In a patient with Wolff-Parkinson-White syndrome who develops a wide-complex tachycardia under anesthesia, which drug is most appropriate to control the heart rate?

In a patient with Wolff-Parkinson-White syndrome who develops a wide-complex tachycardia under anesthesia, which drug is most appropriate to control the heart rate?

• A. Verapamil
• B. Esmolol
• C. Adenosine
• D. Procainamide

Answer: (D)

In Wolff-Parkinson-White syndrome the tachycardia often travels through an accessory pathway that bypasses the AV node. The goal is not just to slow the AV node but to increase the refractory period of the accessory pathway and slow conduction there. Drugs that block the AV node, like verapamil or beta-blockers, can push more conduction through the accessory pathway to the ventricles, potentially worsening rate and risking dangerous rhythms such as ventricular fibrillation. Adenosine can terminate AVN-dependent tachycardias but may be ineffective or unsafe in preexcited rhythms and can precipitate dangerous outcomes in WPW. Procainamide is a class IA antiarrhythmic that blocks sodium channels and prolongs the action potential, thereby slowing conduction and increasing refractory periods in both atrial tissue and the accessory pathway. This makes it effective for terminating antidromic AVRT and controlling the rate in wide-complex tachycardias associated with WPW during anesthesia.

In Wolff-Parkinson-White syndrome the tachycardia often travels through an accessory pathway that bypasses the AV node. The goal is not just to slow the AV node but to increase the refractory period of the accessory pathway and slow conduction there. Drugs that block the AV node, like verapamil or beta-blockers, can push more conduction through the accessory pathway to the ventricles, potentially worsening rate and risking dangerous rhythms such as ventricular fibrillation. Adenosine can terminate AVN-dependent tachycardias but may be ineffective or unsafe in preexcited rhythms and can precipitate dangerous outcomes in WPW.

Procainamide is a class IA antiarrhythmic that blocks sodium channels and prolongs the action potential, thereby slowing conduction and increasing refractory periods in both atrial tissue and the accessory pathway. This makes it effective for terminating antidromic AVRT and controlling the rate in wide-complex tachycardias associated with WPW during anesthesia.