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Class IA antiarrhythmics
Class IA antiarrhythmics are used to treat a wide variety of atrialand ventricular arrhythmias. Class IA antiarrhythmics include:
· quinidine (sulfate and gluconate).
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.
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.
Class IA antiarrhythmics control arrhythmias by altering the my-ocardial cell membrane and interfering with autonomic nervous system control of pacemaker cells.
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 in-crease the conduction rate of the AV node.
This increase in the conduction rate can produce dangerous in-creases in the ventricular heart rate if rapid atrial activity is pre-sent, 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.
Class IA antiarrhythmics are prescribed to treat such arrhythmias as premature ventricular contractions, ventricular tachycardia, atrial fibrillation, atrial flutter, and paroxysmal atrial tachycardia.
Class IA antiarrhythmics can interact with other drugs:
· Disopyramide taken with macrolide antibiotics, such as clar-ithromycin and erythromycin, increases the patient’s risk of devel-oping a prolonged QT interval. In turn, this may lead to an in-creased risk of arrhythmias, especially polymorphic ventricular tachycardia.
· Disopyramide plus verapamil may increase myocardial depres-sion and should be avoided in patients with heart failure.
· Other antiarrhythmics, such as beta-adrenergic blockers, in-crease 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 an-tiarrhythmics. (See Adverse reactions to class IA antiarrhyth-mics.)
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