Hypokalemia unmasking underlying premature ventricular contraction induced polymorphic ventricular tachycardia: Low potassium is not always the culprit!

Figures

• 

  Fig. 1. EKG upon arrival to our hospital (A), showing sinus rhythm with LBBB and frequent ectopy of two different morphologies. EKG after potassium and magnesium repletion (B).

• 

  Fig. 2. PVC arising from antero-lateral papillary muscle (A) and para-Hisian (B) triggering PMVT. Recurrent episode of PMVT (C) despite normal serum potassium and QTc, initiated by a PVC from the antero-lateral papillary muscle.

• 

  Fig. 3. A: 12-lead EKG in the electrophysiology lab showing a sinus beat with LBBB, the para-Hisian PVC and anterolateral papillary muscle PVC. B: Site of earliest activation of the para Hisian PVC, on the basal RV septum (a little below the His electrogram). Channels are, from top to bottom: surface ECG leads I, III, aVF, V1, and V5; decapolar coronary sinus catheter, from proximal to distal; ablation proximal and distal; unipolar electrogram from the distal ablation catheter (note the connection is reversed from conventional, resulting in a positive deflection); and a quadripolar catheter in the right ventricular apex, proximal to distal.

• 

  Fig. 4. Electroanatomic activation map (Carto 3, Biosense Webster, Diamond Bar, CA) in right anterior oblique projection showing the site of ablation of the paraHisian PVC. The yellow dots denote the His bundle and proximal right bundle electrograms; the pink and red dots represent ablation lesions. Radiofrequency current was initially delivered slightly further into the ventricle without effect. On mapping on the annulus, an earlier, low amplitude signal was seen. The green dot represents the site of successful ablation.