Image for Cardiovascular Pharmacology Concepts, Richard E Klabunde PhD

Cardiovascular Pharmacology Concepts

Richard E. Klabunde, PhD

Clinical Disorders:

Therapeutic Classes:

Mechanism Classes:

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Cardiovascular Physiology Concepts textbook cover

Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2011)


Cardiovascular Physiology Concepts textbook cover

Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)


Antiarrhythmic Drugs

Therapeutic Use and Rationale

The ultimate goal of antiarrhythmic drug therapy is to restore normal rhythm and conduction. When it is not possible to revert to normal sinus rhythm, drugs may be used to prevent more serious and possibly lethal arrhythmias from occurring. Antiarrhythmic drugs are used to:

All antiarrhythmic drugs directly or indirectly alter membrane ion conductances, which in turn 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 especially the effective refractory period. By prolonging the effective refractory period, reentry tachycardias can often be abolished. These drugs typically affect 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.

In the case of 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.

Sometimes ventricular rate is excessively high because it is being driven by atrial flutter or fibrillation. Because it is very important to reverse ventricular tachycardia, drugs are often used to slow AV nodal conduction. Calcium channel blockers and beta-blockers are useful for this indication. Digitalis, because of its ability to activate the vagus nerve (parasympathomimetic effect), can also be used to reduce AV conduction velocity in an attempt to normalize ventricular rate during atrial flutter or fibrillation.

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:

Click here to see a table summarizing the types of drugs that may be used to treat different types of arrhythmias.

Revised 03/14/07

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.