Why rapid recognition, treatment of Wolff-Parkinson-White syndrome is important

Atrial fibrillation in WPW can lead to ventricular fibrillation so don't delay treatment with cardioversion or medications

Article updated August 4, 2017

Your patient, in shock from a cardiac dysrhythmia, needs immediate treatment.

Fortunately, you already have an IV line to work with and quickly determine the patient’s weight to be 60 kg. You then administer 0.2-0.3 mg/kg (15 mg) of etomidate. While it takes effect, your partner attaches the defibrillation pads and you prepare an oral airway and bag-valve-mask in case they are needed. After confirming that the patient is adequately sedated and reconfirming the rhythm, you charge and deliver a single synchronized defibrillation (cardioversion). This terminates the arrythmia resulting in a normal sinus rhythm at 95 beats per minute.

You identify confirming delta waves throughout the EKG and monitor it for changes during transport.

On the way to the hospital, the patient recovers from the sedation with a complete return of normal vital signs. By the time you arrive at the hospital, she is talking normally while sitting up and tells you that she has never had a heart problem before. The emergency department physician looks at the EKG while you give him a report. He warmly congratulates you for saving this patient’s life. Your accurate, decisive and prompt actions have undoubtedly saved the patient from cardiac arrest.

Wolff-Parkinson-White syndrome

Wolff-Parkinson-White syndrome is a relatively uncommon congenital heart defect. A large percentage of WPW patients will present a tachyarrythmia. Of this subgroup of patients, 20 percent will have atrial fibrillation.

Atrial fibrillation in WPW is particularly dangerous because the normal rate-limiting function of the AV node is bypassed with an accessory tract. The atrial fibrillation can jump across the accessory tract or pathway into the ventricles, which may cause ventricular fibrillation. The risk for ventricular fibrillation increases with higher heart rates, especially if it exceeds 200 beats per minute.

In WPW-AF, it is not wise to delay cardioversion any longer than is necessary! Once the arrythmia was identified in this case, it was treated rapidly. Taking a moment to sedate the patient is ethical and appropriate.

If cardioversion is not possible, then procainamide or amiodarone are the preferred pharmacologic agents. These will provide rate control of the ventricles without significantly enhancing the underlying acessory pathway, the cause of the increased ventricular rate.

There may be some disagreement among readers with our findings of WPW-AF over Torsades de Pointes (also a wide complex tachycardia). The case presented shows a rapid rate and a very irregularly-irregular pattern, with leads III, aVL, and aVF providing distinct non-polymorphic ECG complexes. These factors provide differentiation between WPW-AF and Torsades de Pointes in this patient.

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