Overview

• Wolff–Parkinson–White (WPW) syndrome is cardiac pre-excitation caused by an accessory pathway (Bundle of Kent) that can bypass the AV node and alter ventricular activation and arrhythmia risk.
• Often asymptomatic and found incidentally on ECG, but can produce reentrant supraventricular tachycardia or dangerous rapid ventricular rates when atrial fibrillation occurs.

Anatomy & basic pathophysiology

• The Bundle of Kent connects atria to ventricles outside the AV node, allowing earlier ventricular activation (pre-excitation).
• In normal conduction: SA node → AV node → ventricles. In WPW, accessory pathway can deliver impulses faster to ventricles, competing with AV nodal conduction.
• Pre-excitation short-circuits normal delay at the AV node and can form reentrant circuits when dual conduction pathways exist.

Key ECG features in sinus rhythm (WPW pattern)

• Delta wave: a slurred upstroke of the QRS due to early ventricular activation via the accessory pathway.
• Short PR interval: impulse reaches ventricles earlier than via AV node.
• Widened QRS: because initial activation is abnormal and full ventricular depolarization follows a longer route.
• The delta wave may be subtle or intermittent; careful inspection of ECG leads is required.

Reentrant tachycardias in WPW

Orthodromic AVRT (most common SVT in WPW)

• Reentry travels anterograde through the AV node and retrograde via the Bundle of Kent, forming a continuous loop.
• Produces a narrow-complex tachycardia because ventricular activation runs through the normal His–Purkinje system.
• Delta wave is absent during the tachycardia (pre-excitation not seen because anterograde conduction uses AV node).
• Typical rate: about \(160\)–\(170\) bpm; patients report sudden palpitations.
• Acute treatment: AV nodal blocking agents such as adenosine or calcium channel blockers are effective because they interrupt the anterograde limb of the circuit.

Antidromic AVRT

• Reentry goes anterograde through the Bundle of Kent and retrograde through the AV node.
• Results in a wide-complex tachycardia because ventricles are activated via the accessory pathway.
• Do NOT use adenosine or AV-nodal blocking drugs here—blocking the AV node can force all conduction down the accessory pathway and precipitate ventricular tachyarrhythmia.
• Preferred acute pharmacologic therapy: procainamide (stabilizes conduction via accessory pathway).

WPW with atrial fibrillation (AF)

• AF can produce very fast atrial rates (e.g., around \(400\) beats per minute).
• The AV node normally limits how many impulses reach the ventricles; the accessory pathway often lacks the same rate-limiting refractory properties.
• Giving AV nodal blockers (calcium channel blockers, digoxin, beta blockers) can block the AV node and divert conduction to the accessory pathway, risking extremely rapid ventricular rates, ventricular tachycardia, or ventricular fibrillation.
• AV nodal blockers are contraindicated in WPW with AF. Use agents that slow conduction through or modify the accessory pathway (e.g., procainamide) or perform urgent electrical cardioversion if unstable.

Acute management summary

• Unstable patient (hypotension, ischemia, shock, altered mental status): immediate synchronized electrical cardioversion.
• Stable patient with narrow-complex orthodromic AVRT: adenosine or AV node blockers (if not contraindicated) to interrupt the circuit.
• Stable patient with wide-complex tachycardia suspicious for antidromic AVRT or WPW with pre-excited AF: avoid AV nodal blockers; use procainamide or consult electrophysiology.

Definitive treatment

• Catheter ablation of the accessory pathway is the definitive therapy and is curative in most patients.
• Ablation is indicated for symptomatic patients, recurrent tachyarrhythmias, or high-risk accessory pathways.

Clinical pearls

• Always differentiate orthodromic (narrow QRS, treat with AV nodal blockers) from antidromic/pre-excited arrhythmia (wide QRS, avoid AV nodal blockers).
• In any WPW patient with AF or an irregular wide-complex tachycardia, do not give AV nodal blockers; think accessory-pathway conduction and consider procainamide or cardioversion.
• Delta waves may be subtle—young, asymptomatic patients can still harbor a dangerous pathway.

Quick algorithm (stable vs unstable)

1. Assess stability: if unstable → synchronized cardioversion.
2. If stable and narrow-complex SVT consistent with orthodromic AVRT → adenosine or other AV nodal blocker.
3. If wide-complex tachycardia, pre-excited AF, or antidromic AVRT suspected → avoid AV node blockers; use procainamide and consult EP.
4. Consider catheter ablation for definitive management.