Wolf-Parkinson-White (WPW) syndrome is a form of a pre-excitation syndrome secondary to an abnormal accessory pathway within the heart. The abnormal accessory pathway forms during embryological development and exists between the atria and ventricle, which is known as the Kent bundle. Electrical impulses within the accessory pathway do not follow the normal conduction pathway through the AV node, instead they by pass the AV node and set the heart up for irregular rhythms which can potentially decompensate the fatal arrhythmias (i.e. VFib). Approximately 0.15%-.20% of the population is affected by WPW, it has a male predominance and is commonly found is seemingly healthy individuals. Management of patients with WPW depends upon the presentation, EKG and stability of the patient. Patients with WPW, most commonly develop atrial fibrillation (Afib) and circus movement tachycardia (CMT). The treatment of each is not the same as it would be for a patient without WPW.
In patients presenting with non-WPW Afib, the goal of therapy is to slow conduction through the AV node, by increasing the refractory period of the AV node. In these patients, drugs such calcium channel blockers and beta blockers are indicated. In patients, with WPW Afib, calcium channel blockers and beta blockers may actually worsen the arrhythmia and the patient may decompensate in VFib and cardiac arrest. In WPW, the accessory pathway conducts the impulse is an anterograde direction but much faster than the usual conduction pathway, this activates the ventricular and also blocks conduction through the AVN. So, by further blocking the AV node, by using CCBs or BBs, the accessory pathway will actually speed up. The goal of treatment, in WPW Afib, depends primarily how stable the patient is. If unstable, direct cardioversion is indicated. If stable, then procainamide may be used to help block conduction through the accessory pathway and increase conduction through the AVnode. Procainamide tends to take 30-60 to work and may cause hypotension. In terms of the actual EKG, WPW Afib on tends to have bizarre, wide-complex and irregular tachycardia with rates often in the 250 bpm range or higher.
Patients with WPW may also present with CMT. CMT occurs when a premature atrial contraction occurs while the accessory pathway is in its refractory period. The beats then travels down the AV node, activating the ventricles and then traveling retrograde through the accessory pathway. EKG tends to look very regular and the QRS is narrow because of the normal activation via normal conduction system. Conduction in CMT can also occur antidromic, but is much less likely. Antidromic EKGs are still regular, but usually faster with a wide QRS. Treatment for CMT again depends on the stability of the patient. If unstable, direct cardioversion is the treatment of choice. If a patient is stable, the treatment then depends on the type of CMT. CMT that is regular and narrow QRS complex can be given a trail of adenosine (6mg then 12mg) to try and break the arrhythmia, but the ability to cardiovert must be immediately available at bedside. Wide complex CMT needs to first be distinguished from VTach. Direct cardioversion is usual indicated. If patient goes into cardiac arrest then the usual ACLS guideline are followed.
In the patient presented above, he was not in any arrhythmia and was stable. ED intervention revolved around keeping him on telemetry monitoring and getting an EP evaluation. Patient ended up getting admitted to the telemetry unit. His ECHO was essentially normal and he underwent ablation of his accessory pathway and was discharged 4 days later with a normal EKG.
KEY POINTS:
1. Get an EKG for syncope/near syncope
2. Look for WPW, Brugada's syndrome, or prolonged QT syndrome in young patients with syncope
3. Risk stratify all patients with syncope
