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Differentiating AVNRT from really regular Af + use of adenosine


BushyFromOz

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i must have missed the point where anyone said anything about going against medical direction or protocol.....

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If i extrapolate you post out, if i am presented with said difficult rhythm and a decompensated patient, do i sit on my hands because i cant decide to revert it with adenosine or amiodarone, or, do i wait for them to declare themselves and either better or get worse, and if they do deteriorate and hope they sync cardiovert successfully?

This is a judgment call. There's always a risk of giving adenosine to a seemingly regular NCT and finding out later that it was a.fib. There are some theoretical risks if an accessory pathway is present, but this is difficult to identify when the rate is fast.

Personally, I'd have the pads on, draw up some sedation / analgesia (probably some ketamine), and push the adenosine. If it's a.fib, I'd expect a transient slowing, and possibly to visualise some fib waves. If the patient acutely decompensates I have the option to defibrillate (if appropriate), cardiovert with sedation, and cardiovert without.

If we identify a.fib after the adenosine, then I'd probably give some metoprolol if the pressure is anything close to reasonable.

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  • 3 weeks later...

In my county we have quite liberal protocols, and while our MD in the past did not like to have us use adenosine as a diagnostic tool to see if we could see the a-fib when the heart rate slowed down he recently OK'd it (mainly because a lot of us were doing it anyway :). For me it's fairly simple when I get a supraventricular tachydysrhythmia; if it's regular I give adenocard, if it's irregular I give a calcium channel blocker (our MD prefers diltiazem but sometimes its unavailable so we have a back-up protocol for verapamil).

As to your particular patient, I know I've seen ED docs countless times give adenocard to not only see if it would help, but also as a diagnostic tool to see if it was a-fib or SVT, as it's much easier to tell when the rate slows down. I don't know off the top of my head what the AHA says but I'm pretty sure there's no evidence to suggest that giving adenosine as a diagnostic is harmful. In fact I think that adenosine is a preferred medication because of the extremely short half life. I know one of the reasons our MD changed the protocol was because they were finding that adenosine was converting some wide complex tachycardias. I know in thirteen years I've never once had an adverse event from adenosine administration.

I guess my answer is that adenosine is probably safer to give to a-fib than it is to give a calcium channel blocker to SVT. Calcium channel blockers have some pretty significant side effects. I've had a few patients whos BP bottomed out after treating a-fib. Sorry for the long rant.

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...and while our MD in the past did not like to have us use adenosine as a diagnostic tool to see if we could see the a-fib when the heart rate slowed down he recently OK'd it (mainly because a lot of us were doing it anyway :).

I find this statement concerning.

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Wondering how many people here have had the chance to diagnose WPW with AFib in the field ... I can see this a bit difficult to catch... Though would be the time you'd really not want to use adenosine....

Yeah, good point, certainly its not something that would be routinely done here, and to be honest im not sure if we as a body (as in the service i work for) are across WPW enough to diagnose it as often as we should. Ill let you know when i start my post grad though.

Another thing that does not get talked about often is ruling out a previous heart transplant.

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Why would you need to rule out possible heart transplant. The only cardiac drug I know for a fact may not work for heart transplant is atropine.

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  • 4 weeks later...

I'm not sure if this has anything to do with the Adenosine/heart transplant but here you go. Sounds like there is a significant increase in effect.

Here is a key part of this study the donor sinus node demonstrated a threefold to fourfold increased response to adenosine as compared with the recipient sinus node and a threefold to sixfold increased response as compared with control subjects.

I'm not up to date on the response to adenosine in normal hearts but it appears that the results fo the study show a 3-6fold increase response versus non-transplanted patients.

Someone who is smarter than me care to explain more - Chbare????

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