The double microelectrode technique of intracellular constant current application and intracellular transmembrane voltage recording, which permits quantitative definition of the components of cardiac excitability, was employed to assess the effect of lidocaine in a concentration equivalent to clinically effective antiarrhythmic plasma levels (5 .mu.g/ml), on membrane characteristics, cable properties, strength-duration curves and charge-duration curves in long sheep Purkinje fibers in normal Tyrode''s solution at [K]0 = 4.0 mM. As determined by small hyperpolarizing pulses, lidocaine increased membrane conductance (GM) where GM approximates membrane K conductance (GM .simeq. GK .simeq. gK1) and decreased both the membrane length (.lambda.m) and time constants. Lidocaine shifted non-normalized strength-duration curves (threshold current, Ith, vs. current duration, t) and charge-duration curves (charge threshold Qth, vs. t) upward without altering either the resting transmembrane voltage (Vr) or threshold voltage (Vth). Normalized strength-duration curves and charge-duration curves, were superimposable during the control and lidocaine periods. This is best explained by lidocaine altering passive resistance-capacitance properties by increasing membrane K conductance without influencing active generator properties dependent on Na conductance. Lidocaine did not alter the passive or active membrane properties relevant to conduction velocity. By increasing membrane K conductance, lidocaine decreases excitability in long Purkinje fibers by increasing Ith without altering Vr or Vth, by increasing Qth; by decreasing .lambda.m and by rendering local circuit currents less effectual in eliciting an action potential.