Sodium channel blockers are used in the treatment of
cardiac arrhythmia. They are classified as "Type I" in the
Vaughan Williams classification. Class I antiarrhythmic agents interfere with the
(Na+) channel. Class I agents are grouped by their effect on the Na+ channel, and by their effect on cardiac
action potentials. Class I agents are called Membrane Stabilizing Agents. 'Stabilizing' refers to the decrease of excitogenicity of the plasma membrane affected by these agents. A few class II agents,
propranolol for example, also have a
membrane stabilizing effect.
Class Ia agents 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. Agents in this class also cause decreased conductivity and increased
refractoriness. Indications for Class Ia agents are
supraventricular tachycardia,
ventricular tachycardia, symptomatic ventricular premature beats, and prevention of
ventricular fibrillation.
Procainamide can be used to treat
atrial fibrillation in the setting of
Wolff–Parkinson–White syndrome, and to treat wide complex hemodynamically stable
tachycardias. Oral procainamide is no longer being manufactured in the US, but intravenous formulations are still available. 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. Class Ia agents include
quinidine,
procainamide and
disopyramide.
Class Ib agents Class Ib antiarrhythmic agents are sodium channel blockers. They have fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates. Class Ib agents shorten the action potential duration and reduce refractoriness. These agents will decrease Vmax in partially depolarized cells with fast response action potentials. They either do not change the action potential duration, or they may decrease the action potential duration. Class Ib drugs tend to be more specific for voltage gated Na channels than Ia.
Lidocaine in particular is highly frequency dependent, in that it has more activity with increasing heart rates. This is because lidocaine selectively blocks Na channels in their open and inactive states and has little binding capability in the resting state. Class Ib agents are indicated for the treatment of ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation. Class Ib agents include
lidocaine,
mexiletine,
tocainide, and
phenytoin.
Class Ic agents Class Ic antiarrhythmic agents markedly depress the phase 0 depolarization (decreasing Vmax). They decrease conductivity, but have a minimal effect on the action potential duration. Of the sodium channel blocking antiarrhythmic agents (the class I antiarrhythmic agents), the class Ic agents have the most potent sodium channel blocking effects. Class Ic agents are indicated for supraventricular arrhythmias (i.e.
atrial fibrillation) and as a last line treatment for refractory life-threatening ventricular tachycardia or ventricular fibrillation. These agents are potentially pro-arrhythmic, especially in settings of structural heart disease (e.g. post-
myocardial infarction), and are contraindicated in such settings. Class Ic agents include
encainide,
flecainide,
moricizine, and
propafenone. Encainide is not available in the United States. ==Other uses==