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Yr 4 - CCC > Cardiology: Acute Coronary Syndrome > Flashcards

Cardiology: Acute Coronary Syndrome Flashcards

1
Q

What usually causes acute coronary syndrome (ACS)?

A

The result of a thrombus from an atherosclerotic plaque blocking a coronary artery

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2
Q

What is a arterial thrombus mainly made of?

A

Platelets

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3
Q

Mainstay of treatment of arterial thrombi?

How does this differ from venous thrombi?

A

Arterial –> antiplatelets e.g. aspirin, clopidogrel and ticagrelor

Venous –> anticoagulants e.g. DOACs, heparin

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4
Q

What are the 3 types of ACS?

A

1) Unstable angina

2) ST-elevation myocardial infarction (STEMI)

3) Non-ST-elevation myocardial infarction (NSTEMI)

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5
Q

What does the right coronary artery supply?

A

1) Right atrium

2) Right ventricle

3) Inferior aspect of the left ventricle

4) Posterior septal area

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6
Q

What does the left coronary artery become?

A

Left circumflex artery and left anterior descending artery.

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7
Q

What does the left anterior descending (LAD) supply?

A

Travels down the middle of the heart and supplies:

1) Anterior aspect of the left ventricle

2) Anterior aspect of the septum

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8
Q

What does the circumflex artery supply?

A

Curves around the top, left and back of the heart and supplies the:

1) Left atrium

2) Posterior aspect of the left ventricle

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9
Q

ACS generally develops in patients who have ischaemic heart disease (IHD).

What is IHD?

A

IHD is a term synonymous with coronary heart disease and coronary artery disease.

It describes the gradually build up of fatty plaques within the walls of the coronary arteries.

There are 2 main problems:

1) Gradual narrowing –> less blood and therefore oxygen reaching the myocardium at times of increased demand (angina)

2) Risk of sudden plaque rupture –> may lead to sudden occlusion of the artery. This can result in no blood/oxygen reaching the area of myocardium.

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10
Q

Changes seen in IHD:

A

1) initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia

2) this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability

3) fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles

4) monocytes migrate from the blood and differentiate into macrophages.
These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.

5) smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

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11
Q

What is 1st step of atherosclerosis?

A

initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia

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12
Q

What infiltrates the subendothelial space in atherosclerosis?

A

low-density lipoprotein (LDL) particles (fatty infiltration)

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13
Q

What are foam cells?

A

Foam cells are a type of cell that contain cholesterol:

1) monocytes migrate from the blood and differentiate into macrophages

2) These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’.

3) As these macrophages die the result can further propagate the inflammatory process.

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14
Q

Symptoms of ACS?

A

Main feature is central, constricting chest pain.

This is often associated with:
1) Pain radiating to the jaw or arms
2) Nausea and vomiting
3) Sweating and clamminess
4) Feeling of impending doom
5) Shortness of breath
6) Palpitations

These symptoms should continue at rest for more than 15 minutes.

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15
Q

What is a silent MI?

A

when someone does not experience typical chest pain during acute coronary syndrome

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16
Q

Who is at risk of a silent MI?

A

Diabetics, elderly

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17
Q

What are the 2 most important investigations when assessing a patient with chest pain?

A

1) ECG
2) cardiac markers e.g. troponin

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18
Q

What are the 2 main ECG changes in a STEMI?

A

1) ST-segment elevation
2) New left bundle branch block

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19
Q

What are the 2 main ECG changes in an NSTEMI?

A

1) ST segment depression
2) T wave inversion

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20
Q

What do pathological Q waves indicate?

When do they appear?

A

Suggest a deep infarction involving the full thickness of the heart muscle (transmural)

Typically appear 6 or more hours after the onset of symptoms.

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21
Q

Which artery supplies the anterior aspect of heart?

A

Left anterior descending

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22
Q

Which artery supplies the anterolateral aspect of heart?

A

Left coronary artery

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23
Q

Which artery supplies the lateral aspect of heart?

A

Circumflex

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24
Q

Which artery supplies the inferior aspect of heart?

A

Right coronary artery

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25
Q

What leads can ECG changes be seen in and what artery is affected for the following aspects of the heart:

a) anterior
b) inferior
c) lateral
d) anterolateral

A

a) V1-V4, left anterior descending

b) II, III, aVF, right coronary

c) I, aVL, V5-V6, left cirumflex

d) I, aVL, V3-V6, left coronary artery

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26
Q

An MI affecting the left anterior descending would cause ECG changes in which leads?

A

V1-V4

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27
Q

An MI causing changes in leads II, III and aVF indicates damage to what aspect of the heart?

A

Inferior (right coronary artery)

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28
Q

An MI affecting the circumflex would cause ECG changes in which leads?

A

I, aVL, V5-V6

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29
Q

What is troponin?

A

Troponin is a protein in cardiac muscle (myocardium) and skeletal muscle.

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30
Q

What does a rise in troponin indicate?

A

myocardial ischaemia (released from the ischaemic muscle tissue)

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31
Q

Troponin results are used to diagnosse which type of ACS?

A

NSTEMI (they are not required to diagnose a STEMI, as this is diagnosed based on the clinical presentation and ECG findings)

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32
Q

A high troponin or a rising troponin on repeat tests, in the context of suspected ACS indicates what?

A

NSTEMI

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33
Q

Troponin is a non-specific marker, meaning that a raised troponin does not automatically imply acute coronary syndrome.

What are some other causes of a raised troponin?

A

1) CKD
2) Sepsis
3) Myocarditis
4) Aortic dissection
5) Pulmonary embolism

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34
Q

Investigations in ACS?

A

1) ECG
2) Cardiac markers e.g. troponin
3) Baseline bloods, including FBC, U&E, LFT, lipids and glucose
4) CXRto investigate for pulmonary oedema and other causes of chest pain
5) Echocardiogram once stable to assess the functional damage to the heart, specifically the left ventricular function

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35
Q

What investigation can be done once stable to assess the functional damage to the heart in ACS?

A

Echo (specifically the left ventricular function)

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36
Q

a STEMI can be diagnosed when the ECG shows either:

A

1) ST elevation
2) New left bundle branch block

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37
Q

How is an NSTEMI diagnosed?

A

When there is a raised troponin, with either:

1) A normal ECG
2) Other ECG changes (ST depression or T wave inversion)

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38
Q

When is unstable angina diagnosed?

A

When the symptoms suggest ACS, the troponin is normal, and either:

1) A normal ECG
2) Other ECG changes (ST depression or T wave inversion)

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39
Q

Describe troponin levels in unstable angina?

A

NORMAL

40
Q

When a patient is presenting with chest pain and the troponin and ECG are normal, what are the possible causes?

A

1) unstable angina
2) another cause, such as musculoskeletal chest pain.

41
Q

Initial managment of ACS?

Mneumonic: MONA

A

M - Morphine
O - Oxygen
N - Nitrates (GTN)
A - Aspirin

42
Q

If a patient with suspected ACS is now pain free, but the pain occurred within the past 72 hours, what is the management?

A

They need to be referred to the hospital for same-day assessment, usually to be seen by the medical team in the Ambulatory Care Unit

43
Q

When should oxygen be given in ACS?

A

if the oxygen saturations are < 94%.

44
Q

What is the difference between a STEMI and a NSTEMI blockage?

A

STEMI –> complete occlusion of coronary artery

NSTEMI –> partial blockage (e.g. severe narrowing) of coronary artery

45
Q

Priority of management in STEMI?

A

reopen, or revascularise, the blocked vessel.

46
Q

Management of STEMI?

A

1) MONA

2) Give a 2nd antiplatelet e.g. clopidogrel, ticagrelo

3) Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)

4) Thrombolysis (if PCI is not available within 2 hours)

47
Q

When is a PCI done in a STEMI?

A

If available within 2 hours of presenting

AND

Patients presented within 12 hours of onset

48
Q

What is done if PCI is not available within 2 hours of presenting?

A

Thrombolysis

49
Q

What is PCI?

A

1) Putting a catheter into the patient’s radial or femoral artery (radial is preferred), feeding it up to the coronary arteries under x-ray guidance

2) Injecting contrast to identify the area of blockage (angiography)

3) Blockages can be treated using balloons to widen the lumen (angioplasty) or devices to remove or aspirate the blockage.

4) Usually, a stent is inserted to keep the artery open.

50
Q

What does thrombolysis involve

A

involves injecting a fibrinolytic agent –> breaks down fibrin in blood clots

51
Q

Risks of thrombolysis?

A

significant risk of bleeding

52
Q

Give 3 examples of thromolytic agents

A

1) streptokinase

2) alteplase

3) tenecteplase

53
Q

Medical management of NSTEMI?

Mneumonic: BATMAN

A

B – Base the decision about angiography and PCI on the GRACE score

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)

M – Morphine titrated to control pain

A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)

N – Nitrate (GTN)

54
Q

What dose of aspirin is given in ACS?

A

300mg

55
Q

What does of ticagrelor is given in NSTEMI?

A

180mg

56
Q

Which antiplatelet carries a higher bleeding risk: clopidogrel or ticagrelor?

A

Ticareglor (give clopidogrel in patients at bleeding risk)

57
Q

What score is used to determine risk in NSTEMI?

A

Grace score

58
Q

Define angiography

A

Contrast injected into blood vessels to highlight problems

59
Q

What invesitgations should UNSTABLE patients with NSTEMI be considered for?

A

Immediate angiography

60
Q

What does the GRACE score give?

A

gives a 6-month probability of death after having an NSTEMI

61
Q

What Grace score indicated low risk?

A

3% or less

62
Q

What Grace score indicated medium to high risk?

A

Above 3%

63
Q

Which NSTEMI patients are considered for early angiography with PCI (within 72 hours) in NSTEMI?

A

Patients at medium or high risk (>3% Grace score)

64
Q

Patients who’ve had an ACS require lifelong drug therapy to help reduce the risk of a further event.

2ary prevention in ACS?

Mneumonic: 6 A’s

A

Aspirin 75mg once daily indefinitely

Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months

Atorvastatin 80mg once daily

ACE inhibitors (e.g. ramipril) titrated as high as tolerated

Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated

Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

65
Q

What does of aspirin is given lifelong in ACS?

A

75mg once daily

66
Q

What does of atorvastatin is given lifelong in ACS?

A

80mg once daily

67
Q

What is it important to monitor in patients taking ACE inhibitors and aldosterone antagonists?

A

Renal function –> both can cause hyperkalaemia

68
Q

What electrolyte abnormality can ACEi lead to?

A

Hyperkalaemia

69
Q

Give 2 examples of aldosterone antagonists (also called potassium sparing diuretics)

A

1) eplerenone
2) spironolactone

70
Q

What is risk of using ACEi and K+ sparing diuretic?

A

Hyperkalaemia

71
Q

Potential complications of MI?

A

1) Death

2) Rupture of the heart septum or papillary muscles

3) Heart failure

4) Arrhythmias

5) Aneurysm

6) Dressler’s syndrome

72
Q

What is Dressler’s syndrome?

When does it occur?

A

It is caused by a localised immune response that results in inflammation of the pericardium (pericarditis).

Dressler’s syndrome tends to occur around 2-6 weeks following a MI.

73
Q

Management of Dressler’s?

A

NSAIDs

74
Q

What are the symptoms of Dresser’s?

A

1) fever
2) pleuritic chest pain
3) pericardial effusion
4) raised ESR
5) pericardial rub on auscultation
6) pericardial tamponade (rare)

75
Q

What is a pericardial rub?

A

a rubbing, scratching sound that occurs alongside the heart sound

76
Q

What investigations are needed in the diagnosis of Dressler’s syndrome?

A

1) ECG

2) Echo

3) Inflammatory markers (raised)

77
Q

What can be seen in an ECG in Dressler’s syndrome?

A

global ST elevation and T wave inversion

78
Q

What can be seen in an echo in Dressler’s syndrome?

A

pericardial effusion

79
Q

There are 4 types of MI.

What is type 1?

A

Traditional MI due to an acute coronary event

80
Q

what is a type 2 MI?

A

Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

81
Q

What is a type 3 MI?

A

Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

82
Q

What is a type 4 MI?

A

MI associated with procedures such as PCI, coronary stenting and CABG

83
Q

What are some complications of an MI?

A

1) Cardiac arrest
2) Cardiogenic shock
3) Chronic heart failure
4) Tachyarrhythmias
5) Bradyarrhythmias
6) Pericarditis
7) Left ventricular aneurysm
8) Left ventricular free wall rupture
9) Ventricular septal defect
10) Acute mitral regurgitation

84
Q

What is the most common cause of death following an MI?

A

Ventricular fibrillation causes cardiac arrest

85
Q

What causes cardiogenic shock post MI?

A

If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock.

Can cause be caused by ‘mechanical’ complications such as left ventricular free wall rupture.

86
Q

What can cause heart failure post MI?

A

The ventricular myocardium may be dysfunctional

87
Q

Atrioventricular block is more common post MI affecting which aspect of the heart?

A

Inferior

88
Q

Acute mitral regurgiation is more common post MI affecting which aspect of the heart?

A

Infero-posterior infarction

89
Q

What can be heard on auscultation in acute mitral regurg?

A

An early-to-mid systolic murmur is typically heard.

90
Q

What system is used to stratify risk post myocardial infarction?

A

Killip class

91
Q

Describe Killip class I-IV:

A

I - No clinical signs heart failure (mortality 6%)

II - Lung crackles, S3 (17%)

III - Frank pulmonary oedema (38%)

IV - Cardiogenic shock (81%)

92
Q

What does a new left bundle branch block (LBBB) point in the direction of?

A

ACS

93
Q

What is often the first ECG sign in an MI?

A

hyperacute T waves - but often only persists for a few minutes

94
Q

ECG changes in an MI?

A

1) hyperacute waves (but only persist for a few minutes)

2) ST elevation may develop

3) T waves typically become inverted within the first 24 hours (this can last days to months)

4) pathological Q waves develop after several hours to days (usually indefinitely)

95
Q

What ECG sign usually persists indefinitely?

A

Pathological Q waves

96
Q
A

Yr 4 - CCC (54 decks)

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