Great point Jeff! Mitral Valve Rupture could account for this too any hx of endocarditits and if it wasnt said by now, Is there a Balloon Pump available???

Hey Getoverit

Lemme answer some of your questions:

Ooo good question.

In fact he has had "fast heart", as he calls it, a few times, he has never gone to the doctor about it because it always went away

Lung sounds are normal. No labs since we are at his house

Goof question Jeff

Nothing obvious on the heart sounds.

OK

So it looks like many people are questioning the EKG but not wanting to come out and give the specifics

Here is the EKG with some pointers i made to show some things:


The EKG Review

So on the EKG we see two things.

1) an R-R that isnt equidistant which = irregular
With his history this should make you think A fib. Vtach is always regular so its quickly ruled out.

2) Rates > 300 at times which very very rare for Vtach. > 300 is indicitive of an accesory pathway conduction problem.

Some other things you will note is that Josephson's sign and Brugada's sign (not the syndrome thing) are not there. These are two cardinal Vtach Signs.

Josephson's = Presence of a notch on the downstroke of the S wave. Its used to distinguish an abbarently (LBB conducted SVT vs Vtach

Brugada's = A distance of 0.10 seconds from onset of QRS comples to the very bottom of the S wave that is present in complexes of ventricular origin.

So... We have ruled out Vtach with abbarency (like a BB. We have an irregularly Irregular rhythm with an accesory pathway conduction problem where we have identified delta waves. That means WPW until proven otherwise.

So now the EKG is cleared up (At the end i have one post conversion thats shows his normal rhythm).

What drugs are appropriate and why? What are absolutely not appropriate?

Why is cardioversion in this case where the patients appears to be "stable", considered the first line tx when if it was any other combination it wouldnt be?

What do you mean by any other combination? I am guessing because this has the high potential to decompensate to VFIB. Also, would not want to give IV dig, verapamil, or lido because of the same reason by potentially increasing the ventricular response, could end up in decompensation by increased lengths of very high ventricular rates.

Hey Hoss

What i meant was that in any other case where you had a stable patient with a rhythms that made you unhappy (and them) you would consider pharmacology before electricity. In this particular combo. of Afib and WPW there is some danger in meds.

You are totally correct about those Rx as they would increase rates and worsen this guy!

When we think of the basic treatment principle in WPW AFib is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate. This is in direct contradistinction to the goal of treatment of non-WPW AFib, which is to slow the refractory period of the AVN.

Currently, the meds of choice are in contraversy. Amiod vs Procainamide. Procainamide blocks the accessory pathway, but it has the added effect of increasing transmission through the AV node. So, although procainamide may control the AFib rate through the accessory pathway, it may create a potentially dangerous conventional AFib that may require treatment with other medications and/or cardioversion.

Essentially, the current reccomendation is that patients with Afib/WPW who are somewhat stable or not, should be cardioverted to fix both rhythm issues. Consideration of medical management for this combo should only be in the presence of a cardiologist.

Scary stuff but it highlights the need to know they "whys" eh?

Ahhh, yes. Thx, good case! So, are you ready to tell us what you did and how it went? How did this guy do? Did you go to the cardiac center, etc...

"Essentially, the current reccomendation is that patients with Afib/WPW who are somewhat stable or not, should be cardioverted to fix both rhythm issues. Consideration of medical management for this combo should only be in the presence of a cardiologist."

Mike,

Could you please touch a bit more on concerns of cardioversion/rhythym converion in a patient who may have been in persistant A-Fib for a long period of time. I see that he is not on an anticoagulant (unless you consider ASA one).

Is there a grave risk of conversion to sinus rhythym and the R Atrium pumping clots into the lungs/coronary arteries/brain?

Please let me know your thoughts on this.

Thanks,

SFM

Hey

SooperFLTMedic:

huhuh. You are the only one who noticed that! Actually, i forgot to put that in the meds section! He has a Hx of afib so he was on coumadin! Nice catch!

If this was a random new afib which cane with a WPW (which can happen) we would still cardiovert as it would be a new afib. Anyone with an old afib should be on anticoagulant as you noted! You have a keen eye!

As for the Final result

This patient was cardioverted as soon as the delta waves with an irregular rhythm was noted. He converted on the first attempt and was absolutely asymptomatic en route to a level 1 cardiac center.

Here is his post EKG:


The Post Cardioversion EKG

Its a bit small, but you can see the underlying delta waves and therefore WPW (which had been undiagnosed. Also, no afib on the monitor.

Great and interesting case study. The rule for cardioverting Afib with our facility is they have been in Afib more than 2 hours they get anticoagulated before cardioversion. Less than 2 hours they can get the juice.

WHAT A FANTASTIC CASE STUDY!!!

THESE ARE AMAZING LEARNING TOOLS!!!

THANK YOU MIKE!!!!!!!!!!!!!!

SFM

Im glad everyone likes them

My initial plan for this was simply to setup a way that flight crews could do an interactive review of difficult cases. Essentially, keep fresh on medicine. It also does exactly the same thing for me, and then some!

What it has turned into is an AWESOME way to have excellent clinical discourse with some of the best people in EMS

Special thanks to MDEMT-P and Randy for their input. It is excellent to have physician involvement on this site and i only wish there was more!

Awesome work everyone!

Hey Mike ( and anyone else you may want to throw in on this question...)

Although you didn't say he was on coumadin, you did note that he took ASA. Knowing this, is that a proper level of "anticoagulant" therapy? In other words, I would have thought that throwing an embolism had a low chance because of the ASA. Would anyone else be nervous in thinking this way? Please enlighten me everyone!!

Great case, Mike.

Fly safe everyone...

New to the forum. Question. When individuals offer a treatment modality does this suggest that it is done prehospital? For example, this case, are you suggesting this individual be cardioverted prehospital?

Thanks in advance for taking time to school the newbie.

Brush after you Barf!

Hey

just noticed yer post

He actually was on coumadin but i forgot to write it in, super caught it tho. And no, ASA isnt good enough

Hey

Ij this particular case the tx would be to cardiovert pre hospital for sure.

I am way late on this, but I have a comment to Mike's "unstable" vs "stable"
Isn't it what AHA feels is unstable vs stable. If I can remember, if a pt is having chest pain, is diaphoretic, hypotensive etc, these all fit the "unstable" criteria. Granted he is mentating, so i would go with cardioversion.