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Physiology > Myocardial Ischaemia Epidemiology and Aetiology > Flashcards

Myocardial Ischaemia Epidemiology and Aetiology Flashcards

1
Q

ischaemic heart disease other names (4)

A

coronary artery disease (CAD), coronary heart disease, heart disease, micro-vascular heart disease

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2
Q

heart disease that is more prevalent in women

A

micro-vascular heart disease

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3
Q

CAD symptoms (2)

A

none or angina pectoris

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4
Q

angina pectoris

A

chest strangling

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5
Q

no symptoms

A

silent

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6
Q

angina pectoris pain due to

A

lactate and adenosine activation of pain nerve endings

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7
Q

CAD mortality rates peaked in

A

1966

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8
Q

CAD mortality started to decrease after

A

coronary bypass surgery

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9
Q

Framingham study started

A

1945-50

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10
Q

CAD mortality rate linked to smoking

A

1955

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11
Q

Coronary care units set up in Australia

A

1960-65

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12
Q

Coronary bypass surgery used after MI

A

1970

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13
Q

beta blockers first used for hypertension

A

1975

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14
Q

MONICA study starts

A

1980-85

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15
Q

Framingham shows 50% increase in MI with hypertension

A

1980-85

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16
Q

Statins lower cholesterol

A

1985-90

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17
Q

Statins and ACE inhibitors available PBS

A

1985-90

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18
Q

statins most prescribed drug on PBS

A

2000-2005

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19
Q

Leading causee of disease worldwide

A

CHD

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20
Q

CHD deaths : dementia/stroke

A

2:1

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21
Q

Number of Australians dying daily from CHD

A

48

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22
Q

Cardiovascular disease with the most hospitalisations

A

CHD

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23
Q

hospitalisation for CAD

A

men > women

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24
Q

More deaths compared to hospitalisation

A

women

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25
Q

what is ischaemic heart disease

A

imbalance between oxygen supply and demand

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26
Q

Oxygen supply to the heart factors (3)

A

diastolic pressure, coronary oxygen resistance, carrying capacity

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27
Q

Oxygen demand factors (3)

A

ventricular wall stress, heart rate, contractility

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28
Q

increased muscle mass leads to

A

increased oxygen demand

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29
Q

ventricular wall stress that leads to increased oxygen consumption

A

intraventricular pressure (stretch) and systolic pressure (afterloading)

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30
Q

Ventricular wall stress that leads to decreased oxygen consumption

A

increased wall thickness

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31
Q

How heart rate increases oxygen demand

A

cardiac cycle energy expenditure

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32
Q

cardiac cycle energy expenditure

A

ATP splitting

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33
Q

ATP splitting (2)

A

Calcium homeostatis and cross bridge activity

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34
Q

how contractility leads to increased oxygen demand

A

increased ionotropic state (increased energy expenditure) andsympathetic modulation

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35
Q

when is coronary flow maximised

A

diastole

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36
Q

what determines coronary perfusion

A

aortic diastolic pressure

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37
Q

normal aortic diastolic pressure

A

60 mmHg

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38
Q

what is oxygen carrying capacity dependent on (2)

A

Haemoglobin levels and oxygen saturation (stability)

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39
Q

oxygen extraction in the heart is

A

maximised

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40
Q

what increases coronary resistance

A

vessel compression (maximised in systole)

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41
Q

vascular tone is

A

autoregulated

42
Q

coronary resistance can lead to

A

vessel obstruction

43
Q

Metabolic constrictor

A

oxygen

44
Q

metabolic dilators (4)

A

adenosine, lactate, Hydrogen ions, carbon dioxide

45
Q

Endothelial constrictors

A

Endothelin 1

46
Q

What produces Endothelin 1 (2)

A

shear force and Angiotensin II stimulation

47
Q

Endothelial dilators (2)

A

nitric oxide and prostacyclin

48
Q

neural/hormonal constrictors

A

alpha 1 receptors

49
Q

neural/hormonal dilators

A

beta 2 receptors

50
Q

coronary dysfunction can lead to

A

autoregulatory failure

51
Q

contributors to coronary dysfunction (3)

A

endothelial cell dysfunction, unopposed vasoconstriction, imbalance

52
Q

what leads to endothelial cell dysfunction

A

nitric oxide defficiency

53
Q

autoregulatory failure means (4)

A

increased cardiac work, irregular coronary flow, oxygen demand/supply mismatch, clots

54
Q

what can cause clots in autoregulatory failure

A

loss of nitric oxide mediated suppression of platelet aggregation

55
Q

Main features of coronary pathology (2)

A

atherosclerosis and thrombi formation

56
Q

thrombus

A

clot

57
Q

Normal arterial wall layers (3)

A

endothelial cells, elastic connective tissue, smooth muscle cells

58
Q

Fatty streak features (3)

A

LDL cholesterol, macrophages, muscle cells

59
Q

How is a fatty streak formed (3)

A

macrophages ingest lipids, streak forms, smooth muscle migration

60
Q

Stable plaque features (4)

A

lipid core expansion, smooth muscle proliferation and thickening, plaque bulge, fibrous scar tissue cap

61
Q

Vulnerable plaques (6)

A

plaque cap ruptures, collagen exposed, platelets aggregate, thrombus formation, downstream blood flow occlusion, calcifications

62
Q

Anterior heart surface anatomy (7)

A

superior vena cava, right atrium, right auricle, left atrium, aorta, pulmonary artery, conus arteriosus, right ventricle, left ventricle

63
Q

RCA

A

right coronary artery

64
Q

LAD

A

left anterior descending branch of the left coronary artery

65
Q

RCA runs between

A

right atrium and right ventricle

66
Q

LAD runs between

A

Right ventricle and left ventricle

67
Q

what is present in MI histology

A

calcifications

68
Q

Plaque obstruction

A

stenosis

69
Q

<70% stenosis

A

minimal effect on flow and compensatory dilation

70
Q

70-90% stenosis

A

espisodic ischaemia

71
Q

> 90% stenosis

A

basal ischaemia

72
Q

100% total occlusion

A

thrombosis

73
Q

partial transient occlusion

A

hibernation

74
Q

partial maintained occlusion

A

hibernation

75
Q

total transient occlusion

A

stunning

76
Q

total maintained occlusion

A

stunning

77
Q

hibernation

A

chronic metabolism suppression

78
Q

hibernation recovery

A

Re flow

79
Q

stunning

A

prolonged contractile depression

80
Q

stunning recovery

A

delayed

81
Q

infarct

A

irreversible myocardium necrosis

82
Q

what causes infarct

A

prolonged intense ischaemia

83
Q

How is excitation contraction coupling maintained

A

ion flow (particularly calcium) and pumps

84
Q

In depolarisation of a cardiomyocyte how does calcium enter the cell

A

sarcolemmal T tubule L type Ca channels

85
Q

what does intracellular calcium do in a cardiomyocyte (2)

A

stimulates myofilament contraction and activates sarcoplasmic reticular calcium release

86
Q

how is intracellular calcium reuptaken

A

SERCA pumps and ATP

87
Q

What is required for calcium to be pumped out of a cardiomyocyte

A

ATP

88
Q

How does sodium come into a cell

A

in exchange for hydrogen ions (elevates cardiomyocyte pH)

89
Q

how does sodium leave a cell

A

sodium potassium exchanger or sodium calcium exchanger

90
Q

What is there a reduction of in ischaemia (3)

A

oxygen, pH, ATP

91
Q

What is there an increase of in ischaemia (3)

A

hydrogen, calcium and sodium ions

92
Q

what is inhibited in ischaemia (5)

A

calcium pumps, sodium potassium exchanger, SERCA channels, mitochondrial function, myofilament contraction

93
Q

Myocardial hypoxia leads to decreased (3)

A

ATPase pump activity, SR Ca uptake, cell pH

94
Q

Myocardial hypoxia leads to increased (2)

A

sodium calcium exchanger and anaerobic metabolism

95
Q

reduced ATPase and SR Ca uptake coupled with increased sodium calcium exchanger leads to (3)

A

increased calcium in, potassium out and sodium in

96
Q

increased calcium in, potassium out and sodium in leads to (2)

A

lipase and protease activation and altered RMP

97
Q

RMP

A

resting membrane potential

98
Q

increased anaerobic metabolism coupled with decreased cell pH leads to

A

chromatin clumping and protein denaturation

99
Q

altered RMP can lead to

A

arrythmias

100
Q

lipase and protease activation coupled with chromatin clumping and protein denaturation can lead to

A

cell death

Physiology (9 decks)

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