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iaskdumbquestions

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I'd like to get a sense of your common aggravations with the emergency department and their management of cardiac conditions. What do you see commonly that you wish they would do differently, what do you see that you think is well done (or even above and beyond) regarding what you would expect, and what do you see that is downright dangerous?

I think I'll add specific questions to this thread later on as they come to me, but for now:

1) What is your opinion on electrical cardioversion of a-fib with rvr, stable, no chest pain in a patient who has known a-fib that is well controlled for years on b-blockers until ~10 hour episode. Would you agree with sedation and synch cardioversion or would you prefer the ED use pharm? Also, where do you land on anticoagulation for a patient like this assuming they are returned to NSR and discharged from ED with cardio follow up within 3-5 days (assuming they are not on anticoagulation or maybe just Aspirin?

2) I have sat in many IM rounds where the troponin ordered in the ED is ridiculed heavily. Some ED docs will reflexively order the trop with any patient with CP (though I might disagree), but in a patient with a-fib + rvr, or brady with chest pains would a trop not be wise?

Thank you for your insight. I'll ask lots of dumb questions around these forums I think. Seems like a good resource.

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I'd like to get a sense of your common aggravations with the emergency department and their management of cardiac conditions. What do you see commonly that you wish they would do differently, what do you see that you think is well done (or even above and beyond) regarding what you would expect, and what do you see that is downright dangerous?

I think I'll add specific questions to this thread later on as they come to me, but for now:

1) What is your opinion on electrical cardioversion of a-fib with rvr, stable, no chest pain in a patient who has known a-fib that is well controlled for years on b-blockers until ~10 hour episode. Would you agree with sedation and synch cardioversion or would you prefer the ED use pharm? Also, where do you land on anticoagulation for a patient like this assuming they are returned to NSR and discharged from ED with cardio follow up within 3-5 days (assuming they are not on anticoagulation or maybe just Aspirin?

2) I have sat in many IM rounds where the troponin ordered in the ED is ridiculed heavily. Some ED docs will reflexively order the trop with any patient with CP (though I might disagree), but in a patient with a-fib + rvr, or brady with chest pains would a trop not be wise?

Thank you for your insight. I'll ask lots of dumb questions around these forums I think. Seems like a good resource.

The things that really piss me off is when I get consulted and the ED doc hasn't seen the patient or there is no workup. Just because someone has a history of a heart problem doesn't mean you should call me without starting the workup. If you've done your due diligence and have some questions, great. But if you are just calling to check off a check box stop wasting my time. As to your specific questions:

1) I am assuming you mean the patient has been rate controlled for years? If so, treat pharmacologically. If they have been in sinus for years and now slipped back into AF, it is reasonable to cardiovert. This is tempered by atrial size, MR degree and the like. There are guidelines for anticoagulation after cardioversion.

2) Troponins are the bane of cardiology consults, especially when they are ordered for BS reasons. 90 year old guy who comes in altered, shouldn't have troponins. Septic and hypotensice shouldn't have troponins. ESRD who skips dialysis for a week and comes volume overloaded and short of breath shouldn't have troponins.

As to your direct questions about AF RVR- is it compensatory (ie always in AF and septic)? If so, no troponin. Otherwise, maybe. Bradycardia and troponin depends on the clinical context and baseline diseased state of the conduction system. If it an 80 year old who had a RBBB and LAFB with a first degree AVB a month ago and is in CHB now, probably doesn't need troponins.
 
Thank you for responding. I can't believe someone would consult you without any workup at all! Regarding:

1) Patient was rhythm controlled for years. This was an unusual episode. I'll look up those guidelines.

2) Septic + hypotensive + chest pain = troponin?? I'm not trying to determine every single case that would need troponin, I'm just trying to get a better understanding so that I can apply it appropriately in the future. I agree that a positive troponin in a patient that doesn't really show clinical signs of ischemia would be a pain because now something must be done about it, I'm still just a little unclear about it.

3) Sounds good. I read that paper on SVT and troponin leak and why it doesn't mean infarction. ED docs vary in their workups, some are conservative others are liberal. But all of them are trying to do right by their patients. I'm just trying to get all sides of the issues.

Thank you again.
 
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I agree that a positive troponin in a patient that doesn't really show clinical signs of ischemia would be a pain because now something must be done about it, I'm still just a little unclear about it.
Actually, it's a pain because probably nothing will be done about it. The fundamental question to ask when ordering any test is: what am I going to do with the result? Of what use will it be? In the case of, let's say, an elderly sick patient with urosepsis and an elevated creatinine who is not overtly presenting like an ACS, of what use will a troponin be? You can just assume it's at least mildly elevated. If you have a hard time imagining that a cardiologist will be interested in taking a patient to the cath lab, think twice about ordering the troponin.
 
amen, echo that sentiment. sadly, the indiscriminate ordering of troponins will never go away. given variable presentations of ACS (anginal equivalents, silent MI), it's such a quick and easy screen with bigger consequences if missed. as for septic, afib or ckd/ESRD pts with elevated troponins, 9/10 times the etiology is supply/demand but i also believe in hickum's dictum and the burden to prove or disprove falls on us.
 
amen, echo that sentiment. sadly, the indiscriminate ordering of troponins will never go away. given variable presentations of ACS (anginal equivalents, silent MI), it's such a quick and easy screen with bigger consequences if missed. as for septic, afib or ckd/ESRD pts with elevated troponins, 9/10 times the etiology is supply/demand but i also believe in hickum's dictum and the burden to prove or disprove falls on us.
Your third sentence seems to go against the "sadly" of your second sentence. And, as an EM doc, I don't order "indiscriminately". And, if it even 1/10 for the later group you mention, that's robust enough for me. As long as there are anginal equivalents and silent MIs, I'll order the troponin; indeed, it is quick and easy screen with bigger consequences if missed.

Sorry if a late reply.
 
Your third sentence seems to go against the "sadly" of your second sentence. And, as an EM doc, I don't order "indiscriminately". And, if it even 1/10 for the later group you mention, that's robust enough for me. As long as there are anginal equivalents and silent MIs, I'll order the troponin; indeed, it is quick and easy screen with bigger consequences if missed.

Sorry if a late reply.

There are a lot of people who get bull**** troponins ordered. I had one ordered on a 20 year old who had nausea because it might represent an "anginal equivalent".

Let's not pretend that there's much science behind this and just acknowledge its all done to avoid liability.
 
There are a lot of people who get bull**** troponins ordered. I had one ordered on a 20 year old who had nausea because it might represent an "anginal equivalent".

Let's not pretend that there's much science behind this and just acknowledge its all done to avoid liability.
That's kinda REALLY cynical, because, even if the liability issue is there, it is quite tightly tied to an actual patient, who is having an issue that is causing their troponin to rise. You really think that there is "very little science"?

I work in the community, where there are no fellows, and no academics, and the only time I call cardiology is for a transfer for a pacer or the cath lab. Fellows get all the chaff, but the wheat is for the attending time. And, was the troponin positive in the 20 year old? Or is that just your anecdote?

As Einstein said, "there are two ways to look at the world - that nothing is a miracle, or everything is". Apologies for any mangled quote. I do medicine because I like it - not just a workman like "to get a paycheck, and not get sued, and that's all".
 
I understand the whole feeling of now wanting to miss an MI, and with our current highly sensitive troponins we pick up on a lot of subclinical or frankly clinical irrelevant supposed "myocardial injury" than we had in the past. But are we truly missing MI's?

I'll have to find it but a while ago I listened to an EM podcast that I trust on the issue of troponins/chest pain in the ER and on a review of the data including outcomes and legal issues one of the takeaways seemed to be that that the issue of "missing an MI" is really overblown and that just isn't really happening. I'll have to find the episode and post a link.
 
That said, honestly I'm to the point where I don't fault the ED and ultimately these consults are going to pay the bills. This is why I did fellowship training, to be the expert in the field who can answer the "what is going on here" question and whether something is significant or not. Honestly I'm sure I consult other specialists about issues that they view the same way, medicine is too complex and nuanced for one field to get everything correct right off the bat.

I guess back to the topic of the thread... one thing I do wish the ED would improve one is maybe not automatically assuming a cardiac cause of the patient's issue. At least in my shop I think there's certainly an extra emphasis on cardiac issues because of the nature of our hospital but then that means that the SOB is automatically cardiac and not a PNA with elevated WBCs and focal infiltrate on CXR, or that hypotensive patient with an infiltrate or UTI is automatically tamponade instead of septic shock.

Again, it's annoying initially during training though I've gotten to the point where they have a separate set of headaches and concerns in the ED and I don't envy their job. It's tough and we're all just trying to take care of patients. And in the end these consults are going to pay the bills.
 
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I guess back to the topic of the thread... one thing I do wish the ED would improve one is maybe not automatically assuming a cardiac cause of the patient's issue. At least in my shop I think there's certainly an extra emphasis on cardiac issues because of the nature of our hospital but then that means that the SOB is automatically cardiac and not a PNA with elevated WBCs and focal infiltrate on CXR, or that hypotensive patient with an infiltrate or UTI is automatically tamponade instead of septic shock.
Once I realized that these troponins were being ordered as part of a protocol for basically any chief complaint above the diaphragm, I quit getting worked up about them. Made the rest of my training much less painful.
 
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At least in my shop I think there's certainly an extra emphasis on cardiac issues because of the nature of our hospital but then that means that the SOB is automatically cardiac and not a PNA with elevated WBCs and focal infiltrate on CXR, or that hypotensive patient with an infiltrate or UTI is automatically tamponade instead of septic shock.
Maybe someday I'll get over it, but it still drives me nuts how frequently "CHF" is used as a synonym for "shortness of breath." I'm very frequently reassuring patients that no, they actually don't have congestive heart failure.
 
Maybe someday I'll get over it, but it still drives me nuts how frequently "CHF" is used as a synonym for "shortness of breath." I'm very frequently reassuring patients that no, they actually don't have congestive heart failure.

I find myself doing the opposite: no he doesn't have asthma/copd/pneumonia, it's just his heart failure again. Please stop the fluids and steroids. Please restart the diuretics.
 
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Once I realized that these troponins were being ordered as part of a protocol for basically any chief complaint above the diaphragm, I quit getting worked up about them. Made the rest of my training much less painful.

Haha. It helps when you're not the one getting consulted for it.:)
 
Haha. It helps when you're not the one getting consulted for it.:)
Out of curiosity, what happens after you are consulted for it? Do you have to Obs/Admit for serial troponin, or can you discharge but now the burden is on you? What's the next step?
 
Out of curiosity, what happens after you are consulted for it? Do you have to Obs/Admit for serial troponin, or can you discharge but now the burden is on you? What's the next step?

Depends on the reason they have a positive troponin- old guy with sepsis or AMS- it just wastes my time and they go to the MICU. Old guy with renal failure- it just wastes my time and they go to nephrology. These two probably make up 25-50% of my consults for troponins.

Heart failure, arrhythmia, true type I NSTEMI or any true cardiac etiology, I admit. It is rare that a positive troponin gets discharged and our ER refuses to put people in OBS who have a positive troponin- even if they have a known non-ischemic etiology of their troponin.
 
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