MedicineCardiologyPharmacologyElectrophysiologyLocal AnesthesiaPharmacodynamicsAtrial ElectrophysiologyCardiovascular PharmacodynamicsAction Potential WaveformAtrial RepolarizationDrug Effects On Cardiac Action PotentialsElectrophysiologic EffectsMembrane RepolarizationSinoatrial BlockSinoatrial Node Action PotentialsSinoatrial Node Function
The effects of lidocaine (L), 1 x 10-7 to 5 x10-4 M, were studied on various cell types in isolated rabbit atrial preparations and on cells from canine Bachmann's bundle preparations. High concentrations of L diminished the sinoatrial node rate by only 14% and lower concentrations had little effect. L, ≤ 1 x 10-5 M, had little effect on action potential duration, configuration, rate of rise or amplitude. Exposure to 1 x 10-4 M L was associated with a decrease in action potential amplitude and rate of rise and, with exposure to 5 x 10-4 M L, there also was prolongation of terminal repolarization. All effects of L on action potential characteristics could be abolished with perfusion with drug-free Tyrode's solution. The effective refractory period of Bachmann's bundle was prolonged by L, ≥ 1 x 10-6 M. The effective refractory period of ordinary atrial fibers was not changed until exposure to ≥ 1 x 10-4 M when it too was prolonged. Membrane responsiveness of Bachmann's bundle and ordinary atrial fibers was unaffected by L, ≤ 1 x 10-5 M. Exposure to ≥ 1 x 10-4 M was associated with a decrease in peak dv/dt of phase 0 and a shift of the S curve on the voltage exis. Ectopic atrial rhythms were abolished only after exposure to ≥ 1 x 10-4 M L. L's minimal effects on membrane responsiveness, rate of rise of phase 0, effective refractory period and automatically in various atrial cell types suggest that it may be an ineffective agent in the treatment of atrial arrhythmias.