Antiarrhythmic drugs

Antiarrhythmic drugs
Antiarrhythmic drugs are used to treat arrhythmias, disturbances of the normal heart rhythm.


Troublemakers
Unfortunately, many antiarrhythmics are also capable of worsening or causing the very arrhythmias they’re supposed to treat. The benefits need to be weighed carefully against the risks of antiarrhythmic therapy.
A touch of class
Antiarrhythmics are categorized into four classes:
  • I (which includes classes IA, IB, and IC)
  • II
  • III
  • IV.
Class I antiarrhythmics consist of sodium channel blockers. This is the largest group of antiarrhythmics. Class I agents are frequently subdivided into classes IA, IB, and IC. One drug, adenosine (an AV nodal blocking agent used to treat paroxysmal supraventricular tachycardia), doesn’t fall into any of these classes.
The mechanisms of action of antiarrhythmics vary widely, and a few drugs exhibit properties common to more than one class.
Class IA antiarrhythmics
Class IA antiarrhythmics are used to treat a wide variety of atrial and ventricular arrhythmias. Class IA antiarrhythmics include:
  • disopyramide
  • procainamide
  • quinidine (sulfate and gluconate).
Pharmacokinetics
When administered orally, class IA drugs are rapidly absorbed and metabolized. Because they work so quickly, sustained-release forms of these drugs were developed to help maintain therapeutic levels.

A shot to the head
These drugs are distributed through all body tissues. Quinidine, however, is the only one that crosses the blood-brain barrier.
All class IA antiarrhythmics are metabolized in the liver and are excreted unchanged by the kidneys. Acidic urine increases the excretion of quinidine.


Pharmacodynamics
Class IA antiarrhythmics control arrhythmias by altering the myocardial cell membrane and interfering with autonomic nervous system control of pacemaker cells.
No (para)sympathy
Class IA antiarrhythmics also block parasympathetic stimulation of the sinoatrial (SA) and AV nodes. Because stimulation of the parasympathetic nervous system causes the heart rate to slow down, drugs that block the parasympathetic nervous system increase the conduction rate of the AV node.
Rhythmic risks
This increase in the conduction rate can produce dangerous increases in the ventricular heart rate if rapid atrial activity is present, as in a patient with atrial fibrillation. In turn, the increased ventricular heart rate can offset the ability of the antiarrhythmics to convert atrial arrhythmias to a regular rhythm.
 
Pharmacotherapeutics
Class IA antiarrhythmics are prescribed to treat such arrhythmias as premature ventricular contractions, ventricular tachycardia, atrial fibrillation, atrial flutter, and paroxysmal atrial tachycardia.
Drug interactions
Class IA antiarrhythmics can interact with other drugs:
  • Disopyramide taken with macrolide antibiotics, such as clarithromycin and erythromycin, increases the patient’s risk of developing a prolonged QT interval. In turn, this may lead to an increased risk of arrhythmias, especially polymorphic ventricular tachycardia.
  • Disopyramide plus verapamil may increase myocardial depression and should be avoided in patients with heart failure.
  • Other antiarrhythmics, such as beta-adrenergic blockers, increase the risk of arrhythmias.
  • Quinidine plus neuromuscular blockers may cause increased skeletal muscle relaxation.
  • Quinidine increases the risk of digoxin toxicity.
  • Rifampin, phenytoin, and phenobarbital can reduce the effects of quinidine and disopyramide.
GI symptoms are a common adverse reaction to class IA antiarrhythmics.

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