Here is the powerpoint presentation with audio:
For those who would rather read than watch/listen to the powerpoint slide show:
You have a 30 year old male with a chief complaint of chest pain. You obtain the 12 lead above…What would you call this rhythm? You might just call this a monomorphic ventricular tachycardia or SVT with aberrancy. The treatment for this specific rhythm is incredibly important. It can mean life or death for your patient (du… du.. du..). If you read the title of this, you would know this is neither of those options and is in fact atrial fibrillation with preexcitation syndrome (WPW)
What is a Preexcitation Syndrome?
Preexcitation refers to an early activation of the ventricles using an accessory pathway that bypasses the AV node. It usually develops during the cardiac development. Three different types of accessory pathways:
- Antegrade- impulses head down the “normal” way from atria to ventricles
- Retrograde- impulses head away from the ventricle
- Both directions (Antegrade and Retrograde)
There are three types of preexcitation syndromes
2. Lown-Ganong-Levine syndrome
3. Mahaim-type tachycardia
Below is a normal cardiac conduction system:
Now in a WPW patient, there is an accessory pathway called the Bundle of Kent that freely allows impulses to go through it and does not block out impulses like the AV node.
General Information of WPW
- 1-3.1 per 1,000 people have WPW
- Around 20% of WPW patients experience A-fib with WPW
- WPW is often present at birth but not detected until later in life
- Peak incidence is 30-40 years old
- Short PR interval (less than 120ms)
- Delta waves
- Widened QRS (Delta wave causes the QRS to appear wider)
- Different morphologies (this occurs in atrial fibrillation with WPW and we will hit on that a little bit later)
Type A: Positive delta wave and a prominent R wave in V1. Left sided bypass tract
There are normally T wave inversions in V1 and sometimes in V2 due to secondary abnormal ventricular depolarization. You can see the extremely short PRI and a slurred upstroke at the beginning of the QRS complex which is the delta wave.
Type B: Negative delta waves in V1-V2 and dominant S wave in V1. Right sided bypass tract.
In V1 you’ll notice a slightly negative slurring which is the delta wave. The delta wave is also able to be seen in other leads.
Atrial Fibrillation with WPW
Now that you know more about this syndrome, you look at this ECG and say to yourself “I don’t see any short PRI or any delta waves”. You have a point, but when these critical patients have atrial fibrillation with WPW, you need to know it’s not just atrial fibrillation with aberrancy or VT. Look close at the long lead II strip, you’ll see a wide complex tachycardia (rates nearing 300 BPM) that’s irregularly irregular with varying QRS morphologies. They vary in size and shape due to some impulses going down the normal conduction pathway, some going down the accessory pathway and to the ventricles, and some going down the accessory pathway and linking back up to the normal conduction system.
Important fact: in atrial fibrillation, the two atrias are fibrillating and producing impulses from 300 to even 600 BPM. What causes the ventricles to only conduct less than 300 BPM? The AV node squashes the rest of the impulses and acts as a gatekeeper.
Now what do you give these patients? Lidocaine? Digoxin? Adenosine? Amiodarone? Procainamide? Well if you give 4/5 of these medications you should expect to see this:
As I mentioned before, the AV node is very important in squashing 300+ impulses from hitting the ventricles and sending the patient into ventricular fibrillation. So lidocaine and adenosine are out. When digoxin is administered, though it won’t kill them immediately, the patient can deteriorate into ventricular fibrillation within a few hours. Now the choices are amiodarone and procainamide. Everyone loves amiodarone, but unfortunately this will kill your patient. Amiodarone is typically classified as a class III antiarrhythmic drug that primarily focuses on the potassium channels of the heart that are responsible for the repolarization process in the phase 3 of cardiac action potential. Amiodarone is normally not marketed this way, but it also acts on beta-adrenergic receptors, calcium channels, and sodium channels. The beta-adrenergic effect on the AV node will send the patient into ventricular fibrillation.
Procainamide does not affect the AV node and will only impact the accessory pathway. This should be the only medication given to a stable atrial fibrillation patient with WPW. The safest way to deal with any tachyarrhythmia is sedation followed by 200 Joules. Synchronized cardioversion is always the safest way to deal with this rhythm and all of the other lethal tachyarrhythmias.
This site is meant to be used for educational use only. We strive to push evidence based medicine with no bias to help you obtain all the important information. You should always follow your protocols that have been set in place.
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–Scopeducation Team (Matt)
Check out Amal Mattu’s site if you want amazing access to advanced ECG cases: https://ecgweekly.com/
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