The electrophysiological effects of flecainide were tested using the two-microelectrode voltage-clamp technique and Vmax-measurements in isolated rabbit cardiac Purkinje fibres. Flecainide predominantly unfolds its sodium-channel blocking action during the upstroke phase of the cardiac action potential, because its Vmax-depressant effects are independent of the duration of the depolarizing interval. Very long lasting depolarizations caused a second, very slow blocking activity. Starting from a steady-state block, recovery from block was tested and yielded a time constant of 7.3 s for a membrane potential of -105 mV. The strong blockade of sodium-channels combined with a delayed recovery behaviour of the drug-associated channels gives reasons for the observation of a marked use-dependent block. This block increased when the cycle length was shortened or the holding potential was less negative. Additional application of lidocaine in several concentrations did not significantly increase or attenuate the phasic block caused by flecainide alone. Under special conditions we investigated flecainide's depression and shift of the Vmax/Vm-relation and we observed that the concentration dependence of both parameters could be described by simple 1:1 binding reaction. The effects of flecainide are largely reversible often greater than or equal to 15 min. Flecainide could be characterized as an open channel blocker with a very slow inactivated channel blocking activity. For the qualitative description of the sodium-channel block by flecainide we used the "modulated-receptor hypothesis", whereas for reconstructions of the use-dependent action we applied the "guarded-receptor hypothesis", which enables computations of phasic block with the knowledge of only one forward and one reverse rate constant.