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Flashcards in Acute Coronary Syndromes Deck (62)
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31

Q-wave MI

Transmural infarction

32

Non q-wave MI.

Subendocardial ischemia -- few collaterals there and exposed to highest pressures from ventricle

33

Presentation of ACS?

Ischemic discomfort at rest

34

Sign of ACS

Either ST segment elevation or non ST segment elevation

35

Non ST segment elevation ACS

Can be unstable angina, Non-q wave MI, or even a Q wave MI (very rarely)

36

ST segment elevation ACS

Generally a q-wave MI, but sometimes (rare) can be a non-q wave MI.

37

Nonocclusive ruptured plaque leading to thrombus causes

Unstable angina, NSTEMI

38

Occlusive ruptured plaque leading to thrombus causes

STEMI.

39

Increasing severity of ACS

Unstable angina -> NSTEMI -> STEMI

40

Most critical distinction to make

NSTEMI or STEMI

41

Clinical symptoms of MI

Chest pain more severe, longer duration, with greater radiation than normal. Does not improve with rest or nitroglycerin.
Sympathetic discharge (diaphoresis, tachycardia, nausea, clammy skin)
Shortness of breath (LV volume rises, so backs up to lungs)

42

Who is likely to have an MI without symptoms?

Diabetics

43

Physical findings of MI

S4 (noncompliant LV)
S3 (volume overload and systolic dysfunction)
Systolic murmur (may come from papillary muscle dysfunction leading to MR)
Fever

44

Why can an MI cause MR?

Because papillary muscle doesn't function properly.

45

Differential for MI

Pericarditis, pleuritis (pain w/inspiration and diffuse ST ele)
Aortic dissection (ripping pain, BP asymmetry, widened mediastinum on CXR)
PE
Acute cholecystitis

46

ECG findings of USA or NSTEMI

T wave inversion, ST depression or normal

47

Are biomarkers elevated in USA?

No

48

Are biomarkers elevated in NSTEMI

yes

49

ECG evolution with STEMi

See slides

50

Definition of STEMI

Prolonged chest discomfort unrelieved by nitroglycerin with ST segment elevation on EKG and rise in cardiac markers

51

Definition of NSTEMI

Angina at rest for longer than 20 minutes without ST segment elevation but with cardiac biomarkers.

52

Pathophysiology of STEMI

Total or near total occlusion of coronary artery

53

Pathophys of NSTEMI

Abrupt decrease in myocardial O2, thrombus formation or an atherosclerotic plaque

54

Management of STEMI

Immediate reperfusion with a preferred door to balloon time of <90 minutes

55

Management of NSTEMI

Depends on TIMI score

56

Cardiac biomarkers

Troponin (T, I, or C)
Creatine Kinase Myocardial Band (CK-MB)
Myoglobin

57

Troponins

Control calcium mediated interactions between actin and myosin that are released into circulation from muscle and cytosolic reserves during necrosis. TNI and TNT are highly sensitive and specific for myocardial necrosis.

58

Where is troponin released from first?

Cytosolic pool, but if injury persists, then muscular pool

59

When do levels of troponin rise and peak?

Rise within 3-4 hours. Peak at 18-36 and decline slowly

60

Creatine Kinase

Enzyme involved in ATP generation. Found in heart (CK-MB) but also in muscle (MM) and brain (BB). Also in uterus prostate gut.