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Study Notes - Cardiology > *Ischaemic heart disease (2) - MI > Flashcards

*Ischaemic heart disease (2) - MI Flashcards

1
Q

What are the 4 main progressive steps involved in atherogenesis?

A

Normal -> fatty streak -> atheromatous plaque -> atherosclerotic plaque

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2
Q

What is atherosclerosis?

A

A disease of the arteries characterized by the deposition of fatty material on their inner walls causing progressive narrowing and hardening

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3
Q

What is an atheroma?

A

A fatty deposit in the intima

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4
Q

Risk factors for coronary heart disease?

A 
Gender 
Age
Drug abuse
alcohol
Smoking
Stress
Hypertension
High cholesterol
Obesity
Family history
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5
Q

What is chronic stable angina?

A

Chest pain caused by demand led ischaemia due to fixed stenosis which occurs in a predictable manner

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6
Q

What is the immediate treatment of chest pain due to chronic stable angina?

A

Stop
Sit
Spray

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7
Q

What is an acute coronary syndrome in general?

A

Any acute presentation of coronary artery disease
Only a provisional diagnosis that covers a spectrum of conditions
Like stable angina it is caused by ischaemia caused by atherosclerosis

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8
Q

What conditions are classified as acute coronary syndromes?

A

Unstable angina
NSTEMI
STEMI

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9
Q

What are 2 older alternative names for a NSTEMI?

A

Non-Q wave

Sub-endocardial MI

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10
Q

What are 2 older alternative names for a STEMI?

A 
Acute MI (not called this anymore)
Q wave MI
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11
Q

What are the 2 types of MI?

A

ST elevation MI

Non ST elevation MI

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12
Q

Does a fatty streak cause symptoms?

A

No - it is clinically silent

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13
Q

What is the pathogenesis surrounding unstable coronary syndrome?

A

Plaque rupture/ fissure and thrombosis

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14
Q

What can happen to the plaque which bridges between an atherosclerotic plaque and plaque rupture/ fissure and thrombosis?

A

Fibrous cap forms over the fatty core

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15
Q

What type of stenosis does acute coronary syndrome have?

Type of ischaemia?

A 
Dynamic stenosis (subtotal or complete occlusion)
Supply led ischaemia
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16
Q

What are the stages of the platelet cascade?

A

Initiation
Adhesion
Activation

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17
Q

What causes initiation of the platelet cascade?

A

Spontaneous plaque rupture which leads to exposed tissue elements (sub endothelial collagen and Von Willebrand factor)

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18
Q

What are factors affecting plaque rupture/ fissure? (6)

A

Lipid content of plaque
Thickness of fibrous cap
Sudden changes in intraluminal pressure or tone
Bending and twisting of an artery during each heart contraction
Plaque shape
Mechanical injury

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19
Q

What is von willebrand factor?

A

A glycoprotein that plays an important role in stopping the escape of blood from vessels

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20
Q

What is involved in adhesion (platelet cascade)?

A

Platelet recruitment and adhesion at the site of injury forming a monolayer

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21
Q

What is involved in activation (platelet cascade)?

A

Activators are released (ADP and Thromboxane A2)
They bind to surface receptors on platelets
Platelet activation accelerates resulting in platelet aggregation
Activated platelets express adhesion receptors for leukocytes (P-selectin and CD40 ligand) = inflammation
Organised fibrin-rich thrombus forms
(This leads to vascular blockage = acute MI/ stroke)

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22
Q

How is ADP and other activators released during platelet cascade?

A

Through degranulation

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23
Q

How is thromboxane A2 generated?

A

Via cycloxygenase

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24
Q

What adhesion receptors for leukocytes do activated platelets express (2)?

A

P-selectin

CD40 ligand

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25
Q

Difference between unstable angina and NSTEMI?

A

There is no elevation in cardiac enzymes in unstable angina where as there will be an elevation in cardiac enzymes in an NSTEMI (infarction does not occur- pre-MI which can lead to an MI)

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26
Q

Difference between a STEMI and NSTEMI?

A

There is only partial damage in heart muscle with an NSTEMI compared to full thickness damage to heart muscle with a STEMI - due to this full thickness damage ST elevation occurs on the ECG

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27
Q

What are ECG changes that are seen with a STEMI?

A

ST elevation
T wave inversion
Pathological Q waves

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28
Q

What must be present on an ECG to confirm a STEMI? (either one of 3 of)

A

Greater than or equal to 1mm ST elevation in 2 adjacent limb leads
Greater than or equal to 2mm elevation in at least 2 adjacent precordial leads
New onset bundle branch block (usually left bundle branch block)

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29
Q

What changes in Q waves indicate a problem?

A

> 40 ms (1 mm) wide
2 mm deep
25% of depth of QRS complex
-Seen in leads V1-3

30
Q

What changes in ECG are seen in the first few hours of a STEMI?

A

ST elevation

31
Q

What changes in ECG are seen in the first day?

A

pathological Q wave formation and T wave inversion

32
Q

What ECG changes are suggestive of an old MI?

A

Q waves +/- inverted T waves

33
Q

What leads have pathologies that indicate an inferior MI?

A

II, III and aVF

34
Q

What leads have pathologies which indicate an anteroseptal MI?

A

V1-V4

35
Q

What leads have pathologies indicating an anterolateral MI?

A

I, aVL, V1-V6

36
Q

What is the cardiac enzyme?
When does its levels peak post-MI?
Where is this also present?

A

CK (creatinine kinase)
24 hours
In skeletal muscle and brain

37
Q

What is the cardiac protein marker?
Specific/ not specific?
Sensitive/ not sensitive?

A

Troponin
Highly specific
Can detect tiny small amounts of myocardial necrosis

38
Q

Is CK or Tn better?

A

Tn

39
Q

Difference between NSTEMI and UA?

A

NSTEMI will cause an elevation in cardiac enzymes due to necrosis, which will not be present in UA (as the muscle is not dying)

40
Q

Management of acute coronary syndrome pre-hospital?

A

Emergency ambulance
300mg aspirin
GTN
Morphine (e.g. 5-10mg morphine IV)
Anti-emetics (e.g. 10mg IV metoclopramide)
O2 if required
If 45 minutes or longer road time to hospital, pre-hospital thrombolysis

41
Q

Management of STEMI?

A 
300mg aspirin
GTN (if BP greater than 90mmhg)
Morphine (e.g. 5-10mg morphine IV)
Anti-emetics (e.g. 10mg IV metoclopramide)
O2 (if hypoxic)
300mg clopidogrel
PCI
Thrombolysis if angioplasty not available within 90 minutes
42
Q

What are the indications for repercussion therapy (thrombolysis or PCI) for acute coronary syndrome?

A

Chest pain suggestive of acute MI (more than 20 minutes but less than 12 hours)
Ecg changes (acute ST elevation/ new left bundle branch block)
No contraindicaitons

43
Q

When is thrombolysis performed instead of PCI?

A

Patients who can’t undergo PCI in a timely fashion - diagnosis to angioplasty time is greater than 90 minutes

44
Q

Risk of thrombolysis?

A

Failure to re-perfuse
Haemorrhage
Hypersensitivity

45
Q

What are the 4 categories of complications from an MI?

A

Death
Arrhythmic complicaitons
Structural complications
Functional complications

46
Q

Arrhythmic complications from a MI?

A

Ventricular fibrillation

47
Q

Structural complications from an MI?

A 
Cardiac rupture
Ventricular septal defect
Mitral valve regurgitation
Left ventricular aneurysm
Mural thrombus +/- systemic emboli
Inflammation
Acute pericarditis
Dressler's syndrome
48
Q

What are the functional complications of an MI?

A

Acute ventricular failure (left, right, both)
Chronic cardiac failure
Cardiogenic shock

49
Q

What classification system can be used to determine in-hospital mortality post-MI?

A

Killip Classification

50
Q

Killip classification?

A 
I = no signs of heart failure (6%)
II = crepitations less than 50% of lung fields (17%)
III = crepitations greater than 50% of lung fields (38%)
IV = cardiogenic shock (81%)
51
Q

Routine observations post-MI?

A 
Cardiac monitor - rhythm?
How does the patient feel?
Pulse and blood pressure
Heart sounds especially added sounds
Murmurs especially new murmurs
pulmonary crepitations
Fluid balance especially uric output
52
Q

What is extremely important to remember about the ECG of a patient with an NSTEMI?

A

It may be normal

53
Q

What are the different isotopes of troponin present in the body and where are these present?

A

Troponin C = heart and skeletal muscle
Troponin I = cardiac specific
Troponin T = cardiac specific

54
Q

What are the preferred isoforms of troponin used as a biomarker?

A

TnT or TnI (high cardiac specificity)

55
Q

What happens to the TnT or TnI levels over time?

A

Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days

56
Q

What other conditions can cause an elevation in TnT levels?

A 
CCF
Hypertensive crisis
Renal failure
PE
Sepsis
Stroke/ TIA
Pericarditis/ myocarditis
Post arrhythmia
57
Q

How many different classifications of MI are there according to the new clinical classification of MI?

A

6 (1, 2, 3, 4a, 4b, 5)

58
Q

What is a class 1 MI?

A

Spontaneous MI related to ischaemia due to a primary coronary event, such as plaque erosion and/or rupture, fissuring or dissection

59
Q

What is a class 2 MI?

A

MI secondary to ischaemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolic, anaemia, arrhythmias, hypertension or hypotension

60
Q

What is a class 3 MI?

A

Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggesting ischaemia with new ST-segment elevation, ew left bundle branch block, or pathological or angiographic evidence of fresh coronary thrombus - in the absence of reliable biomarker findings

61
Q

What is a class 4a MI?

A

MI associated with PCI

62
Q

What is a class 4b MI?

A

MI associated with documented in-stent thrombosis

63
Q

What is a class 5 MI?

A

MI associated with CABG surgery

64
Q

Treatment of NSTEMI?

A

Long term aspirin
Clopidogrel therapy (continued for 3 months)
Patients should receive coronary angioplasty within 72 hours of admission

65
Q

How should patients with STEMI treated with thrombolysis be further treated?

A

Early coronary angiography and revasculirisation

66
Q

What are the 4 phases of cardiac rehabilitation?

A

Phase 1 = in-patietn
Phase 2 = early post discharge period
Phase 3 = structured exercise programme - usually hospital based
Phase 4 = long term maintenance of physical activity and lifestyle change - usually community based

67
Q

What is the aim of blood pressure post MI?

A

Less than 140/85mmHg unless diabetic, renal disease or target organ damage = less than 130/80 mmHg

68
Q

4 examples of thrombolytic drugs?

A

Streptokinase
Altepase
Reteplase
Tenectaplase

69
Q

Apart from MONA-C, how is an NSTEMI treated?

A

Low weight heparin or fondaparinux given

Angiography within 72 hours to determine best next steps e.g. PCI, CABG

70
Q

Management of UA once in hospital?

A

Aspirin and other anti-platlet agent e.g. clopidogrel
Low weight heparin or factor Xa inhibitor e.g. fondaparinux
Opiates and anti-emetics
May need IV nitrates for pain
Secondary prevention with statin, ACEI and beta blocker
If high risk of reoccurrence, revascularisaiton

71
Q

Medicaitons after an MI?

A 
75mg aspirin OD for life
Additional anti-playlet agent for over 1 year e.g. clopidogrel
Statins
ACEI
Beta blocker

Study Notes - Cardiology (25 decks)

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