Antiarrhythmic Drugs

Therapeutic Use and Rationale

The goal of antiarrhythmic drug therapy is to restore normal rhythm and conduction. They are also used to prevent more serious and 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
• suppress abnormal automaticity

All antiarrhythmic drugs directly or indirectly alter membrane ion conductances, which alters the physical characteristics of cardiac action potentials. For example, some drugs are used to block fast sodium channels. These channels determine how fast the membrane depolarizes (phase 0) during an action potential. Since conduction velocity is related to how fast the membrane depolarizes, sodium channel blockers reduce conduction velocity. Decreasing conduction velocity can help to abolish tachyarrhythmias caused by reentry circuits. Other types of antiarrhythmic drugs affect the duration of action potentials and the effective refractory period. By prolonging the effective refractory period, reentry tachycardias can often be abolished. These drugs typically block potassium channels and delay repolarization of action potentials (phase 3). Drugs that block slow inward calcium channels are used to reduce pacemaker firing rate by slowing the rate of rise of depolarizing pacemaker potentials (phase 4 depolarization). These drugs also reduce conduction velocity at the AV node because those cells, like SA nodal cells, depend on the inward movement of calcium ions to depolarize. 

Because sympathetic activity can precipitate arrhythmias, drugs that block beta₁-adrenoceptors are used to inhibit sympathetic effects on the heart. Because beta-adrenoceptors are coupled to ion channels through defined signal transduction pathways, beta-blockers indirectly alter membrane ion conductance, particularly calcium and potassium conductance.

With AV block, drugs that block vagal influences (e.g., atropine, a muscarinic receptor antagonist) are sometimes used. AV block can occur during beta-blocker treatment, and therefore simply removing a beta-blocker in patients being treated with such drugs may normalize AV conduction.

Occasionally, the ventricular rate is excessively high because atrial flutter or fibrillation is driving it. Therefore, drugs can be used to slow AV nodal conduction to control ventricular rate. Calcium channel blockers and beta-blockers are useful for this indication. Digoxin, because of its ability to activate the vagus nerve (parasympathomimetic effect), can also reduce AV conduction velocity to normalize ventricular rate during atrial flutter or fibrillation, particularly in heart failure patients.

Classes of Drugs Used to Treat Arrhythmias

Classes of drugs used in the treatment of arrhythmias are given below. Clicking on the drug class will link you to the page describing the pharmacology of that drug class and specific drugs. Please note that many of the drugs comprising the first five listed classes have considerable overlap in their pharmacologic properties.

Antiarrhythmic drug classes:

• Class I - Sodium-channel blockers
• Class II - Beta-blockers
• Class III - Potassium-channel blockers
• Class IV - Calcium-channel blockers
• Miscellaneous - adenosine
  - electrolyte supplement (magnesium and potassium salts)
  - digitalis compounds (cardiac glycosides)
  - atropine (muscarinic receptor antagonist)

Click here to see a table summarizing the drugs that may treat different arrhythmias.

Revised 11/29/2023