question about NSTEMI and posterior MI
- 0Feb 28, '13 by skylarkPlease help, I'm studying for CEN and getting very confused here.
The more I read, the more confused I am!
Here's where I am having trouble -
I'm trying to be clear about ECG interpretation and on the whole I was clear what I was doing, until I started studying today : )
But then I'm reading that the ECG presentation of a posterior MI is ST depression in V1-3 and flipped T waves.
I'm also reading that a NSTEMI shows ST depression in V1-3, with the flipped Ts.
And I'm still having trouble defining the difference between NSTEMI and UA.
Both involve ischemia but not infarction, is that right or have I gone into total meltdown here?
Sorry to trouble you folks, but I am more muddled now than when I started.
- 3,087 Visits
- 5Mar 1, '13 by turnforthenurseRNWith a posterior MI, you will ONLY see reciprocal changes, as in ST-depression with T-wave inversion. You may also see a large R wave with tall T's and ST-depression, but those large R waves are essentially a Q wave, upside down. A reciprocal change s when you see ST elevation in two or more contiguous leads and ST depression in other leads. If you have reciprocal changes, you are having an MI. 50% of inferior wall MI's will also have posterior wall involvement, so if you see changes in leads II, III and aVF (inferior) with those reciprocal changes in leads V1 & V2, you have yourself a posteroinferior MI.
UA is an acute coronary syndrome that results from decreased blood flow to the myocardium. UA is not relieved by rest or nitroglycerine. Cardiac enzymes are normal. UA can lead to NSTEMI or STEMI depending on the severity of the blockage.
In an NSTEMI (or non Q-wave MI), there is subendocardial damage, meaning that NOT all muscle layers of the heart are affected. This is caused by a non-occlusive thrombus. There is a decrease in blood flow but the vessel is not completely occluded. In an NSTEMI, you will see normal R-wave progression and no Q-waves (hence the other name, "non Q-wave MI.") and no ST-elevation. You will see an elevation in cardiac enzymes. The goal here is to stabilize that non-occlusive thrombus and of course open up that vessel(s). tPA is NOT used to treat a patient with an NSTEMI and can actually increase bleeding complications in patients with an NSTEMI.
UA can also lead to a STEMI (Q-wave MI) where there is transmural damage - the entire thickness of the myocardium is injured (ST elevation) and will soon be infarcted (Q waves) if you do not act quickly. This is caused by an occlusive thrombus, or complete blockage of a coronary artery. You will see a loss of R-wave progression and ST-segment elevation with Q wave formation. tPA can be used to treat a STEMI, unlike with an NSTEMI.
- 2Mar 2, '13 by hodgieRNIf you are studying for the CEN, you might want to make a quick note of ischemia vs infarction. They like asking all about MIs and then throw some vague ST depression questions on there, making you want to go with infarct answers. Know the differences between unstable angina, ischemia, infarction, etc. Those are good curve balls. Know what an EKG will show 24 hrs after an MI. Know what cardiac enzymes go up first (or are more sensitive) and know how long they last. For example, how many hours will a troponin stay elevated vs CK or myoglobin. What goes down first and how quick? You may need to identify a case where the pt had a MI a day ago. They usually like to ask about treatment for new-onset LBBB (it's treated as an MI). Also know what rhythms to expect with certain MI's. Which ones cause bradycardia, 2nd and 3rd degree blocks? Know the treatment of a right-sided MI vs left-sided MI. And make sure you learn the what coronary artery is associated with elevation. People study ST elevation over and over and learn all the different leads and changes, but can't recall which coronary artery is blocked. An inferior MI has what artery blocked? And anterior MI has which artery blocked. What EKG changes would you see with circumflex blockage?