Antiarrhythmic Drugs

See also the following individual entries:

Calcium Channel Blocking Agents



Diltiazem hydrochloride Flecainide acetate Lidocaine hydrochloride Moricizine hydrochloride Phenytoin Phenytoin sodium

Procainamide hydrochloride Propranolol hydrochloride Quinidine gluconate Tocainide hydrochloride Verapamil General Statement: Cardiac arrhythmias are altered patterns of contraction or marked increases or decreases in the rate of the heart which reduce the ability of the heart to pump blood. Some examples of cardiac arrhythmias are premature ventricular beats, ventricular tachycardia, atrial flutter, atrial fibrillation, ventricular fibrillation, and atrioventricular heart block. Action/Kinetics: The various anti-arrhythmic drugs are classified according to both their mechanism of action and their effects on the action potential of cardiac cells. Importantly, one drug in a particular class may be more effective and safer in an individual client. The antiarrhythmic drugs are classified as follows:

1. Group I. These drugs decrease the rate of entry of sodium into the cell during cardiac membrane depolarization which prevents depolarization and transmission of nerve impulses. Drugs classified as group I are further listed in subgroups (according to their effects on action potential duration) as follows:

• Group IA: Prolong the duration of the action potential. Examples: Dis-opyramide, procainamide, and qui-nidine.

• Group IB: Are thought to shorten the action potential. Examples: Lido-caine, phenytoin, and tocainide.

• Group IC: Significant slowing of conduction without really affecting the action potential. Examples: Flecai-nide, indecainide, and propafenone.

NOTE: Moricizine is classified as a group I agent but it has characteristics of agents in groups IA, B, and C.

2. Group II. These drugs competitively block beta-adrenergic receptors and depress phase 4 depolarization. Examples: Acebutolol, esmolol, and propranolol.

3. Group III. These drugs prolong the duration of the membrane action potential (relative refractory period) without changing the phase of depolarization or the resting membrane potential. Examples: Amiodarone, bretylium, and sotalol.

4. Group IV. Verapamil, a calcium channel blocker that slows conduction velocity and increases the refractoriness of the AV node.

Two other drugs, adenosine and digoxin, are also used to treat arrhythmias. Adenosine slows conduction time through the AV node and can interrupt the reentry pathways through the AV node. Digoxin causes a decrease in maximal diastolic potential and duration of the action potential; it also increases the slope of phase 4 depolarization. Special Concerns: Monitor serum levels of antiarrhythmic drugs since some drugs can cause toxic side effects which can be confused with the purpose for which the drug is used. For example, toxicity from quinidine can result in cardiac arrhythmias. Antiarrhythmic drugs may cause new or worsening of arrhythmias, ranging from an increase in frequency of PVCs to severe ventricular tachycardia, ventricular fibrillation, or tachycardia that is more sustained and rapid. Such situations (called proarrhythmic effect) may make it difficult to distinguish the proarrhythmic effect from the underlying rhythm disorder.

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