In arrhythmias associated with emotional stress, the antiarrhythmic effect in patients without serious heart diseases can be sedative (sedative, tranquilizing) drugs. Anti-arrhythmic activity is possessed to some extent by many neurotropic drugs (holinoblockers and cholinomimetics, adrenoblockers and adrenomimetics, local anesthetics, some anticonvulsants with antiepileptic activity), preparations containing potassium salts, antagonists of calcium ions, etc. At the same time, there are some drugs, the primary pharmacological property of which is the normalizing effect on the rhythm of the heart for various types of arrhythmias. These substances, along with beta-adrenoblockers and calcium ion antagonists, some local anesthetics and others, in connection with their pronounced antiarrhythmic activity are combined into a group of antiarrhythmic drugs.
In the mechanism of action of all antiarrhythmic drugs, their effect on cell membranes, transport of ions (sodium, potassium, calcium) plays a leading role and the associated changes in the depolarization of the membrane potential of cardiomyocytes and other electrophysiological processes in the myocardium. Different groups of antiarrhythmic drugs and individual drugs differ in their influence on these processes. Thus, preparations of subgroup IA and IC suppress the transport of sodium ions through the “fast” sodium channels of the cell membrane. Medication of IB subset increases the permeability of membranes for potassium ions. Quinidine simultaneously with the inhibition of transport of sodium ions reduces the flow of calcium ions into the cardiomyocytes. Quinidine-like substances lessen the maximum depolarization rate, increase the threshold of excitability, impede conduction along the bundle of the Hisnia and Purkinje fibers, slow the restoration of reactivity of the membranes of cardiomyocytes.