Effects of lidocaine on shock-induced vulnerability and defibrillation

Lidocaine is known to increase monophasic shock (MS) defibrillation threshold (DFT). We investigated the underlying mechanisms using optical mapping of the shock-induced arrhythmias in Langendorf-perfused rabbit hearts. MS were delivered from two mesh electrodes during pacing. Vulnerability was assessed as vulnerable window (VW) within shock strengths of 15 V-150 V and vulnerable period (VP) within coupling intervals of 0-100% of action potential duration (%APD). Lidocaine caused significant increase in both VW (51±16 V vs 100±16 V, p<0.01) and VP (44±21 V vs 49±17 V, p<0.01). Lidocaine had no effect on virtual electrode polarization (AV.). In contrast, the conduction velocity (CV) slowed significantly by lidocaine during both pacing (0.58±0.08 m/s vs 0.44±0.05 m/s, p<0.01) and shock-induced reentry (0.34±0.07 m/s vs 0.19±0.08 m/s, p<0.01). Slowing of the conduction caused by lidocaine resulted in increased dispersion of repolarization. In conclusion, lidocaine increased vulnerability due to the slowing of shock-induced wavefront, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no significant effect on shock-induced ΔV_m.