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BDS2 - BAMS > acute coronary syndromes > Flashcards

acute coronary syndromes Flashcards

1
Q

what are the 2 processes in which acute coronary syndromes can occur

A
  • blood vessel narrowing

- blood vessel occlusion

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2
Q

what is blood vessel narrowing

A
  • vessel narrowed due to an atheroma forming in the vessel blocking part of it
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3
Q

what is the consequence of blood vessel narrowing

A
  • small narrowing can have a large effect

- inadequate O2 delivery for tissue needs, causing cramp in the affected muscle/tissue

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4
Q

what can happen when you have narrowing of blood vessels

A
  • can get a pain in your chest (angina) when you exercise beyond the ability for O2 to get round body
  • it is completely reversible at first but over time it will lead to damage to the heart (hypoxia) due to lactic acid build up
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5
Q

what is blood vessel occlusion

A
  • no delivery of O2 to tissue
  • have atherosclerotic lesion which causes a change to the endothelial wall of blood vessel causing them to open to the blood flow which platelets then stick to ad eventually block the flow or break off and become lodged elsewhere
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6
Q

what can happen due to blood vessel occlusion

A
  • tissue death

- instead of hypoxia you get cell death as their is no O2

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7
Q

what is more severe; blood vessel occlusion or narrowing

A
  • occlusion
  • has more severe pain due to death of tissue/muscle
  • get loss of function of that tissue
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8
Q

what is the reversible side of ischaemia

A

angina and peripheral vascular disease

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9
Q

what is a myocardial infarction

A

tissue death as a consequence of blockage of arteries

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10
Q

what can be different about the diagnosis of acute coronary syndromes

A

different patients feel different things

- need their medical history

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11
Q

what are the 2 ECG findings for ACS

A
  • STEMI = ST segment elevation myocardial infarction

- NSTEMI= non-ST segment elevation myocardial infarction

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12
Q

what are the biomarkers of myocardial infarction

A
  • troponin mainly
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13
Q

what is atherosclerosis

A
  • gradual build up of plaque in blood vessels which eventually cause the vessel to become blocked or the atherosclerotic lesion can break off and become lodges elsewhere in the body
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14
Q

what can atherosclerosis lead to

A
  • unstable angina
  • acute myocardial infarction
  • death from coronary disease
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15
Q

where do coronary arteries sit

A

they come away from the aorta behind where the artic valve opens

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16
Q

what can sometimes happen in an increased HR

A

can miss the coronary artery as there is less time for the blood to flow through

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17
Q

what can happen in coronary artery disease in relation to atherosclerosis

A
  • can make blood vessels narrower

- makes heart function harder than it should be

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18
Q

what is angina pectoris

A

reversible ischaemia of one or more coronary arteries

- narrowing of one or more coronary arteries

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19
Q

where is angina pectoris

A

angina in the chest

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20
Q

what makes ‘classical’ angina worse

A

exercise

- chest pain that feels like a heart attack but will stop at rest

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21
Q

what is ‘unstable’ angina

A
  • symptoms at rest with no biomarkers
  • angina pain with no exercise
  • can have loose flap of atherosclerotic tissue that flaps down then up, narrowing the vessel
  • don’t have permanent muscle damage but presents like a MI
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22
Q

what are the symptoms of angina

A
  • described as a ‘central crushing pain’
  • radiation to the arm, back or jaw possible
  • pain is blood vessel pain = autonomic NS in heart, mainly on the left side as left forms the aorta etc and embryologically formed the same
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23
Q

what are some ‘classical’ angina symptoms

A
  • no pain at rest
  • pain with certain level of exercise = pain felt once used up all O2 around the heart
  • pain relieved by rest
  • patient lives within limits of tolerance = they will learn what they are able to do
  • gradual deterioration as progresses = will only be able to do less and less exercise before resting
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24
Q

what are some ‘classical’ angina signs

A
  • often none

- occasionally hyper dynamic circulation = anaemia, hyperthyroidism, hypovolaemia

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25
Q

what are investigations for angina

A
  • ECG = at both rest and exercise, shows area of myocardial ischaemia, angina will cause ST segment depression
  • need to eliminate other possible diseases
  • angiography
  • echocardiography
  • isotope studies (function assessment)
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26
Q

what does a coronary artery blockage do

A

restrict blood flow

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27
Q

what are some angina treatment

A
  • reduce O2 demands of the heart

- increasing O2 delivery to tissues

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28
Q

how can you reduce O2 demand to the hear

A
  • reduce after load (blood pressure)

- reduce preload (venous pressure)

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29
Q

how can you increase O2 demand to the tissues

A
  • dilate blocked/narrowed vessels = angioplasty, stretches bv’s
  • bypass blocked/narrowed vessels = CABG
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30
Q

what is CABG

A
  • coronary artery bypass grafting
  • add extra bv to avoid damaged one
  • it is a one off operation as there is a risk of the heart not starting again
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31
Q

why is angioplasty not good by itself

A
  • it does not keep the vessel open once stretched
  • need to use something that will maintain stretch
  • use stent = angioplasty and stenting is much better fix
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32
Q

what is some non-drug therapy for angina

A
  • explanation of illness = live within limitations

- modify the risk factors = stop smoking, graded exercise programme, improve diet/ control cholesterol

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33
Q

what is the drug therapy used for angina

A
  • reduce MI risk = use aspirin
  • for hypertension = use diuretics, Ca channel antagonists, ace inhibitors, beta blockers
  • to reduce preload = use nitrates, short acting and long lasting
  • for emergency treatment = use GTN spray/tablet, but has a short shelf life
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34
Q

what do nitrates do to help angina

A
  • reduce preload

- dilate coronary vessels

35
Q

what is the surgical therapy used for angina

A
  • CABG

- angioplasty and stenting

36
Q

how does CABG work

A
  • get part of patients leg vein (big vein - femoral)
  • need to ensure it is put in the correct way as veins have valves only flow in one direction
  • benefit of CABG not always obtained
  • around 10 year benefit
  • has a mortality risk as it is a major surgery
37
Q

how does angioplasty and stenting work

A
  • put tube in and dye to find plaque
  • put ballon in to flatten plaque
  • then slide a metal slot in where the balloon was and slot should clock once locked into place
  • deflate balloon and remove
  • lower risk procedure but has lower benefit
  • there is a risk fo vessel rupture though during procedure
  • is a PCI
38
Q

what is a PCI

A

percutaneous intervention

39
Q

what is peripheral vascular disease

A

angina of the tissues

40
Q

where is peripheral vascular disease most common

A

lower limb

- atheroma forms in the femoral or popliteal vessels

41
Q

what is claudication

A

condition where cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries

42
Q

what is a common symptom of peripheral vascular disease

A

claudication pain in the lower limb on exercise and stops at rest

43
Q

how is peripheral vascular disease managed

A

same way as angina

44
Q

what does PVD indicate

A

indicates arteriopath - you are at risk of an MI

45
Q

what can be an effect of PVD

A
  • limitation of function
  • poor wound healing
  • tissue necrosis and gangrene = leading to amputation
46
Q

how can PVD cause poor wound healing

A
  • femoral artery supplies all blood to the leg so if it has poor blood flow, then cuts etc may not heal due to lack of O2 and can cause limbs to be amputated
  • so if not treated can have major consequences
47
Q

what aggravates PVD

A

aggravated by CV risk factors

48
Q

what is an atheroma in vessels

A
  • ulcerated plaques with platelet aggregates

- thrombosis occurs on the surface

49
Q

how does thrombosis block vessels

A

it can enlarge to block the vessels

50
Q

what happens to the plaque once it has formed

A
  • detach from the vessel wall
  • travel downstream and block vessels
  • cause no blood flow to that tissue causing infarction
51
Q

what are the difference infarctions that can occur

A
  • heart = coronary artery atheroma
  • limb = femoral and popliteal arteries
  • brain = carotid arteries
52
Q

what is a myocardial infarction

A

result of a blocked artery (left anterior descending coronary artery for example)
- in the heart can get areas of blockage and then any tissue under that area will die because it is receiving no blood supply

53
Q

how many types of MI can you get

A

5

54
Q

what is the most common type of MI

A

type 1

55
Q

what is a type 1 MI

A
  • spontaneous

- primary coronary event = plaque fissure/ rupture

56
Q

what is a type 2 MI

A
  • MI secondary to ischaemia
  • balance of supply and demand
  • chronic ischaemia for a long time = will get infarction eventually
57
Q

what is a type 3 MI

A
  • sudden death
  • from symptoms of ischaemia and evidence of ST elevation of thrombus (PCI/autopsy)
  • chest pain then fall over and die
  • not due to dead tissue but from electrical conductivity being upset so there is an abnormal rhythm caused
58
Q

what is a type 4 or 5 MI

A
  • caused from CV treatment
  • MI from PCI for example
  • such as balloon in stenting blown up inside you and gets stuck for too long then tissue will be blocked
  • type 4 = from PCI
  • type 5 = from CABG
  • like a normal blockage but from a CV treatment
59
Q

what are some treatments for infarction

A
  • reduce tissue loss from necrosis

- prevent a further episode

60
Q

how can you reduce tissue loss from necrosis

A
  • open blood flow to ischaemic tissue = by thrombolysis (drugs given intravenously), or by angioplasty and stenting (good if able to do in short amount of time)
  • bypass obstruction = CABG, femoral popliteal bypass
61
Q

how long do you have to do a angioplasty and stenting from occurrence of MI

A
  • 3hrs
62
Q

how long do you have to do thrombolysis from event of MI

A
  • 6hrs
63
Q

how can you prevent a further MI episode

A
  • risk factor management = in the long run, more muscle functioning means fewer complications, MI will lead onto HF if lose a lot of muscle
  • aspirin = has no effect on current HA but will prevent a second one from occurring
64
Q

what is done to treat a limb infarction

A
  • medical/surgical emergency
  • thrombolysis
  • easier to get to than the heart so are more likely to be able to salvage tissue
65
Q

what can occur from limb infarctions

A
  • may lead to acute limb necrosis
  • if don’t get attention quickly (3-6hrs) from infarction then tissue will die
  • may need amputation
66
Q

what is another name for a brain infarction

A

stroke

- usually an embolism from atheroma, occasionally a cerebral bleed

67
Q

why is treatment of a stroke complicated

A
  • because of the 2 possibilities it could be = stroke or bleed
68
Q

what is a transient ischaemic attack

A

short duration stroke (less than 24hours)

  • an athero breaks off and moves up and blocks part of the brain
  • it is removed in the same way as a normal clot so within 30 minutes patient will begin to feel better and then within 24 hours they will be back to normal
  • warns you are at risk of a proper stroke though
69
Q

what is a common deficit caused by a stroke

A
  • usually loss of function
  • depends on the brain region involved
  • usually some recovery with time
70
Q

what is the treatment for a stroke

A
  • specialist centres/trials
71
Q

what are the symptoms and signs of an MI

A
  • pain, nausea, pale, sweaty
  • have a ‘going to die’ feeling as that’s how nerves work so make you feel like you are going to die
  • can get silent MI’s though = no pain felt at all
72
Q

what is the effect of an MI

A
  • death = not due to blockage, but from electrical instability leading to VF, go from sinus rhythm to VF
  • functional limitation = can’t pump blood around as well from heart as muscle not as good
73
Q

what are the investigations take for a MI

A
  • ECG
  • ST segment elevation/ T wave abnormalities = varies in with where infarction is
  • Q waves depression will only indicate old MI’s = will dip below the baseline
  • cardiac enzymes
  • look for troponin
  • creatine kinase (CKmb) = this and troponin specific to heart muscle
  • LDH and AST increase = not specific to heart muscle though
74
Q

what is the treatment of a MI

A
  • primary care

- hospital

75
Q

what is the primary care for an MI

A
  • aim to get patient to hospital to get managed properly
  • analgesia, aspirin and reassurance = not much you can reassure them of however
  • basic life support if needed = cardiac arrest situation
76
Q

what treatment is undertake in the hospital for a MI

A
  • primary PCI = acute angioplasty and stenting
  • if not within 3hours then do thrombolysis = will open vessel in couple hours, use streptokinase TPA, most effective if done early
  • drug treatment to reduce tissue damage
  • prevent recurrences/complications = aspirin, secondary prevention
77
Q

what is TPA

A

tissue plasminogen activator

78
Q

what are some contraindications of thrombolysis

A
  • injury/ surgery/ IM injections
  • severe hypertension, PVD
  • diabetic eye disease, liver disease
79
Q

what are some complications from an MI

A
  • death
  • arrhythmias = can happen because of conductive tissue affected by MI
  • heart failure
  • ventricular hypo function and thrombosis = papillary muscle rupture, valve disease
  • DVT and pulmonary embolism = can be due to lack of movement being in hospital bed for days
  • complications of thrombolysis
80
Q

what is the medical management of MI

A
  • prevent the next MI

- treat complications

81
Q

how can you prevent the next MI

A
  • risk modification and aspirin (secondary prevention)
  • beta blocker
  • ACE inhibitor = will make you live longer
82
Q

what complications may you have to treat from an MI

A
  • heart failure
  • arrhythmias
  • psychological distress = big aspect of having MI
83
Q

what are the dental aspects of an MI

A
  • emergency management
  • risk assessment before treating = is this patient going to have an MI, angina attack, sudden cardiac death, stroke
  • most people who have an MI in your surgery will have never had one before

BDS2 - BAMS (18 decks)

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