Question 15.3 from the second paper of 2017, Question 14.1 from the second paper of 2015, Question 3.1 from the first paper of 2009 and  Question 14  from the first paper of 2002 all asked about Wolff- Parkinson-White syndrome. It appeared again in Question 26.1 from the first paper of 2016, where it was complicated by AF. Specific issues asked about have included the characteristic ECG findings (short PR and delta waves), contraindicated drugs (AV nodal blockers like digoxin), and complications (SVT and sudden cardiac death). In brief, that's all you need to know. But of course many people (among them college examiners) would not be satisfied with a single sentence answer.  To address the issues of WPW in greater detail, one may need to refer to published literature. If one were pressed for time, one may safely limit one's reading to the LITFL page on WPW. If one were for some reason in need of greater detail, one might instead read the  UpToDate chapter on WPW.

Pathophysiology and ECG features of WPW

WPW is characterised by the presence of the Bundle of Kent, an accessory conducting pathway which is closer to the SA node than the AV node is. The atria are well-behaved, and they politely conduct the impulse from the SA node along the usual fast conduits. The P wave, therefore, is normal in appearance. Then, the impulse reaches the Bundle of Kent, and it conducts the impulse first, before the AV node has a chance.

The result is a short AV conduction time, and an abnormal pattern of depolarisation, with some of the ventricular mass depolarising some milliseconds before the rest. Electrophysiology findings are diagnostic, but one does not need EPS to make the diagnosis (SVT and characteristic sinus ECG findings seem to be enough). Thus, the 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.

Complications of WPW

What could go wrong:

• 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? Turns out, yes. Orthodromic SVT in WPW can be treated much like any other SVT (adenosine, vagal manoeuvres etc), whereas in antidromic SVT many of the usual drugs are contraindicated.
• AF  is disturbingly common in WPW- 10 to 30% of patients will have it at some point. Question 26.1 from the first paper of 2016  demonstrates what this looks like:
  
  
  • 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.

The model answer to Question 3.1 from the first paper of 2009 lists digoxin and verapamil. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Generally speaking many of the AV node  blockers are at least relatively contraindicated in WPW - certainly in AF, and in AVRT unless it is confidently known to be orthodromic AVRT.  The table below has been compiled with the use of the belowlisted references and the UpToDate article on this topic

Management of acute arrhythmia in WPW

Narrow complexes:

• Same as any SVT: vagal manoeuvres, adenosine, verapamil, ß-blockers

Broad complexes:

• vagal manoeuvres
• Procainamide or amiodarone
• DC cardioversion
• Flecainide for long term management

Atrial fibrillation:

• vagal manoeuvres
• Procainamide or ibutilide acutely
• DC synchronised cardioversion
• Flecainide or propafenone are used in long term management. Amiodarone also OK - but the side effect profile in long term use is not very nice for younger patients.