Atrial fibrillation (AF) is a medical emergency when rapid antegrade conduction over an accessory pathway occurs in Wolff-Parkinson-White (WPW) syndrome.

In manifest WPW syndrome, antegrade conduction occurs over the accessory pathway. If AF develops, the normal rate-limiting effects of the atrioventricular (AV) node are bypassed, and the resultant excessive ventricular rates (sometimes 200 to 240 beats/min) may lead to ventricular fibrillation (see Fig. 15: Arrhythmias and Conduction Disorders: Atrial fibrillation in Wolff-Parkinson-White syndrome.) and sudden death. Patients with concealed WPW syndrome are not at risk because in them, antegrade conduction does not occur over the accessory connection.

Fig. 15
Atrial fibrillation in Wolff-Parkinson-White syndrome. Ventricular response is very fast (RR intervals minimum of 160 msec). Shortly thereafter, ventricular fibrillation develops (lead II continuous rhythm strip at bottom).

Pearls & Pitfalls Do not give digoxin or nondihydropyridine Ca channel blockers (eg, verapamil, diltiazem) to patients with atrial fibrillation and WPW because these drugs may trigger ventricular fibrillation.

The treatment of choice is direct-current cardioversion. The usual rate-slowing drugs used in AF are not effective, and digoxin and the nondihydropyridine Ca channel blockers (eg, verapamil, diltiazem) are contraindicated because they may increase the ventricular rate and cause ventricular fibrillation. If cardioversion is impossible, drugs that prolong the refractory period of the accessory connection should be used. IV procainamide or amiodarone is preferred, but any class Ia, class Ic, or class III antiarrhythmic can be used.

Last full review/revision July 2012 by L. Brent Mitchell, MD