Sodium channel blocker

Sodium channel blockers are drugs which impair the conduction of sodium ions (Na+) through sodium channels. Sodium channel blockers are drugs which impair the conduction of sodium ions (Na+) through sodium channels. The following naturally-produced substances block sodium channels by binding to and occluding the extracellular pore opening of the channel: Drugs which block sodium channels by blocking from the intracellular side of the channel include: 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 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.