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CVS (Semester 2) > Ischaemic Heart Disease > Flashcards

Ischaemic Heart Disease Flashcards

1
Q

What condition does a sharp pain in the chest usually associate with?

A

Pericarditis

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2
Q

What type of pain typically evolves during myocardial ischaemia?

A

Tightening pain

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3
Q

What pain is likely to be felt during aortic dissection?

A

Tearing

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4
Q

What condition can be associated with MI and no pain?

A

Diabetes.

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5
Q

What is myocardial ischaemia?

A

This is where blood supply is not sufficient to meet O2 demand.

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6
Q

Which cells of the heart are at highest risk of ischaemia?

A

Endocardial cells as blood flow is from epi to endocardium so these are at the end of the arteries.

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7
Q

What type of heart beat worsens ischaemia and why?

A

Tachycardia worsens ischaemia because the arteries fill during diastole and this is shortened when the heart is beating faster.

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8
Q

What is the most common cause of myocardial ischaemia?

A

Atherosclerosis, a fixed narrowing of the blood vessel. These are particularly problematic in the heart due to the lack of collaterals.

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9
Q

What factors affecting supply to myocardium can cause ischaemia?

A

Wall tension - preload vs afterload, heart rate and contractility.

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10
Q

What factors associated with demand can cause coronary ischaemia?

A

The o2 carrying capacity of the blood, coronary artery resistance, perfusion pressure.

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11
Q

Name non-modifiable risk factors for coronary artery disease.

A

Age, gender, family history.

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12
Q

What risk factors for coronary artery disease are modifiable?

A

Diet, high Cholestrol, smoking, hypertension, diabetes mellitus, obesity, lack of exercise, psychological factors, low fruit and veg intake.

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13
Q

What is an atheromatous plaque?

A

This has a necrotic centre and a fibrous cap

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14
Q

Describe the appearance of a vulnerable atheromatous plaque.

A

This will have a large necrotic centre and a thin fibrous cap. it is therefore more likely to fissure.

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15
Q

What is fissuring?

A

This is when an atheromatous plaque breaks through into the lumen of the blood vessel, leaving a rough surface which leads to thrombus formation.

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16
Q

What happens if a thrombus either partially of fully blocks the coronary blood vessel?

A

partial blockage leads to NSTEMI, full blockage leads to STEMI

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17
Q

What is stable angina?

A

This is when there is a stable plaque, and no symptoms at rest but on exertion, typical pain precipitates due to ischaemia. This is relieved on rest.

18
Q

What changes might be seen on an exercise ECG for a patient with stable angina?

A

ST depression due to sub-endocardial ischaemia.

19
Q

What drugs might be used long term to treat stable angina?

A

Ca channel blockers, beta blockers, long acting nitrates, statins or aspirin. These all help to reduce the workload of the heart or the risk of thrombus formation.

20
Q

What is an angioplasty?

A

This is opening of a blood vessel and is usually followed by stenting to keep the lumen open.

21
Q

What vessels are used for coronary artery grafts?

A

Internal mammary artery, radial artery and saphenous vein.

22
Q

What conditions are included in acute coronary syndrome?

A

Unstable angina and acute myocardial infarction.

23
Q

What are all acute coronary syndromes caused by?

A

These are all caused by fissuring of an atheromatous plaque into the lumen and subsequent thrombus formation.

24
Q

What happens in a STEMI?

A

In STEMI, there is a transmural (full thickness) infarction, and this leads to ST elevation in the leads facing the affected area.

25
Q

How can we distinguish between unstable angina and NSTEMI?

A

In unstable angina, there are no blood markers for necrosis.

26
Q

What ECG changes are seen in NSTEMI and unstable angina?

A

There can be ST depression, T inversion or normal.

27
Q

Why is injury limited to sub-endocardial areas in NSTEMI?

A

There is some collateral circulation present and only partial occlusion of the artery.

28
Q

How can worsening angina present?

A

In some cases it shows a slow, gradual progression and includes pain at rest, however in other cases it presents like an acute MI.

29
Q

What biochemical marker is used for NSTEMI/STEMI?

A

Troponin I or T.

30
Q

In acute MI, what will not relieve symptoms?

A

Rest or nitrates.

31
Q

How will a patient having an MI present?

A

They will be anxious or distressed and they will be sweating, have pallor, cold and clammy.

32
Q

In acute MI, comment on the heart rate and blood pressure.

A

The patient is likely to be Tachycardic, with a low BP.

33
Q

Name three ECG changes seen in a STEMI.

A

Pathological Q waves, T inversion and ST segment elevation.

34
Q

What is CK-MB?

A

This is the heart isoenzymes for creatinine kinase and is present in the blood 3-8 hours after MI till around 48-72 hours.

35
Q

When is creatinine kinase of significance?

A

In patients who have had Mi in last 10 days, troponin will still be raised so we can test for creatinine kinase instead.

36
Q

How is a STEMI treated?

A

Urgent PCI is needed. If not available, then fibrinolysis.

37
Q

What type of treatment is given to people with partial coronary artery occlusion?

A

Antithrombotic therapy to prevent formation of an excessive thrombus.

38
Q

What is anti-ischaemic therapy?

A

This reduces workload of the heart to prevent ischaemia and includes nitrates and B blockers.

39
Q

Why is aspirin given in acute coronary syndrome treatment?

A

It is anti-platelet and so reduces the number of platelets and therefore clot formation.

40
Q

Name some long term treatments which might be started after an MI.

A

Aspirin, ace inhibitors, statins, b blockers

41
Q

What complication of MI can cause sudden cardiac death?

A

Ventricular fibrillation

42
Q

What complications of MI can occur?

A

Arrhythmias, heart failure and cardiogenic shock.

CVS (Semester 2) (17 decks)

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