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Emergency and Acute Medicine – Wolff–Parkinson–White (WPW) Syndrome
Wolff–Parkinson–White syndrome (WPW) is a cardiac conduction disorder caused by the presence of an accessory pathway (Kent bundle) that bypasses the atrioventricular (AV) node, allowing premature ventricular activation (pre-excitation). On ECG, the WPW pattern is characterized by a short PR interval (<0.12 sec), a delta (Δ) wave representing early ventricular depolarization, and a widened QRS complex (>0.10 sec). While the ECG pattern alone is termed WPW pattern, the diagnosis of WPW syndrome requires both these findings and associated tachydysrhythmias.
Accessory pathways occur in approximately 0.1–0.3% of the population and are most commonly located along the left lateral free wall, followed by the posteroseptal region. Conduction through these pathways may occur in antegrade, retrograde, or bidirectional fashion. The most common arrhythmia associated with WPW is orthodromic atrioventricular re-entrant tachycardia (AVRT) (≈70%), where impulses travel down the AV node and return via the accessory pathway, producing a narrow complex tachycardia. Less commonly, antidromic AVRT (≈30%) occurs, with conduction down the accessory pathway and back through the AV node, resulting in a wide complex tachycardia. WPW can also precipitate atrial fibrillation with rapid ventricular response, which carries a risk of degeneration into ventricular fibrillation and sudden death.
Patients may be asymptomatic or present with palpitations, chest pain, dyspnea, dizziness, diaphoresis, or syncope. Physical findings depend on the rhythm and hemodynamic status, ranging from stable tachycardia to signs of instability such as hypotension, altered mental status, cyanosis, or pulmonary edema. Sudden cardiac death is rare but can occur (approximately 1 per 1,000 patient-years).
Diagnosis is based primarily on ECG findings. During sinus rhythm, the classic triad includes short PR interval, delta wave, and widened QRS complex. During tachyarrhythmias, ECG patterns vary depending on the mechanism: orthodromic AVRT typically produces a narrow complex tachycardia (150–250 bpm), while antidromic AVRT produces a wide complex tachycardia. Atrial fibrillation in WPW appears as an irregular wide complex rhythm with variable QRS morphology, which is a dangerous presentation.
Management depends on patient stability and rhythm type. Unstable patients (hypotension, chest pain, altered mental status) require immediate synchronized cardioversion, starting at 100 J and escalating as needed. In stable patients, initial management includes vagal maneuvers such as the Valsalva maneuver or carotid sinus massage (if no contraindications).
For narrow complex tachycardia (orthodromic AVRT), pharmacologic therapy includes Adenosine (6 mg rapid IV bolus, followed by 12 mg if needed; pediatric: 0.1–0.2 mg/kg) or calcium channel blockers when the diagnosis is certain. For wide complex tachycardia or suspected WPW with atrial fibrillation, Amiodarone (150 mg IV over 10 minutes, followed by infusion) or Procainamide (6–13 mg/kg IV infusion) are preferred.
Critically important: AV nodal–blocking agents such as β-blockers, calcium channel blockers, digoxin, and lidocaine must be avoided in patients with WPW and wide complex tachycardia or atrial fibrillation, as they may enhance conduction through the accessory pathway and precipitate fatal ventricular arrhythmias.
Disposition depends on clinical presentation. Patients with instability, syncope, or refractory arrhythmias require admission and monitoring. Most stable patients who convert to sinus rhythm can be discharged with cardiology follow-up, including consideration of electrophysiologic studies and radiofrequency ablation, which offers definitive treatment.
Key clinical pearls include maintaining a high suspicion for WPW in any tachydysrhythmia, avoiding AV nodal blockers in uncertain wide complex rhythms, and addressing anticoagulation if arrhythmia duration exceeds 48 hours due to embolic risk.
Wolff–Parkinson–White syndrome (WPW) is a cardiac conduction disorder caused by the presence of an accessory pathway (Kent bundle) that bypasses the atrioventricular (AV) node, allowing premature ventricular activation (pre-excitation). On ECG, the WPW pattern is characterized by a short PR interval (<0.12 sec), a delta (Δ) wave representing early ventricular depolarization, and a widened QRS complex (>0.10 sec). While the ECG pattern alone is termed WPW pattern, the diagnosis of WPW syndrome requires both these findings and associated tachydysrhythmias.
Accessory pathways occur in approximately 0.1–0.3% of the population and are most commonly located along the left lateral free wall, followed by the posteroseptal region. Conduction through these pathways may occur in antegrade, retrograde, or bidirectional fashion. The most common arrhythmia associated with WPW is orthodromic atrioventricular re-entrant tachycardia (AVRT) (≈70%), where impulses travel down the AV node and return via the accessory pathway, producing a narrow complex tachycardia. Less commonly, antidromic AVRT (≈30%) occurs, with conduction down the accessory pathway and back through the AV node, resulting in a wide complex tachycardia. WPW can also precipitate atrial fibrillation with rapid ventricular response, which carries a risk of degeneration into ventricular fibrillation and sudden death.
Patients may be asymptomatic or present with palpitations, chest pain, dyspnea, dizziness, diaphoresis, or syncope. Physical findings depend on the rhythm and hemodynamic status, ranging from stable tachycardia to signs of instability such as hypotension, altered mental status, cyanosis, or pulmonary edema. Sudden cardiac death is rare but can occur (approximately 1 per 1,000 patient-years).
Diagnosis is based primarily on ECG findings. During sinus rhythm, the classic triad includes short PR interval, delta wave, and widened QRS complex. During tachyarrhythmias, ECG patterns vary depending on the mechanism: orthodromic AVRT typically produces a narrow complex tachycardia (150–250 bpm), while antidromic AVRT produces a wide complex tachycardia. Atrial fibrillation in WPW appears as an irregular wide complex rhythm with variable QRS morphology, which is a dangerous presentation.
Management depends on patient stability and rhythm type. Unstable patients (hypotension, chest pain, altered mental status) require immediate synchronized cardioversion, starting at 100 J and escalating as needed. In stable patients, initial management includes vagal maneuvers such as the Valsalva maneuver or carotid sinus massage (if no contraindications).
For narrow complex tachycardia (orthodromic AVRT), pharmacologic therapy includes Adenosine (6 mg rapid IV bolus, followed by 12 mg if needed; pediatric: 0.1–0.2 mg/kg) or calcium channel blockers when the diagnosis is certain. For wide complex tachycardia or suspected WPW with atrial fibrillation, Amiodarone (150 mg IV over 10 minutes, followed by infusion) or Procainamide (6–13 mg/kg IV infusion) are preferred.
Critically important: AV nodal–blocking agents such as β-blockers, calcium channel blockers, digoxin, and lidocaine must be avoided in patients with WPW and wide complex tachycardia or atrial fibrillation, as they may enhance conduction through the accessory pathway and precipitate fatal ventricular arrhythmias.
Disposition depends on clinical presentation. Patients with instability, syncope, or refractory arrhythmias require admission and monitoring. Most stable patients who convert to sinus rhythm can be discharged with cardiology follow-up, including consideration of electrophysiologic studies and radiofrequency ablation, which offers definitive treatment.
Key clinical pearls include maintaining a high suspicion for WPW in any tachydysrhythmia, avoiding AV nodal blockers in uncertain wide complex rhythms, and addressing anticoagulation if arrhythmia duration exceeds 48 hours due to embolic risk.
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