Introduction: Lidocaine is known to increase the defibrillation threshold (DFT) of monophasic shocks (MS) and have no effect on DFT of biphasic shocks (BS). The aim of this study was to enhance our understanding of the mechanisms of vulnerability and defibrillation through the investigation of this difference.
Methods and Results: We studied the effect of 15 μM lidocaine on shock-induced vulnerability using fluorescent imaging of Langendorff-perfused rabbit hearts. Vulnerability was assessed as vulnerable window with shock strengths of 15 to 150 V and vulnerable period (VP) with shock delivery phase of 0% to 100% of action potential duration (% APD). With MS, lidocaine caused a significant increase in both the upper limit of vulnerability (ULV, 71 ± 17 V vs 120 ± 1.5 V, P < 0.01) and upper limit of VP (91 ± 8.0% APD vs 110 ± 4.2% APD, P < 0.01). With BS, lidocaine had no effect on ULV (40 ± 3.4 V vs 45 ± 4.5 V) and did not increase the upper limit of VP (78 ± 8.9% APD vs 96 ± 12% APD, P < 0.01). Lidocaine caused reduction of the conduction velocity during pacing (0.58 ± 0.08 m/s vs 0.44 ± 0.05 m/s, P < 0.01), shock-induced break excitation (0.82 ± 0.17 m/s vs 0.30 ± 0.07 m/s, P < 0.01), and postshock reentry (0.34 ± 0.07 m/s vs 0.19 ± 0.08 m/s, P < 0.01). Lidocaine had no effect on shock-induced virtual electrode polarization.
Conclusion: Lidocaine increased MS ULV due to slowing of shock-induced break-excitation wavefronts, which resulted in enhanced probability of survival of virtual electrode induced phase singularity. Lidocaine had no effect on BS ULV because no break excitation was induced by BS. Reduction of conduction velocity by lidocaine resulted in increased dispersion of repolarization and led to upper limit of VP increase for both MS and BS. (J Cardiovasc Electrophysiol, Vol. 14, pp. S237-S248, October 2003, Suppl.)