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Atrial fibrillation is a medical emergency in the setting of antegrade conduction over an accessory pathway in Wolff-Parkinson-White syndrome.

In manifest Wolff-Parkinson-White (WPW) syndrome, antegrade conduction occurs over the accessory pathway. If atrial fibrillation (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. 14: 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. 14
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).

The treatment of choice is direct-current cardioversion. The usual rate-slowing drugs used in AF are not effective, and digoxin Some Trade Names
DIGITEK
LANOXIN
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and the nondihydropyridine Ca channel blockers (eg, verapamil Some Trade Names
CALAN
ISOPTIN
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, diltiazem Some Trade Names
CARDIZEM
CARTIA
DILACOR
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) 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 Some Trade Names
PROCAN SR
PRONESTYL
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or amiodarone Some Trade Names
CORDARONE
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is preferred, but any class Ia, class Ic, or class III antiarrhythmic can be used.

Last full review/revision January 2008 by L. Brent Mitchell, MD

Content last modified January 2008