Unstable Ischemic Coronary Syndromes Flashcards Preview

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Flashcards in Unstable Ischemic Coronary Syndromes Deck (28):
1

What's the difference between ischemia and infarction?

In infarction, cells are dead or dying.

2

What distinguishes unstable angina from non-ST elevation MI (NSTEMI)?

In NSTEMI, cardiac enzymes will be elevated, as cells are dying.
Otherwise (by ECG, etc.) these look pretty similar.

3

3 outcomes of plaque rupture in a coronary artery?

Thrombus formation -> spontaneous lysis -> return to stable angina (or... asymptomatic CAD).
Thrombus formation -> healing / incorporation -> progression of stenosis.
Thrombus formation -> occlusion of coronary artery -> MI.

4

What pathophysiology underlies most acute coronary syndrome? What are 2 other causes?

Most common: plaque rupture.
Less common: intravascular thrombosis (i.e. emboli) and vasospasm.

5

Review: What's the most important variable for the risk of an individual plaque rupturing?
Can we actually assess this risk?

Fibrous cap thickness. Thinner is riskier.
No, we can't asses the risk of individual plaques rupturing at this point.

6

Does stenosis predict plaque rupture?

Nope. Extent of stenosis of coronary arteries can give you some sense of overall atherosclerotic burden, but it's often not the most stenotic lesion that's going to rupture.

7

What's important in a history suggesting high-risk unstable angina or NSTEMI?

Change in angina pattern, or new onset of angina type chest pain. (more frequently, with less exertion, more severe, etc.)

8

What does physical exam of a patient with high-risk unstable angina or NSTEMI reveal?

May be normal or show hemodynamic compromise (cardiogenic "pre-shock" or shock)

9

What does an ECG of a patient with high-risk unstable angina or NSTEMI show?

ST segment depression or T wave inversion

10

How are biomarkers changed in high-risk unstable angina or NSTEMI?

High-risk unstable angina: biomarkers are normal.
NSTEM: biomarkers elevated, indicating cellular death.

11

How does epicardial (i.e. transmural) ischemia appear in ECG?

ST segment elevation.
If you see ST elevation, it's likely a STEMI.

12

What's a key cardiac biomarker to remember?

Troponin.
(Others, like creatine kinase and myoglobin are used... but he really emphasizes troponin)

13

How long after MI is troponin released?
When do levels peak, and how long afterward are the detectable?

Released at 20-30mins of ischemia.
Peak at 12 hours.
Detectable for 7 days.
(Says Wikipedia. Not important to know the exact numbers)

14

Are troponin levels correlated with increased mortality?

Yes, higher troponin means more cell death, and this is bad.

15

3 aspects of acute care of acute coronary syndromes (ACS)? (excluding STEMI, I guess)

Anti-ischemic therapy (Nitroglycerin, beta-blockers, CCBs).
Anti-thrombotics (antiplatelets, anticoagulents).
Reperfusion (PCI or CABG)

16

Does adding clopidogrel to aspirin improve outcomes?

Yep.

17

Review: What's the MoA of clopidogrel, plasugrel, and ticagrelor?

Inhibition of P2Y(12) - a receptor on platelets.

18

Does combining platelet inhibitors (eg. GP IIb/IIIa inhibitors) with PCI improve outcomes?

Yes.

19

Is invasive therapy recommended for NSTEMI?

Yes. PCI definitely improves outcomes.

20

Does NSTEMI or STEMI carry a greater risk of recurrent ischemia?

NSTEMI has a greater risk of recurrent ischemia.

21

Does NSTEMI or STEMI carry a greater risk of reduced LV function and CHF?

STEMI is more likely to cause LV dysfunction and CHF.

22

Classic symptoms of MI (not all will necessarily be present)?

Chest pain (pretty much always happens... except in neuropathy, transplanted hearts).
Diaphoresis, nausea, arm pain.
SOB (due to pulm. edema, acute MR, arrhythmia).
Hypotension.

23

Physical exam finding during MI?

(may all be negative, but...)
Cool and clammy skin.
Evelated or decreased BP and/or HR.
Increased JVP.
"Late systolic bulge." (asynchronous contraction)
Increased S3
Mitral regurg..
Pulm. edema.
Pericardial friction rub.

24

3 things ECG can tell you about acute MI?

Diagnosing it.
Localizing it.
Determining eventual size.

25

What will you see in ECG of early STEMI?

ST elevation

26

What appears in ECG of later STEMI, once irreversible damage has occurred?

Q waves.

27

What's perhaps the most important part of STEMI treatment?

Reperfusion via fibrinolytics, PCI, or CABG.
(PCI is preferred, if possible)

28

What are some factors that can prevent against myocardial necrosis in MI?

Ischemic preconditioning.
Presence of collateral bloodflow from chronic ischemia.