Question 3.1

a.   List 3 abnormalities on this ECG

b.  Name 2 drugs which are contraindicated in this disorder

c.   Name 2 complications of this disorder

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College Answer

a.   List 3 abnormalities on this ECG

°    Short PR

°    Delta wave

°    Wide QRS

°    J wave (candidates mentioning this also received credit)

°    Tall R wave in V1

b.  Name 2 drugs which are contraindicated in this disorder

°    Verapamil

°    Digoxin

c.   Name 2 complications of this disorder

°    VF arrest

°    Syncope

°    AF/tachyarrhythmias


This is WPW. The short PR, long QRS and delta waves all suggest that an accessory conduction pathway is present. The J wave is a bit of a red herring here, and is certainly not part of the syndrome; its presence can be a normal variant, which is what I think is happening here (unless this patient was cooled).

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.

Complications of WPW include:

  • 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.

What can we say about the safety of AV nodal blockers in WPW?

  • Theoretically, AV nodal blockers should be safe in WPW-associated SVT, be it antidromic or orthodromic. If one thinks for a minute about the epidemiology of SVT, one will come to the conclusion that a large proportion of SVT is in fact caused by WPW or some other sort of preexcitaton syndrome, which is usually not known at the time of their first presentation. Many of these people get adenosine, which then reveals their delta waves to the horrified emergency personnel. Most of them do not die of VF. On the basis of this, we may conclude that it is probably reasonably safe.
  • Practically, antidromic SVT in WPW may be difficult to discriminate from AF or VT. Broad complexes and 300+ heart rates could be anything in WPW. Sure, it could be supraventricular, and respond to adenosine. Or it could be AF, and turn into VF. Or it could be VT, which will not benefit from an AV nodal blocker, in which case you have wasted precious time.

On this basis, the authorities tend to recommend the use of Class I or Class III agents instead of AV nodal blockers. The model answer to Question 3.1 from the first paper of 2009 lists procainamide and amiodarone as first-line agents, whereas digoxin and verapamil are contraindicated. Digoxin decreases the refractory period of the accessory pathway and verapimil tends to accelerate the ventricular response to AF by a similar mechanism. Since 2009, public opinion has also drifted away from amiodarone. As an acute infusion it is basically a beta-blocker with some AV nodal specificity. It is therefore the wrong drug for acute management of WPW SVT; or rather, it will probably be safe in the narrow-complex-obviously-orthodromic population, with the aforementioned caveats. In the long term, it becomes more useful, as its Class III and Class I effects begin to develop, slowing conduction down the accessory pathway.