Sodium channel blocker

Class Ia agents block the fast sodium channel, which depresses the phase 0 depolarization (i.e. reduces Vmax), which prolongs the action potential duration by slowing conduction.

While procainamide and quinidine may be used in the conversion of atrial fibrillation to normal sinus rhythm, they should only be used in conjunction with an AV node blocking agent such as digoxin or verapamil, or a beta blocker, because procainamide and quinidine can increase the conduction through the AV node and may cause 1:1 conduction of atrial fibrillation, causing an increase in the ventricular rate.

These agents will decrease Vmax in partially depolarized cells with fast response action potentials.

Class Ib drugs tend to be more specific for voltage gated Na channels than Ia.

Class Ic antiarrhythmic agents markedly depress the phase 0 depolarization (decreasing Vmax).

[5] Sodium channel blockers have been proposed for use in the treatment of cystic fibrosis,[6] but current evidence is mixed.

[7] It has been suggested that the analgesic effects of some antidepressants may be mediated in part via sodium channel blockade.

Class Ia agent decreasing V max , thereby increasing action potential duration.
Effect of class Ib antiarrhythmic agents on the cardiac action potential.
Effect of class Ic antiarrhythmic agent on cardiac action potential.