Wolff-Parkinson-White Syndrome

Origin of name?

  • First described in 1930 by Louis Wolff, John Parkinson and Paul Dudley White.

What is it?

  • combination of the presence of a congenital accessory pathway (Bundle of Kent/ atrioventricular bypass tract) and episodes of tachyarrhythmia.
  • Incidence 0.1 – 3.0 per 1000

Why we should know?

  • small risk of sudden cardiac death.
  • can cause tachyarrhytmia.

What it do?

  • can causePre-excitation:  early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway (bypass tracts, are abnormal conduction pathways formed during cardiac development and can exist in a variety of anatomical locations and in some patients there may be multiple pathways)
  • this accessory pathway can conduct impulse both direction (most of the case), antegrade only(rare) or retrograde only(15%) – will affect appearance of the ECG.
    • PR interval <120ms

    • Delta wave – slurring slow rise of initial portion of the QRS

    • QRS prolongation >110ms

    • ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex.Pseudo-infarction pattern can be seen in up to 70% of patients – due to negatively deflected delta waves in the inferior / anterior leads (“pseudo-Q waves”), or as a prominent R wave in V1-3 (mimicking posterior infarction).no 4. : deflected delta wave at inferior lead.

    • pre-excitation may be subtle, or present only intermittently.

    • Pre-excitation may be more pronounced with increased vagal tone e.g. during Valsalva manoeuvres, or with AV blockade e.g. drug therapy.

    • 2 types. Types A or B.Type A has a positive delta wave in all precordial leads with R/S > 1 in V1Type B has a negative delta wave in leads V1 and V2 (cause pseudo Q-wave)In patients with retrograde-only accessory conduction all antegrade conduction occurs via the AV node, thus no features of WPW are seen on the ECG in sinus rhythm (as no pre-excitation occurs). This is termed a “concealed pathway”. Still can experience tachyarrythmias as the pathway can still form part of a re-entry circuit.

  • facilitate Tachyarrhytmia, by the formation of a reentry circuit involving the accessory pathway, termed atrioventricular reentry tachycardias (AVRT). – part of large group tachyarrhytmias  called paroxysmal SVT
  • or by passing AV nodes and cause atrial fibrillation or atrial flutter in conjunction with WPW.


Treatment of WPW associated arrhythmias comprises the following:

  • Radiofrequency ablation of the accessory pathway.
  • Antiarrhythmic drugs to slow accessory pathway conduction
    • Long-term antiarrhythmic therapyOral medication is the mainstay of therapy in patients not undergoing radiofrequency ablation, although the response to long-term antiarrhythmic therapy for the prevention of further episodes of tachycardia in patients with WPW syndrome remains quite variable and unpredictable. Choices include the following:
      • Class Ic drugs (eg, flecainide, propafenone), typically used with an AV nodal blocking agent in low doses to avoid atrial flutter with a 1:1 conduction.
      • Class III drugs (eg, amiodarone, sotalol), although these are less effective for altering accessory pathway conduction properties.
      • In pregnancy, sotalol (class B) or flecainide (class C).
  • Typically, AV node-conduction blocking medicationsare avoided in the acute setting of WPW.
  • For adult WPW patients, address the triggers that perpetuate the dysrhythmia, which include coronary heart disease (CAD), ischemia, cardiomyopathy, pericarditis, electrolyte disturbances, thyroid disease, and anemia

Termination of acute episodes

Decide: Stable or Unstable


Narrow-complex AV reentrant tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT) are treated by blocking AV node conduction with the following:

  • Vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage, splashing cold water or ice water on the face)
  • Adults: IV adenosine 6mg, then 12 mg, then another 12 mg if fail, with 1-2 minute interval, via a large-bore line (the drug has a very short half-life: 10 seconds)
  • Adults: IVI verapamil 1mg/min up to 20mg or IV diltiazem 2.5/min every 3 minutes max 50 mg.

Atrial flutter/fibrillation or wide-complex tachycardia is treated as follows:

  • IV procainamide (blocked both AV node and accessory pathway) or amiodarone (controversial-AV nodal blocking may occur preferentially)
  • Avoid ABCD drugs (amiodarone, beta blocker, calcium channel blocker, digoxin). As this will promote conduction through accessory bundle without protective refractory period of the AV node.

The initial treatment of choice for hemodynamically unstable tachycardia is direct-current synchronized electrical cardioversion, biphasic, as follows:

  • A level of 50 J (biphasic) initially
  • 100, 150, 200J subsequently

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