Goal of antiarrhythmic drug therapy is to restore normal rhythm and conduction.
Attempts to revert to normal sinus rhythm, or are used to prevent more serious and possibly lethal arrhythmias from occurring.
Antiarrhythmic drugs are used to:decrease or increase conduction velocity, alter the excitability of cardiac cells by changing the duration of the effective refractory period, or suppress abnormal automaticity.
Directly or indirectly alter membrane ion conductances, and in turn alters the physical characteristics of cardiac action potentials.
Comprise many different drug classes and have several different mechanisms of action.
Some classes and even some specific drugs within a class are effective with only certain types of arrhythmias.
Vaughan-Williams is the most common classification of antiarrhymic drugs.
Therapeutic Classes include: Antianginal, Antiarrhythmic, Antihypertensive, Cardioinhibitory, Cardiostimulatory, Diuretic, Pressor, Thrombolytic, Vasoconstrictor, and Vasodilator.
Class Basic Mechanism Comments
Class I agents are sodium channel blockers which slow conduction by blocking the Na+ channel and are divided into 3 subclasses a, b and c.
Class Ia slows phase 0 depolarization in the ventricles and increases the absolute refractory period.
IA moderate-Moderate reduction in phase 0 slope; increase action potential duration; increase effective refractory period.
Procainamide, quinidineand disopyramide are Class Ia agents.
Class 1b drugs shorten phase 3 repolarization, and include Lidocaine, Mexiletine and Phenytoin.
IB weak Small reduction in phase 0 slope; reduce action potential duration; decrease effective refractory period.
Class Ic greatly slow phase 0 depolarization in the ventricles, but have no effect on the refractory period.
Flecainide,moricizine and propafenone are Class Ic agents.
IC strong with pronounced reduction in phase 0 slope; no effect on action potential duration or effective refractory period.
II beta-blockade block sympathetic activity; reduce rate and conduction.
Class II agents are beta blockers which inhibit SA and AV node depolarization and slow heart rate.
Class Ii agents also decrease cardiac oxygen demand and can prevent cardiac remodeling.
Not all beta blockers are the same, some are cardio selective, affecting only beta 1 receptors, while others are non-selective, affecting beta 1 and 2 receptors.
Beta blockers that target the beta-1 receptor are called cardio selective because beta-1 is responsible for increasing heart rate; hence a beta blocker will slow the heart rate.
III potassium-channel blockade delay repolarization (phase 3) and thereby increase action potential duration and effective refractory period.
Class III agents prolong repolarization by blocking outward K+ current.
Amiodarone and sotalol are effective Class III agents.
Ibutilide is another Class III agent but has a different mechanism of action.
IV calcium-channel blockade Block L-type calcium-channels; most effective at SA and AV nodes; reduce rate and conduction.
Type IV agents are calcium channel blockers that work by inhibiting the action potential of the SA and AV nodes
Miscellaneous agents include adenosine, electrolyte supplements, digitalis compounds, atropine.
Classifications limited bt the fact that many of the drugs have shared mechanisms of action found in other classes.
Are proarrhythmogenic and can trigger life-threatening ventricular arrhythmias in 1 to 3.5% of patients with normal hearts and in up to 15% of patients with reduced ventricular function and/or history of ventricular arrhythmias.