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Cardiovascular system > Coronary syndromes > Flashcards

Coronary syndromes Flashcards

1
Q

How do plaques develop?

A

fatty streak - endothelial dysfunction, lipoprotein entry + modification, leukocyte recruitment, foam cell formation

plaque progression - smooth muscle cell migration, altered matrix synthesis and degradation

plaque disruption - disrupted plaque integrity, thrombus formation

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2
Q

CAD modifiable risk factors

A

smoking
hypertension
high cholesterol
diabetes

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3
Q

CAD non-modifiable risk factors

A

age
gender
family history
ethnicity

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4
Q

What calculator is used to assess cardiovascular disease risk?

A

QRISK2

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5
Q

What is atherosclerosis?

A

chronic disease characterised by inflammation and lipid deposition affecting the intima

affects large and medium sized muscular and elastic arteries

branch points and bifurcations are particularly at risk (due to more turbulent blood flow)

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6
Q

What 2 factors cause ischaemia in stable angina?

A

fixed vessel narrowing
abnormal vascular tone

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7
Q

What does the effect of a stenosis on blood flow depend on?

A

degree of narrowing of epicardial vessel

amount of compensatory vasodilation that the arterioles can achieve

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8
Q

What does abnormal vascular tone result in?

A

(endothelial dysfunction causes abnormal vascular tone)

results in:
- inappropriate vasoconstriction of coronary arteries
- loss of normal antithrombotic properties

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9
Q

What are 4 broad characteristics of angina?

A

location
character
precipitating and relieving factors
duration

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10
Q

Angina location

A

retrosternal
diffuse
may involve both sides of chest (L>R), arms (L>R), neck, lower jaw, upper abdomen

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11
Q

Angina character

A

pressure, tightness of heavy weight
sometimes burning

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12
Q

Angina precipitating and relieving factors

A

provoked by exertion (walking uphill)
more easily provoked after heavy meal/cold weather
rapid relief (2 mins) with GTN

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13
Q

Angina duration

A

attacks last a few minutes (not very brief or very prolonged)

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14
Q

Describe a stable angina artery

A

lumen narrowed by plaque
inappropriate vasoconstriction

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15
Q

Describe an unstable angina artery

A

plaque rupture
platelet aggregation
thrombus formation
unopposed vasoconstriction

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16
Q

Describe a variant angina artery

A

no overt plaques
intense vasospasm

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17
Q

Cardiac causes of recurrent chest pain

A

angina
pericarditis

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18
Q

GI causes of recurrent chest pain

A

reflux (GORD)
peptic ulcer
oesophageal spasm
biliary colic

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19
Q

MSK causes of recurrent chest pain

A

costochondral syndrome
cervical radiculitis

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20
Q

Diagnostic tests for coronary artery disease

A

ECG
Stress tests - exercise ECG, myocardial perfusion imaging, stress echocardiography, stress MRI
Imaging - Non-invasive = CT coronary angiogram, Invasive = coronary angiogram

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21
Q

Define myocardial ischaemia

A

reduced blood supply to the heart

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22
Q

Define myocardial infarction

A

necrosis of myocardial cells

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23
Q

What does transmural MI mean?

A

full thickness

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24
Q

What are acute coronary syndromes usually due to?

A

plaque rupture

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25
Q

What are the 2 types of plaques?

A

stable
vulnerable

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26
Q

Describe a stable plaque

A

thick fibrous cap, small lipid pool

27
Q

Describe a vulnerable plaque

A

thin fibrous cap, large lipid pool

28
Q

What does plaque rupture cause?

A

exposes thrombogenic extracellular matrix and lipid core to circulation
–> platelet aggregation and thrombus formation

29
Q

What are the 2 types of ACS?

A

ST elevation (STEMI)
Non-ST elevation (NSTEMI)

30
Q

How can an ECG appear in a STEMI? (and how does it change over time)

A

Acute = ST elevation
hours = ST elevation, reduced R wave, Q wave begins
days 1-2 = T wave inversion, Q wave deeper
days later = ST normalises, T wave inverted
weeks later = ST + T normal, Q wave persists

31
Q

How can an ECG appear in an NSTEMI? (and how does it change over time)

A

Acute = T wave inversion or ST depression
weeks later = ST + T normal, no Q waves

32
Q

Post MI complications

A

ACT RAPID

Arrhythmias
Congestive cardiac failure/cardiogenic shock
Thromboembolism

Rupture (ventricular free wall, septum, papillary muscle)
Aneurysm
Pericarditis
Ischaemia
Death/Dressler’s syndrome

main late complications = arrhythmias and heart failure

33
Q

If there is partial occlusion of a coronary artery, what is this called?

A

NSTEMI

34
Q

If there if complete occlusion of a coronary artery, what is this called?

A

STEMI

35
Q

Symptomatic treatment for stable coronary artery disease

A

lifestyle
drugs - antianginals, nitrates
revascularisation (eg. PCI)

36
Q

Prognostic benefit treatment for stable coronary artery disease

A

lifestyle (stop smoking)
drugs - statins, aspirin, beta blockers, ACE inhibitors
revascularisation eg. CABG

37
Q

Define ischaemia

A

inadequate oxygen supply to myocardial tissue

38
Q

What factors could affect supply of oxygen to myocardial tissue?

A

coronary stenosis
anaemia
lung problems

39
Q

What factors could affect demand of oxygen supply to myocardial tissue?

A

tachycardia
preload (venous return)
afterload (BP)
muscle mass (eg. hypertrophy, infarcted)
muscle contractility

40
Q

What investigations can be done to confirm angina?

A

exercise stress test (low sensitivity and specificity)
MIBI
CTCA (anatomical test)
stress MRI
dobutamine stress echo
coronary angiogram

CTCA (CT coronary angiogram) = first line for most patients

41
Q

What is PCI?

A

percutaneous coronary intervention

42
Q

Indications for PCI

A

stable angina:
- limiting symptoms despite 2 anti-anginals

ACS:
- NSTEMI = urgent
- STEMI = emergency treatment

43
Q

Indications for CABG

A

‘surgical disease’:
- left main stem
- LM equivalent
- proximal 3 vessel disease

especially if:
- left ventricular dysfunction
- diabetes
- complex disease (high risk score - syntax score)

44
Q

NSTEMI drugs

A

dual antiplatelet (aspirin, ticagrelor)
anticoagulant
beta blocker
statin

long term = consider ACE-i/ARB

45
Q

What would the troponin be in unstable angina?

A

near normal

46
Q

If chest pain radiates to back, what needs to be ruled out?

A

aortic dissection - tenni ball sign seen on CT

47
Q

What can PE cause a rise in?

A

troponin (due to right heart strain)

48
Q

What other events can cause ST elevation (other than STEMI)?

A

brain events (eg. subarachnoid haemorrhage)

49
Q

Modifiable biomedical risk factors for coronary heart disease

A

diabetes
high blood cholesterol
hypertension

50
Q

Lifestyle/behavioural risk factors for coronary heart disease

A

smoking
sedentary lifestyle
obesity
diet
alcohol
stress

51
Q

Non-modifiable risk factors for coronary heart disease

A

family history
gender
ethnicity
age

52
Q

What family history increases risk of coronary heart disease

A

1st degree female relative under 65
1st degree male relative under 55

risk increases 1.5x if one relative
risk increases 1.5-2x if more than one relative
familial hypercholesterolaemia

53
Q

Secondary prevention of coronary heart disease

A

anti-platelets (aspirin, clopidogrel, ticagrelor)
beta-blockers
statin
ACE-i
lifestyle modification
psychosocial factors
cardiac rehabilitation

54
Q

Lifestyle modifications to reduce blood pressure

A

weight loss
mediterranean diet
reduced salt intake
physical activity
moderate alcohol

55
Q

HDLs function

A

(high density lipoproteins)
carry cholesterol away from arteries and back to liver, then excreted from the body

56
Q

LDLs function

A

(low density lipoproteins)
build up in the walls of the arteries to form thick, hard deposits that narrow the arteries and make them less flexible

57
Q

Triglycerides function

A

main storage form of LDL

58
Q

What lifestyle modifications can improve lipid profile?

A

diet
aerobic exercise
resistance training

59
Q

What is obesity associated with?

A

raised BP
raised LDL and triglycerides
low HDL
impaired glucose tolerance
increased insulin resistance

60
Q

Diet modifications to reduce coronary heart disease risk

A

pile on fruit and vegetables
choose healthy fats
pick seeds, nuts and legumes
focus on fish and chicken over red meat
add herbs and spices rather than salt

61
Q

What is cardiac rehabilitation?

A

comprehensive, long-term programs involving medical evaluation, prescribed exercise, cardiac risk factor modification, education and counselling

designed to limit physiologic and psychological effects of cardiac illness, reduce the risk for sudden death or re-infarction, control cardiac symptoms, reverse/stabilise atherosclerotic process and enhance vocational status of patients

62
Q

6 core components of BACPR

A

health behaviour change and education
lifestyle risk factor management
psychosocial health
medical risk management
long-term strategies
audit and evaluation

63
Q

What is the heart manual?

A

home based exercise program
trained facilitators
inclusion/exclusion criteria

principles of self-management:
- gain understanding and acceptance of condition
- pace themselves
- set short, medium and long-term goals
- promote realistic exercise and activity
- self monitor progress and condition
- maintain behaviour change
- deal with setbacks

64
Q

What types of fat should you eat?

A

MUFA/PUFA (monounsaturated/polyunsaturated fatty acids)

reduce amounts of saturated fat eaten

Cardiovascular system (33 decks)

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