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WPW syndrome

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Wolff-Parkinson-White (WPW) Syndrome

Definition

WPW syndrome is defined as a pre-excited QRS during sinus rhythm combined with episodes of paroxysmal supraventricular tachycardia (PSVT). It results from the presence of an accessory pathway (AP) - an abnormal strand of myocardium that bypasses the AV node and connects the atria directly to the ventricles (Bundle of Kent). - Harrison's Principles of Internal Medicine, 22E, p. 1984

Pathophysiology

In normal conduction, the AV node delays the impulse before activating the ventricles. In WPW, the AP conducts the impulse faster than the AV node, causing pre-excitation - the ventricles begin depolarizing early (from the AP insertion point), while the rest of the ventricle activates normally via the AV node/His-Purkinje system. This creates a fusion QRS on ECG.

WPW conduction pathways and associated rhythms - Rosen's Emergency Medicine

ECG Features (Classic Triad)

Feature	Description
Short PR interval	<120 ms (bypass of AV node delay)
Delta wave	Slurred upstroke at the beginning of QRS
Wide QRS	>120 ms (due to fusion of AP + normal conduction)

The delta wave polarity varies by AP location and can mimic myocardial infarction or bundle branch block - e.g., negative delta waves in inferior leads can look like inferior MI Q waves.

Accessory Pathway Locations

Pathways can be located around the mitral or tricuspid annulus. Common sites include:

Left lateral (most common) - negative delta in aVL
Right free wall - positive delta in V1
Posteroseptal - negative delta in II, III, aVF (mimics inferior MI)
Anteroseptal

Accessory pathway locations and corresponding ECG delta wave patterns - Harrison's, 22E

Associated Conditions

WPW can be idiopathic or associated with structural heart disease (Box from Rosen's Emergency Medicine):

Hypertrophic cardiomyopathy (most common structural association)
Ebstein anomaly
Transposition of great vessels
Mitral valve prolapse
Endocardial fibroelastosis
Tricuspid atresia

Tachyarrhythmias in WPW

1. Orthodromic AV Reentrant Tachycardia (AVRT) - Most Common (~95%)

Impulse travels antegrade via AV node → ventricles → retrograde via AP → atria
Narrow QRS tachycardia (no pre-excitation during tachycardia)
P waves follow QRS (in ST segment), with short RP interval
Rate: typically 150-250 bpm

2. Antidromic AVRT - Uncommon (~5%)

Impulse travels antegrade via AP → ventricles → retrograde via AV node
Wide, bizarre QRS - often indistinguishable from VT
Pre-excitation is maximal (entire QRS through AP)

3. WPW with Atrial Fibrillation - Most Dangerous

AF impulses bypass the rate-limiting AV node and conduct rapidly down the AP
Ventricular rates can reach 250-300+ bpm
Can degenerate into ventricular fibrillation and sudden cardiac death
~25% of APs have minimum R-R intervals <250 ms during AF, conferring higher SCD risk - Harrison's 22E

Variants

Concealed AP: Only retrograde conduction (ventricle → atrium). No pre-excitation in sinus rhythm, but orthodromic SVT can occur.
Mahaim fibers (Atriofascicular pathways): Duplicate AV node/His-Purkinje system connecting right atrium to right bundle branch → wide LBBB-pattern tachycardia.
PJRT (Permanent Junctional Reciprocating Tachycardia): Slowly conducting posteroseptal AP → near-incessant orthodromic SVT → can cause tachycardia-induced cardiomyopathy.

Management

Acute Tachycardia (Orthodromic AVRT - narrow complex)

Vagal maneuvers (Valsalva, carotid sinus massage)
IV adenosine (drug of choice - blocks AV node, terminates reentry)
IV verapamil or beta-blockers if no pre-excitation present

Acute WPW + AF (Wide complex, pre-excited AF) - EMERGENCY

Hemodynamically unstable: Immediate DC cardioversion
Hemodynamically stable: IV procainamide or ibutilide (slow AP conduction)
CONTRAINDICATED: Digoxin, verapamil, diltiazem, beta-blockers, adenosine, IV amiodarone
- These agents block the AV node but NOT the AP - they can paradoxically accelerate conduction through the AP, precipitating VF and cardiac arrest - Braunwald's Heart Disease; Harrison's 22E

Definitive Treatment

Radiofrequency catheter ablation of the accessory pathway
- Success rate: >95% for most AP locations
- Very low risk of major complications
- AF typically does not recur after successful ablation (since it was often triggered by AVRT degenerating into AF)
- Preferred for symptomatic patients and those with high-risk APs - Braunwald's Heart Disease

Risk Stratification (Asymptomatic WPW)

EP study to measure the shortest pre-excited R-R interval during AF and the AP effective refractory period
High-risk features: AP refractory period <250 ms, multiple APs, Ebstein anomaly
Ablation may be considered in high-risk asymptomatic patients (e.g., athletes, competitive sports)

Key teaching point: Never give AV nodal blocking drugs (verapamil, diltiazem, digoxin, adenosine) in pre-excited AF - this is a potentially fatal error. The only safe acute agents are procainamide/ibutilide, or cardioversion.

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