Educate me more on troponin

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mrhunt

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So. heres what i know about troponin.

Its a cardiac enzyme that Appears when a pt has Damage to the heart or various other issues such as acute kidney damage, Sepsis, PE, Heart Failure or more.
Normal levels are 0 to 0.4 (im assuming thats flexible depending on where / who you talk to???)

Ive transported so many pt's that are "NSTEMI" because of elevated trop but No cardiac history but oh jeez, Turns out theyre new onset Renal failure. Or my most recent guy was having a panic attack and had a stable non-operable AAA that the hospital was just watching (didnt even know THAT was a thing.huh!)

So why do dr's tend to make this their clinical dx with an elevated trop if theres other issues causing this? It sorta seems to be the "go to" in my area.


Soooooooo What else causes elevated trops that i missed?
How long Does it take to return to normal?
Educate me.

Here to learn. Dont know anything. Not claiming i do. Probally everything above is wrong somehow. Posting this thread to learn [/disclaimer]
 
I'll explain the little that I know, in hopes that others pop in.

Troponin is as you said a cardiac marker. It's kind of like a solder joint on muscle cells. When the cells are damaged this "solder joint" breaks off and can be detected in the blood.

There are multiple types of troponin. When we do testing we try to test for cardiac specific troponin. As you said, many things can cause a false positive, kidney failure being a leading false positive cause.

When patients get a cardiac workup they get serial troponin tests, usually 3. This is to establish a trend of stable, upwards or downward trending levels. With no known cardiac history, a positive troponin is usually enough to buy you an admission for observation. If the patient has cardiac symptoms, it may lead to a NSTEMI diagnosis.

Keep in mind, troponin just indicates muscle damage. In the heart, this may or may not mean a clot. For example, an over worked heart, or a hypoxic heart could both release troponin with no clot. These are called Type 2 MIs.
 
To add to what NPO said:

Cardiac troponin is released from myocytes (cells in the heart) when they are stressed or damaged. The most common cause of this is cardiac ischemia from acute coronary syndrome--NSTEMI or STEMI--but it can be from anything else that causes cardiac damage. Sepsis often causes a form of cardiomyopathy because the inflammatory response causes heart damage. Anemia, especially more acute anemia can raise troponin because it leads to decreased oxygen supply to the heart. Aortic dissection causes cardiac stress, etc. Some causes of troponin elevation are weirder, like strokes, though I forget the exact mechanism. Even marathon running can cause a mild troponin elevation.

Troponin coming from cardiac ischemia and other direct issues with the heart is called a type 1 MI. Troponin coming from global ischemia like anemia is a type 2 MI.

There are three types of acute coronary syndrome, which is itself the most common Type 1 MI. Unstable angina, which is ongoing cardiac chest pain without a rise in troponin or ST segment elevations. NSTEMI is cardiac chest pain WITH troponins, and STEMI is purely an EKG diagnosis, made without troponins (see below for why). The reason misdiagnoses can happen is it's fairly easy to assume that someone with chest pain, a cardiac history, and an elevated troponin is having an NSTEMI when they may in fact be having an aortic dissection or a pulmonary embolism, both of which would require a CT to diagnose.

Renal failure does not cause troponin to be released, but it inhibits the body's ability to clear troponin. There is a tiny amount of troponin released at any given time that is usually undetectable, but it can accumulate in patients with significant kidney disease. While it's a predictor of bad outcomes to have a high troponin and kidney disease, there's not much you can do about it.

Troponin takes a few hours to rise, which is why an acute STEMI may have initially negative troponins. This is also why, as said above, you take several measurements of troponin to insure you aren't missing anything by testing too early. Troponin also clears in a few hours, but in most of these conditions there will be significant ongoing death of cells so in an MI troponin usually takes a few days to fully clear. The PCI itself used to treat a STEMI can also cause a release of troponin.

Hope that helps.
 
My dear friend,
Troponin belongs in the cells,
Not in the blood.
When found where it shouldn't be
A type of MI (N or not-N) it would be.
If the GFR is normal,
And Troponin is up,
A type of NSTEMI,
or STEMI if on EKG,
It will be.
 
When y'all say stressed. What defines stress in cardiac or other functions.
 
DragonClaw said:
When y'all say stressed. What defines stress in cardiac or other functions.
Click to expand...
When cardiac oxygen demand is greater than the oxygen supply.

This can be from a clot, pulmonary disease, or even strenuous exercise. Any condition where the heart wants more oxygen than it's getting.
 
NPO said:
When cardiac oxygen demand is greater than the oxygen supply.

This can be from a clot, pulmonary disease, or even strenuous exercise. Any condition where the heart wants more oxygen than it's getting.
Click to expand...

So it's a oxygen deficit.

In a hypothetical sense, if there's no blockage, would "blood doping" be a treatment if oxygenation is sufficient?

I guess that's the basis of a blood transmission.

How often does getting a hypercarbic pt to calm down and breathe help alleviate symptoms? Or I guess if it's that bad you'd go straight to giving oxygen anyway.

What about sedating a pt so they require less oxygen? Is that a thing?
 
DragonClaw said:
So it's a oxygen deficit.

In a hypothetical sense, if there's no blockage, would "blood doping" be a treatment if oxygenation is sufficient?

I guess that's the basis of a blood transmission.

How often does getting a hypercarbic pt to calm down and breathe help alleviate symptoms? Or I guess if it's that bad you'd go straight to giving oxygen anyway.

What about sedating a pt so they require less oxygen? Is that a thing?
Click to expand...

It all depends on why the oxygen demand mismatch is a problem. For example trauma patients may be at 100% SPO2, but have very low hemoglobin which means their total body oxygen is low. So no matter how much oxygen you throw at them, they will be "hypoxic". This is called anemic hypoxia. The treatment in this case is increasing the oxygen carrying capacity of the blood by adding more blood.

Sometimes sedating a patient may aleviate the problem if they are suffering from some causes of Type 2 MI. For example, if someone has overdoses on sympathomimetics (meth, for example), some benzodiazapines may be appropriate in countering the sympathetic system to reduce heart rate and associated myocardial oxygen demand. Anesthesia is not the goal here, just decreased sympathic drive.
 
NPO said:
It all depends on why the oxygen demand mismatch is a problem. For example trauma patients may be at 100% SPO2, but have very low hemoglobin which means their total body oxygen is low. So no matter how much oxygen you throw at them, they will be "hypoxic". This is called anemic hypoxia. The treatment in this case is increasing the oxygen carrying capacity of the blood by adding more blood.

Sometimes sedating a patient may aleviate the problem if they are suffering from some causes of Type 2 MI. For example, if someone has overdoses on sympathomimetics (meth, for example), some benzodiazapines may be appropriate in countering the sympathetic system to reduce heart rate and associated myocardial oxygen demand. Anesthesia is not the goal here, just decreased sympathic drive.
Click to expand...

And yes, trauma with hypovolemia was a candidate for blood. And I guess hypovolemia without trauma, chronic GI bleed etc.



Of course, decreased oxygen requirements as the hoped result, not effect.
 
Troponin is released in response to the stretching of cardiac myocites aside from ischemia so you will see elevated levels in heart failure with volume overload, massive PE, pericarditis, and even massive ICH. Increased wall tension and stretch causes increased oxygen demand and relative ischemia but the mechanism of Troponin is a little more complex than just MI/ACS
 
mrhunt said:
a stable non-operable AAA that the hospital was just watching (didnt even know THAT was a thing.huh!)
Click to expand...
Risk vs Reward equation, how big is the anuersym and what is that particular patients surgical risk profile. If it is less than 5 cm and remains stable, they do a follow up every 6 months to monitor.
 
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