A patient taking regular flecainide for paroxysmal atrial fibrillation presented with broad complex tachycardia and circulatory compromise. With no history of pacemaker insertion and no pacing spikes visible on the ECG, this was presumed to be ventricular tachycardia and treated with electrical cardioversion, leading to p-wave asystole. An indwelling pacemaker was now recognised and ventricular capture was eventually attained by significantly increasing ventricular lead output. Invasive haemodynamic support was required due to new ventricular systolic dysfunction. Pacing thresholds and ventricular function normalised within 72 h consistent with flecainide toxicity; levels were shown to be toxic. Pacemaker interrogation revealed evidence of an undiagnosed atrial flutter, at presentation this was likely slowed by flecainide toxicity to a rate below the pacemaker mode switch, such that it was tracked in the ventricle at the upper tracking rate (120 bpm). Cardioversion terminated the arrhythmia but raised the capture threshold of the ventricle above the maximum lead output.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550908PMC
http://dx.doi.org/10.1136/bcr-2015-210598DOI Listing

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