BACKGROUND: Bidirectional ventricular tachycardia (BVT), which is characterized 
by an alternating beat-to-beat ECG QRS axis, is a rare but intriguing arrhythmia 
associated with digitalis toxicity, familial catecholaminergic polymorphic 
ventricular tachycardia (CPVT), and several other conditions that predispose 
cardiac myocytes to delayed afterdepolarizations (DADs) and triggered activity. 
Evidence from human and animal studies attributes BVT to alternating ectopic 
foci originating from the distal His-Purkinje system in the left and/or right 
ventricle, respectively.
OBJECTIVE: The purpose of this study was to evaluate a simple "ping pong" model 
of reciprocating bigeminy to explain BVT.
METHODS: We constructed a two-dimensional anatomic model of the rabbit 
ventricles with a simplified His-Purkinje system, in which different sites in 
the His-Purkinje system had different heart rate thresholds for DAD-induced 
bigeminy.
RESULTS: When the heart rate exceeded the threshold for bigeminy at the first 
site in the His-Purkinje system, ventricular bigeminy developed, causing the 
heart rate to accelerate and exceed the threshold for bigeminy at the second 
site. Thus, the triggered beat from the first site induced a triggered beat from 
the second site. The triggered beat from the second site next reciprocated by 
inducing a triggered beat from the first site, and so forth. Bigeminy from two 
sites produced BVT, and that from three or more sites produced polymorphic VT.
CONCLUSION: This "ping pong" mechanism of reciprocating bigeminy readily 
produces the characteristic ECG pattern of BVT and its degeneration to 
polymorphic VT if additional sites develop bigeminy.