Wolff–Parkinson–White syndrome

(Redirected from Wolf Parkinson White (WPW))


Graphic representation of the bundle of Kent in Wolff–Parkinson–White syndrome
  • Abbreviation: WPW
  • Congenital pre-excitation syndrome
  • Presence of an accessory electrical pathway between atria and ventricles predisposing to supraventricular tachycardia
  • Associated with certain genetic predispositions, Ebstein anomaly, and hypokalemic periodic paralysis[1] [2]

Types by Aberrant Pathway Site

  • Type A
    • Pathway between the left atrium and ventricle
    • Delta wave and QRS complex predominantly upright in precordial leads [3]
    • Dominant R wave (greater than S amplitude) in V1 may have appearance of right bundle branch block [4]
  • Type B
    • Pathway between the right atrium and ventricle
    • Delta wave and QRS complex predominantly negative in V1 and V2
    • Delta wave and QRS complex predominantly positive in other precordial leads [5]
    • Appearance of left bundle branch block [6]

Types by Cycle Direction

  • Orthodromic
    • Accessory pathway with retrograde reentry conduction
    • Most common variant (~95% of cases)
    • QRS narrow (delta wave absent)
      • Referred to as 'concealed' accessory pathway [7]
    • May see ST depression, TWI
    • Rate 150-250 bpm
  • Antidromic
    • Accessory pathway with anterograde reentry conduction
    • Least common variant (~5% of cases)
    • QRS wide, delta wave present
    • Rate 160-220 bpm, regular

Atrial Fibrillation and Flutter[8]

  • Atrial fibrillation in up to 20% of patients with WPW
    • Irregular rhythm, wide QRS complexes
    • Changing QRS complexes in shape and morphology
    • Axis remains stable as opposed to polymorphic VT
  • Atrial flutter in ~7% of patients with WPW
    • Similar features to atrial fibrillation with WPW
    • Except regular rhythm
    • Easily mistaken for monomorphic ventricular tachycardia
    • Note that if unclear, always safest to assume VT and treat with shock
  • Treatment with AV nodal blocking agents (adenosine, beta-blockers, calcium-channel blockers, amiodarone, digoxin) may incite ventricular fibrillation or ventricular tachycardia
  • "Manifest WPW" = degeneration into VT or VF

Clinical Features

  • Suspect in any patient with ventricular rate >300
  • Many are asymptomatic


  • Irritability, feeding intolerance
  • CHF
  • Intercurrent febrile illness


  • Chest pain, palpitations
  • Shortness of breath
  • Syncope/near-syncope


  • Sudden onset "racing heart"

Differential Diagnosis

Narrow-complex tachycardia

Wide-complex tachycardia

Assume any wide-complex tachycardia is ventricular tachycardia until proven otherwise (it is safer to incorrectly assume a ventricular dysrhythmia than supraventricular tachycardia with abberancy)

^Fixed or rate-related




Delta wave


12 lead electrocardiogram showing classic findings

Although the ECG and an electrophysiology study are diagnostic, the characteristic features are not always seen on ECG

  • Short PR interval - <0.12sec
  • Delta wave / slurred upstroke
    • Due to early activation of ventricular myocardium
  • QRS duration > 0.10 sec
    • Represents a fusion beat
  • Dominant R wave in V1, Type A WPW
    • Left sided accessory pathway
  • Dominant S wave in V1, Type B WPW
    • Right sided accessory pathway
  • Tall R waves in V1-V3 with T wave inversion
    • Mimic RVH
  • "Negative" delta waves in III and aVF
    • Appear as pseudo-infarct Q waves
    • Mimics prior inferior infarct



Treat like paroxysmal SVT


Treat like ventricular tachycardia

Atrial Fibrillation and Atrial Flutter

  • Stable
  • Unstable - synchronized cardioversion
    • Consider higher joule dosage and frequency of repeats than for stable
  • Avoid AV nodal blocking agents



  • Consider if dysrhythmia was easily terminated and can arrange outpatient EP study with possible RF catheter ablation
  • Consider consulting cardiologist regarding outpatient beta-blockers vs. more potent medications (amiodarone, sotalol, flecainide, etc.)


See Also

External Links