Intramural Virtual Electrodes During Defibrillation Shocks in Left Ventricular Wall Assessed by Optical Mapping of Membrane Potential

BACKGROUND: It is believed that defibrillation is due to shock-induced changes of transmembrane potential (DeltaV(m)) in the bulk of ventricular myocardium (so-called virtual electrodes), but experimental proof of this hypothesis is absent. Here, intramural shock-induced DeltaV(m) were measured for the first time in isolated preparations of left ventricle (LV) by an optical mapping technique. METHODS AND RESULTS: LV preparations were excised from porcine hearts (n=9) and perfused through a coronary artery. Rectangular shocks (duration 10 ms, field strength E approximately 2 to 50 V/cm) were applied across the wall during the action potential plateau by 2 large electrodes. Shock-induced DeltaV(m) were measured on the transmural wall surface with a 16x16 photodiode array (resolution 1.2 mm/diode). Whereas weak shocks (E approximately 2 V/cm) induced negligible DeltaV(m) in the wall middle, stronger shocks produced intramural DeltaV(m) of 2 types. (1) Shocks with E>4 V/cm produced both positive and negative intramural DeltaV(m) that changed their sign on changing shock polarity, possibly reflecting large-scale nonuniformities in the tissue structure; the DeltaV(m) patterns were asymmetrical, with DeltaV-(m)>DeltaV+(m). (2) Shocks with E>34 V/cm produced predominantly negative DeltaV(m) across the whole transmural surface, independent of the shock polarity. These relatively uniform polarizations could be a result of microscopic discontinuities in tissue structure. CONCLUSIONS: Strong defibrillation shocks induce DeltaV(m) in the intramural layers of LV. During action potential plateau, intramural DeltaV(m) are typically asymmetrical (DeltaV-(m)>DeltaV+(m)) and become globally negative during very strong shocks.