Ventricular fibrillation after ablation of a benign arrhythmia. Angry Purkinje syndrome?

Figures

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  Figure 1. A: Sustained ventricular tachycardia (VT), 190 beats/min, detected incidentally prior to a scheduled exercise test. The VT slowed with intravenous amiodarone (not shown). The QRS pattern (right bundle branch morphology with superior axis) and the relatively narrow complexes suggested the diagnosis of verapamil-sensitive fascicular VT.2,3B: Intravenous verapamil restored sinus rhythm with normal QRS morphology.

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  Figure 2. A: Electrocardiogram recorded 2 hours after the ablation procedure in the absence of symptoms. Note the ventricular extrasystoles with right bundle branch block (RBBB)–like morphology, leftward axis, yet fairly narrow QRS complexes (best appreciated at leads V1-V2). The extrasystoles have a very short coupling interval (320 ms). These characteristics indicate that the ectopic beats originate from Purkinje fibers located in the area of ablation within the left posterior fascicle. B: One hour later, polymorphic ventricular tachycardia deteriorating to ventricular fibrillation is triggered by a ventricular extrasystole with short coupling interval. C: After defibrillation there is sinus rhythm with RBBB and ventricular bigeminy with coupling interval of 320 ms. Intravenous quinidine was started at this point.

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  Figure 3. A: Bradyasystolic cardiac arrest that ensued after 24 hours of quinidine therapy. Asystole is followed by a slow escape rhythm with very wide QRS. B: After resuscitation with chest compressions, epinephrine, and atropine, there is sinus rhythm with complete atrioventricular block (arrows show the P waves) with an escape rhythm with left bundle branch block pattern with very wide QRS. C: Sodium bicarbonate, injected intravenously at this point, led to immediate restoration of atrioventricular conduction with narrow QRS.