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Where does it say 15 mins?

And that's Mr. Mighty Mouth to you...(C'mon..say it...SAY IT!! I promise not to tell anyone...)

Dwayne

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I would want to see the XII lead. You can run into many issues with a pacemaker such as failure to sense and so on. Amiodarone is unfortunately, profoundly pro-dysrhythmic and adding it into the mix can lead to a laundry list of issues. However, amiodarone can be used successfully in patients with a low LVEJF. I am not sure I would do much of anything if the patient's haemodynamic and mental status did not change.

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Hmm, here I go replying off the top of my head. . . So as great a drug as Amio is, it has a crazy long half life. So if you have some one who already has conduction issues, and may have a new one, it seems to me to be more appropriate to hang some Lido, and have the ability to still to an electrophysiology study, some time in the next few days vs. Several months if you went the Amio route. If the research shows Amio to only be margionally better in codes, it seems to me there is still a place for our old girl, Lido, here at the ball.

Fireman1037

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What good is blocking intermediate Sodium channels? We are still throwing a medication that is pro-dysrhythmic at a problem that may or may not be conduction related and is by its very nature exceedingly difficult to differentiate.

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Furthermore, lido would only be effective IF the ectopy is ventricular. Obviously, this patient would only be treated if she was symptomatic. For the reasons articulated so effectively by chbare, cardioversion would be the way to go.

Thank you so much all for your contributions. I thought I was really dumb not being able to figure this out, but I feel better knowing that it is indeed a challenging one.

Where does it say 15 mins?

And that's Mr. Mighty Mouth to you...(C'mon..say it...SAY IT!! I promise not to tell anyone...)

Dwayne

Oh for freaks sake Mr. Mighty Mouth - do you have to question EVERYTHING I tell you? are you sure we weren't married at some point?

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...Oh for freaks sake Mr. Mighty Mouth - do you have to question EVERYTHING I tell you? are you sure we weren't married at some point?...

I'm sure we were never married, but I did dream once or twice that we played house...does that count?

It's so good to have you back posting again...I was missing you.

Dwayne

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I use 2 simple methods myself, since I have trouble remembering all the rules in the heat of the momemt at 3am (Though next time i'm calling bieber).

1) Are all the V leads concordant? (All positive or negative). If so.... prolly V-Tach

2) Is there right axis deviation? If so Prolly V-Tach

Consider thier "normal" rythm in this case. If they are a A-Fib look for regularity in your strip. Regular wide strip in a A-Fib patient strongly leans toward V-Tach.

If you are really unsure..... just use Amiodarone! Can`t go wrong

danger! danger will Robinson

amiodarone is used at your patients' peril in patients with Afib wpw. slowing the node in a patient with Ann accessory pathway can produce even nastier rhythms. This may or may not be the case here, but I think it bears remembering that amiodarone is not safe in all cases (and not effective in many)

There are several reports of the danger, but I think this is a good start:

http://www.cjem-online.ca/v7/n4/p262

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danger! danger will Robinson

amiodarone is used at your patients' peril in patients with Afib wpw. slowing the node in a patient with Ann accessory pathway can produce even nastier rhythms. This may or may not be the case here, but I think it bears remembering that amiodarone is not safe in all cases (and not effective in many)

There are several reports of the danger, but I think this is a good start:

http://www.cjem-online.ca/v7/n4/p262

Now we are thinking new onset WPW with A-Fib in a 82 year old with multiple cardiac histories including pacemaker?

I can appreciate you wanting to share some knowledge, but scrambling for zebras in this scenario is just too much....

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Now the question: Given the wide complex, if I am fortunate enough to capture an episode of tachycardia on the monitor, how can I tell if the tachycardia is atrial or ventricular in origin?

You can't reliably, and it's not that important.

It's going to be difficult to distinguish between paced beats, any atrial-initiated complexes that conduct across the AV node, and complexes initiating in the ventricles.

That being said:

- if the WCT is irregular, then it's more likely to be originating in the fibrillating ventricles, and may just be AF.

- The rightward axis, precordial concordance, etc. points towards VT, but isn't 100% sensitive or specific, i.e. in some cases it's there, but it's not VT, in other cases it's not there but it is VT.

- AHA says the morphology criteria for VT are too cumbersome to use routinely in emergency situations and recommends against it for MDs. Most of these have better specificity for VT than sensitivity, i.e. if you see criteria for VT, there's a good chance it is, but the absence of these criteria doesn't mean much.

- Other signs of VT that aren't as applicable here are:

* AV-dissociation (seen on the ECG as buried P waves, or by auscultating heart sounds and hearing an S1 and S2 that don't match; Here unfortunately we have AV dissociation even if the rhythm is supraventricular, because we have a.fib),

* Jugular venous "cannon" waves, which occur when the atrial are contracting against a contracted ventricle (but this is already underlying AF, so we're not seeing that here).

* Capture beats (occasional atrial-origin beats that conduct across the AV node and appear right before the next VT complex, and have a normal QRS morphology, or a QRS that resembles the morphology of previous supraventricular beats.)

* Fusion beats, where an atrial depolarisation and ventricular depolarisation meet. (Again, not going to see this here, because of the AF).

If you're lucky, you might get a nice clear regular VT, that looks nothing like either the paced rhythm or the normal QRS complexes, but even here there's a possibility that you have AV-conducted depolarisations with a rate-dependent bundle branch block. So you're pretty much out of luck there too.

And it's unlikely that you're going to be able to identify WPW from the ECG if there's AF. You might be able to see it, but then again, you might not. Especially if the QRS is wide / abnormal to start with. It means the delta waves have to be a little more blatant before your eye picks them out.

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Now we are thinking new onset WPW with A-Fib in a 82 year old with multiple cardiac histories including pacemaker?

I can appreciate you wanting to share some knowledge, but scrambling for zebras in this scenario is just too much....

It isn't that much of a zebra, WPW definitely happens and usually when you aren't looking for it. You only have to miss this once before you start thinking about it on every patient with wide and tachy rhythms. I've missed it before, and I promised myself I wouldn't again.

As far as the OP: you really can't tell the difference between VT and SVT with abbarency on a 3 lead. Even with a 12 lead it can be very difficult. I would take extreme caution in diagnosing, and especially treating VT as this is an area where you can definitely do some significant harm with the wrong choice. It's been my personal observation that people tend to be a little quick to think they are dealing with VT when it is oftentimes not the case. You should have a high index of suspicion in regards to VT, and really only consider treating those patients who need it immediately.

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