Exact mechanism of STEMI

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hckyplyr

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Hello all,
I've searched online, and this forum, but haven't quite found the answer I was looking for. Does anyone know the exact mechanism of a STEMI, or why the ST segment is elevated? I realize its from ischemia/infarction, but what is actually causing the ST segment to rise?
My best "guess" is since an EKG measures electrical impulses, as well as time, since that one area of the heart is damaged, it takes more time for the electrical impulse to travel around or through the damaged area, leading to an elevation...But that still doesn't answer what actually caused it to rise and fall......Any thoughts? Thanks
 
You're over thinking this.

What causes a p wave? What causes a QRS wave?

Everything is based upon how electricity waves flow towards or away from the leads.

People have watched these waves and learned the patterns they form. One pattern is an STEMI. The heart muscle is damaged in a way that causes the impulse on the leads to read as a ST elevation.

What I've written above is enough knowledge for clinical medicine.
 
An MI is any cardiac insult resulting in an elevation of troponin on testing. So an N-STEMI. This can be stress or demand or ischemic. Regardless, there is sufficient insult to the heart to cause damage resulting in cardiac enzymes leaking in to the serum

An STEMI is when there is an insult to the heart which causes both troponin leak and elevation of the ST segment of the ECG. Typically, this is ischemic in the distribution of one of the cardiac arteries, and the distribution of the ST elevation is significant in diagnosing the location of the infarct. This is because the hypoxic cardiac tissue functions less normal than the surrounding tissue
 
An MI is any cardiac insult resulting in an elevation of troponin on testing. So an N-STEMI. This can be stress or demand or ischemic. Regardless, there is sufficient insult to the heart to cause damage resulting in cardiac enzymes leaking in to the serum

An STEMI is when there is an insult to the heart which causes both troponin leak and elevation of the ST segment of the ECG. Typically, this is ischemic in the distribution of one of the cardiac arteries, and the distribution of the ST elevation is significant in diagnosing the location of the infarct. This is because the hypoxic cardiac tissue functions less normal than the surrounding tissue

Wow that was surprisingly unhelpful.

There are a few thoughts on the issue. The most prevalent:
In ischemia, STE occurs because the ischemic region is depolaraized. So the baseline voltage prior to the QRS will be depressed. Essentially there is a depressed baseline. When the ventricle depolarizes, all the muscle is depolarized so the votage is recorded as the zero point. Thus, the ST segment appears "elevated" as essentially an artifact of a falsely depressed baseline.
 
Wow that was surprisingly unhelpful.

There are a few thoughts on the issue. The most prevalent:
In ischemia, STE occurs because the ischemic region is depolaraized. So the baseline voltage prior to the QRS will be depressed. Essentially there is a depressed baseline. When the ventricle depolarizes, all the muscle is depolarized so the votage is recorded as the zero point. Thus, the ST segment appears "elevated" as essentially an artifact of a falsely depressed baseline.

Thanks for the editorial comment.

Your statement is false. The qrs segment is the depolarization phase, st is repolarization. St elevation happens in ischemic tissue, or tissue blocked by an artery that is occluded, because of early repolarization.

The ecg is simply a measurement of the electrochemical vectors that occur within the heart. The 12 - lead arrangement is meant to help the physician localize the lesion based on normal physiology.
 
Thanks for the editorial comment.

Your statement is false. The qrs segment is the depolarization phase, st is repolarization. St elevation happens in ischemic tissue, or tissue blocked by an artery that is occluded, because of early repolarization.

The ecg is simply a measurement of the electrochemical vectors that occur within the heart. The 12 - lead arrangement is meant to help the physician localize the lesion based on normal physiology.

Actually @Instatewaiter is correct. The ischemic region is partially depolarized, creating a potential difference between it and the healthy tissue at rest (area between T and P wave). The EKG machine is calibrated to designate this the zero point. So during the ST segment, when both the healthy and damaged tissue are both completely depolarized, no potential difference exists and this should be our normal, isoelectric ST located at zero. However we already defined our zero point as when there was a potential difference, so any change from this i.e. no potential difference, will show up as a deflection from isoelectric on EKG, giving rise to elevated ST
 
Thanks for the editorial comment.

Your statement is false. The qrs segment is the depolarization phase, st is repolarization. St elevation happens in ischemic tissue, or tissue blocked by an artery that is occluded, because of early repolarization.

The ecg is simply a measurement of the electrochemical vectors that occur within the heart. The 12 - lead arrangement is meant to help the physician localize the lesion based on normal physiology.

Thank you for the insight into the EKG. If you stick to the brain, I'll stick to the other side of the vagus nerve

Ischemic cells depolarize. This causes a lower TQ segment. This in turn, appears as ST elevation because the EKG recorders in clinical practice use amplifiers that automatically set the baseline and compensate for a negative shift in the supposedly isoelectric TQ segement. You don't see this during the QRS because all of the myocardium depolarizes to meet the injured myocardium and when it tries to repolarize, you see the damage. This is called the diastolic current of injury.

As I said before, there is some diagreement. This comes in because there is also a systolic currrent of injury some have found in experiments while others have not. Some have claimed this comes from a shortening of the plateau of the action potential (basically what you said) or a slower AP upstroke. Regardless this can establish a current of injury between normal and ischemic zones during the ST directed toward this ischemic region. Thus positive STs in the location of injury.
 
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I stick to my earlier comment.

It's a pattern and that's enough for clinicians. Excluding cardiologists, which is something you can focus on pgy2-6.
 
I am a cardiology fellow. Thank you for the insight into the EKG. If you stick to the brain, I'll stick to the other side of the vagus nerve

Ischemic cells depolarize. This causes a lower TQ segment. This in turn, appears as ST elevation because the EKG recorders in clinical practice use amplifiers that automatically set the baseline and compensate for a negative shift in the supposedly isoelectric TQ segement. You don't see this during the QRS because all of the myocardium depolarizes to meet the injured myocardium and when it tries to repolarize, you see the damage. This is called the diastolic current of injury.

As I said before, there is some diagreement. This comes in because there is also a systolic currrent of injury some have found in experiments while others have not. Some have claimed this comes from a shortening of the plateau of the action potential (basically what you said) or a slower AP upstroke. Regardless this can establish a current of injury between normal and ischemic zones during the ST directed toward this ischemic region. Thus positive STs in the location of injury.

Really appreciate you taking the time to comment, as this makes a lot of sense. I am having difficulty reasoning why subendocardial ischemia results in ST depression? It seems to me that these are just reversibly injured heart cells and should also be depolarized. Thoughts?
 
Really appreciate you taking the time to comment, as this makes a lot of sense. I am having difficulty reasoning why subendocardial ischemia results in ST depression? It seems to me that these are just reversibly injured heart cells and should also be depolarized. Thoughts?

Wow. Down the path of low yield.
 
My cardiology teacher said the mechanism is unimportant. When I told her some proposed mechanisms I read, some of them people already mentioned here, she said that sometimes STEMI doesn't originate from that mechanism, and sometimes that mechanism doesn't cause STEMI.
 
It's not about high or low yield but trying to understand why things are the way they are. I find that I retain concepts much better than facts and it's easier to remember things if I can reason through it. Integrating knowledge and applying it is more important than memorizing facts and regurgitating it onto a computer screen. We're studying to be doctors, not Step 1 test takers.
 
I find there's not much to retain in terms of the mechanisms behind elevated and depressed ST segments on the EKG becausethe concepts are more complex than the answer. Reasoning through it can lead to wrong answers if you're not intimately familiar with it. The stuff that needs to be retained by your method is figuring out axis, figuring out which leads point to which anatomical location, etc. That's stuff where the explanations are simpler and can aid in memorizing the facts you need to know. But as far as STEMI and NSTEMI go, the explanation is more likely to get in the way of than it will aid in diagnostics. And if I want to get that STEMI to the cath lab in 90 minutes, it's much more important to get the pattern recognition down than anything else.

Now if people want to know about it, great, get a cardiologist to explain it. It's academic. Maybe it's fun or cool to know. Just don't belittle someone trying to say that it's low yield =p It really is, as is a lot in medicine.
 
Get a life. If you don't like the content of the thread then just ignore it. Not everything is about being high or low yield. I was curious about something and asked someone who is skilled at explaining it.

I was curious about the content also, until I saw were it was going. Hence I commented on it. I do understand your type, so it was as much a comment as it was a warning - but oh well.

As for the usefulness of high/low yield, talk to me again after your clinic years / Step 1 or even an EKG course, anything pertaining to this topic. EDIT: after reading/quoting some replies below, it appears others are echoing my sentiments.

I'm just wondering why the allo forum has suddenly turned into the physio homework help forum...

+1

It's not about high or low yield but trying to understand why things are the way they are. I find that I retain concepts much better than facts and it's easier to remember things if I can reason through it. Integrating knowledge and applying it is more important than memorizing facts and regurgitating it onto a computer screen. We're studying to be doctors, not Step 1 test takers.

Haha. I wasn't advising you to focus on how to be better on tests - my personality is the opposite of that.

Instead, I was telling you to learn what's clinically applicable (i.e. be a good doctor, not a test taker/academic). I know most the physicians I've worked with outside of cardiology couldn't explain this. In this thread, a neurosurgeon + cardiologist didn't agree on the exact mechanism. I too learn best with concepts, but in this case it's not advisable.

There are so many more important concepts to learn. Take for example the best internal medicine book for medical students, Step Up to Medicine, it won't explain such a concept. Just for fun, I read the STEMI section in Harrison's Principles of Internal Medicine, mind you this is a 4,100 page tome on internal medicine written by the best physicians in the world. Guess what, their explanation of a STEMI is essentially what I said, it's a pattern from the direction the tissue is depolarizing.

To your statement, "We're studying to be doctors, not Step 1 test takers." Oh, how misinformed you are. This has nothing to do with being a good physician. If you can't even find it in Harrisons, then I would question how important it will be for you clinically (especially as a med student!). Most residents don't even have time to read through Harrisons.

Whatever though, I guess med students will be med students.

My cardiology teacher said the mechanism is unimportant. When I told her some proposed mechanisms I read, some of them people already mentioned here, she said that sometimes STEMI doesn't originate from that mechanism, and sometimes that mechanism doesn't cause STEMI.

Exactly. It isn't important.

I find there's not much to retain in terms of the mechanisms behind elevated and depressed ST segments on the EKG becausethe concepts are more complex than the answer. Reasoning through it can lead to wrong answers if you're not intimately familiar with it. The stuff that needs to be retained by your method is figuring out axis, figuring out which leads point to which anatomical location, etc. That's stuff where the explanations are simpler and can aid in memorizing the facts you need to know. But as far as STEMI and NSTEMI go, the explanation is more likely to get in the way of than it will aid in diagnostics. And if I want to get that STEMI to the cath lab in 90 minutes, it's much more important to get the pattern recognition down than anything else.

Now if people want to know about it, great, get a cardiologist to explain it. It's academic. Maybe it's fun or cool to know. Just don't belittle someone trying to say that it's low yield =p It really is, as is a lot in medicine.

Agreed. I may not have been as eloquent in my earlier posts, because they were one-liners. Honestly wasn't trying to belittle anyone. I apologize if anyone thought I was attacking them personally.
 
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I definitely wish I was more like you. God forbid I ask a question that interested me. I don't have homework, don't care about whether it is on step 1 or not, just asked a question. I'm so glad two people on an anonymous forum echoed your sentiments, I know your type so that must give you great pleasure
 
Check out Dubin's Rapid Interpretation. It helped me understand the concepts of EKG better (even how to interpret) which has stuck with me long-term.
 
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