WPW

Wolff-Parkinson-White syndrome (WPW) is a disease characterized by an accessory pathway that predisposes the patient to both supraventricular and ventricular arrhythmias. The accessory pathway in WPW in known as the bundle of Kent and has a variable location. Patients may have EKG findings while in a normal sinus rhythm that alerts the provider to the diagnosis, though it is vital to understand how conduction through this accessory pathway is occurring with arrhythmias.

Findings in Sinus Rhythm

The classic findings of a patient in NSR are a delta wave, prolonged QRS, and short PR interval. Patients with these findings commonly have ST segment and T wave changes that are discordant (typical repolarization abnormality with repolarization abnormality). The delta wave is a slow slur on the upstroke of an R wave, though is sometimes seen as a slow slur on the downstroke of a Q/S wave (and therefore, sometimes thought to be pathologic Q waves). Sometimes, this pre-excitation (these EKG findings) are variably present; they tend to be more obvious with more vagal tone. Patients commonly have a pseudo-infarction pattern due to negative delta wave in the inferior leads (producing what appears to be pathologic Q waves) and tall R waves in the anterior leads from the delta wave (similar to posterior infarction pattern).

These findings may be variable primarily due to variable conduction through the accessory pathway. Anterograde conduction is conduction down from the atrial to the ventricles through this pathway. It is often initiated, however, before the QRS (producing a shorter PR interval) as it does not have to go through the AV node. In other words, conduction commonly starts sooner through the accessory pathway and is found earlier on the EKG (producing the short PR interval and delta wave with prolonged QRS). The conduction through the accessory pathway and AV node commonly meet somewhere in the ventricles. However, if the conduction is retrograde (conduction through accessory pathway from ventricles to atria), these findings may be absent. In this instance in a normal sinus rhythm, the accessory pathway is not initiated via the atria and, when it reaches the accessory pathway via the ventricles, the atria are still refractory and conduction 'dies' in the accessory pathway.

It is also common to have discordant ST-T changes (typical of a repolarization abnormality from a depolarization abnormality...) producing ST depressions or T wave inversions.

Orthodromic Conduction Arrhythmias

Arrhythmias commonly occur from the accessory pathway due to its ability to form a reentrant circuit (pathway to allow for continued conduction between the atria and ventricles like a circuit). Orthodromic conduction goes from the atria, down through the AV node to the ventricles, and then may come back up to the atria via the accessory pathway. Patients with these arrhythmias commonly have no EKG findings of WPW while in the arrhythmia and WPW may only be diagnosed after cardioversion to NSR. Because they travel down the AV node, they are still limited by the AV node (usually limit on upper limit of conduction to 150-200bpm, though sometimes up to 220bpm).

SVT is a common arrhythmia found in these patients. SVT with orthodromic conduction produces typical EKG features of SVT and should be treated as one would normally (AV nodal blockers are ok). Atrial fibrillation and atrial flutter are common and should not be treated with AV nodal blocking medications given the ability of the accessory pathway to allow for conduction to the ventricles. When atrial fibrillation or atrial flutter are sending impulses via orthodromic conduction (down the AV node), the EKG will have typical findings of these arrhythmias.

Antidromic Arrhythmias

Antidromic conduction with WPW is much more rare than orthodromic conduction, but is far more likely to be deadly. It is conduction from the atria to the ventricles via the accessory pathway, and then back up the AV node. These can be much more deadly as the accessory pathway does not have the 'checkpoint' ability of the AV node with a maximum rate. Therefore, the ventricles could be stimulated to beat just as fast as the atria. If the impulses from the atria are extremely fast, the ventricles will not have time to fill and have little to no cardiac output. In other words, the ventricular rates with these arrhythmias can be too fast for ventricular filling (up to 300bpm!) with resultant shock and death. Patients that initially have supraventricular arrhythmias with antidromic conduction may easily degenerate into ventricular arrhythmias and sudden death. The rates with these arrhythmias are commonly 200-300bpm and tend to have wide QRS complexes due to the abnormal ventricular depolarization.

SVT will produce a regular wide complex tachycardia with variable QRS morphologies. It, therefore, may be difficult to distinguish from VT; however, patients are commonly younger and not at particular risk for VT otherwise.

Atrial fibrillation and flutter may also produce antidromic conduction as noted above. With antidromic conduction, the rate is commonly >200bpm and there are polymorphic wide QRS complexes. In other words, the QRS complexes will be wide and there will be multiple QRS morphologies. It is easily differentiated from VT due to the rate being irregularly irregular. However, atrial flutter with antidromic conduction may be mistaken for VT as there may be 1:1 conduction. It is vital to not use AV nodal blocking agents (as noted above). These patients are commonly unstable given the extremely rapid ventricular response and, therefore, commonly require electrical cardioversion. Although polymorphic VT has multiple QRS morphologies, WPW with antidromic conduction does not have the repetitive shifting of the axis that is typical of torsades de pointes.

Examples:

Further Reading:

https://litfl.com/pre-excitation-syndromes-ecg-library/

http://hqmeded-ecg.blogspot.com/search/label/WPW

http://hqmeded-ecg.blogspot.com/search/label/wolff%20parkinson%20white%20WPW