Atrial Fibrillation in WPW Syndrome – Pearls and Pitfalls

While the ECG in question can easily be interpreted as Atrial Fibrillation (AF) with rapid ventricular response, there is more to the picture. There is a beat-to-beat variation in QRS width and also variation in the R-R interval. The ventricular rate also approaches 300/min, which is too rapid for this conduction to be occurring through the AV node. The combination of wide, irregular QRS complexes with significant beat-to-beat variation, R-R variation, and very rapid ventricular rate should lead you to consider atrial fibrillation in the setting of Wolff Parkinson White Syndrome (WPW).

Besides AF in WPW, AF with aberrant conduction and polymorphic ventricular tachycardias (including torsades de pointes) are all considerations for this rhythm. Irregularly irregular rhythm, broad and varying QRS complexes, rapid ventricular response often approaching 200/minute, a delta wave are all clues to distinguishing atrial fibrillation in WPW.⁽¹⁾ Distinguishing these rhythms based on an ECG is difficult. Age and medical history should be considered. Young patients with no other medical problems are more likely to have WPW-related AF, where older patients with CAD are more likely to have polymorphic ventricular tachycardia.⁽¹⁾

Polymorphic VT can appear similar to atrial fibrillation in WPW. However some types of polymorphic VT, such as torsades de pointes can appear with an undulating baseline with alternating QRS polarity. This is usually not the case in atrial fibrillation with WPW. See the example below (courtesy of Life in the Fast Lane). This is AF in WPW – it looks similar to polymorphic VT but lacks the undulating baseline seen in torsades de pointes.

LITFL. Life in the Fast Lane Medical Blog. 2018 [cited 2018 Feb ]; Available from: https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes

Atrial fibrillation with aberrant conduction occurs when a patient has a baseline bundle branch block or develops a rate-related block during a rapid ventricular response to AF. Unlike in WPW, while the rate is irregular and QRS complexes are are broad, they usually have a stable beat-to-beat configuration.⁽¹⁾

In WPW syndrome, there is an additional accessory pathway (often called the Bundle of Kent) that can conduct electrical impulses from atrium to ventricle without the use of AV node and His-Purkinje system. This results in a phenomenon called pre-excitation – as an impulse bypasses the slow-conducting AV node, it can initially depolarize the ventricles earlier than when proceeding normally through the AV node. This phenomenon may be represented by a short PR interval and delta wave on an ECG. Impulses can travel anterograde or retrograde through this pathway. Pre-excitation can result in tachydysrhythmias and sudden death.

In a reentrant circuit that is made up of the AV node and accessory pathway, anterograde conduction occurs from the atria through the accessory pathway to the ventricles (without use of His-Purkinje system) and then returns to the atria via the AV node – this is antidromic atrioventricular tachycardia and is rare. Retrograde conduction occurs from the atria through the AV node and His-Purkinje system to the ventricles, and then returns to the atria via the accessory pathway – this is orthodromic atrioventricular tachycardia and is more common.

Clinical ECG Interpretation. [Cited Feb 2018]. Available from <https://ecgwaves.com/pre-excitation-avrt-wolff-parkinson-white-wpw-syndrome/>

Both of these pathways can result in a regular tachydysrhythmia through rapid depolarization of the ventricles using the accessory pathway.⁽³⁾ The direction of the impulse conduction and use of fast-conducting His-Purkinje system determines how the ECG appears (antidromic – wide QRS, orthodromic – narrow QRS). Atrial fibrillation in WPW can be precipitated by AV node reentrant tachycardia or occur alone. Conduction through the accessory pathway is faster than through the AV node and can result in very rapid ventricular response. With ventricular responses at or above 300/minute, the risk for degeneration to ventricular fibrillation is increased.⁽¹⁾

The use of beta blockers, calcium channel blockers, and adenosine all act through slowing or blocking conduction through the AV node. This can enhance conduction through the accessory pathway, resulting in extremely rapid ventricular rates and increased risk for conversion of AF to ventricular fibrillation.

Preferred treatment for unstable patients is immediate electrical cardioversion. Unstable patients include those who have end organ hypoperfusion such as ischemic chest pain, pulmonary edema, or altered mental status.

If your patient is stable, chemical cardioversion can be attempted. Again, AV nodal blocking agents should be avoided. Your options include IV ibutilide, procainamide, and amiodarone.

Ibutilide is a class III antiarrhythmic that acts by prolonging the QT interval and repolarization. It has a fast onset of action (about 20 minutes) and has no dosing concerns for hepatic and renal patients. It also has been shown to have minimal effect on blood pressure in comparison to procainamide.⁽²⁾

Procainamide acts by blocking the inward sodium and outward potassium currents. It slows the refractory period of the atrioventricular and accessory pathway conduction system and slows anterograde and retrograde conduction. It has a risk of severe hypotension, especially with rapid infusion, and should be infused slowly.

Amiodarone is a class III antiarrhythmic and acts by prolonging the repolarization phase of the action potential. Short term infusion has conduction-slowing effect on sinus and AV node properties with little effect on the accessory pathway.⁽¹⁾ While it has traditionally been used in AF in WPW, it has a risk of causing acceleration of the ventricular rate and degeneration to ventricular fibrillation.