How can sodium channel blockers terminate re-entry in cardiac arrhythmia?

Answer 1

Cardiac arrhythmia is cause by the presence of an ectopic focus or a re-entry mechanism where an action potential is delayed for some reason and enters nearby muscle fibres that are no longer refractory causing depolarisation and establishing a circuit movement.

There are three classes of anti-arrhythmic drugs which block sodium channels:

Class IA drugs block open Na+ sodium and can increase the effective refractory period. They produce a frequency-dependent block As they dissociate slowly away from these Na+ channels, they can prevent the Na+ channel from contributing towards an action potential if the frequency is high. Disopyramide one such example. It is used to treat ventricular arrhythmia by resulting in a negative inotropic effect.

Class IB drugs block closed Na+ sodium. It is often used to treat ventricular arrhythmia after an acute myocardial infraction. Lidocaine is one such example. It has little effect on normal cardiac tissues as it dissociates quickly from the Na+ channels. However, many Na+ channels are closed in ischemic cases due to anoxia. Lidocaine can hence act on these closed Na+ channels.

Class IC drugs are the most potent when it comes to blocking Na+ channels. They slowly dissociate from the Na+ channels and it leads to depressed conduction in the myocardium. These agents can prolong the RP and QRS intervals. Flecainide is one such example and it is used the treat atrial fibrillation.