Immediate Management of Atrial Fibrillation: State of the Art

Abstract

During programmed stimulation cardiac arrhythmias are more commonly induced when the applied extrastimulus is near the refractory period. This was illustrated in a study by Wijffels [1] entitled “Atrial Fibrillation Begets Atrial Fibrillation.” In this experiment, a single extrastimulus applied to the right atrium of goats did not induce atrial fibrillation when applied at the atrial refractory period (127 msec). Using pacemaker techniques, atrial fibrillation was induced for 6 hours and an extrastimulus was reapplied. The atrial refractory period was shortened (104 msec) and short runs of atrial fibrillation were induced. With longer inductions of pacemaker induced atrial fibrillation, the atrial refractory period became shorter and induced atrial fibrillation lasted longer. The authors concluded that atrial fibrillation results in electrophysiologic changes of a shorter refractory period which promote the maintenance of atrial fibrillation. The reasons for this electrical remodeling are unclear however they can be reversed. If sinus rhythm is maintained for a week, the electrophysiologic changes return to normal. These results have important implications in the management of patients with acute atrial fibrillation. New onset atrial fibrillation is recognized in three general clinical categories. The first category represents the minority of patients with atrial fibrillation. These are patients who have a rapid ventricular response and hemodynamic compromise. Frequently these patients are brought to the hospital after experiencing dizziness, syncope or some other type of cardiac symptom requiring prompt attention. In these patients the immediate management is direct current cardioversion. In the second clinical setting, atrial fibrillation results in a rapid ventricular response but without hemodynamic compromise. These patients seek medical attention early in the course of symptoms and may complain of dizziness, chest pain, dyspnea, or palpitations. In these patients AV node blocking agents such as digoxin, beta blockers or calcium channel blockers are usually given. Whether oral or intravenous medications are given depends upon the clinical context. For patients with heart rates greater than 120–130 bpm or with patients with severe symptoms, intravenous diltiazem (20–25 mg bolus, 10–15 mg per hour) or intravenous esmolol (0.5 mg/kg over 1 minute followed by 0.05 to 0.1 mg/kg per minute) offer prompt control of the ventricular response in most cases [2,3] and are often preferred over oral agents. IV digoxin could also be considered in these cases but the onset of action is slower. A special case involves the patient with a preexcitation syndrome in which atrial fibrillation occurs with a rapid ventricular response. Direct current countershock is indicated in these patients if hemodynamic instability is present. However, for patients who hemodynamically stable, intravenous procainamide is the drug of choice. This drug slows conduction in the accessory pathway and may convert atrial fibrillation to sinus rhythm. Digoxin and intravenous calcium channel blockers may accelerate conduction across the accessory pathway and should be avoided in this situation. Intravenous procainimide should be given with caution since a main side effect is hypotension. Once the ventricular rate is controlled, the physician needs to determine if the patient should be converted to sinus rhythm. Many patients with atrial fibrillation of less than 48 hours will convert to sinus rhythm spontaneously. Other patients will convert to sinus rhythm while receiving digoxin, calcium blockers, or beta blockers. Although there are data suggesting that intracellular calciumlowering drugs (beta blockers and calcium channel blockers) may prevemt early recurrences of atrial fibrillation after electrical cardioversion [4], these drugs are administered primarily for rate control. Because of the high rate of spontaneous conversion to sinus rhythm, the success rates of antiarrythmic drugs must be evaluated in placebo controlled trials. (Table 1, references 5–9,11–13) Digoxin given in doses of 0.6, 0.4, 0.2 and 0.2 mg at 0, 4, 8, and 14 hours has been shown to convert 50% of patients with new onset atrial fibrillation by 18 hours. However 44% of placebo treated patients converted to sinus rhythm, not a significant difference. The atrial refractory period is shortened by digoxin which may be an undesirable