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Year 6 Cardiology > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What is acute coronary syndrome (ACS)?

A

ACS is an umbrella term covering a number of acute presentations of ischaemic heart disease.

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2
Q

What are the presentations included in ACS?

A

The presentations include ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina.

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3
Q

What is ischaemic heart disease?

A

Ischaemic heart disease is synonymous with coronary heart disease and describes the gradual buildup of fatty plaques within the coronary arteries.

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4
Q

What are the two main problems caused by ischaemic heart disease?

A
  1. Gradual narrowing of arteries leading to angina. 2. Risk of sudden plaque rupture causing occlusion.
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5
Q

What are unmodifiable risk factors for ischaemic heart disease?

A

Unmodifiable risk factors include increasing age, male gender, and family history.

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6
Q

What are modifiable risk factors for ischaemic heart disease?

A

Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolaemia, and obesity.

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7
Q

What triggers initial endothelial dysfunction in ischaemic heart disease?

A

Initial endothelial dysfunction is triggered by factors such as smoking, hypertension, and hyperglycaemia.

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8
Q

What complications can develop from atherosclerosis?

A

Complications include physical blockage of the coronary artery leading to angina and plaque rupture causing myocardial infarction.

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9
Q

What are common symptoms of acute coronary syndrome?

A

Common symptoms include chest pain, dyspnoea, sweating, and nausea.

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10
Q

What are the two most important investigations for chest pain?

A

The two most important investigations are ECG and cardiac markers (e.g., troponin).

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11
Q

What is the mnemonic for the treatment of ACS?

A

The mnemonic is MONA: Morphine, Oxygen, Nitrates, Aspirin.

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12
Q

What is the priority management for a STEMI?

A

The priority is to revascularise the blocked vessel.

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13
Q

What lifelong drug therapy is required after an ACS event?

A

Lifelong therapy includes aspirin, a second antiplatelet (if appropriate), a beta-blocker, an ACE inhibitor, and a statin.

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14
Q

What are the features of acute coronary syndrome (ACS)?

A

Features of acute coronary syndrome (ACS) include: chest pain, dyspnoea, nausea and vomiting, sweating, and palpitations.

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15
Q

Where is chest pain typically located in acute coronary syndrome?

A

Chest pain is classically on the left side of the chest.

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16
Q

Can chest pain in acute coronary syndrome radiate?

A

Yes, it may radiate to the left arm or neck.

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17
Q

Is chest pain always present in acute coronary syndrome?

A

No, chest pain may not always be present.

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18
Q

What factors make atypical presentation of acute coronary syndrome more likely?

A

Being elderly, diabetic, or female makes an atypical presentation more likely.

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19
Q

What is acute coronary syndrome (ACS)?

A

ACS is a common and important presentation in medicine, classified into STEMI, NSTEMI, and unstable angina.

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20
Q

What are the classifications of acute coronary syndrome?

A
  1. ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage.
  2. Non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage.
  3. Unstable angina.
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21
Q

What are the common management strategies for all patients with ACS?

A

Initial drug therapy includes aspirin 300mg, oxygen (if saturations < 94%), morphine (for severe pain), and nitrates (for ongoing chest pain or hypertension).

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22
Q

What are the STEMI criteria?

A

Clinical symptoms consistent with ACS (≥ 20 minutes) with persistent ECG features in ≥ 2 contiguous leads of:
- 2.5 mm ST elevation in leads V2-3 in men under 40 years.
- 2.0 mm ST elevation in leads V2-3 in men over 40 years.
- 1.5 mm ST elevation in V2-3 in women.
- 1 mm ST elevation in other leads.
- New LBBB.

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23
Q

What is the first step after confirming STEMI?

A

Immediately assess eligibility for coronary reperfusion therapy, which includes percutaneous coronary intervention (PCI) and fibrinolysis.

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24
Q

When should PCI be offered for STEMI?

A

PCI should be offered if the presentation is within 12 hours of symptom onset and can be delivered within 120 minutes of when fibrinolysis could have been given.

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25
Q

What is dual antiplatelet therapy prior to PCI?

A

Dual antiplatelet therapy includes aspirin + another drug: prasugrel (if not on oral anticoagulant) or clopidogrel (if on oral anticoagulant).

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26
Q

What should be done if fibrinolysis is administered?

A

An ECG should be repeated after 60-90 minutes to check for resolution of ST elevation. If persistent myocardial ischaemia occurs, consider PCI.

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27
Q

What is the management approach for NSTEMI/unstable angina?

A

Management depends on individual patient factors and risk assessment, including antithrombin treatment and potential for coronary angiography.

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28
Q

What is the Global Registry of Acute Coronary Events (GRACE)?

A

GRACE is a tool for risk assessment that considers age, heart rate, blood pressure, cardiac function, ECG findings, and troponin levels.

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29
Q

When should coronary angiography be performed for NSTEMI/unstable angina?

A

Immediate for clinically unstable patients and within 72 hours for those with a GRACE score > 3%.

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30
Q

What is the further drug therapy for patients with NSTEMI/unstable angina undergoing PCI?

A

Unfractionated heparin and dual antiplatelet therapy (aspirin + another drug) prior to PCI.

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31
Q

What is the conservative management for patients with NSTEMI/unstable angina?

A

Further antiplatelet therapy (aspirin + another drug) based on bleeding risk: ticagrelor (if low risk) or clopidogrel (if high risk).

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32
Q

What study was used to derive regression models for predicting death in patients with acute coronary syndrome?

A

The 2006 Global Registry of Acute Coronary Events (GRACE) study.

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33
Q

What are some poor prognostic factors in acute coronary syndrome?

A

Age, development (or history) of heart failure, peripheral vascular disease, reduced systolic blood pressure, initial serum creatinine concentration, elevated initial cardiac markers, cardiac arrest on admission, ST segment deviation.

34
Q

What is the Killip class?

A

A system used to stratify risk post myocardial infarction.

35
Q

What are the features and 30-day mortality rates for Killip class I?

A

No clinical signs of heart failure; 30-day mortality is 6%.

36
Q

What are the features and 30-day mortality rates for Killip class II?

A

Lung crackles, S3; 30-day mortality is 17%.

37
Q

What are the features and 30-day mortality rates for Killip class III?

A

Frank pulmonary oedema; 30-day mortality is 38%.

38
Q

What are the features and 30-day mortality rates for Killip class IV?

A

Cardiogenic shock; 30-day mortality is 81%.

39
Q

What are the immediate complications following a myocardial infarction?

A

Patients are at risk of cardiac arrest, cardiogenic shock, tachyarrhythmias, bradyarrhythmias, and pericarditis.

40
Q

What is the most common cause of death following a myocardial infarction?

A

Cardiac arrest due to ventricular fibrillation.

41
Q

How is cardiac arrest managed after a myocardial infarction?

A

Patients are managed as per the ALS protocol with defibrillation.

42
Q

What is cardiogenic shock?

A

A condition where the ejection fraction decreases significantly due to extensive damage to the ventricular myocardium.

43
Q

What treatments may be required for cardiogenic shock?

A

Patients may require inotropic support and/or an intra-aortic balloon pump.

44
Q

What can result from surviving the acute phase of a myocardial infarction?

A

Chronic heart failure due to dysfunctional ventricular myocardium.

45
Q

What medications can improve the long-term prognosis of chronic heart failure?

A

Loop diuretics, ACE-inhibitors, and beta-blockers.

46
Q

What are common arrhythmias following a myocardial infarction?

A

Ventricular fibrillation and ventricular tachycardia.

47
Q

What is a common complication following inferior myocardial infarctions?

A

Atrioventricular block.

48
Q

What is pericarditis and when is it common after a myocardial infarction?

A

Pericarditis is common in the first 48 hours following a transmural MI, affecting around 10% of patients.

49
Q

What are the symptoms of pericarditis?

A

Typical pain worsens when lying flat, a pericardial rub may be heard, and a pericardial effusion may be demonstrated with an echocardiogram.

50
Q

What is Dressler’s syndrome?

A

An autoimmune reaction occurring 2-6 weeks after a MI, characterized by fever, pleuritic pain, pericardial effusion, and raised ESR.

51
Q

How is Dressler’s syndrome treated?

A

It is treated with NSAIDs.

52
Q

What is a left ventricular aneurysm?

A

A condition where ischaemic damage weakens the myocardium, typically associated with persistent ST elevation and left ventricular failure.

53
Q

What is the risk associated with a left ventricular aneurysm?

A

Thrombus formation within the aneurysm increases the risk of stroke, requiring anticoagulation.

54
Q

What is left ventricular free wall rupture?

A

A complication seen in around 3% of MIs, occurring 1-2 weeks after, presenting with acute heart failure secondary to cardiac tamponade.

55
Q

What is the treatment for left ventricular free wall rupture?

A

Urgent pericardiocentesis and thoracotomy are required.

56
Q

What is a ventricular septal defect?

A

Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients.

57
Q

What are the features of a ventricular septal defect?

A

Acute heart failure associated with a pan-systolic murmur; an echocardiogram is diagnostic.

58
Q

What is acute mitral regurgitation?

A

More common with infero-posterior infarction, potentially due to ischaemia or rupture of the papillary muscle.

59
Q

What symptoms may occur with acute mitral regurgitation?

A

Acute hypotension and pulmonary oedema may occur, with an early-to-mid systolic murmur typically heard.

60
Q

How is acute mitral regurgitation treated?

A

Patients are treated with vasodilator therapy but often require emergency surgical repair.

61
Q

What are the key drugs offered to all patients after a myocardial infarction?

A

Patients should be offered dual antiplatelet therapy (aspirin plus a second antiplatelet agent), an ACE inhibitor, a beta-blocker, and a statin.

62
Q

What dietary changes are recommended for patients after a myocardial infarction?

A

Advise a Mediterranean style diet, switching butter and cheese for plant oil-based products. Do not recommend omega-3 supplements or eating oily fish.

63
Q

What is the recommended exercise for patients post-myocardial infarction?

A

Advise 20-30 minutes of exercise a day until patients are ‘slightly breathless’.

64
Q

When can sexual activity resume after an uncomplicated myocardial infarction?

A

Sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI.

65
Q

What is the recommendation for PDE5 inhibitors after a myocardial infarction?

A

PDE5 inhibitors (e.g., sildenafil) may be used 6 months after a MI but should be avoided in patients prescribed either nitrates or nicorandil.

66
Q

What is the current recommendation for dual antiplatelet therapy (DAPT) after acute coronary syndrome?

A

Post-acute coronary syndrome (medically managed): add ticagrelor to aspirin and stop ticagrelor after 12 months. Post-percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin and stop the second antiplatelet after 12 months.

67
Q

What should be considered for patients at high-risk of bleeding or further ischaemic events regarding DAPT duration?

A

The 12-month period for DAPT may be altered for people at high-risk of bleeding or those at high-risk of further ischaemic events.

68
Q

When should aldosterone antagonists be initiated after an acute myocardial infarction?

A

Aldosterone antagonists should be initiated within 3-14 days of the MI for patients with symptoms and/or signs of heart failure and left ventricular systolic dysfunction, preferably after ACE inhibitor therapy.

69
Q
A

Diagram showing the progression of atherosclerosis in the coronary arteries with associated complications on the right.

70
Q
A

Slide showing a markedly narrowed coronary artery secondary to atherosclerosis. Stained with Masson’s trichrome.

71
Q
A

Ruptured coronary artery plaque resulting in thrombosis and associated myocardial infarction.

72
Q
A

Pathological specimen showing infarction of the anteroseptal and lateral wall of the left ventricle. There is a background of biventricular myocardial hypertrophy.

73
Q
A

ECG showing a ST elevation myocardial infarction (STEMI). Note by how looking at which leads are affected (in this case II, III and aVF) we are able to tell which coronary arteries are blocked (the right coronary artery in this case). A blockage of the left anterior descending (LAD) artery would cause elevation of V1-V4, what is often termed an ‘anterior’ myocardial infarction.

74
Q
A

ECG showing a non-ST elevation myocardial infarction (NSTEMI). On the ECG there is deep ST depression in I-III, aVF, and V3-V6. aVR also has ST elevation. Deep and widespread ST depression is associated with very high mortality because it signifies severe ischemia usually of LAD or left main stem.

75
Q
A

Diagram showing the correlation between ECG changes and coronary territories in acute coronary syndrome

76
Q
A

Normal coronary artery

77
Q
A

Slightly stenosed coronary artery

78
Q
A

Moderately stenosed coronary artery

79
Q
A

Severely stenosed coronary artery

80
Q
A

Recanalised old atherothrombotic occlusion of a coronary artery. Numerous small neolumina recanalising the organised occluding thrombus (indicated with arrows)

Year 6 Cardiology (36 decks)

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