Modelling induction of a rotor in cardiac muscle by perpendicular electric shocks.

A strong, properly timed shock applied perpendicularly to a propagating wavefront causes a rotor in the canine myocardium. Experimental data indicate that the induction of this rotor relies on the shock exciting tissue away from the electrodes. The computational study reproduced such direct excitation in a two-dimensional model of a 2.7 x 3 cm sheet of cardiac muscle. The model used experimentally measured extracellular potentials to represent 100 and 150 V shocks delivered through extracellular electrodes. The shock-induced transmembrane potential was computed according to two mechanisms, the activating function and the unit-bundle sawtooth potential. The overall process leading to initiation of a rotor was the same in model and experiment. For the 100 V shock, the directly excited region extended 2.26 cm away from the electrode; the centre of the rotor ('critical point') was 1.28 cm away, where the electric field Ecr was 4.54 Vcm(-1). Increasing the shock strength to 150 V moved the critical point 1.02 cm further and decreased Ecr by 0.39 Vcm(-1). The results are comparable with experimental data. The model suggests that the unit-bundle sawtooth is responsible for the creation of the directly excited region, and the activating function is behind the dependence of Ecr on shock strength.