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Stage 2: Supporting Life > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

1
Q

What is the first step in diagnosing acute MI?

A

ECG

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2
Q

What is the crucial part of the ECG to diagnosing MI?

A

ST segment

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3
Q

What should the normal ST segment look like?

A

Should be the same height as the PR interval and the isoelectric line

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4
Q

What happens to the ST segment in an MI?

A

ST elevation

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5
Q

What else is used to diagnose MI and why?

A

The presence of troponin I or T (cardiac specific) as when heart cells burst/die these proteins are released

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6
Q

What is the coronary flow reserve?

A

Maximum amount of blood in the coronary blood flow

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7
Q

By how much can the coronary flow reserve increase?

A

5 fold

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8
Q

Why does angina happen on exertion?

A

Bc stenosis affects coronary flow reserve

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9
Q

When does coronary flow reserve increase normally?

A

During exercise

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10
Q

How does stenosis affect coronary blood flow?

A

After about 50% stenosis, the coronary flow reserve decreases so coronary blood flow can no longer increase as much - CFR decreases with increasing % stenosis

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11
Q

What causes the stenosis to increase from 50% to 100% in AMI?

A

Unstable clot/plaque - RBCs caught in fibrin net

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12
Q

What is chest pain due to in AMI?

A

Sensation of myocardial ischaemia

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13
Q

Where else is pain felt during an AMI?

A

Anterior chest, left arm, neck

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14
Q

Is the pain diffuse or localised and why?

A

Diffuse → nerve supply is somatic, no dermatomes, visceral nerve supply

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15
Q

What is the character of pain in AMI?

A

Tight, pressure, weight, constriction, dull

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16
Q

What triggers angina?

A

Exercise, cold, meals, psychological stress

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17
Q

What is relief for angina?

A

Rest, GTN

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18
Q

What causes shortness of breath in an MI?

A

Pulmonary oedema

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19
Q

What happens as the heart becomes increasing failing?

A

As LV EDP increases, CO increases less

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20
Q

Why does oedema occur?

A

Pressure on the venule end of capillaries → mean pressure increases → hydrostatic pressure increases

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21
Q

What happens when atherosclerotic plaque ruptures?

A

1) Endothelial layer feels back under sheer stress of exercise
2) Platelets starts accumulating on exposed atherosclerotic plaque which initiates the clotting casade

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22
Q

What is the difference between stable and unstable atherosclerotic plaque?

A

Stable plaque is separated from the lumen by a fibrous cap however in unstable plaque the fibrous cap is eroded

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23
Q

What state is the plaque in at body temp?

A

Liquid

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24
Q

What happens to unstable plaque?

A

1) Fibrous cap is eroded and communicated with the lumen
2) Cholesterol liquid is replaced by a blood clot
3) Intraplaque haemorrhage occurs which extends into the lumen of the coronary artery

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25
Q

What are 3 treatments for atherosclerotic plaque?

A

1) Statins (cholesterol lowering)
2) Anti-platelet drugs
3) Clot busters

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26
Q

How does cholesterol cause plaque?

A

1) Oxidised LDL is attacked by macrophages which think it is a foreign body
2) Activated macrophages induce intimal smooth muscle cell death and degrade matrix in the fibrous cap
3) Intimal smooth muscle cells become senescent

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27
Q

What drugs are used to lower LDL cholesterol by preventing the above process?

A

Statins

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28
Q

Why do you need anti-platelet drugs to treat plaque?

A

Because platelets aggregate at the site of rupture/erosin

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29
Q

What are anti-platelet drugs?

A

Aspirin and other drugs which work together with aspirin

30
Q

When is aspirin given to treat AMI?

A

Immediately after ST elevation is seen on ECG (done in ambulance)

31
Q

How much aspirin is given and how?

A

300mg orally (bc it is absorbed in buccal mucosa)

32
Q

What happens after platelets aggregate at the site of rupture?

A

Thrombus forms and extends into the lumen and plaque

33
Q

What is an example of a clot buster drug (thrombolytic) used for PE and stroke?

A

tPA (tissue plasminogen activator)

34
Q

What is the problem with used a thrombolytic e.g. tPA?

A

You are marinating the body in a v potent drug which goes around the whole body and stops clotting aka the healing process around the body → risk of GI and intracranial haemorrhage

35
Q

What happens when MI patient arrives at hospital?

A

Go to heart attack centre and direct to catheter labs for mechanical reperfusion (bypass A&E) bc time is muscle

36
Q

Why is mechanical reperfusion better than pharmacological?

A

1) Faster reperfusion
2) Higher % reperfusion
3) Less stroke and bleeds
4) Lower mortality

37
Q

What is mechanical reperfusion?

A

Inserting a stent?

38
Q

What is the name of the mechanical reperfusion process used to treat MI?

A

Primary percutaneous coronary intervention

39
Q

What is the most common presentation of AMI?

A

Chest pain

40
Q

What are the two main types of MI?

A

1) STEMI (ST elevated MI)

2) NSTEMI (non-ST elevated MI)

41
Q

Which type of MI is more serious?

A

STEMI

42
Q

What are the two most important investigations when suspecting an MI?

A

ECG and troponin

43
Q

What is used to diagnose a NSTEMI without ST elevation?

A

Troponin release

44
Q

What is the diagnosis if there is no ST elevation and the troponin is negative?

A

Unstable angina

45
Q

What is the diagnosis if there is ST elevation but the troponin is negative?

A

Aborted MI (v rare)

46
Q

What do you do if someone has ST elevation?

A

Risk of MI but heart is in process of dying → medical emergency, take straight to cath lab for mechanical reperfusion

47
Q

What do you do if someone has no ST elevation?

A

No occluded epicardial coronary artery so not a medical emergency until troponin comes back positive

48
Q

How long does it take for troponin results to come back?

A

60 minutes

49
Q

What do you need before making diagnosis of MI?

A

Troponin release shown

50
Q

What is a myocardial infarction?

A

When there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischaemia

51
Q

How do you diagnose MI?

A
  • Detection of rise and/or fall of cardiac biomarkers (troponin) with at least one value >99th percentile of the URL together with evidence of myocardial ischaemia with at least one of…
    1) Symptoms of ischaemia
    2) ECG changes indicative of new ischaemia (ST or LBBB)
    3) Development of pathological Q waves
    4) Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
    5) Identification of intracoronary thrombus by angiography or autopsy
52
Q

What are the types of MI?

A

1) Spontaneous MI (plaque rupture, ulceration, erosion or dissection)
2) MI secondary to ischaemic imbalance (endothelial dysfunction, spasm, coronary embolism, fast or slow arrhythmias, anaemia, hypoxia, hypotension, high BP ± LVH (perioperative))
3) MI causing death before biomarkers available
4a) MI related to PCI
4b) MI related to stent thrombosis
5) MI related to CBG

53
Q

What causes don’t lead to an MI?

A

Myocarditis, chemotherapy, cardioversion, trauma

54
Q

What drugs improve supply demand balance of the heart?

A

Anti-anginals

1) Beta-adrenoreceptor blockers
2) L-type calcium channel blockers
3) Nitrates
4) ATP-sensitive potassium channel openers
5) Funny current channel blockers

55
Q

What needs to happen/be given to stop a second heart attack or developing heart failure?

A

1) Lower cholesterol
2) Lower BP (ACE-I and beta blocker)
3) Aspirin ± ADP receptor antagonist → stops platelet activation
4) Beta blockers
5) Statins
6) Stopping smoking
7) Managing diabetes

56
Q

What are examples of the big 5 classes of cardiology drugs which prolong life (secondary intervention?

A

1) Atorvastatin
2) Ramipril
3) Bisoprolol
4) Aspirin
5) Ticagrelor

57
Q

Give an example of an ACE inhibitor

A

Ramipril

58
Q

Give an example of a beta blocker

A

Bisoprolol

59
Q

Give an example of a platelet ADP receptor antagonist

A

Ticagrelor

60
Q

Given an example of a statin

A

Atorvastatin

61
Q

What investigation usually leads to patients being advised to take statins?

A

CT coronary angiogram

62
Q

What happens to the heart after an MI?

A

The heart dilates

63
Q

What happens hours to days after an MI?

A

Expansion of infarct (ventricular remodelling)

64
Q

What happens days to months after an MI?

A

Global (ventricular) remodelling

65
Q

What accelerates ventricular modelling (heart dilation)?

A

Further plaque rupture

66
Q

What happens to the cardiac wall after an MI?

A

The wall of the apex of the heart is much thinner after one apical anterior MI due to cardiac dilation? (good areas are those away from the area of infarction)

67
Q

How many people in the UK aged >45 have definite HF?

A

650,000

68
Q

What is the readmission rate in older patients?

A

Up to 50% in 6 months following discharge §

69
Q

What are the non-modifiable CV risk factors?

A

Family history, age, sex

70
Q

What are the modifiable CV risk factors?

A

Smoking, high cholesterol, high BP, diabetes, obesity, diet, exercise, excess alcohol

Stage 2: Supporting Life (30 decks)

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