Wolff-Parkinson-White Syndrome, or WPW, is one of the pre-excitation syndromes caused by an accessory pathway, or bypass tract, between the atria and ventricles. The normal AV node acts like a guard gate, slowing down the impulse before it enters the ventricles.
The accessory pathway bypasses the AV node, allowing an impulse to enter the ventricles prematurely, preexciting part of the ventricular muscle. Accessory pathways are able to conduct in an antegrade — toward the ventricles — direction, a retrograde — away from the ventricles — direction, or more commonly, in both directions.
The accessory pathway in WPW, called the Bundle of Kent, can be on the right or left side of the heart. The Bundle of Kent can combine with the normal pathway through the AV node and form a circuit, giving rise to reentrant tachycardias.
History of WPW
Wolff-Parkinson-White Syndrome was first described in 1930 by Louis Wolff, John Parkinson and Paul Dudley White. They reported a series of young patients who experienced paroxysms of supraventricular tachycardia and had characteristic ECG changes.
Now, WPW Syndrome is defined by the presence of a congenital bypass tract combined with episodes of tachyarrhythmia. WPW is associated with a small risk of sudden cardiac death which occurs in approximately 1 to 3 per thousand people. Patients may experience the first signs of WPW Syndrome any time from infancy to early middle age.
Preexcitation on the ECG
When an impulse travels forward along the Bundle of Kent into the ventricles, it arrives slightly before the impulse that travels through the slower AV node. The ECG sign of this preexcitation of the ventricles in WPW is called a delta wave.
The delta wave is a slurred slow rise of the QRS that arises from the end of the P wave. This causes a short PR interval (<120 ms) and a prolonged QRS (>110 ms). In this ECG, the delta waves can best be seen in Leads I, II, aVR, and aVL, as well as in V1, V2, and V3.
WPW also causes discordant ST and T wave changes, with the ST and T in the opposite direction of the QRS complex. On the ECG, the discordant ST segments appear abnormally flat and slightly elevated or depressed.
When antegrade conduction occurs in the AV node, and retrograde conduction occurs in the accessory pathway, the patient is said to have a concealed pathway. No delta wave will occur, as there is no preexcitation of the ventricles, but the patient is still at risk for developing a reentrant tachycardia.
WPW Syndrome and tachyarrhythmias
People with WPW are prone to bouts of supraventricular tachycardia, called AV reentry tachycardia (AVRT). When a circular pathway forms between the normal AV pathways and the accessory pathway, it causes one impulse to depolarize the ventricles and return to the atria in a rapidly repeating cycle. This is called reentry. AVRT often begins with a premature atrial or ventricular contraction.
WPW clinical signs and symptoms
Patients experiencing WPW Syndrome may present with new-onset PSVT, recurrent PSVT, or signs of congestive heart failure. Symptoms are not usually present during periods of normal rate. During tachydysrhythmias symptoms will depend on the age of the patient. Infants often present with tachypnea, feeding problems, and irritability. Verbal children, teens and adults may complain of “pounding chest,” rapid heart rate, shortness of breath and exercise intolerance.
AVRT with orthodromic conduction
When reentrant tachycardia occurs with antegrade conduction in the AV node and retrograde conduction through the accessory pathway, the AVRT is called orthodromic. ECG features of orthodromic AVRT include:
- Rate usually between 200-300 bpm
- P waves retrograde, and usually buried in the preceding T wave
- QRS complexes usually less than 120 ms, unless there is also bundle branch block or rate-dependent aberrancy
- QRS Alternans which is variation in amplitude of the QRS complexes
- Discordant ST and T wave changes
AVRT with antidromic conduction
When reentrant tachycardia occurs with antegrade conduction in the accessory pathway and retrograde conduction in the AV node, the AVRT is called antidromic. ECG features of antidromic AVRT include:
- Rate usually between 200-300 bpm
- Wide QRS complexes due to preexitation via the accessory pathway
Prehospital treatment of AVRT
Orthodromic AVRT should be treated using your PSVT protocols. Valsalva maneuvers, adenosine and calcium-channel blockers are used in the stable patient, while synchronized DC cardioversion is recommended for the unstable patient.
Antidromic AVRT may be mistaken for ventricular tachycardia. Wide-complex tachycardias should always be treated as VT until proven to be supraventricular. The VT protocols that include amiodarone or procainamide for stable patients and DC cardioversion for unstable patients will usually serve the preexcited AVRT patient well.
A real danger
Tachyarrhythmias can also form when impulses from atrial flutter or atrial fibrillation rapidly enter the ventricles through the accessory pathway without the filtering effect of the AV node. The extremely rapid rates produced in these situations can quickly lead to deterioration and ventricular fibrillation. Atrial fibrillation occurs in up to 20 percent of patients with WPW. ECG signs of preexcited atrial fibrillation include:
- Rate greater than 200 bpm
- Irregular rhythm
- QRS complex complexes that change in shape and appearance
- Wide QRS due to preexcitation
- Axis remains stable from beat to beat (unlike polymorphic VT)
Treatment of preexcited atrial fibrillation
If the patient is hemodynamically unstable (likely), urgent synchronized DC cardioversion is needed. Avoid AV nodal blocking drugs like adenosine, Ca-channel blockers, and beta blockers, as they may increase conduction through the accessory pathway, increasing the heart rate.
Long-term treatment
Patients are sometimes managed with drugs to prevent AVNT. A permanent solution for some patients is radiofrequency ablation of the accessory pathway.
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