Effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium of dogs.

The effect of lidocaine on conduction within normal and acutely ischemic ventricular myocardium was studied in 45 dogs in vivo. By recording pairs of local electrograms from the endocardium and epicardium and by stimulating the ventricle close to one of a pair of electrodes, we measured conduction times in the subendocardial layer (Endo 1-2), in the subepicardial layer (Epi 1-2), and from the endocardium to the epicardium (Endo-Epi). We then estimated the effect of lidocaine on each of them. In normal myocardium, lidocaine in a therapeutic dose (serum level 2.5 +/- 0.4 micrograms/ml) did not affect any of the three conduction times, but in a larger dose (serum level 6.5 +/- 0.7 micrograms/ml) it prolonged Endo-Epi significantly (P less than 0.05) and Endo 1-2 and Epi 1-2 slightly. In acutely ischemic myocardium caused by single stage ligation of the left anterior descending coronary artery, lidocaine in a therapeutic dose prolonged Endo 1-2 and Endo-Epi significantly (P less than 0.001) in the early stage after administration but did not affect Epi 1-2 simultaneously. Lidocaine in a larger dose, however, prolonged all three conduction times (P less than 0.001). The data indicate that within normal ventricular myocardium, lidocaine does not influence conduction unless its dose is toxic, and that within acutely ischemic ventricular myocardium, at a therapeutic dose, lidocaine prolongs conduction rapidly, but this effect is produced heterogeneously in the ischemic myocardium and is poor in the subepicardial layer.