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Posted

Hey guys, the physiology of diaphoresis is exceedingly complicated. Sweat glands are heavily innervated by cholinergic receptors but diaphoresis is often the result of a sympathetic response. Clearly, the basic intuition regarding autonomic nervous physiology breaks down. You need not have tachycardia to have diaphoresis; however, being that a sympathetic response is often associated with diaphoresis, it's no surprise that tachycardia is often associated with said response.

Take care,

chbare.

  • Like 2
Posted

Super case study, thanks for having the cohunes to post it.

I'm not quite settled about the treatment choices, however. It seems like amiodarone is still on the list of options (as the default for wide/fast rythms).

Amiodarone has been associated with some less than stellar results in patients with WPW and atrial fibrillation in several case reports, and there doesn't seem to be any evidence that it works or is safe in WPW-afib, and several sources I've seen recommend proving Edison right about the safety of DC.

reviews of the case reports and lack of evidence here:

http://www.ncbi.nlm.nih/pubmed/20437113

http://www.ncbi.nlm.nih.gov/pubmed/17355684

This case isn't quite the same. If I'm understanding correctly, the initial rhythm was likely atrial flutter with WPW. I can find no evidence whatsoever about treating such a condition. All the same, I have to say that I've pretty much scared myself away from trying any pharmacology in a patient like this.

What is the perspective on this from the experienced smart brain trust? Is there really a role for amiodarone in this case?

Posted (edited)
Your honesty should be the gold standard that we judge all scenarios by here. Thanks for sharing brother. I don't think you realize your value to the City...It's massive.
I applaud you as well. This is the biggest reason that I join in on forums - to continue my education so I can learn from others. It's also the reason I was doing the "What would you do" scenarios. I found myself at a crossroad in possible treatments and wanted to see if my peers would have gone the same way, gone the other, and why for either choice. Thanks for putting this out there. Edited by tcripp
Posted

Ahhh, but see, the problem with your answer Ugly is that the pt that I saw it in had a pulse rate of 28 when I first took it.

Also, I've seen many, many, many pts with heart rates above 120 that didn't display diaphoresis at all, much less to this level.

Moral of the story here is that we need to be really care to state, "this is what you need." when in fact it may be only sometimes that it happens, only one thing that you need, or had nothing to do with it in fact and was simply coincidental that it happened at the same time.

Dwayne

Posted

"I did not believe I was looking at VT as the axis is leftward (VT should be extreme rightward), there is no precordial concordance (as seen in VT), the morphology looks asymmetrical and abbarant (not VT), the rate is awful high for VT, and the patient was somewhat young."

This was a great case, but I'm going to clarify one point because it's very important. Ventricular tachycardia can have a frontal plane axis in any quadrant. A right superior axis helps support the diagnosis but absence of that finding does not exclude the diagnosis. Same thing with precordial concordance. There is no safe way to exclude VT based on QRS morphology. On rare occasions you might see ventricular flutter with a rate around 250 but you should suspect an accessory pathway whenever the rate approaches (or exceeds) 250. When it's a regular, monomorphic wide complex tachycardia, in theory it's okay to try adenosine, and in fact it may convert orthodromic or antidromic AVRT (or be diagnositc when the underlying rhythm is atrial flutter). Just remember to hit the PRINT button so you can see what happens during the asystolic pause. The drug of choice for this patient would be procainamide but in these types of situations "edison before medicine" is probably the wisest course of action for the hemodynamically unstable patient.

Thanks for sharing the case, fiznat!

  • Like 2
Posted (edited)
Ventricular tachycardia can have a frontal plane axis in any quadrant. A right superior axis helps support the diagnosis but absence of that finding does not exclude the diagnosis. Same thing with precordial concordance. There is no safe way to exclude VT based on QRS morphology.

What about all of these together in one ECG? I understand that individually they can't be used to exclude VT, but if they are all present I would imagine VT is increasingly less likely....?

Edited by fiznat
Posted

What about all of these together in one ECG? I understand that individually they can't be used to exclude VT, but if they are all present I would imagine VT is increasingly less likely....?

Less likely, from what I've read personally, but like the ACLS guidelines state when in doubt--even if there's just a little bit of doubt--treat as V-tach.

Posted

If the patient has no history of heart disease, and there are RS complexes in the precordial leads, and the start of the R-wave to the nadir of the S-wave is less than 100 ms, and AV dissociation is absent, and there are no fusion or capture complexes, and Wellens' criteria are not positive for VT in leads V1 and V6, then yes, VT is less likely, but cannot be safely excluded, especially when taking into account the problem of inter-observer agreement.

What about all of these together in one ECG? I understand that individually they can't be used to exclude VT, but if they are all present I would imagine VT is increasingly less likely....?

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