Background: One mechanism by which extracellular field shocks (ECFSs) defibrillate the heart is by producing changes in membrane potential (V(m)) at tissue discontinuities. Such virtual electrodes may produce new excitation waves or affect locally propagating action potentials. The rise time of V(m) determines the required duration of a single defibrillation pulse to reach a critical threshold for activation or for the modification of ion channel function, and depends on the electric and microstructural characteristics of the tissue.
Methods and results: We used optical mapping of V(m) in patterned cultures of neonatal rat ventricular myocytes to assess the relationship between cardiac structure and the early time course of V(m) during ECFSs. At monolayer boundaries, the time course of V(m) showed a close fit to the theoretical change predicted by theory, with a membrane time constant of 2.65±0.19 ms (n=13) and a length constant of 159±6 μm (n=10). Experiments in patterned strands, mimicking the resistive boundaries that occur naturally in the heart, explained the observation that the rate of rise and the maximal amplitudes of the V(m) changes are inversely related because of electrotonic interactions between structural boundaries. Interrupting ECFSs by very short intervals diminished V(m), but did not cause major changes in its overall time course.
Conclusions: Interaction between virtual sinks and sources decreases the magnitude of the changes in V(m) but accelerates its time course. For efficient defibrillation, short ECFSs are needed, with an amplitude adapted to match the boundary interaction.