CVS Session 10 Flashcards Preview

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Flashcards in CVS Session 10 Deck (91):
1

How is cardiovascular chest pain located?

Central

2

What type of pain is caused by myocardial ischaemia?

Tightening and diffuse

3

What is the typical radiation of myocardial ischaemic pain?

L and/or R arms/shoulders
Neck
Jaw
Back
Epigastrium

4

What type of pain is caused by pericarditis?

Sharp

5

What type of pain is caused by aortic dissection?

Tearing

6

Where does the pain from an aortic dissection radiate to?

Backwards b/w shoulder blades
Down spine - following aorta

7

Where is respiratory chest pain located?

Lateral - localised to affected side

8

What is pleuritic pain?

Pain which is worse on inspiration and coughing

9

Give three causes of respiratory chest pain.

Pneumonia
Pulmonary embolism
Pneumothorax

10

Where is GI chest pain localised?

Chest and epigastrium

11

What makes GI chest pain worse?

Bending and/or lying down

12

Give four causes of GI chest pain.

Reflux oesophagitis
Gastric disease
Gall bladder disease
Pancreatic disease

13

What indicates that chest pain is due to musculoskeletal injury?

Hx of trauma
Hx of excessive use
Movements may increase pain

14

Give three MSK causes of chest pain.

Trauma
Muscle pain
Bone metastases

15

What is the most common cause of myocardial ischaemia?

Atheromatous coronary artery disease

16

What does coronary blood flow depend on?

Coronary artery resistance
Perfusion pressure (diastolic BP)

17

What does myocardial oxygen supply depend on?

Coronary blood flow
Oxygen carrying capacity of blood

18

What does myocardial oxygen demand depend on?

HR
Wall tension
Contractility

19

What determines wall tension?

Pre load
After load

20

Give a circumstance when after load will be increased.

Pumping against stenosis

21

Which area of cardiac muscle is most vulnerable to ischaemia?

Subendocardial

22

Describe the collateral circulation of the heart.

Absent between major arteries
Present between smaller coronary arteries and arterioles

23

How does the collateral circulation change with ischaemia?

Expansion and development of new collaterals over time

24

What can cause IHD if coronary circulation is perfect?

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

25

What are non-modifiable risk factors for CAD?

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

26

What are modifiable risk factors for CAD?

Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes mellitus

27

What is the structure of a stable atheromatous plaque?

Atheroma with a small necrotic core and thick fibrous cap

28

How can a stable atheromatous plaque present clinically?

Asymptomatic
Stable angina

29

Why does thyrotoxicosis increase myocardial oxygen demand?

Increased HR
Increased BMR

30

Is there myocyte injury and necrosis in stable angina?

Nope

31

What is used to determine the cause of chest pain?

Anatomical sieve

32

What is stable angina?

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

33

What does stable angina indicate?

High risk of acute coronary syndrome

34

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

~5 mins

35

What are the specific signs of stable angina on examination?

There are none

36

What is the clinical diagnosis of angina based on?

Hx

37

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

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

38

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

Exercise stress test

39

Describe the exercise stress test for stable angina.

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

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

Speed of development of ST depression correlates

41

What are the 5 mechanisms of stable angina treatment?

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

42

How can oral nitrates be used to treat stable angina?

Decrease preload

43

Why are calcium channel blockers used to treat stable angina?

If beta-blockers cannot be tolerated they decrease afterload

44

How can beta-blockers treat stable angina?

Decrease HR and myocardial contractility

45

How is PCI used to treat stable angina?

Percutaneous coronary intervention by stent
Femoral puncture --> aorta --> coronary artery

46

Which blood vessels can be used in CABG?

Radial artery
Internal mammary artery
Reversed saphenous vein

47

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

So the valves open in the right way

48

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

Angiography

49

Why are statins given to stable angina patients?

Decrease LDL levels
Reduce progression
Less necrotic core

50

Why is aspirin given in stable angina?

Prevent thrombosis

51

What is acute coronary syndrome?

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

How does ACS present?

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

53

Which three conditions does ACS include?

STEMI
Unstable angina
NSTEMI

54

How does sudden plaque fissuring cause a STEMI?

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

55

How does sudden plaque fissuring cause unstable angina/NSTEMI?

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

56

What treatments are used for a STEMI?

Aspirin and colpidogrel
IV nitrates
Beta-blockers
ACEI
Statins

57

Why are ACEI used in treatment for a STEMI?

To prevent harmful heart remodelling in L ventricle dysfunction

58

Which areas of the heart are affected by a STEMI?

Sub-endocardial to sub-epicardial

59

What are the three types of unstable angina?

Crescendo
Angina at rest
Recent onset of new, effort limiting

60

What is crescendo unstable angina?

More frequent, more severe and longer lasting angina pain

61

What treatments are used for unstable angina/NSTEMI?

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

62

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

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

63

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

Subendocardial areas

64

What ECG changes are seen in NSTEMI and unstable angina?

ST depression

65

What percentage of arterial occlusion is considered total artery occlusion?

90

66

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

Cardiac troponin I and T

67

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

4 hrs after onset of pain

68

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

18-36 hrs after initial pain

69

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

Up to 10-14 days

70

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

V. Specific and sensitive

71

What is the cardiac isoenzyme of creating kinase?

CK-MB

72

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

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

73

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

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

74

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

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

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

Decrease mortality
Decrease risk of reinfarction

76

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

Increase survival

77

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

Management of risk factors

78

Why are pathological Q waves seen in myocyte damage?

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

79

What is the criteria of a pathological Q wave?

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

80

Why are pathological Q waves not always deep?

Not always followed by R wave

81

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

Ischaemia

82

Describe the progression of ECG changes with myocyte damage.

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

What are the complications of MI?

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

84

What is cardiogenic shock?

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

85

What causes heart failure as a complication of MI?

Decreased contractility

86

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

II, III, aVF
RCA

87

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

V1-V2
LAD

88

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

Anteroapical
LAD (distal)

89

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?

Anterolateral
Cm

90

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

Extensive anterior
I, aVL, V2-V6

91

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

True posterior
Heightened R wave