CVD (2) Flashcards

1
Q

What is the most common type of heart disease?

A

Coronary heart disease

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2
Q

How often does someone get a heart attack in the US?

A

Every 43 seconds

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3
Q

How many deaths are due to heart disease in US?

A

1 in 4

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4
Q

What are the non modifiable risk factors of CVD?

A

Male sex

Age (males > 40, females > 50)

Heredity

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5
Q

What are the modifiable risk factors of CVD?

A

Hypertension

Tobacco

Elevated blood glucose

Physical inactivity

Obesity

Dyslipidemia (high cholesterol)

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6
Q

Can emotions contribute to CVD?

A

Yes

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7
Q

What is atherosclerosis?

A

Dynamic chronic inflammatory response of the arterial wall to endothelial injury

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8
Q

What is the pathogenesis of atherosclerosis?

A

Lipids, thrombosis, elements of vascular wall, and immune cells

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9
Q

What are some characteristics about atherosclerosis?

A

Slow progressive disease that starts early in life where plaques are distributed and increase in number and size with age

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10
Q

What is the innermost layer of the arterial wall called?

A

Intima

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11
Q

What is located in the intima?

A

Endothelial cells

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12
Q

What is the middle layer of the arterial wall called?

A

Media (smooth muscle cells)

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13
Q

What is the outermost layer of the arterial wall called?

A

Adventitia (connective tissue that surrounds arterial wall)

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14
Q

What is atherosclerosis in simplified terms?

A

Injury to endothelial cells which causes inflammatory process which leads to ECM production and then atherosclerotic plaque production

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15
Q

What are the 3 main pathological stages of atherosclerosis?

A

Fatty streak

Plaque progression

Plaque disruption

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16
Q

What occurs during the fatty streak stage?

A

Endothelial dysfunction

Lipoprotein entry

Leukocyte recruitment

Foam cell formation

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17
Q

What occurs during the plaque progression stage?

A

SMC migration and altered matrix synthesis and degradation

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18
Q

What occurs during the plaque disruption stage?

A

Thrombus formation

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19
Q

What do EC cells normally produce?

A

Anti thrombotic molecules to prevent blood clots

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20
Q

What may EC produce when subjected to various stressors?

A

Pro thrombotic molecules

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21
Q

How do EC modulate the immune response?

A

Resisting leukocyte adhesion which inhibits inflammation

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22
Q

What occurs as a result of disturbed Hemodynamic stress in endothelial dysfunction?

A

Increased permeability

Increase inflammatory cytokines

Increased leukocyte adhesion molecule

Decreased vasodilatory molecules

Decreased anti thrombotic molecules

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23
Q

What happens to the endothelium with lipoprotein entry and modification?

A

It no longer serves as an effective barrier to circulating lipoproteins

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24
Q

What does increased permeability allow the LDL to do?

A

Enter the intima where they become trapped and undergo chemical modifications

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25
Q

What may promote the retention of LDL in the intima?

A

Hypertension

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26
Q

Foam cells, activated platelets, and EC secrete substances that do what?

A

Signal SMC migration

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27
Q

What is SMC migration followed by?

A

Proliferation and secretion of matrix macromolecules

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28
Q

What occurs with plaque profession?

A

Outward remodeling of arterial wall with preservation of lumen (growth is inward restricting blood flow)

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29
Q

What does collagen synthesis favor?

A

Fortification of fibrous cap (stable)

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30
Q

What does collagen degradation favor?

A

Vulnerable plaques

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31
Q

What are some complications of atherosclerosis?

A

Calcification of atherosclerotic plaque (pipe like rigidity increasing its vulnerability)

Rupture leading to thrombus formation

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32
Q

What does a hemorrhage into the plaque result in?

A

Further narrowing

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33
Q

What does weakening of the vessel wall result in?

A

Aneurysm

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34
Q

What are some types of ischemic heart diseases?

A

Coronary artery disease

Atherosclerotic heart disease

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35
Q

What is ischemic heart disease?

A

Condition of imbalance between myocardial O2 supply and demand often caused by atherosclerosis of coronary arteries

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36
Q

What conditions increase wall stress (Afterload)?

A

Hypertension or aortic stenosis

37
Q

What do conditions that increase LV filling raise?.

A

Wall stress and O2 consumption (mitral valve regurgitation)

38
Q

What is the pathophysiolohy of ischemia?

A

Fixed vessel narrowing and endothelial dysfunction

39
Q

Why is there decreased perfusion pressure in ischemia?

A

Due to hypotension

40
Q

What is severely decreased in ischemia?

A

Blood oxygen contetn

41
Q

What is increased in ischemia?

A

Myocardial oxygen demand

42
Q

What are ischemic syndromes?

A

Stable angina

Unstable angina

Variant angina

Silent ischemia

Microvascular angina

43
Q

What is silent ischemia?

A

Ischemia in the absence of discomfort or pain (diabetes)

44
Q

What is microvascular angina?

A

Angina in the absence of atherosclerotic stenosis

45
Q

What is microvascular angina due to?

A

Inadequate vasodilatory reserve in the coronary resistance vessels (better prognosis)

46
Q

Stable angina

A

Chest pain with increased activity

47
Q

Unstable angina

A

Chest pain at rest

48
Q

How does pain present in stable angina?

A

Heaviness, tightness, pressure, burning that is more discomfort than pain (gradually builds and leaves in 2-5 minutes)

49
Q

Is stable angina diffused or localized?

A

Diffused

50
Q

What are symptoms of stable angina due to sympathetic and parasympathetic stimulation?

A

Tachycardia

Sweating

Nausea

51
Q

Ischemia results in dysfunctional diastolic relaxation which then results in what?

A

Elevated LV diastolic pressure that is transmitted to the pulmonary vessels and causes Dyspnea

52
Q

How can stable angina be precipitated?

A

By conditions that increase MVO2 demand like exercise, anger, or cold weather

53
Q

What are ECG abnormalities to look for with subendocardial ischemia?

A

ST depression (horizontal or downsloping)

T wave inversion

54
Q

What are ECG abnormalities to look for with transmural ischemia?

A

ST elevation

55
Q

What are the drugs used for ischemic heart disease?

A

Organic nitrates

Beta blockers

Calcium channel blockers

Ranolazine

56
Q

What are the different types of calcium channel blockers used to treat ischemic heart disease?

A

Nondihydropyridines (central)

Dihydropyridines (peripheral)

57
Q

When should patients do revascularization therapy for ischemic heart disease?

A

They do not respond to drugs or have side effects from them

Patient has high risk coronary disease

58
Q

What are the types of revascularization therapies for ischemic heart disease?

A

Percutaneous coronary intervention

Coronary artery bypass graft

59
Q

What is the success rate of Percutaneous transluminal coronary angioplasty?

A

80-90% with 30% restenosis within 6 months

60
Q

Why are coronary stents becoming the preferred treatment?

A

Reduces rate of stents

61
Q

What are the two types of stents used?

A

Drug eluting stent (thrombogenic- must be on anticoagulants)

Non drug eluting stent (higher rate of restenosis- no need for anticoagulants)

62
Q

What types of grafts are used in coronary artery bypass graft?

A

Saphenous vein and left internal mammary artery

63
Q

What are the characteristics of a saphenous vein graft?

A

Patency rate of 80% at 12 months but is vulnerable to accelerated atherosclerosis (>50% occlusion 10 years after surgery)

64
Q

What are the characteristics of left internal mammary artery graft?

A

Patency rate of 90% at 10 years and resistant to atherosclerosis

65
Q

What are acute coronary syndromes?

A

Unstable angina which can develop into non ST elevation MI or ST elevation MI

66
Q

Do males have a higher prevalence of MI than females?

A

Yes

67
Q

What do acute coronary syndromes result from?

A

Disruption of atherosclerotic coronary plaque and formation of a thrombus

68
Q

What occurs in partially occlusive thrombus?

A

Unstable angina and NSTEMI

69
Q

What occurs in complete occlusion thrombus?

A

STEMI

70
Q

What is the difference between partial and complete occlusion thrombus?

A

The presence of myocardial necrosis

71
Q

What is myocardial infarction?

A

Cell death in the heart muscle caused by complete and prolonged occlusion of a coronary artery

72
Q

What is the wave front phenomenon?

A

Tissue furthest away from the heart dies first and moves inward like a wave until it covers the thickness of the myocardium

73
Q

What are functional alterations post MI?

A

Impaired contractility and compliance

Stunned myocardium

Hibernating myocardium

Ischemic preconditioning

74
Q

What is hibernating myocardium?

A

Chronic contractile dysfunction due to persistently poor blood supply

75
Q

What may happen to ventricles post MI?

A

Expansion which can lead to wall stress, impaired contractile function, and increased likelihood of aneurysms

76
Q

What is the timeline of an MI?

A

20 min= no necrosis

20-60 min= subendocardial necrosis

1-3 hours= necrosis extends into myocardium

3-6 hours= transmural infarction

77
Q

How long do symptoms at rest occur in unstable angina?

A

> 20 min

78
Q

What is unstable angina a precursor to?

A

MI

79
Q

What are the pain signs of MI?

A

Severe and persistent (substernal)

80
Q

What are the sympathetic signs of MI?

A

Sweating and cold clammy skin

81
Q

What are the parasympathetic signs of MI?

A

Nausea and weakness

82
Q

What are the cardiac findings in MI?

A

S4 (S3 if systolic dysfunction present)

Dyskinetic bulge

Systolic murmur

83
Q

What is the disease progression of MI?

A

Can progress or regress based on secondary prevention of risk factors

84
Q

What is the frequency of exercise for inpatient cardiac rehab?

A

2-4 sessions a day for first 3 days

85
Q

What is intensity of exercise for inpatient cardiac rehab?

A

HR should be 20-30 bpm above resting HR and RPE < 13 (submaximal)

86
Q

What is the time of exercise for inpatient cardiac rehab?

A

Bouts of 10 minutes each

87
Q

How should outpatient cardiac rehab be administered?

A

Moderate intensity aerobic of 30-45 min 3-5 days a week (40-80% VO2 and RPE of 12-16)

88
Q

Should resistance training be incorporated for outpatient cardiac rehab?

A

Yes, 40-60% 1RM and RPE 11-13 (consider eccentrics to keep BP low)