocal and multifocal premature systoles). This suggests that, in these patients, electric shock acted to increase ventricular irritability, even though there were no cases of ventricular fibrillation or tachycardia in this small group. Furthermore, in those patients who were not receiving toxic doses of digitalis, the dose of digitalis being used did not appear to be an important factor in determining which patients would develop new ventricular arrhythmias. Ventricular arrhythmias were more frequent after multiple shocks and high levels of energy. This may have been due either to a dose-dependent pro-arrhythmic effect of electric shock or to the severity of the underlying heart disease that necessitated multiple shocks of high energy, or to both.

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Irreversible electroporation: Proceed with caution
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Citation Excerpt :
Electrical shock is an effective therapy against atrial fibrillation (AF) and ventricular fibrillation (VF). However, despite significant improvement in defibrillation efficacy, which has resulted in a radical reduction of defibrillation thresholds and myocardial damage, there are still extensive clinical and basic electrophysiology data indicating that defibrillation shocks are accompanied by adverse effects: (1) transient ectopy, tachycardia, or reinduction of VF1–5 and AF6; (2) bradycardia, complete heart block, and increased pacing thresholds4,7,8; (3) atrial and ventricular electrical and mechanical dysfunction (stunning), which is directly related to the strength of shocks.9–17 These effects are likely to be associated with shock-induced electroporation, which is characterized by the formation of aqueous pores in the cellular lipid matrix.18
Defibrillation shock is known to induce atrial stunning, which is electrical and mechanical dysfunction.
We hypothesized that atrial stunning is caused by higher atrial susceptibility to electroporation vs ventricles. We also hypothesize that electroporation may be responsible for early recurrence of atrial fibrillation.
We investigated electroporation induced by 10-ms epicardial high-intensity shocks applied locally in atria and ventricles of Langendorff-perfused rabbit hearts (n = 12) using optical mapping.
Electroporation was centered at the electrode and was evident from transient diastolic depolarization and reduction of action potential amplitude and maximum upstroke derivative. Electroporation was voltage-dependent and polarity-dependent and was significantly more pronounced in the atria vs ventricles (P <.01), with a summary 50% of Effective Dose (ED50) for main measured parameters of 9.2 ± 3.6 V/cm and 13.6 ± 3.2 V/cm in the atria vs 37.4 ± 1.5 V/cm and 48.4 ± 2.8 V/cm in the ventricles, for anodal and cathodal stimuli, respectively. In atria (n = 5), shocks of both polarities (27.2 ± 1.1 V/cm) transiently induced conduction block and reentry around the inexcitable area. Electroporation-induced ectopic activity was a possible trigger for reentry. However, in the thicker ventricles, electroporation and resulting conduction slowing and block were restricted to the surface only, preventing complete block and arrhythmia. The upstroke morphology revealed that the wave front dived below the electroporated region and resurfaced into unaffected epicardial tissue.
We showed that the atria are more vulnerable to electroporation and resulting block and arrhythmia than the ventricles.
Elective cardioversion in the presence of conduction disturbances
1984, Journal of Electrocardiology
Elective cardioversion of supraventricular arrhythmias has been demonstrated to be an effective procedure which can be performed with minimal risk.^1–5. The risks of cardioversion are increased in the presence of digoxin intoxication,^5–7 failure of synchronization,² conversion in the presence of high energies,^8,9 long standing atrial fibrillation,^8,9 atrial fibrillation with slow ventricular rates,^2,3 and dysrhythmias in association with ischemic heart disease or cardiomyopathy.⁸ However, the risk of cardioversion of supraventricular arrhythmias in the presence of conduction disturbances, although thought to be increased,³ has never been carefully studied.
This study was designed to examine the effects of conduction disturbances (CD) on the success and risk of elective cardioversion of supraventricular arrhythmias (atrial fibrillation and atrial flutter) and to define the role of temporary pacemakers prior to cardioversion in these patients.
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1980, American Heart Journal
The use of electrical energy for the immediate treatment of atrial and ventricular arrhythmias is practical and easily applied. The method, though simple, is the most effective method for terminating cardiac arrhythmias and is associated with only a low risk if properly employed. In symptomatic patients, the utilization of cardioversion reduces patient discomfort and complications which may occur while awaiting pharmacologic reversion of arrhythmia. At present, transthoracic defibrillation is the only practical method for terminating VF. Despite the safety of electrical reversion, proper precautions are necessary to prevent complications. In particular, the discharge of excessive energies, especially in the presence of digitalis toxicity, primises grave and life-threatening consequences. The use of antiarrhythmic medications is not supplanted by cardioversion and defibrillation. Rather, ongoing drug therapy is frequently necessary to prevent recurrence of arrhythmia.
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1970, Progress in Cardiovascular Diseases
Complicating the recognition of digitalis toxicity are certain electrophysiological phenomena which may result in arrhythmias which mimic toxic effects of the glycosides. In particular, the “rule of bigeminy”, aberrancy of intraventricular conduction, ”concealed” toxicity, concealed conduction into the AV junction, and exit block complicate the diagnosis of excessive digitalization.
Of the various arrhythmias indued by digitalis, atrial tachycardia with block, nonparoxysmal junctional tachycardia, bidirectional “ventricular” tachycardia, ventricular premature systoles, ventricular tachycardias, multiple ectopic arrhythmias, AV dissociation, and the coexistance of conduction defects with ectopic beats or rhythms are of particular interest either (1) because of a high degree of correlation with digitalis toxicity or (2) because the recognition of the arrhythmia may present complexities which need consideration.
The discussion in this review focuses on these complexities of arrhythmia interpretation as a manifestation of digitalis toxicity.

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^☆: Supported in part by Grant Nos. 2T1 HE 5240-06, FR-O 5500-04, and HE-22,699-01 from the United States Public Health Service.

^∗: Address: Cardiology Division, The Mount Sinai Hospital, 100th St. and Fifth Ave., New York, N. Y., 10029.

^∗∗: United States Public Health Service Postdoctoral Fellow.

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Clinical communicationVentricular arrhythmias after precordial electric shock☆

Abstract

Circulation

Am. Heart J.

J.A.M.A.

Canad. M. A. J.

Circulation Res.

Circulation

AC and DC countershock for arrhythmias

J.A.M.A.

“Cardioversion” of arrhythmias, I

Mod. Concepts Cardiovas. Dis.

“Cardioversion” of arrhythmias, II

Mod. Concepts Cardiovas. Dis.

Synchronized DC precordial shock for arrhythmias

J.A.M.A.

Further experience of electrical conversion of atrial fibrillation to sinus rhythm

Lancet

Post-cardioversion ventricular tachycardia

Am. J. Cardiol.

Clinical communication
Ventricular arrhythmias after precordial electric shock☆