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BDS2 BAMS > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

2 pathology processes of acute coronary syndromes

A
  • blood vessel narrowing

- blood vessel occlusion

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2
Q

what is felt if blood vessel narrows?

A
  • inadequate oxygen delivery for tissue needs
  • cramp’ in affected tissue/muscle
  • no residual deficit at first
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3
Q

what is felt if blood vessel occludes?

A
  • no oxygen delivery - tissue death
  • more severe pain
  • loss of function of tissue
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4
Q

how will muscle metabolise when there is insufficient blood flow?

A

anaerobically

Stop doing exercise and allow requirements to drop
- Make up lactic acid debt and return to normal

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5
Q

what can happen over time if there is a lactic acid build up?

A

damage (10+ years)

- hypoxia leading to less effective cardiac muscle

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6
Q

what is key in treatment of acute coronary syndromes?

A

early effective treatment

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7
Q

what are 3 points in ACS diagnosis?

A
  • history
  • ECG findings
  • biomarkers
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8
Q

what should be gathered from history taking for ACS?

A
  • what can the patient tell you about their issues
  • how the patient feels conditions differently
    helpful information but not exclusive
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9
Q

what are the 2 classes of ECG findings in ACS diagnosis?

A
  • STEMI

- NSTEMI

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10
Q

STEMI ECG finding

A

ST segment elevation myocardial infarction

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11
Q

NSTEMI ECG finding

A

no ST segment elevation myocardial infarction

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12
Q

biomarkers in ACS diagnosis

A
  • released from damaged cells
  • released into blood circulation
  • increase with time and tissue damage
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13
Q

factors that influence artherosclerosis occurring

A

genetic mainly

can be worsened by lifestyle factors
- family history is good to assess

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14
Q

where do coronary arteries come away from?

A

the aorta, aortic valves cover the openings to coronary arteries

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15
Q

when does blood flow into coronary arteries?

A

during diastole

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16
Q

what causes a significant increase in inadequate blood flow to coronary arteries?

A

increased heart rate as shorter diastole

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17
Q

what are the 3 main coronary arteries?

A
  • right
  • left
  • circumflex
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18
Q

what happens if there is a blockage in one of the coronary arteries?

A

can lead to low oxygen supply to part of cardiac muscle
- can be lethal

poorly designed

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19
Q

what is angina pectoris?

A

reversible ischaemia of heart muscle

  • narrowing of one or more coronary arteries
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20
Q

how to differentiate ‘classical’ angina from ‘unstable’ angina?

A

‘classical’ angina gets worse with exercise

‘unstable’ angina has symptoms at rest with no biomarkers

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21
Q

what is the symptom of angina? (both classical and unstable)

A

‘central crushing chest pain’

- radiation to arm, back, jaw possible

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22
Q

‘classical’ angina symptoms

A
  • No pain at rest
  • pain with certain level of exertion (worse with cold weather/emotion)
  • pain relieved by rest (Use up all spare muscle around heart muscle; Get chest pain; Stop pain dissipates)
  • patient lives within limits of tolerance (avoids generating pain)
  • gradual deterioration
  • As disease gets worse exercise tolerance gets less and less
    Easily reproduced defined change
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23
Q

what are ‘classical’ angina signs?

A

Often none
- They don’t push themselves far enough to generate pain

Occasionally hyperdynamic circulation 
- anaemia 
- hyperthyroidism 
- hypovolaemia 
(less O2 in blood supply worsens these)
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24
Q

4 types of investigations used for angina

A
  • ECG (resting and exercise)
  • angiography
  • echocardiography
  • isotope studies (function assessment)

eliminate other diseases (thyroid; anaemia; valve)

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25
Q

what does a resting and exercise ECG tell you about angina?

A

shows area of myocardial ischaemia

at rest ECG should be normal and then with gradual increased exercise can see change (increase pace and inclination of treadmill)
- can see changes happening before pain in chest generated

infarction causes ECG changes all the time

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26
Q

what does an angiography tell you about angina?

A

dye injected to see if there is a narrowing

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27
Q

what do isotope studies tell you about angina?

A

function assessment

radioisotope in cardiac chambers and assess how efficient heart is at pumping out

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28
Q

what is an ischaemic episode on an ECG?

A

ST depression

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29
Q

what can an agiogram show you?

A

narrowing of coronary artery, potentially coronary artery blockage

  • if narrowing blood flow will be restricted but not blocked - dye can still pass beyond narrowing
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30
Q

4 methods of angina treatment

A
  • reduce oxygen demands to the heart
  • increase oxygen delivery to the tissues
  • dilate blocked/narrowed vessels
  • bypass blocked/narrowed vessels

surgical, drug and non-drug

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31
Q

how can you reduce oxygen demands of the heart to treat angina?

A 
reduce afterload (blood pressure)
- Higher BP in aorta more pressure in ventricles to pump out - so lower BP as lower afterload

reduce preload (venous pressure)

  • Preload is the pressure of blood filling heart (Starlings law - more pressure in more pressure out )
  • Reduce in –> reduce CO –> reduce heart’s demands
32
Q

how can you dilate blocked/narrowed vessels to treat angina?

A

angioplasty

open blockage up - inc blood flow - more O2 can pass through
- stretching blood vessels

33
Q

how can you bypass blocked/narrowed vessels to treat angina?

A

Coronary Artery Bypass Grafting (CABG)

  • extra loop past narrowing
  • no heart bypass
34
Q

what are non-drug therapy options for angina patients?

A

Explanation of illness

  • live within limitations
  • maybe because unwilling, unable, past treatable point

Modify risk factors

  • stop smoking
  • graded exercise programme to match tissue - improve diet/control cholesterol
35
Q

drug therapy methods for angina patients

A

Reduce MI risk
– ASPIRIN

Hypertension

  • diuretics, Ca channel antagonists
  • ace inhibitors, beta blockers

reduce preload / dilate coronary vessels
- nitrates - short acting & long acting

Emergency treatment - GTN spray/tab
(short shelf life)

36
Q

2 main surgical therapies for angina

A

CABG - coronary artery bypass graft

Angioplasty & stenting

37
Q

what are the negatives of CABG?

A
  • benefit not always obtained
  • major surgery - mortality risk – have to stop heart to preform;
  • limited benefit - 10 years - doesn’t fix the problem, makes it less bad
  • less in smokers who continue to smoke

one off operation

38
Q

what are the negatives of angioplasty and stenting?

A

Precutaneous Intervention (PCI)

lower risk but lower benefit

risk of vessel rupture during procedure

  • Stretching opening the narrowing
  • Gradually close again - can re-stretch
  • Need to put something in to keep open - stent

Less suitable for some patients

More permanent fix usually

Need dual antiplatelet therapy
- Duration varies with stent type

39
Q

process of coronary artery bypass graft CABG

A
  • Vein from patient’s leg
  • Sewn onto aorta
  • Go around the blockage
  • Veins doing the jobs of arteries - put in backwards as valves need to be in artery direction
40
Q

process of angioplasty & stenting

A
  • Tube in arm
  • Feed into heart
  • Out aorta into coronary artery
  • Dye in to identify block
  • Blow balloon up to stretch (If pops issue)
  • Frame clicks and locks into scaffold position (Metal in artery can attract clots need anti platelet drugs)
41
Q

what is peripheral vascular disease?

A

‘angina’ of the tissues
- same process and symptoms as angina but not in chest

  • usually lower limb
  • atheroma in femoral/popliteal vessels
  • ‘claudication’ pain in limb on exercise (claudication distance; pain relieved with rest )
42
Q

how is peripheral vascular disease managed?

A

in same way as angina

  • indicates artheropath (MI risk)
43
Q

what are consequences of having peripheral vascular disease?

A

Limitation of Function

Poor wound healing

  • Blister improve in a few days but ulcer may not heal if poor flow
  • If not treated can be very significant consequences - amputation

May lead to tissue necrosis & gangrene

  • Chronic slow process
  • Amputation

Aggravated by CV risk factors

44
Q

arteriosclerosis is a disease of…..

A

the whole body

if patient has peripheral vascular disease will be at risk of MI in surgery as will affect heart too

45
Q

atheroma in vessels is

A

ulcerated plaque with platelet aggregates

-thrombosis on the surface

46
Q

3 ways how can ischeamia lead to infarction?

A

Atheroma in vessels

  • ulcerated plaques with platelet aggregates
  • thrombosis on the surface

Thrombosis can enlarge rapidly to block vessel
- coronary artery 2-3mm lumen, can be completely occluded

Plaque surface/ platelets detach

  • travel downstream and BLOCK vessels
  • no blood flow to that area - infarction
47
Q

infarction in heart

A

coronary artery atheroma

can effect neck, platelets get broken off and block brain - stroke

48
Q

infarction in limb

A

femoral and popliteal arteries

49
Q

infarction in brain

A

carotid bodies

50
Q

5 ways of myocardial infarction

A

Spontaneous

  • primary coronary event
  • plaque fissure/rupture
  • most common

MI secondary to ischaemia
- balance of supply and demand
e.g. Chronic ischaemia for long period of time will get infarction
(severe anaemia for long time)

Sudden death with symptoms of ischaemia and evidence of ST elevation or thrombus (PCI/autopsy)

  • Chest pain and then collapse
  • Upset electrical conductivity of heart – abnormal heart rhythm, usually

MI from PCI (percutaneous intervention)
- thrombolysis – leave balloon inflated for too long, no O2 delivery downstream

MI from CABG

51
Q

3 strategies for myocardial infarction treatment and management

A
  • reduce tissue loss from necrosis
  • bypass obstruction
  • prevent further episodes

treatment depends on timing and accessibility

52
Q

how to reduce tissue loss from necrosis in myocardial treatment and management?

A

open blood flow to ischaemic tissue

thrombolysis
- drugs will dissolve away blood clot, allowing flow (up to 6 hours but angioplasty and stenting best possible option)

Angioplasty
- treatment of choice if you can do it quickly (within 3 hours best outcome)

53
Q

how to bypass obstruction in myocardial infarction treatment and management?

A
  • CABG

- fem/pop bypass

54
Q

how to prevent a further myocardial infarction episode?

A
  • risk factor management

- aspirin

55
Q

what is a limb infarction classified as?

A

medical/surgical emergency

  • thrombolysis
  • salvage surgery

may result in acute limb necorsos
- amputation

timing is key - need access within 3-6 hours to save tissue (limb easier access than cardiac muscle)

56
Q

what is a brain infarction?

A

stroke

57
Q

how does a brain infarction/stoke occur?

A
  • usually embolism from atheroma
  • occasionally a cerebral bleed
  • rarely vessel thrombosis (good collateral blood supply - left/right and vertebral artery)
58
Q

what is the consequence of having a stroke?

A

Deficit variable - usually loss of function

  • depends of brain region involved
  • usually some recovery with time

Short duration in some patients (<24hrs)
- Transient Ischaemic attacks

59
Q

what are the treatment options for strokes?

A
  • specialist centres

- trials

60
Q

symptoms and signs of myocardial infarction

A
  • pain, nausea, pale, sweaty
  • ‘going to die’
    Autonomic nerves go through basal ganglia (thalamus)
  • Only tell brain when something has gone wrong unlike somatic system As autonomic messages are only in issue – cause more anxiety and concern to brain
  • silent MIs (no pain at all)
61
Q

what are the consequences of MIs?

A

death
- due to electrical instability usually

functional limitations
- survive initial problem but compromised cardiac function as less muscle ability

62
Q

4 ways to investigate and treat MIs

A
  • ECG
  • Cardiac enzymes
  • primary care
  • hosptial
63
Q

how can ECGs be used to investigate MIs?

A

ST segment elevation/T wave abnormalities

  • varies in position with infarct
  • may be normal

Q waves only indicate OLD MI
- dip down more before R peak

64
Q

how can cardiac enzymes be used to investigate MIs?

A

Troponin

Creatinine Kinase (CKmb)

LDH & AST increase - not specific

65
Q

how is primary care used in MI investigations?

A

aim to get patient to hospital!

Analgesia, Aspirin & reassurance

Basic life support if required (Cardiac arrest situation = no repsonse)

66
Q

how is hospital care used in MI incidences?

A

Primary PCI
- acute angioplasty & stenting (if available)

thrombolysis if unable to do PCI (Open Vessel. Streptokinase or TPA; ‘window of opportunity’; most effective if given very early)

drug treatment to reduce tissue damage (aspirin)

prevent recurrence/complications
- Secondary prevention

67
Q

contraindications of thrombolysis for MI cases

A
  • injury/surgery/IM injections
  • severe hypertension, active PUD
  • diabetic eye disease, liver disease, pregnancy

so unable to have medicines needed for thrombolysis
- streptokinase or TPA

68
Q

complications of MIs

A
  • Death
  • Arrhythmias
  • Heart Failure due to loss of ventricular muscle
  • Ventricular hypofunction & thrombosis (papillary muscle rupture - valve disease)
  • DVT & pulmonary embolism due to inactivity
  • Complications of thrombolysis
69
Q

medical management of MI - preventing future episode

A
  • risk modification & aspirin
  • beta blocker will reduce risk of abnormal heart rhythm
  • ACE inhibitor - live longer
70
Q

things that may need managed if MI complications occurred

A
  • heart failure
  • arrhythmias
  • psychological distress
71
Q

acute coronary symptoms - dental aspects

A

Emergency management

Risk assessment

  • is this patient going to have a……… MI; angina attack; sudden cardiac death; stroke
  • is hospital setting safer for treatment?

Dentists role in promoting good health!
- see patient when well - try and encourage keeping there

72
Q

how can you have an MI secondary to ischaemia?

A

balance of supply and demand

E.g. Chronic ischaemia for long period of time will get infarction
- severe anaemia for long time

73
Q

what is the most common route for an MI to occur?

A

spontaneous

  • primary coronary event
  • plaque fissure/rupture
74
Q

what are 2 key points when trying to treat infarction?

A
  • how much tissue is necrotic
  • diagnosis - how certain are you of MI infarction?

timing and accessibility dictates treatment plan

75
Q

how does extent of tissue necrosis impact on prognosis of infarction treatment?

A

Less tissue necrosis = better prognosis

Long run the more functioning muscle there the less complications – want to maintain as can lead to heart failure if lose significant amount of muscle

76
Q

complication of treating infarction of the brain (stroke)

A

Usually treat infarction by dissolving clot/embolism but if there is a bleed can make bleed worse

  • So brain infarction need to differentiate between bleed and blockage to decide treatment
  • Hard to be confident – need good MRI scan

BDS2 BAMS (54 decks)

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