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MEDS5009 > Pathophysiology of CVD > Flashcards

Pathophysiology of CVD Flashcards

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1
Q

cardiovascular disease

A

pathologic process commonly associated with atherosclerotic process, that causes disease of the heart, coronary and systemic circulation

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2
Q

atherosclerosis

A

build up of fatty deposits inside the arteries, associated with all CVD

development of atheromatous lesions within intimal lining of large and medium-sized arteries that protrude into and eventually obstruct blood flow

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3
Q

types of CVD

A

coronary heart disease (CHD, ischemic heart disease, myocardial infarction, angina pectoris), cerebrovascular disease (stroke, TIA), hypertensive heart disease, peripheral vascular disease, heart failure, rheumatic heart disease, congenital heart disease, cardiomyopathies

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4
Q

cardiovascular system

A

heart, arteries, veins and capillaries make it up. These structures transport life-supporting oxygen and nutrients to cells, remove metabolic waste products and carry hormones from one part of the body to another

plays role in temperature regulation

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5
Q

cardiac output

A

stroke volume x HR

measures the efficiency of the heart

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6
Q

stroke volume

A

how much blood ejected from the left ventricle

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7
Q

phases of heart pumping

A

systole and diastole

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8
Q

systole

A

contraction

isovolumetric contraction and ventricular filling

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9
Q

diastole

A

relaxation

isovolumetric relaxation, ventricular filling and arterial contraction

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10
Q

right side of heart

A

pumps deoxygenated blood to lungs

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11
Q

pulmonary arteries

A

carry deoxygenated blood from right ventrical to lungs

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12
Q

pulmonary veins

A

carry oxygenated blood from lungs to left atrium

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13
Q

left side of heart

A

pumps oxygenated blood to rest of body

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14
Q

windkessel effect

A

describes how the elasticity of the aorta and large arteries smooths the pulsatile blood flow from the heart, ensuring a more continuous flow to the smaller arteries and capillaries

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15
Q

hemodynamics

A

principles that govern blood flow in the circulatory system

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16
Q

blood flow

A

movement of specific volume of fluid within a defined time

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17
Q

blood flow regulation

A

CO, peripheral vascular resistance, viscosity, size, laminar vs turbulent flow, wall tension and compliance

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18
Q

cardiac reserve

A

maximum percentage of increase in CO that can be achieved

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19
Q

ability of heart to increase output depends on

A
  • preload or ventricular filling
  • afterload or resistance to ejection of blood from heart
  • cardiac contractility
  • heart rate
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20
Q

arteries

A

thick walled vessels with large amounts of elastic fibres, which allows them to stretch during systole and recoil during diastole

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21
Q

arterioles

A

predominately smooth muscle, serve as resistance vessels. Act as control valves through which blood is released as it moves into capillaries

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22
Q

venous system

A

low pressure that returns blood to heart

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23
Q

venules

A

collect blood from capillaries

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24
Q

veins

A

transport blood back to the right heart

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25
central venous pressure
pressure in the right atrium
26
right atrial pressure
regulated by ability of right ventricle to pump blood into lungs and tendency of blood to flow from peripheral veins into right atrium
27
progressive process of atherosclerotic lesions
1. endothelial cell injury 2. migration of inflammatory cells 3. smooth muscle cells proliferative and lipid deposition 4. gradual development of atheromatous plaque with liquid core
28
endothelium
protective layer inside blood vessels
28
endothelial cell injury
external factors (smoking, hypertension, high LDL) damage endothelium causing increased permeability which allows harmful substances to enter the arterial wall.
29
migration of inflammatory cells
monocytes and platelets stick to damaged endothelium and monocytes adhere to endothelium to move into arterial wall to transform into macrophages macrophages engulf LDL-C which forms foam cells
30
lipid accumulation
foam cells create fatty deposits
31
smooth muscle proliferation
accumulation of foam cells promotes SMC migration into plaque, which helps stabilise plaque and contributes to further growth
32
plaque structure and growth
fibrous cap protects plaque from rupturing, and necrotic core is full of dead foam cells and fatty debris if fibrous cap ruptures the plaque releases contents into blood stream = blood clot formation = blockage
33
mature plaque
consists of foam cells, smooth muscle cells, macrophages and extracellular matrix components of collagen
34
thrombosis
blood clot formation
35
clinical manifestations of atherosclerosis
- narrowing of vessels and production of ischemia - sudden vessel obstruction due to plaque hemorrhage - thrombosis and formation of emboli resulting from damage to vessel endothelium - aneurysm formation due to weakening of vessel wall
36
subclinical CVD
below the clinical threshold and undetectable symptoms, therefore crucial time for prevention and intervention measured by biomarkers, MRI, CT and DEXA symptoms - non-obstructive plaques, subclinical inflammation, endothelial dysfunction
37
valvular heart defects
dysfunction of heart valves causing a disruption in blood flow. caused by cognetial defects, trauma, ischemic heart disease, degenerative changes and inflammation
38
regurgitant valvular defect
leaking blood when valve is closed
39
stenotic valvular defect
narrowing causing decreased blood flow through valve and therefore impaired emptying and increase work demands of heart chamber that empties blood across diseased valve
40
arrythmia
irregular heart beat due to fault in the hearts electrical system
41
coronary heart disease
impaired coronary blood flow often caused by atherosclerosis
42
possible consequences of CHD
myocardial ischemia, angina, myocardial infarction, arrhythmia, conduction defects, heart failure, sudden death
43
risk factors of CHD
non-modifiable - genetics, age, race/ethnicity and sex modifiable - smoking, high BP, high cholesterol, high lipoproteins, lack of exercise, diabetes, thrombosis, obesity/overweight, family history, excessive alcohol, stress
44
anterior STEMI
left coronary artery
45
inferior STEMI
right coronary artery
46
assessment of CHD
ECG, exercise stress testing, echocardiography and doppler imaging, cardiac MRI and CT, cardiac catheterisation and angiography, serum biomarkers
47
myocardial ischemia
occurs when ability of coronary arteries to supply blood is inadequate to meet the metabolic demands of the heart
48
unstable angina
plaque disruption and platelet aggregation, unstable plaque no serum markers for myocardial damage
49
NSTEMI
non-ST-segment elevation myocardial infarction partial blockage (plaque + thrombosis), diagnosed by serum markers of myocardial injury present
50
pathogenesis of UA/NSTEMI
1. unstable plaque ruptures or erodes with thrombosis 2. obstruction (spasm, constriction, dysfunction or adrenergic stimuli) 3. severe narrowing of coronary lumen 4. inflammation (thin fibrous cap = vulnerable to rupture) 5. physiological state (fever, hypotension) causing ischemia
51
pain associated with UA/NSTEMI
persistent pain: - occurring at rest, more than 20 mins - severe, frank pain (New onset) - severe, prolonged or frequent
52
STEMI
ischemic death of myocardial tissue associated with athersclerotic disease of coronary arteries heart attack
53
extent of STEMI damage
depends on location, extent of occlusion, amount of hart tissue supplied by vessel, duration, metabolic needs of affected tissue, extent of collateral circulation, HR, BP, cardiac rhythm
54
transmural infarcts
involve full thickness of wall
55
myocardial necrosis
irreversible myocardial cell death that occurs after 20-40 mins of severe ischemia and 1 hour after irreversible cell injury
56
ventricular remodelling
progressive changes in size, shape and thickness, comprising early wall thinning, healing, hypertrophy and dilation of infarcted and non-infarcted areas of ventricle
57
STEMI clinical presentation
abrupt or progression post NSTEMI - prolonged pain (crushing and severe) - radiating from left arm, neck or jaw - gastrointestinal complaints (vomiting, nausea) - fatigue and weakness in limbs - tachycardia, restlessness, anxiety - feelings of impending doom - productive cough (frothy pink) - pale, moist skin - hypotension and shock
58
management of CHD
-recognition of symptoms - prompt emergency team, transport and seeking help - timing key - implementation of therapy within 60-90 mins to avoid irreversible damage - oxygen, pain control , pharmacological therapies - reperfusion strategies
59
reperfusion
reestablishment of blood through use of pharmacologic agents, percutaneous coronary intervention or coronary artery bypass grafting
59
cardiac rehabilitation
exercise, nutrition, smoking cessation, psychological management and education
60
chronic stable angina
fixed coronary obstruction that produces disparity between coronary blood flor and metabolic demands of myocardium
61
angina pectoris
precipitated by situations that increase work demands of heart (exercise, exposure to cold, emotional stress) therefore, lots of people don't develop due to sedentary lifestyle, development of adequate collateral circulation or inability to perceive pain
62
heart failure
complex syndrome resulting from any functional or structural disorder of the heart that results in increased risk of developing manifestations of low CO and pulmonary or systemic congestion produced by any heart condition that reduces ability to pump blood
63
causes of heart failure
CHD, hypertension, dilated cardiomyopathy, valvular heart disease
64
right side heart failure
leads to congestion of peripheral tissues - edema and ascites - GI tract congestion - liver congestion
65
left side heart failure
decreased CO (activity intolerance and tissue perfusion) and pulmonary congestion (impaired gas exchange, pulmonary edema)
66
dyspnea
perceived shortness of breath, when related to increase activity it is exertional
67
orthopnea
shortness of breath when lying down
68
paroxysmal nocturnal dyspnea
sudden attack of dyspnea that occurs during sleep
69
Cheyne-stokes respiration
pattern of periodic breathing characterised by gradual increase in depth of breathing to max, followed by decrease = apnea
70
right side heart failure clinical presentation
swelling, weight gain, edema, large neck veins, lethargic, irregular heart rate, nausea, girth of abdomen increased
71
left side heart failure clinical presentation
difficulty breathing, rales, orthopnea, weakness, nocturnal paroxysmal dyspnea, increased HR, nagging cough, gain weight
72
class 1 heart failure
people with known heart disease without symptoms during ordinary activity
73
class 2 heart failure
people who have heart disease who have slight limitations but no extreme fatigue, palpitations, dyspnea or angina pain during regular activity
74
class 3 heart failure
people with heart disease who are comfortable at rest but ordinary activity does result in fatigue, palpitations, dyspnea or chest pain
75
class 4 heart failure
people who have marked progressive cardiac disease and are not comfortable at rest or minimal activity
76
diagnosis of heart failure
risk factor assessment, history, physical exam, lab studies (anemia and electrolyte imbalances, check liver congestion), ECG, chest radiography, echocardiography, cardiac MRI need to know if connected to left or right side to assess symptoms
77
pharmacological treatment approach
mechanical support device (intra-aortic ballon pump), ventricular assist device, heart transplantation (end-stage)
78
non-pharmacological approach
individualised exercise training (improve intolerance, low intensity), sodium and fluid restriction, weight management

MEDS5009 (19 decks)

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