02.16 Acute Coronary Syndrome Flashcards Preview

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Flashcards in 02.16 Acute Coronary Syndrome Deck (80):
1

Caused by complete obstruction of a coronary artery

STEMI

2

Results in damage or necrosis of the full thickness of the heart muscles

STEMI

3

Caused by partial obstruction of a coronary artery

NSTEMI

4

Resulting necrosis only involves a partial thickness of the heart muscle

NSTEMI

5

2 main components of atherosclerotic plaques

Soft, lipid-rick core
Hard, collagen-rich fibrous cap

6

Thick fibrous cap may represent >70% of plaque volume

Stable plaque

7

Lipid-rich core may represent the majority of the plaque volume

Unstable plaque

8

Due to inflammation by foam cells and other inflammatory mediators that make the plaque more vulnerable to rupture

Plaque destabilization

9

Where does plaque destabilization commonly occur

At the junction of the plaque and the less diseased vessel wall

10

Primary cause of a heart attack

Rupture of unstable plaques

11

Usually >20 minutes in duration
Sudden chest pain patient is at rest

Rest angina

12

Markedly limits physical activity

New onset angina

13

More frequent, longer in duration or occurs with less exertion than previous angiina

Increasing angina

14

Symptoms of acute coronary syndrome

Prolonged pain
Usually retrosternal location, radiating to the left chest, arm
Nausea, vomiting
Palpitations
Diaphoresis
Sense of impending doom

15

Acute coronary syndrome

STEMI
NSTEMI
US

16

Risk factors of ACS

Advanced age
Smoking
Hypertension
DM
Dyslipidemia
Family history of early MI
Known CAD

17

PE of ACS

Anxious and restless
Pallor with cold sweats and cold extermities
Sympathetic hyperactivity
3th and 4th heart sound
Friction rub
Signs of congestion

18

If ST deviations are on V3, V4, then the problem is at the ____

LAD, anterior of the heart

19

If ST deviations are on V5, V6, the problem is at the _____

LCX, lateral of the heart

20

If ST deviation is on II, III and aVF, then the patient has _______

Right coronary artery problem

21

Established CAD by angiography, history of CABG or PCI, history of MI, CHF, Multiple CAD risk factors are likely to have _____

US/NSTEMI

22

Normal or nonspecific ST T wave changes
ST depression
T wave inversion

US/NSTEMI

23

Cardiac markers for US/NSTEMI

Cardiac troponin I and T
CK-MB (4-6 hours)

24

Diagnostic approach to US/NSTEMI

ECG, Cardiac markers, Treadmill exercise testing, CT angiogram

25

TIMI Risk stratification

Age >/= 65 years
>/= 3 CAD risk factors
Prior stenosis >50%
ST deviation
>/= 2 anginal events = 24h
ASA in last 7 days
Elevated cardiac markers

26

Pharma intervention for plaque rupture

Statins

27

Pharma intervention for platelet adhesion

ASA, clopidogel, GP IIb/IIa inhibitors

28

Pharma intervention for activation of clotting cascade

Anticoagulant agents

29

Pharma intervention for myocardial ischemia

Beta blockers
Nitrates
Calcium antagonists

30

Treatment of US/NSTEMI

Bed rest
Nirates
B-blockers
CCB
Morphine sulfate

31

Limited by hypotension and bradycardia
CI if with pulmonary congestion and severe reactive airways disease

Beta-blockers (metaprolol)

32

Used when betablockers are not effective

CCB (Diltiazem, verapamil)

33

Used for persistent angina

Morphine sulfate

34

Prevent the progression of intracoronary thrombi
Promote stabilization of the atherosclerostic plaque, thereby reducing myocardial ischemia and preventing further complications such as death or MI

Antithrombotic therapy

35

Antiplatelet drugs

Aspirin
Clopidogrel
GP IIb/IIa antagonists (Abciximab, eptifibatie, tirofiban)
Prasugrel
Ticagrelor

36

Only for PCI patients

Prasugrel

37

Reduced mortality
Increased risk of bleeding
Reversible

Ticagrelor

38

Anticoagulant agents

Unfractioned heparin
Low molecular weight heparin (Enoxaparin)
Fondaparinux
Bivalirudin

39

Standard therapy, continuous IV infusion
Requires periodic monitoring of prothrombin time
To prolong pTT

Unfractioned heparin

40

Longer acting
Subcutaneous administration
No need for PTT monitoring

Low molecular weight heparin (enoxaparin)

41

Once a day administration
Less bledding than enoxaparin
Direct factor X inhibitor

Fondaparinux

42

Direct thrombin inhibitor

Bivalirudin

43

Indications for use of an early invasive strategy in patients with NSTEMI

Recurrent angina at rest/low-level activity despite treatment
Elevated TnT or TnI
New ST-segment depression
CHF symptoms, rales MR
EF < 0.40
SustainedVT
PCI < 6 months, prior CABG
High risk findings from noninvasive testing
Hemodynamic instability
Mild-to-moderate renal dysfunction
DM
High TIMI Risk SCore (>3)

44

In coronary angiogram, catheter is introduced either via the ____ or ____

Brachial artery
Femoral artery

45

Coronary angioplasty/stenting

Stent insertion
Stent expansion
Stent remains in the coronary artery

46

Stent has a drug coating that controls recovery to prevent re-narrowing

Drug-eluting stents

47

Long term management for UA/NSTEMI

ASA
Clopidogrel
Statins
ACEI or ARB (LV remodeling)
Lifestyle modification

48

Ischemic pain at rest caused by spasm of the coronary artery
Transient ST elevation on ECG
Hypercontractility of vascular smooth muscle

Prinzmetal angina

49

Treatment of Prinzmetal angina

Smoking cessation
Calcium antagonists
Addition of long acting nitrates to CCb

50

Detection of rise and fall of cardiac biomarker valus with at least one value above the 99th upper reference limit and at least one of the following: symptoms of ischemia, new or presumed new significant ST segment T wave changes or new left bundle branch block, development of pathologic Q waves in ECG, imaging evidence, identification of an intracoronary thrombus

AMI

51

Spontaneous MI

Type 1

52

MI secondar to ischemic imbalance

Type 2

53

MI resulting in death when biomarkers aren't available

Type 3

54

MI related to PCI

Type 4a

55

MI related to stent thrombosis

Type 4b

56

Mi related to CABG

Type 5

57

Symptoms associated with AMI

Prolonged pain
Usually retrosternal location, radiating to left chest, arm
Nausea/vomiting
Palpitations
Diaphoresis
Sense of impending doom

58

In distress, levine sign
HR, pulse, RR variable
BP variable
Low-grade fever
Examination of JVP
Pulmonary crackles
S4 gallop
S3 gallop
Murmurs

STEMI

59

Useful adjunct for chest pain patient with non-diagnostic or uninterpretable ECG
Can identify regional wall motion

2D echo

60

Early presentation
Invasive strategy not an option
Delay to stratery > prolonged transport, door-to-balloon time > 90 minutes

Fibrinolysis

61

Skilled PCI lab available with surgical back-up
Door-to-balloon time < 90 minutes
High risk patients
Late presentation
STEMI diagnosis in doubt

Primary PCI

62

General measures to address STEMI

Morphine
Oxygen
Aspirin
Nitrate

63

Main goal of fibrinolytic therapy

Full coronary patency

64

Reduces infarct size, limits LV dysfunction, and reduces incidence of serious complications: septal rupture, cardiogenic shock, malignant ventricular arrhythmias

Fibrinolytic therapy

65

Absolute CI of fibrinolytic therapy

Hx of cardiovascular hermorrhage
CVA within the past year
BP > 180 systolic or 110 diastolic
Aortic dissection
Active internal bledding

66

Relative CI of fibrinolytic therapy

Current anticoagulant use
Invasive surgery within 2 weeks
Prolonged CPR
Known bleeding diathesis
Hemorrhagic opthalmic condition
Active peptic ulcer disease
Sever HTN concurrently actively controlled

67

Most frequent and potentially most serious complication of fibrinolytic therapy

Hemorrhage

68

Reduce mortality after STEMI
Greatest benefit in patients with large anterior infarctions prior M, globally reduced LV systolic function
Reduces ventricular remodeling and subsequent risk of congestive heart failure

ACE or ARBs

69

Complication of STEMI common in patients with multi-vessel disease
Managements include vasopressors/inotropes, inaortic balloon counter pulsation, early reperfusion/revascularization

Cardiogenic shock

70

1/3 of inferior wall MI have _____, commonly manifested as hypotension, distended neck veins, clear lung fields. In ECG; ST elevation on right sided precordial leads, In 2D echo: RV dilatation and dysfunction

Right ventricular infarction

71

Treatment of right ventricular infarction

Volume expansion to improve LV filling

72

Pericarditis post MI

Dressler syndrome

73

Complication of STEMI that may lead to stroke

Thromboembolism

74

What to give to patients with ventricular premature beats

Beta-blockers

75

One of the worst complications of STEMI
Can occur within the first 24 hours of STEMI without warning arrhythmias

Ventricular fibrillation/tachycardia

76

Treatment for sustained VT

IV amiodarone

77

Treatment for VF or hemodynamically unstable VT

DC cardioversion

78

Treatment for VF/VT after 48 hours

ICD/Defib

79

Post infaction risk stratification and management

Submaximal stress test (hospital) or full stress test (4-6 w after discharge)
2D echo to assess LV systolic function

80

Secondary prevention of STEMI

Antiplatelet therapy
AC-I, ARB
B-blockers
Statin therapy
Risk factor modification