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
What may promote the retention of LDL in the intima?
Hypertension
26
Foam cells, activated platelets, and EC secrete substances that do what?
Signal SMC migration
27
What is SMC migration followed by?
Proliferation and secretion of matrix macromolecules
28
What occurs with plaque profession?
Outward remodeling of arterial wall with preservation of lumen (growth is inward restricting blood flow)
29
What does collagen synthesis favor?
Fortification of fibrous cap (stable)
30
What does collagen degradation favor?
Vulnerable plaques
31
What are some complications of atherosclerosis?
Calcification of atherosclerotic plaque (pipe like rigidity increasing its vulnerability) Rupture leading to thrombus formation
32
What does a hemorrhage into the plaque result in?
Further narrowing
33
What does weakening of the vessel wall result in?
Aneurysm
34
What are some types of ischemic heart diseases?
Coronary artery disease Atherosclerotic heart disease
35
What is ischemic heart disease?
Condition of imbalance between myocardial O2 supply and demand often caused by atherosclerosis of coronary arteries
36
What conditions increase wall stress (Afterload)?
Hypertension or aortic stenosis
37
What do conditions that increase LV filling raise?.
Wall stress and O2 consumption (mitral valve regurgitation)
38
What is the pathophysiolohy of ischemia?
Fixed vessel narrowing and endothelial dysfunction
39
Why is there decreased perfusion pressure in ischemia?
Due to hypotension
40
What is severely decreased in ischemia?
Blood oxygen contetn
41
What is increased in ischemia?
Myocardial oxygen demand
42
What are ischemic syndromes?
Stable angina Unstable angina Variant angina Silent ischemia Microvascular angina
43
What is silent ischemia?
Ischemia in the absence of discomfort or pain (diabetes)
44
What is microvascular angina?
Angina in the absence of atherosclerotic stenosis
45
What is microvascular angina due to?
Inadequate vasodilatory reserve in the coronary resistance vessels (better prognosis)
46
Stable angina
Chest pain with increased activity
47
Unstable angina
Chest pain at rest
48
How does pain present in stable angina?
Heaviness, tightness, pressure, burning that is more discomfort than pain (gradually builds and leaves in 2-5 minutes)
49
Is stable angina diffused or localized?
Diffused
50
What are symptoms of stable angina due to sympathetic and parasympathetic stimulation?
Tachycardia Sweating Nausea
51
Ischemia results in dysfunctional diastolic relaxation which then results in what?
Elevated LV diastolic pressure that is transmitted to the pulmonary vessels and causes Dyspnea
52
How can stable angina be precipitated?
By conditions that increase MVO2 demand like exercise, anger, or cold weather
53
What are ECG abnormalities to look for with subendocardial ischemia?
ST depression (horizontal or downsloping) T wave inversion
54
What are ECG abnormalities to look for with transmural ischemia?
ST elevation
55
What are the drugs used for ischemic heart disease?
Organic nitrates Beta blockers Calcium channel blockers Ranolazine
56
What are the different types of calcium channel blockers used to treat ischemic heart disease?
Nondihydropyridines (central) Dihydropyridines (peripheral)
57
When should patients do revascularization therapy for ischemic heart disease?
They do not respond to drugs or have side effects from them Patient has high risk coronary disease
58
What are the types of revascularization therapies for ischemic heart disease?
Percutaneous coronary intervention Coronary artery bypass graft
59
What is the success rate of Percutaneous transluminal coronary angioplasty?
80-90% with 30% restenosis within 6 months
60
Why are coronary stents becoming the preferred treatment?
Reduces rate of stents
61
What are the two types of stents used?
Drug eluting stent (thrombogenic- must be on anticoagulants) Non drug eluting stent (higher rate of restenosis- no need for anticoagulants)
62
What types of grafts are used in coronary artery bypass graft?
Saphenous vein and left internal mammary artery
63
What are the characteristics of a saphenous vein graft?
Patency rate of 80% at 12 months but is vulnerable to accelerated atherosclerosis (>50% occlusion 10 years after surgery)
64
What are the characteristics of left internal mammary artery graft?
Patency rate of 90% at 10 years and resistant to atherosclerosis
65
What are acute coronary syndromes?
Unstable angina which can develop into non ST elevation MI or ST elevation MI
66
Do males have a higher prevalence of MI than females?
Yes
67
What do acute coronary syndromes result from?
Disruption of atherosclerotic coronary plaque and formation of a thrombus
68
What occurs in partially occlusive thrombus?
Unstable angina and NSTEMI
69
What occurs in complete occlusion thrombus?
STEMI
70
What is the difference between partial and complete occlusion thrombus?
The presence of myocardial necrosis
71
What is myocardial infarction?
Cell death in the heart muscle caused by complete and prolonged occlusion of a coronary artery
72
What is the wave front phenomenon?
Tissue furthest away from the heart dies first and moves inward like a wave until it covers the thickness of the myocardium
73
What are functional alterations post MI?
Impaired contractility and compliance Stunned myocardium Hibernating myocardium Ischemic preconditioning
74
What is hibernating myocardium?
Chronic contractile dysfunction due to persistently poor blood supply
75
What may happen to ventricles post MI?
Expansion which can lead to wall stress, impaired contractile function, and increased likelihood of aneurysms
76
What is the timeline of an MI?
20 min= no necrosis 20-60 min= subendocardial necrosis 1-3 hours= necrosis extends into myocardium 3-6 hours= transmural infarction
77
How long do symptoms at rest occur in unstable angina?
> 20 min
78
What is unstable angina a precursor to?
MI
79
What are the pain signs of MI?
Severe and persistent (substernal)
80
What are the sympathetic signs of MI?
Sweating and cold clammy skin
81
What are the parasympathetic signs of MI?
Nausea and weakness
82
What are the cardiac findings in MI?
S4 (S3 if systolic dysfunction present) Dyskinetic bulge Systolic murmur
83
What is the disease progression of MI?
Can progress or regress based on secondary prevention of risk factors
84
What is the frequency of exercise for inpatient cardiac rehab?
2-4 sessions a day for first 3 days
85
What is intensity of exercise for inpatient cardiac rehab?
HR should be 20-30 bpm above resting HR and RPE < 13 (submaximal)
86
What is the time of exercise for inpatient cardiac rehab?
Bouts of 10 minutes each
87
How should outpatient cardiac rehab be administered?
Moderate intensity aerobic of 30-45 min 3-5 days a week (40-80% VO2 and RPE of 12-16)
88
Should resistance training be incorporated for outpatient cardiac rehab?
Yes, 40-60% 1RM and RPE 11-13 (consider eccentrics to keep BP low)