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Semester 2 > CVS Session 10 > Flashcards

CVS Session 10 Flashcards

1
Q

How is cardiovascular chest pain located?

A

Central

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2
Q

What type of pain is caused by myocardial ischaemia?

A

Tightening and diffuse

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3
Q

What is the typical radiation of myocardial ischaemic pain?

A 
L and/or R arms/shoulders
Neck
Jaw
Back
Epigastrium
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4
Q

What type of pain is caused by pericarditis?

A

Sharp

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5
Q

What type of pain is caused by aortic dissection?

A

Tearing

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6
Q

Where does the pain from an aortic dissection radiate to?

A

Backwards b/w shoulder blades

Down spine - following aorta

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7
Q

Where is respiratory chest pain located?

A

Lateral - localised to affected side

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8
Q

What is pleuritic pain?

A

Pain which is worse on inspiration and coughing

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9
Q

Give three causes of respiratory chest pain.

A

Pneumonia
Pulmonary embolism
Pneumothorax

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10
Q

Where is GI chest pain localised?

A

Chest and epigastrium

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11
Q

What makes GI chest pain worse?

A

Bending and/or lying down

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12
Q

Give four causes of GI chest pain.

A

Reflux oesophagitis
Gastric disease
Gall bladder disease
Pancreatic disease

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13
Q

What indicates that chest pain is due to musculoskeletal injury?

A

Hx of trauma
Hx of excessive use
Movements may increase pain

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14
Q

Give three MSK causes of chest pain.

A

Trauma
Muscle pain
Bone metastases

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15
Q

What is the most common cause of myocardial ischaemia?

A

Atheromatous coronary artery disease

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16
Q

What does coronary blood flow depend on?

A 
Coronary artery resistance
Perfusion pressure (diastolic BP)
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17
Q

What does myocardial oxygen supply depend on?

A

Coronary blood flow

Oxygen carrying capacity of blood

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18
Q

What does myocardial oxygen demand depend on?

A

HR
Wall tension
Contractility

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19
Q

What determines wall tension?

A

Pre load

After load

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20
Q

Give a circumstance when after load will be increased.

A

Pumping against stenosis

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21
Q

Which area of cardiac muscle is most vulnerable to ischaemia?

A

Subendocardial

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22
Q

Describe the collateral circulation of the heart.

A

Absent between major arteries

Present between smaller coronary arteries and arterioles

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23
Q

How does the collateral circulation change with ischaemia?

A

Expansion and development of new collaterals over time

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24
Q

What can cause IHD if coronary circulation is perfect?

A 
Severe hypotension
Non-atheromatous causes of coronary artery narrowing 
Severe anaemia
Tachycardia
Aortic stenosis
Thyrotoxicosis
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25
Q

What are non-modifiable risk factors for CAD?

A

Age
Male gender - females catch up after menopause
FHx - especially in 1st degree relatives at an early stage

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26
Q

What are modifiable risk factors for CAD?

A

Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes mellitus

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27
Q

What is the structure of a stable atheromatous plaque?

A

Atheroma with a small necrotic core and thick fibrous cap

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28
Q

How can a stable atheromatous plaque present clinically?

A

Asymptomatic

Stable angina

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29
Q

Why does thyrotoxicosis increase myocardial oxygen demand?

A

Increased HR

Increased BMR

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30
Q

Is there myocyte injury and necrosis in stable angina?

A

Nope

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31
Q

What is used to determine the cause of chest pain?

A

Anatomical sieve

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32
Q

What is stable angina?

A

Transient ischaemia during periods of high oxygen demand
Relieved when demand stops
Can progress to severe, fixed narrowing
Predictable pain

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33
Q

What does stable angina indicate?

A

High risk of acute coronary syndrome

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34
Q

How quickly is the ischaemic pain of stable angina relieved by rest or nitrates?

A

~5 mins

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35
Q

What are the specific signs of stable angina on examination?

A

There are none

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36
Q

What is the clinical diagnosis of angina based on?

A

Hx

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37
Q

What signs of risk factors for stable angina may been seen on presentation?

A

High B.P.
Corneal arcus
Signs of atheroma elsewhere
Left ventricle dysfunction

38
Q

What test can be used if the diagnosis of stable angina is uncertain?

A

Exercise stress test

39
Q

Describe the exercise stress test for stable angina.

A

Patient has ECG continuously taken whilst undertaking graded exercise on a treadmill
Stop when target HR reached/ECG changes/chest pain/ other problems (arhythmias, low BP)
+ve if ST depression > 1 mm

40
Q

How can the exercise stress test be used to determine the prognosis of stable angina?

A

Speed of development of ST depression correlates

41
Q

What are the 5 mechanisms of stable angina treatment?

A

Decease preload and afterload
Decrease HR
Decrease myocardial contractility
Increase blood flow by revascularisation
Prevent progression and thrombosis and stabilise plaque

42
Q

How can oral nitrates be used to treat stable angina?

A

Decrease preload

43
Q

Why are calcium channel blockers used to treat stable angina?

A

If beta-blockers cannot be tolerated they decrease afterload

44
Q

How can beta-blockers treat stable angina?

A

Decrease HR and myocardial contractility

45
Q

How is PCI used to treat stable angina?

A

Percutaneous coronary intervention by stent

Femoral puncture –> aorta –> coronary artery

46
Q

Which blood vessels can be used in CABG?

A

Radial artery
Internal mammary artery
Reversed saphenous vein

47
Q

Why must the saphenous vein be reversed for use in CABG?

A

So the valves open in the right way

48
Q

Which imaging technique influences whether PCI or CABG is used for revascularisation?

A

Angiography

49
Q

Why are statins given to stable angina patients?

A

Decrease LDL levels
Reduce progression
Less necrotic core

50
Q

Why is aspirin given in stable angina?

A

Prevent thrombosis

51
Q

What is acute coronary syndrome?

A

A medical emergency when an atheromatous plaque fissure causes a sudden reduction in artery lumen which may be sufficient to cause myocyte injury/necrosis

52
Q

How does ACS present?

A

Same pain as angina but much more severe
May have had preceding symptoms of atheroma
Can be asymptomatic until point of rupture

53
Q

Which three conditions does ACS include?

A

STEMI
Unstable angina
NSTEMI

54
Q

How does sudden plaque fissuring cause a STEMI?

A

Occlusion complete
Persistent
Large area of myocardium w/out collateral circulation affected
Severe ischaemia w/myocardial necrosis

55
Q

How does sudden plaque fissuring cause unstable angina/NSTEMI?

A 
Non occlusive thrombus
Brief occlusion
Small area of myocardium affected
Collaterals present
Less severe ischaemia +/- necrosis
56
Q

What treatments are used for a STEMI?

A 
Aspirin and colpidogrel
IV nitrates
Beta-blockers
ACEI
Statins
57
Q

Why are ACEI used in treatment for a STEMI?

A

To prevent harmful heart remodelling in L ventricle dysfunction

58
Q

Which areas of the heart are affected by a STEMI?

A

Sub-endocardial to sub-epicardial

59
Q

What are the three types of unstable angina?

A

Crescendo
Angina at rest
Recent onset of new, effort limiting

60
Q

What is crescendo unstable angina?

A

More frequent, more severe and longer lasting angina pain

61
Q

What treatments are used for unstable angina/NSTEMI?

A 
Anticoagulants - heparin
Non-urgent PCI/CABG
Antiplatelets - aspirin
Statins
ACEI
62
Q

How does the presence of biomarkers differ between STEMI, NSTEMI and unstable angina?

A

STEMI: +ve
NSTEMI: +ve
Unstable angina: -ve

63
Q

Which area of the heart is affected in NSTEMI/unstable angina?

A

Subendocardial areas

64
Q

What ECG changes are seen in NSTEMI and unstable angina?

A

ST depression

65
Q

What percentage of arterial occlusion is considered total artery occlusion?

A

90

66
Q

Which proteins present in myocytes that are important in the myosin/actin interaction are released in myocyte death?

A

Cardiac troponin I and T

67
Q

When are cardiac troponin I and T seen in the blood following MI?

A

4 hrs after onset of pain

68
Q

When do cardiac troponin I and T levels peak following MI?

A

18-36 hrs after initial pain

69
Q

How long does it take for cardiac troponin I and T to be returned to normal levels in the blood?

A

Up to 10-14 days

70
Q

Why are cardiac troponin T and I a good biomarker for detecting MI?

A

V. Specific and sensitive

71
Q

What is the cardiac isoenzyme of creating kinase?

A

CK-MB

72
Q

When would CK-MB be used as a biomarker of myocyte damage?

A

When troponins are unavailable e.g. when new episodes of chest pain occur w/in 10 days of initial MI

73
Q

How do the levels of CK-MB vary over time?

A

Rise 3-8 hrs after onset of pain
Peak at 24 hrs
Back to normal after 48-72 hrs

74
Q

What is the typical Hx given by a patient suffering an MI?

A

Central, crushing chest pain w/typical radiation
‘Feeling of impending death’
Persistant pain often w/ no precipitant
Autonomic features e.g. nausea, vomiting, faint
Signs of LV dysfunction - breathlessness, lung base crackles, low BP, S3/S4

75
Q

Why are aspirin, beta-blockers and statins used as long term treatments for MI?

A

Decrease mortality

Decrease risk of reinfarction

76
Q

Why are ACEI used as a long term treatment following MI?

A

Increase survival

77
Q

What non-medicine long term treatment can be used following an MI?

A

Management of risk factors

78
Q

Why are pathological Q waves seen in myocyte damage?

A

‘Window’ created by necrotic tissue so don’t see depol moving towards view

79
Q

What is the criteria of a pathological Q wave?

A 
Wide = >1 small square wide
Deep = >25% of QRS
80
Q

Why are pathological Q waves not always deep?

A

Not always followed by R wave

81
Q

What causes the T wave inversion on an ECG showing myocyte damage?

A

Ischaemia

82
Q

Describe the progression of ECG changes with myocyte damage.

A

Hyperacute T-wave in mins/hrs –> ST elevation in 0-12 hrs –> Q wave in 1-12 hrs –> ST elevation w/T wave inversion in 2-5 days –> recovery after weeks-months

83
Q

What are the complications of MI?

A 
Sudden cardiac death - V. Fib/asystole
Arrhythmias
Heart block
Re-entry circuits/ increased automaticity --> V. tachy/fib
Heart failure
Cardiogenic shock
84
Q

What is cardiogenic shock?

A

When >40% of myocardium is infarcted –> severely decreased cardiac output –> systolic BP

85
Q

What causes heart failure as a complication of MI?

A

Decreased contractility

86
Q

If the area of infarction in MI is inferior, which ECG leads and which artery will be affected?

A

II, III, aVF

RCA

87
Q

If the area of infarction in MI is anteroseptal, which ECG leads and coronary artery will be affected?

A

V1-V2

LAD

88
Q

If changes are visible in the V3-V4 ECG leads, which area of the heart and coronary artery have been affected?

A

Anteroapical

LAD (distal)

89
Q

If the I, aVL, V5-V6 ECG leads have noticeable changes in them following MI, which area of the heart and coronary artery have been affected?

A

Anterolateral

Cm

90
Q

If the proximal LCA has been occluded in MI, which area of the heart and ECG leads will be affected?

A

Extensive anterior

I, aVL, V2-V6

91
Q

If the RCA is occluded in MI, which area of the heart ands hat change is seen in V1?

A

True posterior

Heightened R wave

Semester 2 (45 decks)

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