BIDIRECTIONAL FASCICULAR TACHYCARDIA

The signature VT associated with  digoxin toxicity is bidirectional VT

BIDIRECTIONAL FASCICULAR TACHYCARDIA.

1.       Digoxin toxicity can produce increased ventricular ectopy and, when coupled with bradyarrhythmias caused by digoxin toxicity, may predispose to

a.       sustained polymorphic ventricular arrhythmias

b.      VF

c.       Birectional VT

2.       This unique VT is due to triggered activity associated with calcium overload resulting from the inhibition of Na+,K+-ATPase by digoxin.

3.       See fig--Bidirectional VT originates from the left anterior and posterior fascicles, creating

a.       relatively narrow QRS right bundle branch (RBB) configuration

b.       with  beat-to-beat alternating right and left frontal plane QRS axis.

   

4.       This VT seldom is observed in the absence of digoxin toxicity.

5.       Treatment for bidirectional VT or other hemodynamically significant arrhythmias due to digoxin excess

a.       correction of electrolyte disorders

b.       IV infusion of digoxin-specific Fab fragments.

                                                               i.      antibody fragments will, over the course of 1 hour, bind digoxin and eliminate toxic effects.

                                                             ii.      In the setting of normal renal function, the bound complex is secreted.