Lidocaine consistently prolonged refractoriness of potentially re-entrant pathways in the infarction zone and produced conduction block, abolishing re-entrant ventricular beats and tachycardia.
The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected. The impairment of conduction induced by lidocaine in the RP was directly related to its ability to abolish re-entrant ventricular beats and tachycardia. Gradual slowing of conduction in the RP consistently developed before abolition: lengthening of coupling of extrasystolic beats in surface leads and gradual slowing of ventricular tachycardia rate occurred. The termination of re-entry was characteristically associated with complete block in the RP. A "selectivity hypothesis" for the antiarrhythmic action of lidocaine is proposed.
El‐Sherif et al. (Thu,) conducted a other in Re-entrant ventricular arrhythmias in late myocardial infarction. Lidocaine was evaluated on Effect on re-entrant ventricular arrhythmias and conduction in the re-entrant pathway. Lidocaine consistently prolonged refractoriness of potentially re-entrant pathways in the infarction zone and produced conduction block, abolishing re-entrant ventricular beats and tachycardia.