Outline the diagnostic features, complications and treatment of patients with Wolf- Parkinson-White syndrome.
Diagnosis: history of arrhythmias (palpitations, dizzy, lightheaded), sudden death. ECG in sinus rhythm demonstrates short PR interval and delta waves. Electrophysiological evidence of AV conduction through AV bypass tract (bundle of Kent).
Complications: recurrent arrhythmias (narrow QRS complex orthodromic AV re-entrant tachycardia, wide QRS antidromic AV re-entrant tachycardia, atrial fibrillation (broad complex and may be very fast [> 200/min]), ventricular fibrillation), sudden death.
Treatment: (1) acute treatment of arrhythmias: a) Narrow SVT (as per SVT). b) Wide QRS SVT (procainamide; avoid adenosine, verapamil, digoxin and beta-blockers; treat as if VT). c) Atrial fibrilation: (Appropriate agents include procainamide, amiodarone and flecainide. Avoid agents which might slow AV conduction but not decrease conduction through bypass tract: i.e. adenosine, verapamil, digoxin and beta-blockers). (2) investigation via electrophysiologic evaluation: usually curative ablation of accessory pathway, or no treatment if asymptomatic, or occasionally prophylactic medications.
I would never be able to remember such things if they were not organised into headings and point form.
The below "model answer" is derived almost completely from UpToDate.
- ECG features of WPS are:
- The PR interval is short (less than 0.12 seconds)
- There is a delta wave (a slurred upstroke of the QRS complex)
- Wide QRS (because the delta wave widens it)
- ST Segment and T wave discordant changes: T waves point in the opposite direction to the QRS.
- Pseudo-Q waves: negatively deflected delta waves in the inferior / anterior leads
- prominent R wave in V1-3 (mimicking posterior infarction).
- Ideally, this sort of ECG should come with a history of syncopal episodes.
- Characteristic electrophysiology findings of an accessory pathway (Bundle of Kent) are desirable but non essential.
- ECG features of WPS are:
- SVT, which comes in two flavours. if the complexes are narrow, its orthodromic. If they are wide and with delta-waves, its antidromic. Does that really matter? Probably not.
- AF is disturbingly common in WPW- 10 to 30% of patients will have it at some point. Having AVRT predisposes one to AF in this situation because the reentry circuit via the accessory pathway can cause the atria to contract quite randomly (after all, the accessory pathway is not a serious part of the conducting system, and it doesn’t link into any sort of conduction pathways- its just going to excite any old patch of atrium). The ECG will throw you off. The conduction rate is roughly 1:1.5; the QRS rate is about 180 to 200. It is hard to tell that its irregularly irregular. The QRS complexes will be a mixture of pre-excited delta-waving ones, and normal-looking narrow ones. If the accessory pathway has a short refractory period, it will conduct more often and therefore there will be more broad complexes than narrow ones. The shorter the refractory period of the accessory pathway, the broader the QRS. And the broader the QRS, the greater the chance of this thing degenerating into ventricular fibrillation.
- Atrial flutter can also conduct via the bundle of Kent. There will be 1:1 conduction. Ventricular rate will approach 300. Because this is an antidromic way of conducting impulses, the QRS complexes will be broad and there will be delta waves. Unlike AF, the rate runs with a metronome-like regularity. The patient will likely look dead.
- Ventricular fibrillation is a common cause of sudden cardiac death among the WPWs. So, in AF with WPW conduction, the rate of ventricular contraction is increased, and the regularity is decreased. This fractionates the wavefront of ventricular depolarization. Soon enough, there are numerous wavefronts all moving around the ventricle. This is ventricular fibrillation. If you block the AV node, occasionally the accessory pathway will launch the ventricles into this. It’s a known, and extremely uncommon, complication of adenosine use in WPW.
- Syncope and sudden cardiac death are the natural histories of these arrhythmias in WPW, because they are frequently too fast to be perfusing rhythms. The surviving sufferer is typically saved by their youth, as they may be better able to tolerate hummingbird-like heart rate for sustained periods.
- Management of acute arrhythmias
- vagal manoeuvres
- AVOID ASV node blocking drugs such as adenosine, digoxin, beta blockers and calcium channel blockers
- Procainamide, ibutilide or (maybe) amiodarone are the only antiarrhytmics useful in WPW
- DC synchronised cardioversion
- Long-term management
- Catheter ablation of accessory pathway
- Flecainide or propafenone
- amiodarone also OK - but the side effect profile in long term use is not very nice for younger patients
WPW also crops up in Question 3.1 from the first paper of 2009.
Narula, Onkar S. "Wolff-Parkinson-White Syndrome A Review." Circulation 47.4 (1973): 872-887.
and, somewhat more recently...
Scheinman, Melvin M. "History of Wolff‐Parkinson‐White Syndrome." Pacing and clinical electrophysiology 28.2 (2005): 152-156.
Keating, L., F. P. Morris, and W. J. Brady. "Electrocardiographic features of Wolff-Parkinson-White syndrome." Emergency medicine journal 20.5 (2003): 491-493.