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Podcast 117 - Jumping The Gun - WPW and Adenosine?

WPW is a Cheater

Sprinters are lined up in their starting blocks - the tension builds! The official holds their starter pistol in the air and yells:




....and just before the sound of the shot, a sprinter takes off down the track before anyone else even moves. They jumped the gun - started running before it was the right time. Will they win the race? The rest of the sprinters take off after this rogue runner, and only time will tell. Either way, they cheated - disqualified! To make matters worse, the runner takes a shortcut across the middle of the track.

We can think of Wolff-Parkinson-White (WPW) syndrome as that rogue runner. It takes off before the rest of the electricity even starts, and it takes a shortcut - not staying in the designated lanes. However, most of the time, it still ends up losing the race - why? It's not an athlete - WPW is a very slow runner (most of the time). This is why it quickly becomes overrun. Let's take a look at an example of how this usually works out.

That red part (the delta slur) where WPW jumps the gun and takes a shortcut, is electricity traveling from the atria to the ventricle through an accessory pathway called the Bundle of Kent. It bypasses the AV node, so it's not slowed down at all. We know that the AV node typically pauses the electrical conduction from the SA node, so that the atria have time to contract and move blood into the ventricle. Muscle and blood move slower than electricity, which is why this pause is so important. On the ECG, the P-R interval is the representation of this pause.

But, why is WPW so slow? If electricity can make it down to the ventricle through the Bundle of Kent, shouldn't WPW win the race to depolarize the whole ventricle every time? Although WPW gets a head start and takes a shortcut, it's not efficient at all. The depolarization that occurs in the ventricle after electricity travels through the Bundle of Kent is cell-to-cell - it's not taking any of the fast fibers of the bundle branches or Purkinje fibers. Thus, when the signal is released from the AV node, it overtakes this cell-to-cell conduction and limits the spread.

What I've just described - this delta slur appearance - is what most people associate with WPW, and rightly so! The diagnosis of WPW is most commonly made with the observation of this delta slur, which indicates partial ventricular depolarization through the Bundle of Kent. However, if we can see the delta slur on our baseline ECG, there probably isn't anything crazy going on at the moment. We probably found this WPW pattern by happenstance. Why? If a patient has WPW, won't they always have a delta slur?

Actually, no. The problem with WPW is that the patient can have tachyarrhythmias which appear as "SVT" or "VTACH" type rhythms, but are different in their mechanism and treatment. How so? Let's start with the mechanisms of these tachyarrhythmias and go from there.

Quick Facts

Alright, so I lied. First, a few quick facts about WPW.

-Having "WPW Pattern" on an ECG just means you have the Delta slur, with a short PR interval (<120ms), and a QRS duration >110ms. WPW pattern might be present in up to 0.13 - 0.25% of the population, but can be intermittent and can actually disappear over time.

-Having "WPW Syndrome" is having WPW Pattern, PLUS actually having tachyarrhythmias that are causing the patient to have symptoms. Of those who have the WPW pattern, only a small percent will ever develop WPW syndrome.

-There is a Type A WPW Pattern. This occurs when the Bundle of Kent is on the left side of the heart. Type A presents with positive Delta waves in the precordial leads. There is usually a prominent R wave in V1 which might be confused with a RBBB.

-There is a Type B WPW Pattern. This occurs when the Bundle of Kent is on the right side of the heart. Type B presents with negative Delta waves in V1 and V2 - the rest of the precordial leads might be positive - this pattern may be confused with a LBBB

-WPW can also present with no delta slur due to a 'concealed pathway', which is not possible to observe on the surface ECG. This occurs because the pathway only goes from the ventricle to atria (but can still cause arrhythmias).

-WPW patients can have ST/T abnormalities in the opposite (discordant) direction of the Delta slur.

-Adenosine is NOT contraindicated in WPW, but it IS contraindicated in WPW with A-Fib. More on that later.

Presenting Problems

Back to what causes these patients to actually present to us - tachyarrhythmias! There are two tachyarrhythmias that we want to be aware of. The first is Orthodromic AVRT, and the second is Antidromic AVRT. Let's start with Orthodromic AVRT!

Orthodromic AVRT (AVRT = Atrio-Ventricular reciprocating tachycardia - notice the 'nodal' is missing) looks just like plain old AVNRT (what most people call "SVT"). There is a T wave, narrow complex QRS, T wave, narrow complex QRS, and so on, and on, and on, and on.

Notice how there is no Delta slur? Why not? Because there is no partial depolarization occurring! Once the reentry circuit has formed, the WPW patient will lose their Delta slur. Don't worry, it will come back once you convert them to a sinus rhythm. In an orthodromic AVRT, the reentry circuit goes UP the Bundle of Kent, and DOWN the AV node. This is what makes this rhythm narrow - because it's using very fast conduction through the BOH, RBB, LBB, and Purkinje fibers. I always remember 'ortho'-dromic is narrow complex because the root word 'ortho' means straight or correct. The impulse that contracts the ventricles does use the correct pathways to depolarize (which is why it is narrow complex).

Example ECG of Orthodromic AVRT:

Antidromic AVRT looks like VTACH. Why? In Antidromic AVRT the reentry circuit isn't using any of the fast channels in the heart that Antidromic used to stay narrow. The Antidromic reentry circuit goes UP the AV node and DOWN the Bundle of Kent, using only cell-to-cell conduction (making the rhythm wide and fast like VTACH). I always remember 'anti'-dromic is wide complex because the root word 'anti' means opposed or against. The impulse that contracts the ventricles does not use the correct pathways to depolarize - it goes against normal pathways by traveling up the AV node (which is why it is wide complex).

Example of Antidromic AVRT:

There is one more issue we should be aware of, which is the unfortunate combination of Atrial Fibrillation (or flutter) and WPW. These patients can form a reentry circuit in either direction - they can have either ANTIdromic or ORTHOdromic AVRT. However, they have a dangerous underline A-fib that is waiting to turn that reentry rhythm into V-fib. How?

If a patient has A-fib, their atrium is dealing with over 500 impulses per minute. The ventricles are usually kept safe because the AV node acts as a gatekeeper, only letting a small amount of those impulses through. However, the Bundle of Kent is no gatekeeper - it's an unregulated gap in the fence. If we were to give an agent that blocks the AV node, there is a strong possibility that the A-fib will transfer its impulse rate to the ventricles, and then we would be dealing with V-fib. Anytime you see an irregular tachycardia, regardless of whether it's wide or narrow, think A-fib, and possibly WPW with A-fib.

Example ECG of WPW with A-fib:


We're going to have to separate the treatment of these arrhythmias into their QRS duration. Again, we'll start with orthodromic (it's the most common).

Orthodromic Treatment

Unstable: If they're unstable, guess what the treatment is... synchronized cardioversion. Alright, glad we got that out of the way.

Stable: If they're stable, we can try the traditional 'SVT'-type treatments. First, try vagal maneuvers. But not those crappy ones we usually do. Try a modified valsalva maneuver to actually give it a chance to work.

If a couple of rounds of vagal maneuvers don't work, it's time to try adenosine at standard dosages. Yes, you read that correctly - give adenosine for Orthodromic AVRT. The weak point of this reentry circuit is the AV node. If we cancel part of this reentry circuit, the rest will likely fail. Guess what third-line treatment is? Diltiazem. Seems crazy, right? Again, we're blocking the weak point of the circuit. In the absence of underlining A-fib, Orthodromic AVRT is not treated much differently than a run-of-the-mill AVNRT ('SVT'). If Diltiazem doesn't work, we're probably going to have to perform synchronized cardioversion.

Antidromic Treatment

Unstable: Again, synchronized cardioversion.

Stable: Here's the deal... Antidromic is technically the same problem as Orthodromic, except going in the opposite direction. Any treatment that works for Orthodromic will have a similar chance of working for antidromic. If you're sure the patient has WPW, then you would treat with vagal maneuvers, adenosine, diltiazem, synchronized cardioversion. What if you're not sure if they have WPW or not?

If the patient has an uncertain history, you're going to handle this a little differently. Honestly, you should probably just perform synchronized cardioversion - it's the safest thing to do. However, if you carry procainamide, it would be indicated in this circumstance.

If you're like me, your probably thinking... 'okay... but if the patient looks like they have VTACH with a pulse (because Antidromic AVRT looks like VTACH), and is supposedly stable... isn't everyone going to give Amiodarone 150mg over 10 minutes since they won't know this is WPW? Yes. Probably.

Treatment of Antidromic or Orthodromic AVRT with underlining A-fib

Unstable: Synchronized cardioversion

Stable: If you have procainamide, you can try that. If procainamide is unavailable, synchronized cardioversion.


WPW is an incredibly interesting disease process that can initially cause some trepidation on the part of the clinician due to the perceived nuance of treatment. However, we might just be psyching ourselves out a little bit. If it looks like AVNRT, it's gets treated like AVNRT. Don't be afraid of the adenosine and traditional treatments. If it looks like VTACH and we don't have procainamide, we should probably just perform synchronized cardioversion. What if the patent has an underlying A-fib? DO NOT GIVE ADENOSINE! It turns A-Fib into V-Fib when the patient has WPW. Again, if we don't have procainamide, we should be performing synchronized cardioversion.

See below for some peer reviews and extra content!

Oh, and before you go... a couple of honorable mentions

Just for a sense of completeness.. Lown-Ganong-Levine (LGL) is a syndrome that is always mentioned alongside WPW as another cause of a short PR interval, and it has a bundle all of its own - The James Bundle. This James Bundle runs from (usually) one of the infranodal bundles (the ones that run from the SA to AV node), skips the AV node, and hooks up with the bundle of HIS. Because there is no partial depolarization of the ventricle, this syndrome presents without the delta slur, but with the short PR and tachyarrhythmias (almost always narrow complex unless a BBB is present). The blue line around the AV node and James Bundle signifies where a re-entry circuit would form. Check it out:

Another honorable mention is Mahaim (Mah-high-mmmm) Syndrome. This one doesn't present with a short PR or delta slur (actually sometimes it can have a tiny delta slur), but it is an accessory pathway, so I thought I would throw it in the mix. Mahaim syndrome has something called an Atriofascicular fiber that extends from the RA down to the RBB, where it causes a LBBB appearance on the ECG (because the RBB was stimulated before the LBB). However, the atriofascicular fiber isn't always stimulated, so the ECG can actually look normal a lot of the time. However, the patient can get reentry circuits in the fiber, as well as other tachyarrhythmias that cause a VTACH with LBBB morphology appearance. The blue lines show the usual path of electricity, and why this presents like a LBBB when the accessory pathway is stimulated. Check it out:

Alright, now I'm done. Thanks for reading! Be sure to jump in on the live class version of this inside the paramedic refresher!

Peer review and weird observation by Tyler Christifulli

Ok, so this is not so much of a peer review as it is a weird observation I have made when a patient presents with WPW w/ an underlying afib. It is anecdotal, but it seems like the amplitude of the R wave in the precordial leads and some limb leads is always HUGE when WPW & Afib are concomitant. Take a look at this google search of "afib w/ WPW."

When the rate is this fast, it becomes nearly impossible to tell if it is regular or not. At a quick glance my mind has started to suspect WPW w/ afib when I see a 12 lead that looks like a bad polygraph test.

But anyway, nice blog Sam!

Peer review by Jake Good

Sam... Crushed it. In emergency medicine we are always highly concerned with the clinical item that carries the highest mortality -- in this case it is absolutely WPW with Afib. Like Tyler mentioned, the pattern of that 12 lead is something to commit to memory!

Giving adenosine to a patient in that WPW with afib (ventricular rates around 300) has been termed "a clean kill of emergency medicine" by several prominent FOAMed cardiology peeps. Electricity flows down the path of least resistance, if we block the AV node with adenosine the path of least resistance becomes the bundle of kent! An atrial rate of 500 that makes its way down to the ventricles to a rate of 500 is called vfib!!

Peer Review By J-ROD!

Boom, Motherfucker! If I had to absolutely find something to criticize, it would be that I thought you'd have more emphasis on the adenosine and other "normal treatments" (medication wise) that WILL drop that guillotine blade if given in those A-Fib/Accessory Pathway situations. But, at the same time, I read through was like, "Damn, solid work!" I did fix some grammar and spelling, per Grammarly. Don't worry, I didn't change all it picked up, just stuff that was obvious and didn't seem like a "stylistic" choice.


Can you reference a blog on your own platform? Screw it! Jared Patterson did an awesome job on this subject last year! Patterson, Jared - One Rad Medic - (2020) FOAMfrat

Chhabra L, Goyal A, Benham MD. Wolff Parkinson White Syndrome. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:

Page, R. L., Joglar, J. A., Caldwell, M. A., Calkins, H., Conti, J. B., Deal, B. J., Estes, N. A., 3rd, Field, M. E., Goldberger, Z. D., Hammill, S. C., Indik, J. H., Lindsay, B. D., Olshansky, B., Russo, A. M., Shen, W. K., Tracy, C. M., Al-Khatib, S. M., & Evidence Review Committee Chair‡ (2016). 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation, 133(14), e506–e574.

Exner, D. V., Muzyka, T., & Gillis, A. M. (1995). Proarrhythmia in patients with the Wolff-Parkinson-White syndrome after standard doses of intravenous adenosine. Annals of internal medicine, 122(5), 351–352.

ECG images were taken from Life in the Fast Lane (great website for ECGs!):


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