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Wolff-Parkinson-White Syndrome by mrcpstudy


Wolff-Parkinson-White Syndrome

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									Wolff-Parkinson-White Syndrome
In 1930, Wolff, Parkinson, and White described a series of young patients who experienced paroxysms of
tachycardia and had characteristic abnormalities on electrocardiography (ECG). Currently, Wolff-Parkinson-
White (WPW) syndrome is defined as a congenital condition involving abnormal conductive tissue between
the atria and the ventricles that provides a pathway for a reentrant tachycardia circuit.

Signs and symptoms
Clinical manifestations of WPW syndrome may have their onset at any time from childhood to middle age,
and they can vary in severity from mild chest discomfort or palpitations with or without syncope to severe
cardiopulmonary compromise and cardiac arrest. Presentation varies by patient age.
Infants may present with the following:

      Tachypnea
      Irritability
      Pallor
      Intolerance of feedings
      Evidence of congestive heart failure if the episode has been untreated for several hours
      A history of not behaving as usual for 1-2 days
      An intercurrent febrile illness may be present

A verbal child with WPW syndrome usually reports the following:

      Chest pain
      Palpitations
      Breathing difficulty

Older patients can usually describe the following:

      Sudden onset of a pounding heartbeat
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      Pulse that is regular and “too rapid to count”
      Typically, a concomitant reduction in their tolerance for activity

Physical findings include the following:

      Normal cardiac examination findings in the vast majority of cases
      During tachycardic episodes, the patient may be cool, diaphoretic, and hypotensive
      Crackles in the lungs from pulmonary vascular congestion
      In many young patients, only minimal symptoms (eg, palpitations, weakness, mild dizziness) despite
       exceedingly fast heart rates

Clinical features of associated cardiac defects may be present, such as the following:

      HOCM
      mitral valve prolapse
      Ebstein's anomaly
      thyrotoxicosis
      secundum ASD

The diagnosis of WPW syndrome is typically made with formal ECG monitoring (eg, telemetry, Holter
monitoring) in conjunction with clues from the history and physical examination. Although the ECG
morphology varies widely, the classic ECG features are as follows:
Possible ECG features include:

      short PR interval
      wide QRS complexes with a slurred upstroke - 'delta wave'
      left axis deviation if right-sided accessory pathway*
      right axis deviation if left-sided accessory pathway*

Differentiating between type A and type B

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      type A (left-sided pathway): dominant R wave in V1
      type B (right-sided pathway): no dominant R wave in V1

Electrophysiologic studies (EPS) can be used in patients with WPW syndrome to determine the

      The mechanism of the clinical dysrhythmia
      The electrophysiologic properties (eg, conduction capability, refractory periods) of the accessory
       pathway and the normal atrioventricular (AV) nodal and His Purkinje conduction system
      The number and locations of accessory pathways (necessary for catheter ablation)
      The response to pharmacologic or ablation therapy


      definitive treatment: radiofrequency ablation of the accessory pathway
      medical therapy: sotalol**, amiodarone, flecainide

*in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is
associated with left axis deviation

**sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the
AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular
rate and potentially deteriorating

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