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Cardiac rehabilitation > Cardiac event and intervention > Flashcards

Cardiac event and intervention Flashcards

1
Q

what makes up the left coronary artery?

A

circumflex

left anterior descending

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2
Q

what makes up the right coronary artery?

A

marginal artery

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3
Q

what are the most important factors that can effect the myocardial blood flow? (2)

A

changes in aortic pressure and compression of myocardial vessels during systole

changes in oxygen demand

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4
Q

what is the coronary perfusion problem?

A

pressure in the muscle tissue during systole opposes blood flow. the effect is maximal in the deeper layers thus harder for blood to flow through the deeper layers

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5
Q

what are the limits to coronary perfusion? (4)

A

Tachycardia

low diastolic pressure

ischemic heart disease

increased HR

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6
Q

what are the 3 basic steps in atherosclerosis?

A
  1. tear in artery wall
  2. fatty material is deposited in vessel wall
  3. narrowed artery becomes blocked by a blood clot
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7
Q

what can atherosclerosis cause?

A

stroke and heart attack

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8
Q

what are the two type of cholesterol involved in atherosclerosis?

A

LDL-C (bad)

HDL-C (good)

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9
Q

what are the three layers of an artery wall?

A

tunica intima

tunica media

tunica adventitia

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10
Q

Name some risk factors for atherosclerosis

A

smoking, high BP, diabetes

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11
Q

How does the body try to defend against LDL-C?

A

activating macrophages to consume the LDL-C

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12
Q

what are foam cells?

A

enlarged cholesterol enriched cells

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13
Q

what is a plaque?

A

fatty streaks surrounded by a fibrous capsule

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14
Q

as the plaque grows, how does the body try to preserve blood flow in the artery?

A

The plaque expands in the elastic layer which stretches in order to keep the size of the artery the same

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15
Q

what is a symptom of continued plaque growth?

A

angina

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16
Q

what ion makes the plaque hard and inflexible reducing the ability for expansion?

A

calcium

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17
Q

what is the final stage of atherosclerosis?

A

as the plaque grows it squeezes the blood through another smaller gap which results in increased pressure which may damage the capsule cover which may then rupture leading to a blood clot which can completely block the artery

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18
Q

what is the name of the inner most layer of the artery?

A

The endothelium

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19
Q

name 3 characteristics of the endothelium

A

permeable

produces growth factors

releases platelets aggregation

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20
Q

In atherosclerosis what causes the endothelium to release leukocyte adhesion molecules?

A

LDL oxidised

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21
Q

what type of components does oxidised LDL have?

A

deformed lipoprotein components

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22
Q

what do the surface proteins do?

A

make the endothelium sticky rater than smooth

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23
Q

what are the surface proteins called?

A

vascular cell adhesion molecule

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24
Q

what cells adhere to the VCAM

A

monocytes and lymphocytes

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25
Q

what do monocytes differentiate into and what does this create?

A

macrophages to create more foam cells

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26
Q

what do foam cells do?

A

release chemical messengers that cause m-RNA to produce further inflammatory factors that cause further tissue damage to area

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27
Q

what cells release growth factors that cause proliferation and attraction of smooth muscle cells to area

A

T-cells

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28
Q

what has it been suggested that MI is caused by and how?

A

an inflammatory response - They release inflammatory cytokines (eg TNF) and these reduce stability of plaque making it more likely to rupture

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29
Q

Why do VCAM exacerbate the prothrombotic risk?

A

they make it sticky

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30
Q

What causes instability of the fatty plaque? (3)

A

the stretch of the artery

localised increase in blood pressure

release protease - weakening the wall

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31
Q

what damages the endothelial layer in the first place?

A

Normal microvascular wear and tear

Viral attack

High blood pressure

Turbulent flow

Free radicals

Carbon monoxide

Elevated glucose and blood lipids

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32
Q

where does atherosclerosis lesions often occur and why?

A

at artery intersections of curves - blood flow speed or direction changes creating turbulence

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33
Q

what is stenosis?

A

the narrowing

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34
Q

if we are inactive how blocked can our artery be to still deliver enough blood?

A

90%

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35
Q

what type of plaque is more likely to rupture?

A

fatty plaque

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36
Q

what can make a plaque more stable?

A

a fibrous cap

37
Q

what are the 8 events leading to an MI?

A
  1. atherosclerosis
  2. plaque rupture
  3. platelet aggregation
  4. thrombus formation
  5. vessel occlusion
  6. vasospasm
  7. distal ischemia
  8. ischaemic complications
38
Q

what are the classic symptoms of an acute MI?

A

intense, oppressive chest pressure radiating in left arm

39
Q

what is stable angina?

A

chest pain during exertion resulting from myocardial schema

40
Q

what does an ECG wave show in stable angina?

A

normal, T-wave changes, or ST depression

41
Q

what is unstable angina?

A

chest pain when inactive

42
Q

what does an ECG show with unstable angina?

A

normal, T-wave changes, or ST depression

43
Q

what is ischaemia associated with on an ECG?

A

inverted T waves or S-T segment depression

44
Q

what is non-STEMI and what does it show on an ECG?

A

partial or intermittent blockage of the artery. May show ST depression

45
Q

what is STEMI and what does it show on an ECG?

A

Caused by complete and persisting blockage of the artery - generally associated with S-T segment elevation and T-wave inversion

46
Q

what is an infarct generally associated with on an ECG?

A

Q waves

47
Q

What is ischaemia?

A

ST depression

48
Q

is the ischaemia slow or fast to repolarise?

A

Slow

49
Q

what ion does the cell need to depolarise/repolarise?

A

ATP

50
Q

what ion is there a high concentration of inside the myocyte?

A

K (potassium)

51
Q

what ion is there a high concentration of outside the myocyte?

A

Na (sodium)

52
Q

what is the resting membrane potential?

A

-90mV

53
Q

what causes the myocyte cell to polarize?

A

slow leakage of K from in to out the cell

54
Q

what does Ischaemia do to ATP availability?

A

reduces it

55
Q

what happens to the K+ channels with low ATP availability?

A

K+ channel open

56
Q

what happens when the K+ channels open?

A

K+ quickly leaks out triggering depolarisation then Ca and Na ions flood inwards

57
Q

what happens to the K:Na pump activity with loa ATP availability?

A

reduces the K:Na pump activity - thus K ions increase outside the cell reducing the gradient and cells stay positive for longer

58
Q

At what phase does the ischemic region generate electrical currents?

A

Depolarized

59
Q

what does this pocket of positive electrical signal do?

A

elevates baseline voltage

60
Q

How far below baseline does theST segment depression need to be?

A

> 1mm below baseline

61
Q

what can downsloping ST segment be caused by?

A

digoxin

62
Q

what can upward sloping ST segment depression be caused by?

A

exercise

63
Q

what is injury generally associated with in regard to ST?

A

S-T segment elevation due to broken sodium channels

64
Q

what is normal depolarisation?

A

endocardium to epicardium

65
Q

what is normal depolarisation?

A

epicardium to endocardium

66
Q

what wave is infarction generally associated with?

A

Q waves and T wave inversion

67
Q

what’s a pathological Q wave?

A

Q waves of more than 2mm

68
Q

what is the relationship between EF and subsequent death?

A

Inverse

69
Q

how long do we have to avoid ischemic cells dying?

A

60 minutes

70
Q

how many minutes of ischemia is required for irreversible injury?

A

30 minutes

71
Q

after a heart attack what enzymes do we see a certain increase in? (2)

A

Creatine Kinase and lactate dehydrogenase

72
Q

why do enzymes end up in the blood with cell death?

A

Hole developed in cell membrane thus contents leak dependent on size, solubility

73
Q

what are anti-thrombotic and give an example

A

clot busting drugs e.g. antiplatlet agents (tpa)

74
Q

name some anti-ischemics

A

oxygen, B-blockers, nitrates

75
Q

what is a repercussion drug?

A

PTCA

76
Q

what happens in the first 4-6 hours post-myocardial infarction?

A

poor contraction, loss of systolic power

77
Q

what happens in the 7 days post-myocardial infarction? (3)

A

inflammation, bruising, thinning of ventricular wall and enlargement of infarct site

78
Q

what happens 6-12 weeks post-myocardial infarction?

A

Necrosis (congestive heart failure)

79
Q

What might scarring of the heart cause?

A

Increased stiffness

80
Q

What are the 4 main pharmacological treatments used for MI?

A

Blood thinners
ACE inhibitors
B-blockers
Cholesterol lowering drugs (statins)

81
Q

Give an example of a blood thinner

A

Aspirin

82
Q

what do ACE inhibitors do?

A

decrease peripheral resistance = reduce BP and less heart work

83
Q

what does a angiogram do?

A

Examines any clogged or damaged arteries

84
Q

What does a transluminal extraction extraction device do to plaque in the artery?

A

cuts away at the plaque and the lose plaque is sucked into a tube through a vacuum

85
Q

what does a rotational extraction device do to plaque in the heart?

A

spins at a high speed and pulverises plaque, which is then safely washed away in the blood stream

86
Q

what does CABG stand for?

A

coronary artery bypass graft

87
Q

what is CABG?

A

a procedure to bypass a blocked section of a coronary artery and to deliver oxygen to the heart

88
Q

Name some complications of heart surgery. (5)

A 
Wound infection 
MI 
stroke 
memory loss 
blood clots

Cardiac rehabilitation (13 decks)

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