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Pathophysiology > Adult Cardio 3 (Coronary Artery Disease) > Flashcards

Adult Cardio 3 (Coronary Artery Disease) Flashcards

1
Q

Coronary artery disease is also known as…

A

Ischemic heart disease

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2
Q

Coronary artery disease is caused by a blocked ___ in a branch of the left coronary artery

A

Lumen

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3
Q

___ ___ ___ is the leading cause of death, with coronary artery disease being the largest percentage of that

A

Cardiovascular disease

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4
Q

The creation of ___ drugs started the decline in prevalence of coronary artery disease

A

CABG

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5
Q

____ is an aging process that happens over a long period of time

A

Atherscleorosis

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6
Q

Between ___-___ years of age is when you might start to see the thickening of the endothelium (beginning of the atherosclerosis process)

A

10-20

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7
Q

Massive occlusions caused by atherosclerosis happen between __-__ years of age, typically

A

50-60

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8
Q

Massive occlusions caused by atherosclerosis can cause…

A

-Myocardial infarction
-Ischemia, stroke, TIA
-UA
-Acute limb ischemia
-CV death

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9
Q

___ ___ ___ describes connections or anastomoses between 2 branches of the same coronary artery or connections/branches between the same right coronary artery and left coronary artery

A

Collateral coronary circulation

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10
Q

What is the functional importance of collateral coronary circulation?

A

Protects the heart

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11
Q

Gradual coronary artery ___ results in growth of collaterals

A

Occlusion

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12
Q

What two things will facilitate collateral growth?

A

-Nitric oxide
-Vascular endothelial growth factors

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13
Q

The degree of left ventricle deterioration is ____ related to the presence of collaterals

A

Inversely

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14
Q

The incidence of ventricular aneurysm formation after myocardial infarction is ___ when significant collaterals are present

A

Decreased

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15
Q

The risk for severe dysrhythmias after myocardial infarction is ____ when significant collaterals are present

A

Decreased

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16
Q

The presence of collaterals expands the “window of ___” in which reperfusion strategies are effective after myocardial infarction

A

Time

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17
Q

___ people are more likely to develop collateral circulation because they have more time

A

Older

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18
Q

___ people have more severe and more deadly occlusion (more severe symptoms like crushing chest pain)

A

Younger

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19
Q

Older people might have more ____ symptoms with MI

A

Atypical

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20
Q

Women might also have atypical symptoms because they usually have MI ___ years after men due to estrogen which slows down atherosclerotic process (they have more time for collateral circulation)

A

10

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21
Q

___ ___ is more common in elderly people

A

Unstable angiotensin (blood pressure)

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22
Q

Chest pain is also known as ____

A

Angina

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23
Q

People may have __-__% occlusion before they are symptomatic

A

50-75%

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24
Q

___% what patients have chest pain plus one or more other symptoms

A

90

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25
Q

___-___% may be symptomatic during increased myocardial oxygen demand

A

50-75

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26
Q

Symptoms and outcomes are dependent upon ___ vs ___

A

Ischemia (reduced blood flow); infarction (no blood flow)

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27
Q

Infarction causes ____ activation, aggregation, and adherence

A

Platelet

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28
Q

Common symptoms other than angina:

A

-Dyspnea
-Diaphoresis
-N/V (due to vagus nerve innervation)
-Syncope (due to systolic dysfunction)

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29
Q

The continuum of ischemic heart disease:

A

-Coronary artery disease
-Ischemia
-Myocardial infarction

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30
Q

Definition of coronary artery disease:

A

Any vascular disorder that causes narrowing/occlusion of coronary arteries

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31
Q

Definition of ischemia (angina):

A

Local state in which myocardial O2 supply is diminished to the extent that myocardial cellular metabolism is impaired

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32
Q

What are four types of ischemia?

A

-Stable
-Variant (Prinzmetal’s) (Vasospasm)
-Silent
-Unstable (acute coronary syndrome)

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33
Q

Myocardial infarction is the ___ of acute coronary syndrome

A

Endpoint

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34
Q

Myocardial infarction causes ___ necrosis

A

Myocyte

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35
Q

What are the two types of MI?

A

-ST elevation MI
-Non-ST elevation MI

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36
Q

Within the progression of coronary artery disease, is systolic or diastolic function impaired first?

A

Diastolic

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37
Q

If someone has a normal ___, it does not mean that they definitely don’t have heart issues

A

EKG

38
Q

Ischemia is an imbalance between ___ and ___

A

Supply and demand

39
Q

What can cause increased O2 demand?

A

-Hyperthermia
-Hyperthyroidism
-Sympathomimetic toxicity
-Hypertension
-Anxiety
-AV fistula
-Hypertrophic CMP
-Aortic stenosis
-Dilated CMP
-Tachycardia

40
Q

What can cause decreased O2 supply?

A

-Anemia
-Hypoxemia (pneumonia, asthma, COPD, sleep apnea)
-Sickle cell
-Sympathomimetic toxicity
-Hyperviscosity (polythemia, leukemia)
-Aortic stenosis
-Hypertrophic CMP

41
Q

Acute coronary syndrome starts when atherosclerotic ___ with a lipid-rich core and thin fibrous cap forms

A

Plaque

42
Q

What may cause rupture of this plaque?

A

-Shear force
-Inflammation
-Apoptosis
-Macrophage-derived degradative enzymes

43
Q

After the plaque has ruptured, what may cause thrombus formation over the lesion, plus vasoconstriction of the vessel?

A

-Increased inflammation with release of multiple cytokines
-Platelet activation
-Production of thrombin and vasoconstrictors

44
Q

Acute decrease in coronary blood flow then leads to…

A

-Unstable angina
-Myocardial infarction

45
Q

Mitochondria needs ___ to generate ATP

A

Oxygen

46
Q

When O2 is reduced, there is not enough ___ being produced

A

Energy

47
Q

What are some major users of ATP?

A

-Actin
-Myosin
-Sodium-potassium pump

48
Q

Since actin and myosin are ___ in proximity than the sodium-potassium pump, they will get most of the oxygen (the sodium-potassium pump suffers more)

A

Closer

49
Q

Without the sodium-potassium pump, the ___ of the cell is messed up and the cell will remain in repolarization for longer periods of time

A

Polarity

50
Q

___ would then start and this would indicate ischemia

A

Hypokenesis (smaller range of motion of body)

51
Q

The dysfunction of the sodium-potassium pump cause too much ___ to get into the cells, causing the cell to swell

A

Sodium

52
Q

With too much sodium in the cell, you might go into ____ because energy is being used to get sodium into the cell

A

Acidosis

53
Q

Severe acidosis leads to ___ and lots of damage to nearby cells; you would be able to detect troponin in the blood

A

Necrosis

54
Q

If there is less severe acidosis, you might see ____which would not damage nearby cells (no troponin in the blood)

A

Apoptosis

55
Q

Less severe acidosis might cause problems since it is less symptomatic and might go ____

A

Undetected

56
Q

Characteristics of an unstable plaque:

A

-Inflammatory cells
-Thin fibrous cap
-Few smooth muscle cells
-Eroded endothelium
-Activated macrophages

57
Q

Characteristics of a stable plaque:

A

-Lack of inflammatory cells
-Thick fibrous cao
-More smooth muscle cells
-Intact endothelium
-Foam cells

58
Q

Local risk factors for plaque rupture:

A

-Cap fatigue
-Atheromatous core (size/consistency)
-Coronary hemodynamics
-Cap thickness/consistency
-Mechanical injury
-Cap inflammation

59
Q

Systemic risk factors for plaque rupture:

A

-Smoking
-Cholesterol
-Diabetes Mellitus
-Homocysteine
-Impaired fibrinolysis

60
Q

____ use their membrane to form clots

A

Platelets

61
Q

Platelets are activated because they think there is a ___ in the artery, but there is really just a crack in the endothelial layer of the heart

A

Cut

62
Q

____ is the first line therapy for MI because it is anti-platelet (we want to get rid of the clot)

A

Aspirin

63
Q

If patient has unstable angina, after doing a history, physical exam, ECG, and looking at cardiac markers, you can determine if there is ___ elevation or not

A

ST

64
Q

If someone has ST elevation, is is presumed an ___ ___

A

Acute MI

65
Q

If someone has no ST elevation, look at ___ __ ___ and ECGs

A

Serial marker sampling

66
Q

If someone has positive markers, it is presumed __ __

A

Acute MI

67
Q

If someone has negative markers, it could indicate one of what two things?

A

-Unstable angina
-Noncardiac chest pain

68
Q

____ infarction, also known as (STEMI), involves all 3 muscle layers of the heart

A

Transmural

69
Q

A non-transmural (non-STEMI) infarction can be classified as one of what two things?

A

-Subendocardial
-Subepicardial

70
Q

Subendocardial non-STEMIs involve what two muscle layers?

A

-Endocardium
-Myocardium

71
Q

Subendocardial non-STEMIs are more ____ because blood supply to the endocardium is at greater risk due to the mechanics of systolic compression on these vessels

A

Common

72
Q

Subepicardial non-STEMIs involve what two muscle layers?

A

-Epicardium
-Myocardium

73
Q

STEMI MIs have ___ ___, which is more concerning

A

Full occlusion

74
Q

Non-STEMIs are problematic because they might not be ____

A

Detected

75
Q

What should we look for when diagnosing STEMI vs non-STEMI?

A

-Patient’s story
-Physical exam
-Electrocardiogram
-Cardiac markers

76
Q

What should we look for during history and physical exam?

A

-Precipitating factors
-Chest pain (differentials)
-N/V
-Diarrhea
-Weakness
-Dizziness
-Palpations
-Cold perspiration

77
Q

Pain in the lungs might indicate….

A

-Pneumothorax
-Pulmonary embolism

78
Q

Main in the musculoskeletal regions might indicate…

A

-Non-specific pain
-Cocaine abuse

79
Q

Pain in the heart might indicate…

A

-MI
-Aortic dissection
-Pleural effusion
-Heart failure
-Coronary artery disease
-Heart valve diseases
-Atrial fibrilation

80
Q

GI pain might indicate…

A

-Acid reflux disease
-Esophageal rupture

81
Q

CPK is a cardiac biomarker which would rise 4-8 hours after MI, peak ___-___ hours after, and normalize in 3-4 days

A

12-24

82
Q

CK-MB is a cardiac biomarker which would rise 4-6 hours after MI, peak ___-___ hours after, and normalize 2-3 days after

A

12-24

83
Q

Troponin is a cardiac biomarker that would rise 3-12 hours after MI, peak __-__ days after, and normalize 1-2 weeks after

A

1-2

84
Q

The goal is for EMS to balloon time to be within ___ minutes after the onset of symptoms

A

90

85
Q

Total ischemia time should be less than ___ minutes from time of symptom onset to balloon

A

120

86
Q

Sending a patient to the cath lab __-__ hours after symptoms might be deadly due to reperfusion injury

A

3-4

87
Q

If it has been 304 hours since onset of MI symptoms, sending the patient to the cath lab causes creation of ___ ___ ___ (if the mitochondria does not deactivate the ROS, it goes to the DNA and causes cell death)

A

Reactive oxygen species

88
Q

Reperfusion injury causes ____ levels to skyrocket and cause widespread necrosis which could cause death

A

Troponin

89
Q

___ ___ happens in 50-70% of cases and causes sudden death

A

Ventricular fibrilation

90
Q

With ventricular fibrillation, the heart starts fibrillating instead of ____ (causes death)

A

Contracting

91
Q

____ ___ is another mechanism of how occlusion can lead to death; it causes multiorgan failure

A

Cardiogenic shock

92
Q

With ___ ___, the left ventricle fails, so blood backs up into the lungs and causes breathing problems and death

A

Pulmonary edema

Pathophysiology (18 decks)

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