Please note: The following ECGs have all been recorded at 25 mm/sec and gain setting of 10 mm/mVe 26.1

A 54-year-old female walks into the Emergency Department complaining of palpitations for the past hour Her ECG is shown on page 8 (Figure 1). She has no electrolyte abnormalities.

a) Describe the rhythm disturbance. (20% marks)

b) How would you treat this rhythm disturbance? (10% marks)

c) Name two anti-arrhythmic drugs that are contra-indicated for this rhythm disturbance. (20% marks)

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College Answer

a)

Atrial fibrillation with an accessory pathway                                                                                  

AF / SVT with aberrant conduction acceptable answer.(The rapid rate precludes AF with bundle branch block so no marks should be given for AF with bundle branch block).

b)

Electrical cardioversion (flecainide, ibutilide, propafenone acceptable).

c)

Digoxin, calcium channel blocker, beta-blockers, amiodarone, adenosine or other agents that preferentially block AV node and not accessory pathway.

Discussion

a)

This is WPW, in AF. 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.

b)

Management of this acute arrhythmia has several options:

  • vagal manoeuvres
  • AVOID ASV node blocking drugs such as adenosine, digoxin, beta blockers and calcium channel blockers
  • Procainamide, ibutilide or amiodarone are the only antiarrhytmics useful in WPW
  • 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.

c)

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.

References

Wellens, Hein JJ, and Dirk Durrer. "Effect of digitalis on atrioventricular conduction and circus-movement tachycardias in patients with Wolff-Parkinson-White syndrome." Professor Hein JJ Wellens. Springer Netherlands, 2000. 63-68.

Gulamhusein, S. A. J. A. D., et al. "Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil."Circulation 65.2 (1982): 348-354.

Munger, T. M., et al. "A population study of the natural history of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989."Circulation 87.3 (1993): 866-873.

Svenson, ROBERT H., et al. "Electrophysiological evaluation of the Wolff-Parkinson-White syndrome: problems in assessing antegrade and retrograde conduction over the accessory pathway." Circulation 52.4 (1975): 552-562.

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.