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Cardiology-Exam 2 > ACS > Flashcards

ACS Flashcards

1
Q

Spectrum of cardiac ischemic disorders

A

Acute Coronary Syndrome (ACS)

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2
Q

Major trigger for coronary thrombosis; due to chemical/physical stresses on the lesion

A

Atherosclerotic plaque rupture

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3
Q

Vasoconstriction and diminished anti-thrombotic function can exacerbate…

A

coronary thrombosis

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4
Q

Examples of endogenous anti-thrombotics

A 
Antithrombin III
Protein C and S
Tissue Factor Pathway Inhibitor
tPA
Prostacyclin
NO
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5
Q

Acute Coronary Syndromes that are partially occlusive

A

Unstable Angina

NSTEMI

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6
Q

Approx. _____ minutes of ischemia can cause an infarct

A

30

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7
Q

Myocardial infarctions are usually the result of…

A

plaque changes with coronary thombosis

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8
Q

Frequently, coronary thrombi dissolute within _____ hours

A

24

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9
Q

MIs affect the (LV/RV) more often

A

LV

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10
Q

In a subendocardial infarct, why is it only the innermost layers of the myocardium affected?

A

Poor collateral flow and furthest from epicardial coronaries

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11
Q

Factors that affect the amount of tissue infarcted

A 
Mass of myocardium perfused by the artery
Duration of ischemia
Oxygen demand
Adequacy of collateral flow
Degree of reperfusion
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12
Q

An occlusion in the LAD can infarct what areas of the heart

A

Anterior LV
Anterior septum
Apex

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13
Q

An occlusion in the LCx can infarct what areas of the heart

A

Lateral LV

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14
Q

An occlusion in the RCA can infarct what areas of the heart

A

Posterior LV
Posterior septum
Posterior papillary muscle
Inferior

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15
Q

Why does an MI result in cellular edema and risk of arrhythmias?

A

Decreased ATP synthesis (anaerobic metabolism) makes it harder to regulate ions.

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16
Q

Macroscopic features of infarction: <24 hours

A

Dark mottling

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17
Q

Macroscopic features of infarction: 1-14 days

A

Yellow/tan necrotic center, with possible red borders

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18
Q

Macroscopic features of infarction: 2-8 weeks

A

gray-white scar

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19
Q

Microscopic features of infarction: <24 hours

A

Wavy fibers
Nuclear pyknosis
Early PMNs (intravascular)
Contractile proteins coagulate (band necrosis)

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20
Q

Microscopic features of infarction: 1-3 days

A

Loss of nuclei and striations

Interstitial PMNs

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21
Q

Microscopic features of infarction: 3-14 days

A

Macrophages and granulation tissue

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22
Q

Microscopic features of infarction: 2-8 weeks

A

Loss of cellularity
Increased collagen
Surrounding myocytes are hypertrophied (to compensate)

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23
Q

Examples of systolic dysfunction

A

Hypokinesis
Akinesis
Dyskinesis

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24
Q

When a local region in the ventricle has reduced contraction

A

Hypokinesis

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25
Q

When a local region in the ventricle has no contraction

A

Akinesis

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26
Q

Akinesis

A

Dyskinesis

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27
Q

Prolonged, but gradually reversible period of contractile dysfunction; takes days to weeks to recover

A

Stunned myocardium

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28
Q

When brief ischemia renders tissue more resistant to future episodes of ischemia

A

Ischemic preconditioning

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29
Q

MI complication resulting in left-to-right flow of blood through the septum

A

Septal perforation

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30
Q

MI complication resulting in severe mitral regurgitation due to valve incompetence

A

Papillary muscle rupture

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31
Q

MI complication when the wall bulges outward during systole and the fibrous scar progressively stretches; predisposes to rupture and mural thombosis

A

Ventricular aneurysm

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32
Q

Symptoms of MI

A 
Chest pain (persistent, substernal, can radiate)
Nausea, vomiting, weakness
Diaphoresis, cool/clammy skin
Fever (inflammatory response)
Shortness of breath
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33
Q

Differential diagnosis for chest pain

A 
Ischemia
Pericarditis
Costochondritis
GERD
Peptic ulcers
Pneumonia
PE
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34
Q

EKG abnormalities that hint at ischemia (in the setting of chest pain)

A

New ST elevation >1mm
New ST depression >1mm
New T-wave inversion

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35
Q

If you have the reversal of EKG abnormalities (T wave inversion) shortly after treatment such as nitro, it is suggestive of…

A

Myocardial ischemia

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36
Q

Cardiac biomarker that is released following cell death (necrosis) or injury; typically present in extremely low levels due to slow turnover

A

Troponins

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37
Q

Cardiac biomarker that is a cytosolic enzyme for energy production in cardiac tissues; no longer used for diagnosing MI

A

Creatine Kinase-MB

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38
Q

Why must you collect serial samples to analyze cardiac biomarkers for chest pain patients?

A

Initial set of “negative” does not rule out MI

Values begin to rise at ~3 hours, and fluctuate over days

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39
Q

Non-cardiac causes of Troponin elevation

A 
PE
Shock
Aortic dissection
Myocarditis
Trauma
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40
Q

When does an elevated troponin indicate a MI?

A

> 99th percentile

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41
Q

ST-Elevation in leads II, III and aVF indicate infarction in…

A

inferior portion of heart (RCA)

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42
Q

ST-Elevations in leads V2-V4 indicate infarction in…

A

anterior portion of heart (LAD)

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43
Q

ST-Elevations in lead V4R indicate infarction in…

A

Right ventricle (RCA)

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44
Q

ST-Depressions in leads V1-V2 indicate infarction in…

A

Posterior portion of the heart (RCA)

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45
Q

Diagnostic difference between unstable angina and NSTEMI

A

UA: negative troponin
NSTEMI: positive troponin

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46
Q

Risk score for outcomes and treatment guidelines for potential MIs

A

TIMI Risk Score

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47
Q

UA, NSTEMI or STEMI:

ST elevations; positive troponins; completely occluded coronary artery

A

STEMI

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48
Q

UA, NSTEMI, or STEMI:

No ST elevation; positive troponins; sub-totally occluded coronary artery

A

NSTEMI

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49
Q

UA, NSTEMI, or STEMI:

No ST elevation; negative troponin; sub-totally occluded coronary artery

A

UA

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50
Q

General therapies for Acute Coronary Syndromes

A 
Bed rest
Oxygen
Analgesic
Anti-ischemic (beta blockers, nitrates)
Antiplatelet/thrombotic
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51
Q

If you see a evidence of a STEMI….

A

Open the artery emergently

52
Q

therapy that decreases sympathetic drive on the heart (reduces oxygen demand); enhances electrical stability; target heart rate is <60 bpm

A

Beta blockers (metoprolol)

53
Q

Contraindications for beta blockers

A

Bradycardia
Bronchospam
Hypotension
Acute heart failure

54
Q

therapy that induces venodilation, decreasing preload and wall stress; improves blood flow to coronary arteries; administered sublingual then IV

A

Nitrates

55
Q

Contraindication for nitrates (nitro)

A 
RV infarction (dependent on pre-load, so can cause hypotension)
Sexual enhancement drugs (Viagra)
56
Q

therapy that induces vasodilation, decreased chronotropy/inotropy; used if beta-blockers contraindicated; can’t use in LV systolic dysfunction

A

Non-dihydropyridine Calcium Channel blockers (verapamil, diltiazem)

57
Q

therapy that inhibits platelet synthesis of TxA2, thus platelet activation; given immediately

A

Aspirin

58
Q

therapy that inhibits P2Y12 (ADP receptor) on platelets; used for aspirin-allergic patients; prodrug, so need to measure liver metabolism

A

Clopidogrel (Plavix)

59
Q

therapy that is the most potent antiplatelet agent; blocks fibrinogen linkage; adjunctive therapy with PCI

A

G IIb/IIa inhibitor

60
Q

Anticoagulant therapy that can only be used for when NO PCI is planned

A

Fondaparinux

61
Q

Anticoagulant therapy that is only used in the cath lab for PCI

A

Bivalirudin

62
Q

PCI technique that involves passing a balloon into partially occluded artery and inflating it to widen the opening; faulty because the artery can collapse with time

A

Percutaneous Transluminal Coronary Angioplasty (PTCA) or Plain ol’ balloon angioplasty (POBA)

63
Q

PCI

A

Percutaneous Coronary Intervention

64
Q

PCI therapy that involves a metal cage into an obstructed artery; decreases restenosis compared to balloon angioplasty

A

Bare-metal stent

65
Q

PCI therapy that involves a bare-metal stent that elutes antiproliferative agent, markedly reducing restenosis

A

Drug-eluting stent

66
Q

Goals for treating STEMIs

A

Restore blood flow quickly
Prevent further thombus formation
Restore balance between O2 and demand

67
Q

therapy that accelerates clot lysis, restoring blood flow and salvaging myocardium; transforms plasminogen to active plasmin; if given within 2 hours of onset of symptoms, mortality significantly reduced

A

Fibrinolysis

68
Q

Contraindications to fibrinolysis

A 
Active ulcers
Recent CVA
Recent surgery
Uncontrolled HTN
Very elderly
69
Q

Immediate cardiac catheterization and revascularization; greater survival and less bleeding than fibrinolysis; needs to be performed within 90 minutes of onset

A

PCI (Primary Percutaneous Coronary Intervention)

70
Q

What it is called when you give PCI after fibrinolytics have failed to reperfuse

A

Rescue PCI

71
Q

If the time to PCI is going to be more than ___ hour(s) beyond when lytics could be given, then lytics are favored with immediate transfer to facility

A

1

72
Q

Largely responsible for sudden cardiac death within 48 hours after an MI; most fatalities prior to hospital arrival

A

V-tach

V-fib

73
Q

How can sinus bradycardia result from a MI

A

SA node ischemia (occlusion of RCA)

74
Q

Occlusion in what coronary artery is considered a “widow-maker”

A

LAD (effects the Left Bundle Branch)

75
Q

therapy that helps the left ventricle pump blood, and increases blood flow through coronary arteries

A

Intra-aortic balloon pump (IABP)

76
Q

Signs of right-sided heart failure

A

Elevated jugular venous pressure
Hypotension
Clear lungs

77
Q

A holosystolic murmur is indicative of…

A

(Mitral) Papillary muscle rupture

78
Q

Persistent ST elevation weeks after a STEMI is indicative of…

A

Ventricular aneurysm

79
Q

inflammation of pericardial surfaces; sharp, pleuritic pain, fever, friction rub

A

Acute pericarditis

80
Q

Immune process against necrotic myocardium; develops week later

A

Dressler syndrome

81
Q

Drugs that reduce incidence of heart failure and recurrent ischemia; greatest benefit in those with LV dysfunction

A

ACE inhibitors

82
Q

“Sham” procedures for PCI, very similar to a “placebo”, are only able to be done because..

A

PCI has no improvement of mortality

83
Q

What causes transmural infarct to happen?

A

Prolonged ischemia or total occlusion of coronary artery causes the entire thickness of myocardium to die.

84
Q

What causes subendocardial infarct to happen?

A

Since the innermost layer of myocardium is further away from epicardial coronary artery and collateral blood flow, it doesn’t get enough oxygen supply.

85
Q

What is the process called when there is a change in the size, shape, structure, and function of the heart? Leads to ventricular dilation; “slippage” of myocytes; increases wall stress

A

Ventricular remodeling

86
Q

Ventricular remodeling may result in diminished

A

contractile function (systolic) and stroke volume

87
Q

Examples of Diastolic dysfunction

A
  1. Reduced compliance

2. Elevated ventricular (diastolic) filling pressure

88
Q

What is the complication of AMI that is caused by large infarcts and is most likely to occur in days 3-7 of a MI when wall is weakest?

A

Myocardial Free Wall Rupture

89
Q

What complication can arise from free wall rupture

A

Hemopericardium (blood from wall rupture filling up pericardial cavity), causing cardiac tamponade.

90
Q

What is the complication of AMI that results in conduction disturbances and myocardial irritability leading to sudden death?

A

Arrhythmias

91
Q

What is the complication of AMI that involves infarct in LV and is the result of high grade stenosis of all coronary vessels and can lead up to 90% mortality?

A

Acute left ventricular failure –> cardiogenic shock

92
Q

What is the complication of AMI that results in ongoing/repeat ischemia

A

Extension of Infarct

93
Q

What is the complication of transmural AMI that results in bulging of ventricular wall during systole?

A

Aneurysm

94
Q

What causes aneurysm?

A

Fibrous scar progressively stretching as infarct matures.

* Increased risk for myocardial rupture, causing mural thrombosis

95
Q

What is the complication of AMI that predisposes patients to systemic embolization especially after apical infarcts?

A

Mural thrombosis

96
Q

Chest pain that is pleuritic, positional, sharp, not associated with exertion and is reproducible with palpation is

A

Atypical (not likely to be AMI)

97
Q

Chest pain that radiates to limbs or shoulders, associated with exertion, nausea, vomiting, sweating is

A

Typical (likely to be AMI)

98
Q

Hints for a MI during a physical examination

A
  1. Evidence of Systemic Hypoperfusion

2. Evidence of Heart Failure

99
Q

What are evidences of systemic hypoperfusion?

A

hypotension, tachycardia, impaired cognition, cool extremities, end-organ injury

100
Q

What are evidences of heart failure?

A

elevated JVP, pulmonary crackles, S3/S4 gallops, new murmurs

101
Q

S4 (atrial gallop) indicates

A

compromised ventricular filling due to decreased ventricular wall compliance = increased resistance to filling of ventricle.

102
Q

Ischemia makes the heart stiffer, thus compromising diastolic filling and producing a (S3 or S4) sound

A

S4

103
Q

Change in T wave inversion in the setting of chest pain (from inverted T wave to upright normal T wave) after nitroglycerin treatment is suggestive of

A

Myocardial Ischemia

104
Q

ST depression and T wave inversion is suggestive of

A

Subendocardial ischemia

105
Q

ST elevation on EKG is suggestive of

A

Transmural ischemia

106
Q

ST depression segment points ____ epicardial injury

A

toward

107
Q

ST elevation segment points ____ epicardial injury

A

away from

108
Q

What is the biomarker that was used in the past to diagnose MI?

A

Creatine Kinase-MB

109
Q

What was the function of CK?

A

It was a cytosolic enzyme responsible for energy production in cardiac tissue

110
Q

What are some non-cardiac causes of troponin elevation?

A
  • PE, trauma, shock
  • ICD discharge, myocarditis
  • Heart failure, aortic dissection (tearing)
111
Q

How do you diagnose STEMI?

A

Based on ECG

112
Q

What are the requirements of STEMI diagnosis?

A
  1. presence of >1mm ST elevation in at least two contiguous leads
    OR
  2. > 2mm ST elevation in 2 contiguous precordial leads
    OR
  3. New LBBB
113
Q

ST-elevations in leads V1-V4 indicate infarction in…

A

anteroseptal of heart (LAD)

114
Q

ST-elevations in leads I, aVL, V5, V6 indicate infarction in…

A

lateral (LV) of heart (LCx)

115
Q

LBBB indicate infarction in

A

anterior of heart (LAD)

116
Q

Electrically silent ECG indicate infarction of

A

LCx

117
Q

STEMI is treated with emergent

A

Cardiac Catheterization

118
Q

Pathologic Q waves are indicative of…

A

Previous transmural STEMI

119
Q

Diagnostic criteria for pathologic Q waves are

A
  1. > or = 1mm wide
  2. > 25% of overall QRS complex
  3. present in at least 2 contiguous leads
120
Q

What can cause an unusual transient ST elevations?

A

Variant (Prinzmetal) angina

121
Q

What causes Variant Angina?

A

It’s caused by a spasm in the focal coronary artery in the absence of atherosclerotic lesions. The spasm is due to smooth muscle hyperactivity and endothelial dysfunction.

122
Q

What can increase the risk of variant angina?

A

smoking

123
Q

How do you diagnose Variant (Prinzmetal) Angina?

A

Intracoronary ACh to provoke spasm

*cardiac cath is required to do this.

124
Q

What are ECG abnormalities of UA or NSTEMI?

A

T wave inversion, ST depression

125
Q

What is the most important risk factors of UA or NSTEMI and is denoted on TIMI risk score?

A
  1. ST changes >= 0.5mm

2. elevated cardiac marker

Cardiology-Exam 2 (23 decks)

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