BCR 6 - Angina and Valvular Heart Disease

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Last updated 2:58 PM on 4/17/26
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387 Terms

1
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What is the pathophysiological basis of cardiac chest pain?
Cardiac chest pain is caused by myocardial ischaemia, which occurs when coronary blood flow does not meet myocardial oxygen demand.
2
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How does myocardial ischaemia usually develop?
It usually develops due to reduced coronary blood supply and less commonly due to excessive myocardial oxygen demand.
3
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What form of ischaemic heart disease is the focus of stable chest pain physiology?
The focus is on stable angina rather than myocardial infarction.
4
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What determines myocardial oxygen balance?

The relationship between coronary blood flow and myocardial oxygen demand.

5
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What are epicardial coronary arteries?

Large coronary vessels that lie on the outer surface of the heart and act mainly as conductance vessels.

6
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Why are epicardial arteries described as conductance vessels?
They provide minimal resistance to blood flow under normal conditions.
7
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Which coronary vessels provide most vascular resistance?
Pre arterioles and arterioles provide the major resistance in the coronary circulation.
8
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What is the role of pre arterioles and arterioles in coronary flow?
They change calibre to regulate resistance and control coronary blood flow.
9
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Do capillaries significantly contribute to coronary resistance?
Capillaries and venous vessels make only a small contribution to overall resistance.
10
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What is coronary flow reserve?

The ability of the coronary circulation to increase blood flow to meet increased myocardial demand.

11
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How much can coronary blood flow increase during exercise?
Coronary blood flow can increase up to about five times resting levels during exercise.
12
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What does coronary flow reserve represent physiologically?
It reflects the reserve capacity of the coronary circulation to augment flow.
13
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What is the main role of coronary blood flow?

To deliver oxygen to the myocardium and remove metabolic waste.

14
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What factors influence oxygen delivery to the myocardium?

Coronary blood flow, haemoglobin concentration and arterial oxygen tension.

15
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Why is reduced oxygen carrying capacity rarely the primary cause of ischaemia?
Because coronary blood flow is usually the limiting factor rather than oxygen content.
16
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How can anaemia or hypoxia affect myocardial ischaemia?
They can worsen existing ischaemia by reducing oxygen delivery.
17
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How much oxygen does the heart extract at rest?

60% of available oxygen

18
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How does myocardial oxygen extraction compare to skeletal muscle?

Skeletal muscle extracts only about 20 to 30%

19
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Why must the heart increase blood flow during increased demand?
Because it cannot significantly increase oxygen extraction further.
20
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How does Ohm’s law apply to coronary blood flow?
Flow equals pressure difference divided by resistance.
21
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How can coronary blood flow be increased according to Ohm’s law?
By increasing pressure or decreasing resistance.
22
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Which variable does the coronary circulation mainly adjust?

Resistance

23
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What are the main regulators of coronary blood flow?
Metabolic control, autoregulation, extravascular compression, duration of diastole, hormonal and neural control, and the diastolic pressure gradient.
24
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What is metabolic control of coronary blood flow?
It is regulation of flow by metabolites produced during myocardial metabolism.
25
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Where are coronary arterioles located?
They lie within the metabolising myocardium.
26
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How do metabolites influence coronary arterioles?
They diffuse into smooth muscle and cause vasodilatation.
27
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Which metabolites regulate coronary blood flow?
Adenosine, potassium, pH and oxygen tension.
28
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How is adenosine formed during ischaemia?
ATP is broken down to ADP, AMP and then adenosine.
29
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Why is adenosine important in coronary physiology?
It is a potent vasodilator of coronary arterioles.
30
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How is adenosine used clinically?
It is used during cardiac testing to provoke ischaemia.
31
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What is autoregulation in the coronary circulation?
An intrinsic property of vascular smooth muscle that maintains constant flow across a range of pressures.
32
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Over what pressure range is coronary autoregulation effective?

Approximately 60 to 120 mm/Hg

33
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How does increased pressure affect vascular smooth muscle?
Increased pressure increases smooth muscle tone.
34
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Why does autoregulation stabilise coronary flow?
Because resistance increases proportionally with pressure, keeping flow constant.
35
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Does autoregulation cause exercise induced increases in flow?
No, it stabilises flow rather than increasing it during exercise.
36
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Why is coronary blood flow mainly diastolic?
Because myocardial contraction during systole compresses intramyocardial vessels.
37
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What happens to coronary vessels during systole?
Intramyocardial vessels are compressed, resulting in minimal systolic flow.
38
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Are epicardial vessels affected by systolic compression?
They are largely unaffected.
39
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Why is the sub endocardium particularly vulnerable to ischaemia?
It is furthest from epicardial vessels and fills slowest during diastole.
40
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How does reduced perfusion pressure affect the sub endocardium?
It disproportionately reduces blood flow to this region.
41
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How does tachycardia worsen myocardial ischaemia?
It shortens diastole, increases oxygen demand and maintains elevated left ventricular diastolic pressure.
42
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Why does exercise increase susceptibility to ischaemia?
Because heart rate increases, diastole shortens and myocardial demand rises.
43
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How are coronary resistance vessels innervated?
Pre arterioles and arterioles receive autonomic innervation.
44
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What is the effect of alpha receptor activation on coronary vessels?
It causes vasoconstriction.
45
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Where is alpha receptor activation greater?
It is greater in the epicardium.
46
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Why is alpha mediated vasoconstriction beneficial?
It helps maintain homogeneous blood flow between epicardium and sub endocardium.
47
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What is the effect of beta receptor activation on coronary vessels?
It causes vasodilatation.
48
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When is beta mediated vasodilatation particularly important?
During exercise.
49
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What happens to coronary control after heart transplantation?
Neural connections are lost.
50
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How does loss of innervation affect vasodilator responses?
There is reduced vasodilator response to adenosine.
51
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Why do transplant patients have resting tachycardia?
Due to loss of parasympathetic control.
52
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Why is maximal exercise heart rate reduced after transplantation?
Because of abnormal sympathetic responses.
53
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What role does the endothelium play in coronary flow reserve?
It releases endothelium derived relaxing factor which causes vasodilatation.
54
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What is endothelium derived relaxing factor?
Nitric oxide released by endothelial cells.
55
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How does nitric oxide affect coronary resistance?
It reduces resistance by causing vasodilatation.
56
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What coronary flow reserve is seen in healthy arteries?
Flow can increase up to five times resting levels.
57
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How does early atherosclerosis affect coronary flow reserve?
It impairs nitric oxide production despite minimal mechanical obstruction.
58
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Why can early atheroma reduce flow reserve?
Because endothelial dysfunction limits vasodilatation.
59
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What happens to coronary flow in progressive atherosclerotic lesions?
A trans stenotic pressure gradient develops.
60
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How do distal arterioles respond in moderate coronary disease?
They dilate at rest to maintain blood flow.
61
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What happens to coronary flow reserve in moderate disease?
Flow reserve is reduced.
62
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At what level of stenosis can resting ischaemia occur?

85% diameter reduction

63
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Why does severe stenosis cause resting ischaemia?
Because resistance is increased even at rest.
64
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What is fractional flow reserve?

A minimally invasive measurement of the pressure drop across a coronary stenosis during maximal blood flow.

65
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Why is fractional flow reserve needed?
Because angiography alone does not assess functional significance.
66
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Why do normal epicardial vessels contribute little resistance?
They are large conductance vessels under physiological conditions.
67
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How is maximal coronary flow achieved during FFR measurement?
By inducing distal vasodilatation with adenosine.
68
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What does fractional flow reserve compare?
Distal coronary pressure to proximal pressure across a stenosis.
69
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What FFR value indicates a haemodynamically significant lesion?

An FFR less than 0.80

70
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What does FFR assess clinically?
The functional significance of a coronary lesion rather than its appearance.
71
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Why can patients have angina with normal coronary angiograms?
Because disease may exist in the microvasculature.
72
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What does reduced coronary flow reserve with normal angiography suggest?
Microvascular disease.
73
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Why cannot microvascular disease be seen on angiography?
Because it affects pre arterioles and arterioles rather than large epicardial vessels.
74
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What functional abnormalities occur in microvascular disease?
Reduced vasodilator response and abnormal endothelial function.
75
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What abnormal vascular responses are seen in microvascular disease?
Excessive vasoconstrictor responses.
76
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Which conditions are commonly associated with microvascular disease?
Hypertension and diabetes.
77
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What symptoms can microvascular disease cause?
Angina despite absence of large vessel disease.
78
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What are the long term consequences of microvascular disease?
Increased risk of myocardial infarction, heart failure and death.
79
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Why does myocardial ischaemia cause chest pain? (not cause but function)

Because metabolites stimulate sensory nerve fibres around coronary microvessels.

80
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Where are pain sensing nerve fibres located in the heart?
Around coronary microvessels.
81
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Which metabolite is a key mediator of anginal pain?
Adenosine.
82
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How is the role of adenosine in pain demonstrated clinically?
Intracoronary adenosine infusion can reproduce chest pain.
83
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How are anginal pain signals transmitted to the brain?
Via the spinal cord, thalamus and cerebral cortex.
84
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What is angina pectoris?

Chest pain or discomfort caused by myocardial ischaemia due to an imbalance between oxygen supply and demand.

85
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Why does angina occur?

When myocardial oxygen supply is insufficient to meet myocardial oxygen demand.

86
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Where are anginal symptoms typically felt?
Symptoms are usually felt in the chest, reflected by the term pectoris.
87
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How is anginal pain commonly described?
It is described as tightness, heaviness, pressure, band like or burning discomfort.
88
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How is anginal pain transmitted?
Pain is likely transmitted via sympathetic nerve fibres and is often poorly localised.
89
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What characterises typical anginal pain?
It is predictable, triggered by exertion and relieved by rest within minutes.
90
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What is the most common trigger for angina?
Physical exercise.
91
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Why does rest relieve angina?
Rest reduces myocardial oxygen demand, restoring the balance between supply and demand.
92
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What is the most common cause of angina?
Obstructive epicardial coronary artery disease.
93
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How does epicardial coronary artery disease cause angina?
Narrowing of arteries reduces coronary flow reserve and limits increased blood flow during demand.
94
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At what degree of narrowing does angina commonly occur?
Usually when luminal narrowing is around seventy to eighty five percent or more.
95
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Why is reduced coronary flow reserve important in angina?
It prevents the heart from increasing blood flow during stress or exercise.
96
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What other mechanisms can cause angina besides epicardial disease?
Microvascular disease, coronary artery spasm and increased demand states.
97
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What is microvascular angina?
Angina caused by disease of pre arterioles and arterioles that cannot be visualised on angiography.
98
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What is coronary artery spasm?
Sudden transient narrowing of a normal or mildly diseased coronary artery.
99
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Which conditions increase myocardial oxygen demand and can cause angina?
Hypertrophic cardiomyopathy and severe hypertension.
100
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Why is angina described as a symptom rather than a disease?
Because it represents myocardial ischaemia from multiple possible causes.