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MD3001 > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

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?

A

Decrease HR

24
Q

What is the MOA of Ikf channel inhibitors?

A

Inhibit channels in the SA node –> decrease HR

25
Q

Which vessel is most appropriate for grafting in place of the RCA?

A

Saphenous vein

26
Q

Which vessel is most appropriate for grafting in place of the LAD?

A

LIMA - Left internal mammary artery

27
Q

What percentage of MI sufferers do not make it to hospital?

A

15 - 20%

28
Q

What is MI mortality in hospital?

A

6 - 15%

29
Q

What is the clinical presentation of MI?

A

Severe chest pain radiating to jaw and arm (generally left)
Autonomic symptoms inc. nausea, sweating, terror, etc.
Breathlessness

30
Q

What are the 2 main causes of MI?

A

Plaque rupture

Plaque erosion

31
Q

List 5 events that can modify MI presentation.

A 
o	Time of day
o	Inflammatory activity
o	Infection, especially respiratory
o	Elevation of blood pressure
o	Catacholamines
32
Q

What are the 2 main types of MI?

A

STEMI

NSTEMI

33
Q

How can an MI be clinically diagnosed?

A

Raised cardiomyocyte markers in blood (TROPONIN I/T)
Clinical history
For STEMI: ST elevation in ECG

34
Q

Outline the treatment plan for a STEMI.

A

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
Q

What are two complications of STEMI’s that can occur immediately?

A

Ventricular Arrhythmia and death

Acute Left Heart Failure

36
Q

What are two complications of STEMI’s that can occur early on?

A

Myocardial Rupture
Mitral valve insufficiency
Ventricular Septal defect
Mural thrombus and emobolisation

37
Q

What are two complications of STEMI’s that can occur later on?

A

LV dilatation and heart failure
Arrhythmia
Recurrent myocardial infarction

38
Q

In which age group is NSTEMI most prevalent?

A

The elderly

39
Q

What is a common cause of NSTEMI and therefore can be implied?

A

Sub-endocardial ischaemia

40
Q

What 4 CVS events can predispose to NSTEMI occurrence?

A

Threatened STEMI
Small branch occlusion
Occlusion of well collateralised vessel
Lateral STEMI in territory not well seen by ECG

41
Q

Outline the treatment plan for an NSTEMI

A

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)

MD3001 (63 decks)

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