Loss of coordinated atrial contraction promotes stasis of blood within the left atrium and can lead to the formation of atrial thrombi. Atrial thrombi and the potential for thromboembolic stroke are the most serious clinical dangers of atrial fibrillation. Patients with atrial thrombus are usually treated with anticoagulants.
For long-term anticoagulation therapy, warfarin is most often used. Warfarin is a vitamin K antagonist, with a narrow therapeutic window that necessitates frequent monitoring of clinical effect (international normalized ratio).
Control of ventricular response is typically achieved with drugs that slow AV nodal conduction. The most commonly used drugs for this purpose are -blockers, calcium channel blockers, and digoxin. -Blockers are useful in the prevention of recurrent atrial fibrillation, provide good heart rate control, and reduce symptoms during subsequent episodes of atrial fibrillation.
Pharmacologic cardioversion is most effective if initiated within 7 days of the onset of atrial fibrillation. Several drugs are efficacious in converting atrial fibrillation to sinus rhythm, including amiodarone, propafenone, ibutilide, and sotalol.
The preferred drug for patients with significant heart disease, including ischemic heart disease, left ventricular hypertrophy, left ventricular dysfunction, and heart failure, is amiodarone
If the atrial fibrillation is hemodynamically significant, the treatment is cardioversion. Synchronized cardioversion at 100 to 200 J (biphasic) is indicated. If vital signs are stable, the primary goal should be rate control with a -blocker or calcium channel blocker if there are no clinical contraindications. The drug of choice for rate control in a patient with a known or suspected electrical accessory pathway and preexcitation is procainamide or amiodarone. Pharmacologic conversion to sinus rhythm with intravenous amiodarone may be attempted if vital signs allow.
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