Step I Angina - ST depression/elevation

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Siverhideo1985

Siverhideo1985

Full Member
15+ Year Member
Why does stable angina present with ST depression on ECG but prinzmetal's presents with ST elevation?

no matter what the mechanism is - blood flow is decreased in both so shouldn't the ECG read the same?
 
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Siverhideo1985 said:
Why does stable angina present with ST depression on ECG but prinzmetal's presents with ST elevation?

no matter what the mechanism is - blood flow is decreased in both so shouldn't the ECG read the same?
Click to expand...
The electrical basis for ST depression and elevation is far beyond the scope of Step 1.

That said, you must know that ST elevation MIs (STEMIs) = transmural ischemia, which are usually caused by an ulcerated atheromatous plaque and for which the treatment of choice is stenting/angioplasty or fibrinolytics if >90 minutes from an angio center. These are basically of equal efficacy, but fibrinolytics are much more dangerous. About the only testable adverse effects of angioplasty are femoral hematomas/aneurysms and "blue toe syndrome." If you haven't heard of blue toe, you should look that up and annotate it into your FA.

You may also see ST elevation in other scenarios. Of these, only pericarditis (diffuse elevation in all leads with PR segment depression) is step 1 testable in my opinion, and they would give you wayyy more information than just the ECG (previous viral illness/MI, chest pain relieved by sitting forward, friction rub). You can see "peaked Ts" with hyperkalemia.

ST depression has an absurd number of causes. The most important for step 1 are unstable angina and NSTEMI (non-Q wave MI), which are differentiated from each other by cardiac enzymes (NSTEMI = Trp/CK elevation). The depression in this case is caused by subendocardial ischemia.

Short answer, Prinzmetal's = transmural ischemia and unstable angina is not.
 
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ScubaStarved said:
The electrical basis for ST depression and elevation is far beyond the scope of Step 1.

That said, you must know that ST elevation MIs (STEMIs) = transmural ischemia, which are usually caused by an ulcerated atheromatous plaque and for which the treatment of choice is stenting/angioplasty or fibrinolytics if >90 minutes from an angio center. These are basically of equal efficacy, but fibrinolytics are much more dangerous. About the only testable adverse effects of angioplasty are femoral hematomas/aneurysms and "blue toe syndrome." If you haven't heard of blue toe, you should look that up and annotate it into your FA.

You may also see ST elevation in other scenarios. Of these, only pericarditis (diffuse elevation in all leads with PR segment depression) is step 1 testable in my opinion, and they would give you wayyy more information than just the ECG (previous viral illness/MI, chest pain relieved by sitting forward, friction rub). You can see "peaked Ts" with hyperkalemia.

ST depression has an absurd number of causes. The most important for step 1 are unstable angina and NSTEMI (non-Q wave MI), which are differentiated from each other by cardiac enzymes (NSTEMI = Trp/CK elevation). The depression in this case is caused by subendocardial ischemia (e.g., the endocardium is fed from the heart lumen and outermost muscle is adequately perfused, thus subendocardial).

Short answer, Prinzmetal's = transmural ischemia and unstable angina is not.
Click to expand...

my bad!
 
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Siverhideo1985 said:
Why does stable angina present with ST depression on ECG but prinzmetal's presents with ST elevation?

no matter what the mechanism is - blood flow is decreased in both so shouldn't the ECG read the same?
Click to expand...


In stable angina the deepes layer of myocardium suffers always first, hence ST depression, but if the ischemia is transmural (all layers of myocardium) you will have an ST elevation.
In prinzmetal, vasospasticity in all vessels causes ischemia throughout the myocardium (transmural) causing an ST elevation.

I asked a cardiologist who was giving a lecture about the mechanism of st depression and elevation just to confirm the concept I read in books, that guy did not have a clue, to his defence, he was a clinician.


In ischemia the affected tissue in the innermost layer of the myocardium acts as a cation-sink, so you have an electrical vector going towards the deepest layer of myocardium away from the positive electrode causing an ST depression on the ECG.
If the damage is transmural, cations from neighbouring cells enter the damaged tissue not towards the innermost layer of the myocardium but at an angle from inside towards outside causing an electrical vector going towards the positive electrode leading to an ST elevation.
 
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Maybe the conflict is in definitions? In my textbooks, the endocardium is not part of the myocardium; rather, it's the endothelium between heart lumen and myocardium (and so is fed by the heart lumen). What bbydoc is referring to as the endocardium seems to be what my books call the subendocardium - that is, the myocardium just beneath the luminal endothelium. It seems like you guys are on the same page but using different terminologies...
 
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DuxburyPembroke said:
Maybe the conflict is in definitions? In my textbooks, the endocardium is not part of the myocardium; rather, it's the endothelium between heart lumen and myocardium (and so is fed by the heart lumen). What bbydoc is referring to as the endocardium seems to be what my books call the subendocardium - that is, the myocardium just beneath the luminal endothelium. It seems like you guys are on the same page but using different terminologies...
Click to expand...

thanks for pointing this out!
its my mistake, Im wrongly referring to the deepes layer of the myocardium as the endocardium.
lets start the editing 🙁
 
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bbydoc said:
thanks for pointing this out!
its my mistake, Im wrongly referring to the deepes layer of the myocardium as the endocardium.
lets start the editing 🙁
Click to expand...
Wait, so after all this I was correct about that minor detail the first time?

From someone who has taken the exam, stick to the big picture: understand the differences between STEMI and UA/NSTEMI and the very basic treatment regimens for each.

Memorize the distributions of coronaries and the complications of STEMI (pump failure, septum rupture --> VSD, free wall rupture --> tamponade, aneurysm, ventricular arrhythmias, pericarditis, and so on). Be at least somewhat familiar with murmurs that can arise from papillary muscle failure or IVS rupture. Memorize the timeline for progression of microscopic changes following ischemia. Know the risk factors for ASCVD and the fact that diabetes trumps almost everything.

If you get all that down, then look up blue toe syndrome. 🙂
 
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This may be a dumb question, but why do NSTEMI subendocardial MI's have a higher mortality rate and cause more severe clinical symptoms versus STEMI transmural MI's?
 
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