Drugs that Treat Cardiac Arrhythmias

The Antiarrhythmic Medications

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If you have a cardiac arrhythmia (or heart rhythm disturbance) such as atrial fibrillationsupraventricular tachycardia (SVT)atrial premature complexes (PACs), or ventricular premature complexes (PVCs), your doctor may prescribe a medication aimed at suppressing the arrhythmia. These medications are called antiarrhythmic drugs.

The major antiarrhythmic drugs (those in Class I and Class III), can often produce side effects that outweigh their potential benefits. For this reason, doctors are usually reluctant to prescribe them unless the arrhythmia being treated is very disruptive to a patient's life — and there are no other acceptable alternatives.

Nonetheless, under the right circumstances these drugs can be extremely helpful in controlling a person’s disruptive or dangerous cardiac arrhythmia.

What Do Antiarrhythmic Drugs Do?

Antiarrhythmic drugs work by altering the characteristics of the heart’s electrical impulse.

The electrical impulse and the heart beat. The electrical impulse of the heart is generated by the flow of ions (charged particles) back and forth across the membranes of cardiac cells. The flow of ions, in turn, is controlled by various channels in the cell membrane, that open and close in an organized fashion.

As certain channels open, positively charged sodium ions stream into the cell, causing the cell to “depolarize.” This depolarization (which you can think of as a sudden surge in electrical charge), causes the adjacent cardiac cells to depolarize — and in this way the electrical signal is spread across the heart.

As the heart cells depolarize, they contract — and the heart beats. The spread of the electrical signal across the heart is carefully organized in order to produce an effective and efficient heart beat. You can read details about the heart’s electrical system here.

Antiarrhythmic drugs. Antiarrhythmic drugs work by changing the way ions jump back and forth across the cardiac cell membranes, and thus they change the characteristics of the heart’s electrical signal. 

In the case of automatic cardiac arrhythmias, some antiarrhythmic drugs are useful for suppressing “automaticity” — the tendency of cardiac cells to spontaneously depolarize.

With reentrant cardiac arrhythmias, antiarrhythmic drugs can disrupt the ability of the electrical signal to continuously spin around the reentrant loop.

Thus, by changing the characteristics of the heart’s electrical signal, antiarrhythmic drugs can make cardiac arrhythmias less likely to occur.

Side Effects - Proarrhythmia

The major antiarrhythmic drugs — those in Class I and Class III — are relatively likely to produce side effects. There are many of these drugs, and each of them has a unique side effect profile — so make sure you are aware of the potential side effects of the particular antiarrhythmic drug your doctor is recommending.

But you also need to be aware that there is a potential side effect that many of these drugs share — proarrhythmia, which is the tendency to make arrhythmias worse instead of better.

While it may seem paradoxical that drugs that are meant to suppress arrhythmias can actually potentiate them, if you understand how these drugs work this phenomenon is actually predictable.

There are two general mechanisms of proarrhythmia. First, antiarrhythmic drugs can make reentrant arrhythmias more likely to occur. These drugs work by changing the characteristics of the cardiac electrical signal, and in treating reentrant arrhythmias the idea is to change the signal in such a way as to make reentry less likely to occur. But sometimes the change in the electrical signal caused by the drug will make reentry more likely to occur. There’s actually no way to know ahead of time which of these effects a drug will have on a reentrant arrhythmia, and it often turns out to be a matter of trial and error.

The second mechanism of proarrhythmia is caused by prolonging the QT interval on the ECG — producing the long QT syndrome. Some people are susceptible to dangerous arrhythmias when their QT intervals are prolonged, and several antiarrhythmic drugs actually work by prolonging the QT intervals. 

The phenomenon of proarrhythmia makes doctors relatively reluctant to prescribe antiarrhythmic drugs unless the potential benefits greatly outweigh these (and other) risks. When these drugs are used, doctors need to take every available precaution to prevent harm from being done.

How Antiarrhythmic Drugs Are Classified

Antiarrhythmic drugs are classified according to their specific effects on the various kinds of channels in the cardiac cell membrane that control the flow of ions. These drugs are currently classified into 5 catetories: Class 0 to Class IV.

Class 0 Antiarrhythmic Drugs

Class 0 is reserved for drugs that block a particular channel that controls the “pacemaker current” in the sinus node, thus slowing the heart rate. The only drug currently in this class is ivabradine, which is useful in treating inappropriate sinus tachycardia. Notably, ivabradine does not appear to cause proarrhythmia.

Class I Antiarrhythmic Drugs

Class I antiarrhythmic drugs block channels in a way that slows the heart’s electrical signal as it spreads across the heart, and they also tend to prolong the QT interval. These drugs are most often used in treating reentrant arrhythmias, but because they can produce both kinds of proarrhythmia their usage has fallen off over the past decade or two. The class I drugs include:

  • Disopyramide
  • Flecainide
  • Mexilitine
  • Phenytoin
  • Propafenone
  • Quinidine

Beta Blockers (Class II Antiarrhythmic Drugs)

Beta blockers have many clinical uses. Among these is that, in some circumstances, they can be useful antiarrhythmic drugs. Beta blockers slow the generation of electrical signals by the sinus node, so they can be useful in treating inappropriate sinus tachycardia. They also slow the conduction of the electrical signal across the AV node, so they can slow the heart rate during atrial fibrillation. However, except for these two specific purposes, beta blockers as a class are not particularly effective antiarrhythmic drugs. On the other hand, beta blockers have the major advantage of not producing proarrhythmia. The beta blockers include:

  • Acebutolol
  • Atenolol
  • Betaxolol
  • Bisoprolol
  • Carteolol
  • Carvedilol
  • Labetalol
  • Metoprolol
  • Nadolol
  • Penbutolol
  • Propranolol
  • Timolol

Class III Antiarrhythmic Drugs

The class III antiarrhythmic drugs primarily work by prolonging the QT interval, which accounts for their main proarrhythmia risk. Amiodarone and dronedarone, however, uniquely cause very few episodes of proarrhythmia. The class III antiarrhythmic drugs include:

  • Amiodarone (Amiodarone is a particularly effective — and particularly toxic — antiarrhythmic drug. Read more about amiodarone here.)
  • Dofetilide
  • Dronedarone
  • Ibutilide
  • Sotalol
  • Vernakalant

Calcium Channel Blockers (Class IV Antiarrhythmic Drugs)

Two of the calcium channel blockers, like the beta blockers, are useful in treating arrhythmias that involve the sinus node and AV node. Also like the beta blockers, these drugs do not cause proarrhythmia. The Class IV antiarrhythmic drugs include:

  • Diltiazem
  • Verapamil

A Word From Verywell

Antiarrhythmic drugs can be useful in managing various types of cardiac arrhythmias, but care must be used because the drugs in Class I and Class III tend to produce significant side effects, including the risk of proarrhythmia.

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  • Grant AO. Cardiac Ion Channels. Circ Arrythm Electrophysiol 2009; 2:185.