Wolff-Parkinson-White syndrome

Atrial fibrillation and WPW

Patients with Wolff-Parkinson-White syndrome have an “accessory pathway” or a “bypass tract” that connects the electrical system of the atria directly to the ventricles, thereby allowing conduction to avoid passing through the AV node. In normal individuals, when the sinus node creates an action potential it must pass through the AV node to get to the ventricles. When an accessory pathway is present, the sinus node action potential can pass through the bypass tract before the AV node, which causes the ventricles to become depolarized quickly. This is termed “pre-excitation” and results in a shortened PR interval on the ECG.

The combination of WPW and atrial fibrillation can potentially be fatal, especially if AV blocking agents are given (remember “ABCD” for adenosine/amiodarone, beta-blockers, calcium channel blockers and digoxin). The medical treatment is procainamide, although electrical cardioversion is reasonable, especially if hemodynamically unstable.

In patients with WPW and atrial fibrillation, the erratic atrial action potentials (occurring at 400-600 bpm) can conduct through the accessory pathway very quickly (faster than through the AV node). Therefore, WPW patients who develop atrial fibrillation have higher ventricular rates than those without WPW. If an AV blocking agent is given, fewer atrial action potentials will pass through the AV node and more will pass through the accessory pathway, paradoxically increasing the ventricular rate potentially causing ventricular fibrillation which is a fatal, hemodynamically unstable rhythm. Procainamide or electrical cardioversion is recommended in these situations.