Adenosine in WPW

Parameduck

Parameduck

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What are people's thoughts on adenosine with WPW. I recently watched a lecture on its potential deadly affects for people in afib with rvr with Wolfe parkinson white syndrome. Our protocols don't list that as a contraindication.
 
Our medical director is very adamant that it be not used in WPW patients presenting with any sort of SVT (A-fib included). Certainly it seems like a poor idea in A-fib, if the ectopic sites are firing at 300-400 times per minute and we block the AV node, that probably is not going to do good things when the accessory pathway is activated at such a rate. Vfib seems likely.

Here is an awesome writeup from a favorite blog: http://millhillavecommand.blogspot.com/2014/02/can-you-give-adenosine-to-patient-with.html

As an aside, I am curious about adenosine use in non A-fib SVT (IE regular rate) with WPW. The medical director still seems adamant that it never be used (though if the patient doesn't know, I doubt we'll see a delta wave at that rate). The impulses are still being generated by the SA node, so presumably the rate will be much slower (60-100). So even if the AV node is blocked and the accessory pathway is all that is being used, we aren't looking at the same atrial rate as Afib. As such, I wonder just how terrible it is to use adenosine with a AVRT patient with WPW.
 
Even though it is not listed as a contraindication, it is definitely a terrible thing to administer to the patient with atrial fibrillation with Wolff Parkinson White syndrome.

In Wolff Parkinson White syndrome, there is an accessory pathway. The accessory pathway does not have a delay like the AV node. This is why the P-wave is closer to the QRS complex on the ECG resulting in a decreased PR interval and the ventricles are depolarized early resulting in a delta wave at the beginning of the QRS complex. If the foci is sinus then the rate will be within normal limits (60-100), which is survivable. If there is fibrillation in the atria, the rate will be >350 because of all extrasystolic atrial activity going off at different times going down the accessory pathway without delay. In normal atrial fibrillation (without Wolff Parkinson White syndrome), the AV node would cause delay to the ventricle and help control the heart. If you could, you would want to slow down the ventricle rate, stop the fibrillation, or block the accessory pathway. Blocking the AV node would only encourage electrical activity to go the accessory pathway, which is what you don't want to be using because there is no delay in conduction to the ventricle. Administering Adenosine to a patient in atrial fibrillation with Wolf Parkinson White syndrome likely lead to ventricular fibrillation.

A patient in atrial fibrillation with Wolf Parkinson White syndrome would probably be best treat with electrical cardioversion because these patients are probably going to be unstable anyway. I've heard Amiodarone and Procainamide* being good chemical agents for atrial fibrillation with Wolff Parkinson White syndrome.

It's not necessary to mention the RVR part. It just means rapid ventricular response. The heart rate is >100.

I think the only other suprvantricular tachycardia with Wolff Parkinson White syndrome I wouldn't give Adenosine to is atrial flutter because flutter rates are generally around 250-350. Suppressing the AV node would probably lead to 1:1 atrial flutter. 1 flutter rate for every ventricular activity, heart rate would increase to 250-350, and this could lead to ventricular fibrillation quickly too.

SVTs (order of most common starting with the most common per the AHA)
1. sinus tachycardia - I think it would be OK because the rate would remain the same was the sinus rate
2. atrial fibrillation - not OK for reasons already mentioned
3. atrial flutter - not OK for reasons already mentioned
4. AVNRT - OK because the it is really like an accessory pathway in the AV node so the AV node is the problem. This is what Adenosine is really intended for.
5. accessory pathway mediated tachycardia (like Wolf Parkinson White syndrome, this usually in association with the other rhythms mentioned here)
6. atrial tachycardia - similar to atrial flutter, but the atrial rate is slower. The rate is usually around 150-250 instead.
7. multifocial atrial tachycardia (MAT) - again, would be OK because the rate would stay about the same.
8. junctional tachycardia - I think it wouldn't be affected by an accessory pathway and you probably wouldn't see it.

I'm not sure if all Wolff Parkinson White/accessory pathways would be a problem with Adenosine. Sometimes the accessory pathway does anterograde or retrograde conduction. If it is retrograde conduction only then you won't see the typical signs of Wolff Parkinson White syndrome.

Anyhow, don't give Adenosine to patients with Wolff Parkinson White syndrome with atrial fibrillation or atrial flutter. These patients with fast atrial rate will probably hemodynamically unstable anyhow and would probably warrant electrical cardioversion. Drugs that slow down the ventricular rate or both would be ideal if cardioversion isn't an option or doesn't work eg Amiodarone and Procainamide*.

*I have limited knowledge of Procainamide and never have used it. It is not drug used by EMS out here and therefore only briefly mentioned at paramedic school here.
 
Good review. Thanks Tigger and Aprz.
 
Great timing for this thread! I have had 2 patients with SVT in the past 3 days, one got Adenosine and it worked beautifully, the other converted with vagal maneuvers.

The second patient is the interesting one, she had a hx of A- fib and stated she had episodes of "AVNRT" in the past and has had success converting when she has received Adenosine in the past. The pt stated the palpitations began aprox 30minutes prior to EMS arrival and instantly knew what was happening. The pt had a good BP and was mentating appropriately throughout the event. Here is the initial rhythm captured
EKG 1.jpg

We then began establishing IV access, giving O2 (via N/C), and captured a 12 lead. During this time I also instructed the pt to bear down (while capturing the 12 lead). Here is the 12 lead while the pt was bearing down..
.EKG 2.jpg
As you can see at the end of the strip it turned into a wide complex irregular tachycardia, which is an ABSOLUTE contraindication for Adenosine in our protocols for the same reasons listed in @Aprz 's post. The pt converted into an unremarkable A-fib after bearing down and had no further symptoms. Here is the best tracing of her underlying rhythm...
EKG 3.jpg

My questions is, what would have happened if the pt was given Adenosine while in the SVT? Would she have converted to A-fib or would she have gone into V-fib? The end of the 1st 12 lead really surprised me as I was not expecting the rhythm to change into an irregular wide complex tachycardia. Even if she hadn't converted with the vagal maneuvers I would not have given Adenosine after seeing that rhythm. She got them big pads on her chest and a non emergent ride to the ED without complication.
 
If she had AVNRT, the Adenosine would just stop that and then whatever is her normal pacemaker should takeover. If she is normally in atrial fibrillation then that's what she would be in. I think in your protocol, a wide complex irregular rhythm is "contraindicated" because it is not AVNRT.

There are three types of AVNRT. The most common one presents with "pseudo" s waves in lead III and a "pseudo" s' wave in lead V1. I quote "pseudo" cause it is really just a p-wave/atrial activity. It could be said this probably has a pseudo r' wave, but the pseudo s-wave I am describing cannot be appreciated in this 12-lead due to the patient have a left anterior fascicular block / left axis deviation so they already have an S wave in the QRS in lead III. Also because she says she has had episode of AVNRT and it converted with the valsalva maneuver, I would say this ECG was AVNRT.

Not sure what's up with the wide complex when she converted. It looks like like a regularly irregular (or however they say it when it is not a normal rhythm, but can be predicted) rhythm like a bigeminy to me.
 
We were always taught Adenosine with WPW is safe provided there isn't any A-Fib/Flutter present as mentioned above.

I have given it to a pt with WPW before and it really surprised me how many providers were unaware of the various things to watch out for with WPW and tachyarrhythmias. I found in most pharmacology books it wasn't touched on at all and in emergency medicine books, like Tintinalli, it was only a brief note.
 
Just have some questions:

1) Why won't you want to give adenosine to someone with Afib with RVR? Is it because Adenosine only slows down electrical conduction through AV node, and since A-fib has more foci than AV node, it'll stop conduction through AV node but theres more conduction pathways? Dose that mean it'll hurt the patient more?

2) When cardioverting someone with Afib with RVR, the rhythm is going to be narrow and irregular. That means shock at 120J-200J. How would you (or the machine) know where to shock if the rhythm is irregular? Could there be a moment when it might shock at the wrong place? Why can't you unsynchronize cardiovert this pt?
 
ParamedicStudent said:
1) Why won't you want to give adenosine to someone with Afib with RVR? Is it because Adenosine only slows down electrical conduction through AV node, and since A-fib has more foci than AV node, it'll stop conduction through AV node but theres more conduction pathways? Dose that mean it'll hurt the patient more?
Click to expand...
I wouldn't consider it harmful to give to a patient with atrial fibrillation, but I would consider it pointless. We think Adenosine = treat SVT, but it is actually to treat AVNRT (or an accessory mediated tachycardia/WPW that has like a large circuit due to retrograde conduction or something... you'll end the circuit blocking the AV node). The other rhythms I listed won't be resolved with Adenosine. The good thing about giving Adenosine to an SVT that it can help you figure out which SVT it is too. If it just slows down and goes back up without revealing anything else, it is probably sinus tachycardia. It could cause a higher degree block (eg atrial flutter 2:1 to atrial flutter 4:1) revealing it is an atrial flutter.
ParamedicStudent said:
2) When cardioverting someone with Afib with RVR, the rhythm is going to be narrow and irregular. That means shock at 120J-200J. How would you (or the machine) know where to shock if the rhythm is irregular? Could there be a moment when it might shock at the wrong place? Why can't you unsynchronize cardiovert this pt?
Click to expand...
I have never really thought about this and have no experience on it. It definitely won't sync because the rhythm is irregular. You'd risk an R-on-T phenomenon. If they aren't on any anticoagulant, they would risk a clot dislodging. We don't typically attempt to convert or shock atrial fibrillation just like we don't usually cardiovert sinus tachycardia. You'd only shock them if they are unstable AND you think they are unstable because of their rhythm. Usually the case is that they have atrial fibrillation with RVR secondary to something else like sepsis. If they are symptomatic, but not unstable, drugs to control the rate will be given instead eg calcium channel blockers (diltiazem and verapamil).
 
ParamedicStudent said:
2) When cardioverting someone with Afib with RVR, the rhythm is going to be narrow and irregular. That means shock at 120J-200J. How would you (or the machine) know where to shock if the rhythm is irregular? Could there be a moment when it might shock at the wrong place? Why can't you unsynchronize cardiovert this pt?
Click to expand...
The machine is syncing with the peak of the QRS. And the machine will time when it delivers the shock with the QRS accordingly, which is why you have to actually hold the button down for a bit. Do you want Vfib? Because thats how you get Vfib. (Excuse my Archer reference, I had to.) I cardioverted a woman in afib not too long ago and even got the strip, it syncs perfectly fine.(Its short I know, on my phone and got be up in 5 hours, but thats a dumbed down version.)
 
aaaand just looked and I have very little strip showing the pre-cardioverted rhythm. Dang, thought it was better.
 
I'll try to do it concisely (note, please read the above responses, but read below it you can't fully digest all the info):

Accessory pathways are made of nerve fibers. The AV node is made of muscle. This is by design, because it allows for conduction to slow down from the atrium to the ventricles, like a speed bump.

Electricity takes the path of least resistance. Think about what happens when you block the AV node, and some aberrent conduction is already taking place. If they're in A fib for example, you're now conducting that 250-300+ atrial rate straight to the ventricles.
 
I know ACLS is "entry-level", but I wonder why they don't talk about WPW and Adenosine?
 
ACLS is a set of algorithms that teaches how to treat patients based on very basic ECG findings
  • slow or fast?
  • narrow or wide?
  • regular or irregular?
and their hemodynamic stability. Is any one of the following present?
  • chest pain
  • shortness of breath
  • altered mental status
  • hypotension
Then cardioversion should not be delayed, per ACLS.

I would be very surprised to see a patient well tolerating atrial fibrillation or flutter with an anterograde accessory pathway. From what I've read, these patients' ECG quickly deteriorates to ventricular fibrillation if their rate is not corrected.
 
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