The ECG (Figure 3 shown on page 16) is from a 35-year-old male who presents with paroxysmal tachycardia.
e) What condition is demonstrated? Describe the characteristic features. (30% marks)
f) What would be the possible pharmacological options if his tachycardia were to recur?
e) Wolf-Parkinson-White syndrome
• short PR interval, less than 3 small squares (120 ms)
• slurred upstroke to the QRS indicating pre-excitation (delta wave)
• broad QRS
• secondary ST and T wave changes
f) IV procainamide or amiodarone is preferred, but any class Ia, class Ic, or class III antiarrhythmic can be used
The ECG features of WPS are:
Management of SVT in this condition:
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.
In summary, about the management of acute SVT in WPW:
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.
|Arrhythmia||Drugs contraindicated||Drugs Recommended|
In case you were wondering, WPW patients die sudden cardiac deaths when they develop AF, which is conducted rapidly and erratically through their aberrant pathway, producing VF (Obeyeseker et al, 2012)
Some might ask: why don’t the college want us to just give adenosine for what is likely to be standard narrow-complex-obviously-orthodromic arrhythmias? AHA and UpToDate agree: you treat them as per usual. However, the problem is that you can never exactly know that the SVT is definitely orthodromic. As far as is possible to tell, the recommendation to use procainamide is there as a guideline-maker’s safeguard to protect patients against a mistakenly unrecognised antidromic SVT. They say, “AV node-specific blocking drugs such as adenosine, verapamil, and beta blockers should be avoided unless the tachycardia is definitely known to be antidromic AVRT.” As one can never definitely know that the tachycardia is, to always use the safe agent seems like the right option. To do otherwise may invite weird bedside arguments about the width of QRS complexes.
With regards to 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.
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and, somewhat more recently...
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