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Cardiology > 02.16 Acute Coronary Syndrome > Flashcards

02.16 Acute Coronary Syndrome Flashcards

1
Q

Caused by complete obstruction of a coronary artery

A

STEMI

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2
Q

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

A

STEMI

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3
Q

Caused by partial obstruction of a coronary artery

A

NSTEMI

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4
Q

Resulting necrosis only involves a partial thickness of the heart muscle

A

NSTEMI

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5
Q

2 main components of atherosclerotic plaques

A

Soft, lipid-rick core

Hard, collagen-rich fibrous cap

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6
Q

Thick fibrous cap may represent >70% of plaque volume

A

Stable plaque

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7
Q

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

A

Unstable plaque

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8
Q

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

A

Plaque destabilization

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9
Q

Where does plaque destabilization commonly occur

A

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

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10
Q

Primary cause of a heart attack

A

Rupture of unstable plaques

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11
Q

Usually >20 minutes in duration

Sudden chest pain patient is at rest

A

Rest angina

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12
Q

Markedly limits physical activity

A

New onset angina

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13
Q

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

A

Increasing angina

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14
Q

Symptoms of acute coronary syndrome

A 
Prolonged pain
Usually retrosternal location, radiating to the left chest, arm
Nausea, vomiting
Palpitations
Diaphoresis
Sense of impending doom
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15
Q

Acute coronary syndrome

A

STEMI
NSTEMI
US

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16
Q

Risk factors of ACS

A 
Advanced age
Smoking
Hypertension
DM
Dyslipidemia
Family history of early MI
Known CAD
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17
Q

PE of ACS

A 
Anxious and restless
Pallor with cold sweats and cold extermities
Sympathetic hyperactivity
3th and 4th heart sound
Friction rub
Signs of congestion
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18
Q

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

A

LAD, anterior of the heart

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19
Q

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

A

LCX, lateral of the heart

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20
Q

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

A

Right coronary artery problem

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21
Q

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

A

US/NSTEMI

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22
Q

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

A

US/NSTEMI

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23
Q

Cardiac markers for US/NSTEMI

A

Cardiac troponin I and T

CK-MB (4-6 hours)

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24
Q

Diagnostic approach to US/NSTEMI

A

ECG, Cardiac markers, Treadmill exercise testing, CT angiogram

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25
Q

TIMI Risk stratification

A 
Age >/= 65 years
>/= 3 CAD risk factors
Prior stenosis >50%
ST deviation
>/= 2 anginal events = 24h
ASA in last 7 days
Elevated cardiac markers
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26
Q

Pharma intervention for plaque rupture

A

Statins

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27
Q

Pharma intervention for platelet adhesion

A

ASA, clopidogel, GP IIb/IIa inhibitors

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28
Q

Pharma intervention for activation of clotting cascade

A

Anticoagulant agents

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29
Q

Pharma intervention for myocardial ischemia

A

Beta blockers
Nitrates
Calcium antagonists

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30
Q

Treatment of US/NSTEMI

A 
Bed rest
Nirates
B-blockers
CCB
Morphine sulfate
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31
Q

Limited by hypotension and bradycardia

CI if with pulmonary congestion and severe reactive airways disease

A

Beta-blockers (metaprolol)

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32
Q

Used when betablockers are not effective

A

CCB (Diltiazem, verapamil)

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33
Q

Used for persistent angina

A

Morphine sulfate

34
Q

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

A

Antithrombotic therapy

35
Q

Antiplatelet drugs

A 
Aspirin
Clopidogrel
GP IIb/IIa antagonists (Abciximab, eptifibatie, tirofiban)
Prasugrel
Ticagrelor
36
Q

Only for PCI patients

A

Prasugrel

37
Q

Reduced mortality
Increased risk of bleeding
Reversible

A

Ticagrelor

38
Q

Anticoagulant agents

A

Unfractioned heparin
Low molecular weight heparin (Enoxaparin)
Fondaparinux
Bivalirudin

39
Q

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

A

Unfractioned heparin

40
Q

Longer acting
Subcutaneous administration
No need for PTT monitoring

A

Low molecular weight heparin (enoxaparin)

41
Q

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

A

Fondaparinux

42
Q

Direct thrombin inhibitor

A

Bivalirudin

43
Q

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

A 
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
Q

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

A

Brachial artery

Femoral artery

45
Q

Coronary angioplasty/stenting

A

Stent insertion
Stent expansion
Stent remains in the coronary artery

46
Q

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

A

Drug-eluting stents

47
Q

Long term management for UA/NSTEMI

A 
ASA
Clopidogrel
Statins
ACEI or ARB (LV remodeling)
Lifestyle modification
48
Q

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

A

Prinzmetal angina

49
Q

Treatment of Prinzmetal angina

A

Smoking cessation
Calcium antagonists
Addition of long acting nitrates to CCb

50
Q

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

A

AMI

51
Q

Spontaneous MI

A

Type 1

52
Q

MI secondar to ischemic imbalance

A

Type 2

53
Q

MI resulting in death when biomarkers aren’t available

A

Type 3

54
Q

MI related to PCI

A

Type 4a

55
Q

MI related to stent thrombosis

A

Type 4b

56
Q

Mi related to CABG

A

Type 5

57
Q

Symptoms associated with AMI

A 
Prolonged pain
Usually retrosternal location, radiating to left chest, arm
Nausea/vomiting
Palpitations
Diaphoresis
Sense of impending doom
58
Q 
In distress, levine sign
HR, pulse, RR variable
BP variable
Low-grade fever
Examination of JVP
Pulmonary crackles
S4 gallop 
S3 gallop
Murmurs
A

STEMI

59
Q

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

A

2D echo

60
Q

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

A

Fibrinolysis

61
Q 
Skilled PCI lab available with surgical back-up
Door-to-balloon time < 90 minutes
High risk patients
Late presentation
STEMI diagnosis in doubt
A

Primary PCI

62
Q

General measures to address STEMI

A

Morphine
Oxygen
Aspirin
Nitrate

63
Q

Main goal of fibrinolytic therapy

A

Full coronary patency

64
Q

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

A

Fibrinolytic therapy

65
Q

Absolute CI of fibrinolytic therapy

A 
Hx of cardiovascular hermorrhage
CVA within the past year
BP > 180 systolic or 110 diastolic
Aortic dissection
Active internal bledding
66
Q

Relative CI of fibrinolytic therapy

A 
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
Q

Most frequent and potentially most serious complication of fibrinolytic therapy

A

Hemorrhage

68
Q

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

A

ACE or ARBs

69
Q

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

A

Cardiogenic shock

70
Q

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

A

Right ventricular infarction

71
Q

Treatment of right ventricular infarction

A

Volume expansion to improve LV filling

72
Q

Pericarditis post MI

A

Dressler syndrome

73
Q

Complication of STEMI that may lead to stroke

A

Thromboembolism

74
Q

What to give to patients with ventricular premature beats

A

Beta-blockers

75
Q

One of the worst complications of STEMI

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

A

Ventricular fibrillation/tachycardia

76
Q

Treatment for sustained VT

A

IV amiodarone

77
Q

Treatment for VF or hemodynamically unstable VT

A

DC cardioversion

78
Q

Treatment for VF/VT after 48 hours

A

ICD/Defib

79
Q

Post infaction risk stratification and management

A

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

80
Q

Secondary prevention of STEMI

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

Cardiology (13 decks)

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