Nonsustained polymorphous ventricular tachycardia during amiodarone therapy for atrial fibrillation complicating cardiomyopathy. Management with intravenous magnesium sulfate.

A case is presented in which amiodarone was administered to suppress paroxysmal atrial fibrillation in a patient with an idiopathic cardiomyopathy. Eleven days after initiation of therapy with amiodarone, the patient experienced syncope and was noted to have recurrent episodes of polymorphous ventricular tachycardia. The patient was hospitalized and treated with a bolus as well as continuous infusion of intravenous magnesium sulfate. When the infusion was transiently discontinued, recurrences of polymorphous ventricular tachycardia were noted. The probable proarrhythmic action of amiodarone, although rare, is reviewed along with a discussion of the novel use of intravenous magnesium sulfate therapy.

Setting of relatively low energy outputs may permit implantation of a nonthoracotomy automatic cardioverter defibrillator system when high energy outputs prove ineffective.

At intraoperative testing of defibrillation thresholds during implantation of internal cardioverter defibrillators, standard step-down approaches of energy outputs are used. If relatively high energy outputs are not successful at defibrillating the heart, the electrodes are frequently reconfigured. When attempting implantation of a nonthoracotomy lead system, high defibrillation thresholds may warrant opening of the chest cavity to place one or more epicardial electrodes. A case is presented where a nonthoracotomy system was able to be implanted using relatively low energy outputs which were reproducibly successful at terminating ventricular fibrillation when higher energy outputs were unsuccessful. Mechanisms for this phenomenon and alternate recommendations for defibrillation testing are presented.

Inhibition of bradycardia pacing caused by far-field atrial sensing in a third-generation cardioverter defibrillator with an automatic gain feature.

The diagnostic accuracy of implantable cardioverter defibrillators may be improved by automatically adjusting gain algorithms, which in general reduce the likelihood of oversensing while maintaining the ability to detect the low amplitude signals associated with ventricular fibrillation. We present a patient with a third-generation device who developed prolonged ventricular asystole arising as a complication of the automatic gain feature. During asystole the device automatically increased sensitivity in order to prevent undersensing of ventricular fibrillation, which in this case resulted in far-field sensing of atrial activity and inhibition of ventricular pacing.