Ischaemic Heart Disease Flashcards

(41 cards)

1
Q

What are 4 CVS diseases/problems that atherosclerotic coronary disease can cause?

A
Chronic coronary insufficiency
- angina
Unstable coronary disease
- MI
- sudden ischaemia
Heart failure
Arrhythmias
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2
Q

What is an epicardial coronary artery? Give one example of an epicardial coronary artery.

A
Coronary artery that lies on the outer surface of the heart
Examples:
- LAD
- Circumflex
-
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3
Q

Where therefore does an endocardial coronary artery lie?

A

Inner surface of the heart

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4
Q

What is the subendocardial region?

A

Water-shed area of perfusion and first to become ischaemic

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5
Q

What are the 3 most commonly used types of coronary artery imaging?

A

Coronary angiography
CT
MRI (measures flow)

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6
Q

List some of the risk factors of coronary artery disease.

A
Smoking
Age
Hypertension
Hypercholesterolaemia
Diabetes
Obesity
Physical inactivity
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7
Q

What are the 3 main stages in coronary artery disease pathological development?

A

Fatty streak formation
Fibro-fatty plaque formation
Plaque disruption (rupture/erosion)

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8
Q

How do foam cells form?

A

Monocytes migrate out of the blood to form macrophages and set about ingesting the fat, forming foam cells

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9
Q

What chemical mediator release stimulates the aggregation of smooth muscle cells?

A

Cytokine release

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10
Q

What are some of the symptoms of angina?

A

o Gripping central chest pain
o Radiation to arm and jaw
o Clear and precise relationship to exercise
o Goes 2-10 mins after discontinuation of exercise
o Worse after food. Worse in cold
o No autonomic features
o Flat of hand/fist to describe pain

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11
Q

What is the cause of angina?

A

Sub-endocardial ischaemia

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12
Q

What abnormality is present on an ECG in cases of angina?

A

ST wave depression

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13
Q

What is a key issue in cases of epicardial stenosis?

A

Mismatch of blood supply and demand

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14
Q

What are the two coronary flow regulatory mechanisms?

A

Auto regulation

Metabolic regulation

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15
Q

In order to a 20 fold increase in total body O2 consumption, by how much can coronary blood flow increase?

A

5 fold

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16
Q

What does the Adenosine Hypothesis of Coronary Dilation state?

A

ATP –> AMP – 5-nucleotidase –> adenosine – ADA –> Inosine

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17
Q

What are the 3 main determinants of myocardial oxygen consumption?

A
Tension development (variable per unit mass of tissue)
Contractility (variable)
Heart rate (variable)
Basal activity (fixed)
18
Q

What is the function of angina treating drugs?

A

Reduce myocardial oxygen consumption

19
Q

What are two other more invasive treatments of angina?

A

PCI - Percutaneous Coronary Intervention (stents & balloons)
CABG - Coronary Artery Bypass Grafting

20
Q

List the 4 classes of drug used in angina treatment.

A

Beta blockers
Nitrates
Calcium channel blockers
Ikf channel inhibitors

21
Q

What physiological impact do beta blockers have on the CVS?

A

Reduce BP
Reduce HR
(hence reduce work of heart)

22
Q

What do nitrates cause in the CVS?

A

Venodilation –> reduces LV wall tension –> reduced work of the heart

23
Q

What physiological impact do calcium channel blockers have on the CVS?

24
Q

What is the MOA of Ikf channel inhibitors?

A

Inhibit channels in the SA node –> decrease HR

25
Which vessel is most appropriate for grafting in place of the RCA?
Saphenous vein
26
Which vessel is most appropriate for grafting in place of the LAD?
LIMA - Left internal mammary artery
27
What percentage of MI sufferers do not make it to hospital?
15 - 20%
28
What is MI mortality in hospital?
6 - 15%
29
What is the clinical presentation of MI?
Severe chest pain radiating to jaw and arm (generally left) Autonomic symptoms inc. nausea, sweating, terror, etc. Breathlessness
30
What are the 2 main causes of MI?
Plaque rupture | Plaque erosion
31
List 5 events that can modify MI presentation.
``` o Time of day o Inflammatory activity o Infection, especially respiratory o Elevation of blood pressure o Catacholamines ```
32
What are the 2 main types of MI?
STEMI | NSTEMI
33
How can an MI be clinically diagnosed?
Raised cardiomyocyte markers in blood (TROPONIN I/T) Clinical history For STEMI: ST elevation in ECG
34
Outline the treatment plan for a STEMI.
First... - Antiplatelet agents: Aspirin + Clopidogrel - Immediate revascularisation, i.e. primary PCI or thrombolysis (- clot busting) Then... - Beta blockers (reduce myocardial infarction) - Statin drugs (reduce cholesterol – plaque passivation) - ACE inhibitors (usually a couple of days later to inhibit dilation of the left ventricle)
35
What are two complications of STEMI's that can occur immediately?
Ventricular Arrhythmia and death | Acute Left Heart Failure
36
What are two complications of STEMI's that can occur early on?
Myocardial Rupture Mitral valve insufficiency Ventricular Septal defect Mural thrombus and emobolisation
37
What are two complications of STEMI's that can occur later on?
LV dilatation and heart failure Arrhythmia Recurrent myocardial infarction
38
In which age group is NSTEMI most prevalent?
The elderly
39
What is a common cause of NSTEMI and therefore can be implied?
Sub-endocardial ischaemia
40
What 4 CVS events can predispose to NSTEMI occurrence?
Threatened STEMI Small branch occlusion Occlusion of well collateralised vessel Lateral STEMI in territory not well seen by ECG
41
Outline the treatment plan for an NSTEMI
Antiplatelet therapy (Aspirin and clopidogrel) Anti-ischaemics (beta blockers and nitrates) Statin drugs ACE inhibitors Coronary angiography and revascularisation ---> Early if symptoms continue ---> Early if Troponin raised ---> Risk score (e.g. GRACE)