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Cardiology > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

1
Q

What is the sequence of plaque formation?

A

normal then fatty streak then atheromatous plaque then atherosclerotic plaque

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2
Q

Which stages cause symptoms such as angina?

A
  • atheromatous plaque

- atherosclerotic plaque

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3
Q

What is chronic stable angina?

A
  • chronic stenosis
  • a demand led ischemia
  • safe and predictable
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4
Q

What is an acute coronary syndrome?

A

any acute presentation of coronary artery disease

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5
Q

What is the issue with the term acute coronary syndrome?

A

Only a provisional diagnosis that covers a spectrum of conditions

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6
Q

What is asymptomatic coronary disease?

A

They dont suffer from angina pain but have diseased arteries

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7
Q

What three conditions are underpinned by Acute coronary syndrome?

A
  • unstable angina
  • acute non STEMI
  • STEMI
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8
Q

What two conditions are non STEACS?

A
  • Unstable angina

- Non STEMI

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9
Q

What condition is a STEACS?

A

STEMI

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10
Q

What is a dynamic stenosis?

A

-obstruction suddenly happens

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11
Q

What are the characteristics of acute coronary syndrome?

A
  • dynamic stenosis
  • blood supply led ischemia
  • unpredictable and dangerous
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12
Q

What causes ACS?

A

spontaneous rupture of the atheromatous plaque

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13
Q

What factors affect the plaque rupture?

A
  • lipid content of plaque
  • thickness of fibrous cap
  • sudden changes in intraluminal pressure or tone
  • bending and twisting of an artery during each heart contraction
  • plaque shape
  • mechanical injury
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14
Q

Are newly formed or older plaques more likely to rupture?

A

newly formed are more likely to rupture

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15
Q

What is the surgical procedure used?

A
  • mesh inserted
  • disrupts vascular endothelium
  • platelet reacts to this change
  • platelet formation and activation
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16
Q

How are platelets activated?

A
  • release of ADP and thromboxane A
  • these bind to circulating platelets
  • the platelets activation will accelerate
  • then with this more platelets will be recruited
  • activated platelets express adhesion receptors for leukocytes
  • finally a fibrin rich thrombus is formed
  • vascular blockage
  • ACS
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17
Q

What is aim in treatment for ACS?

A

reduce platelet activation

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18
Q

What occurs if the patient survives a STEMI?

A
  • occlusion of artery
  • death of tissue below the artery
  • scarring o tissue
  • dilation of ventricular volume
  • reduction is volume of blood the ventricle is able to beat
  • LVF
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19
Q

What are the symptoms of LVF?

A
  • cough
  • orthopnoea
  • blood tinged sputum
  • dyspnoea
  • cyanosis
  • paroxysmal nocturnal dyspnoea
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20
Q

history of STEMI?

A
  • severe crushing central chest pain
  • radiating to jaw and arms especially on left
  • does not ease with rest
  • not relieved by GTN
  • sweating, nausea and vomiting
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21
Q

What else can cause chest pain?

A
  • brocho pneumonia
  • pneumothorax
  • muscular skeletal
  • heart burn
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22
Q

What can you see on an ECG in STEMI?

A
  • ST elevation
  • T wave inversion
  • Q waves
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23
Q

What are the necessary components of a STEMI on an ECG?

A
  • more than or equal to 1mm ST elevation in 2 adjacent limb leads
  • more than or equal to 2mm St elevation in at least 2 contiguous precordial leads
  • new onset left bundle branch block
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24
Q

When does ST elevation occur in a STEMI?

A

first few hours

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25
Q

When does Q wave formation and T wave inversion occur?

A

first day

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26
Q

How do you know if someone has had an MI?

A

q waves AND/OR inverted T waves

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27
Q

On which leads will an inferior MI be shown?

A

II, III, AVF

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28
Q

On which leads will an anterior MI be shown?

A

V1-6

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29
Q

which are the anterior leads?

A

V1 and V2

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30
Q

Which are the septal leads?

A

V3 and V4

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31
Q

Which are the lateral leads?

A

V5 and V6, lead I and AVL

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32
Q

What are other tests that could be carried out to diagnose STEMI?

A
  • cardiac enzymes

- protein markers

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33
Q

What are the disadvantages of these other tests?

A
  • may be normal at presentation

- may not have time to wait for test results in a STEMI

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34
Q

What protein do we measure?

A

Troponin as it is highly specific for cardiac muscle damage and it can detect tiny amounts of myocardial necrosis

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35
Q

Why is early treatment key?

A

To avoid muscle damage caused by heart failure in the long term

36
Q

What is the mode of action of STEMI drugs?

A
  • clopidogrel blocks the ADP receptors

- cyclooxygenase is also blocked by aspirin to stop its conversion to thromboxane A2

37
Q

How soon does clopidogrel start to work?

A

Within 2 hours

38
Q

How should ACS be treated?

A

300mg aspirin

39
Q

How should ACS with ECG changes or elevation of cardiac markers be treated?

A

300mg of aspirin

300mg of clopidogrel

40
Q

What at the indications for thrombolysis?

A
  • chest pain suggestive of acute MI (lasting more than 20 minutes in less than 12 hours)
  • ECG changes (ST elevation or new left bundle branch block)
  • no contraindications
41
Q

What are the risk of thrombolysis?

A
  • failure to re-perfuse
  • haemorrhage
  • hypersensitivity
42
Q

What is the probability that thrombolysis will work and open the artery?

A

50%

43
Q

What affect does failed thrombolysis of acute reocculsion have on the body?

A

long term mortality risk doubled

44
Q

What does primary angioplasty involve?

A
  • running a wire through the blocked artery to restore blood flow
  • used in patients that have already taken aspirin and clopidogrel
  • then add a balloon and insert a stent to hold vessel open
  • re perfuse the downstream muscle and prevent necrosis
45
Q

What is the importance of age and time in deciding whether to carry out thrombolysis or angioplasty ?

A
  • younger patients (under 65) have less time before a delay in angioplasty outweighs the risk of thrombolysis
  • older patients have more time
46
Q

What is the optimal time frame for angioplasty?

A

angioplasty inserted within 90 minutes of diagnosis

47
Q

What is the treatment plan for STEMI?

A
  • analgesia
  • anti-emetic
  • aspirin (300mg) clopidogrel (300mg)
  • GTN
  • oxygen (if hypoxic)
  • primary angioplasty
  • thrombolysis (if beyond 90 mins away from hospital)
48
Q

What are the complications of an Acute MI?

A
  • death
  • Arrhythmic complications
  • structural complications
  • functional complications
49
Q

What is an example of an arrhythmic complication?

A

VF

50
Q

What is VF?

A

chaotic, rapid, disordered electrical activity which results in a loss of cardiac output.

51
Q

Infarction will cause VF true or false?

A

true

52
Q

What is the only treatment for VF?

A

defibrillation - shock delivered in an attempt to repolarise the heart to get the sa node to re set the rhythm

53
Q

What are the main structural complications caused by STEMI?

A
  • cardiac rupture
  • ventricular septal defect
  • mitral valve regurgitation (if papillary muscles are damaged)
54
Q

What other structural complications can arise from a STEMI?

A

-Left ventricular aneurysm formation
-mural thrombus
-inflammation resulting in
acute pericarditis
-dressler’s syndrome (rare autoimmune condition - chronic pain following an MI)

55
Q

What are functional complications of a STEMI?

A
  • LVF, RVF, biventricular failure
  • chronic cardiac failure
  • cardiogenic shock
56
Q

What is killip classification in hospital mortality

A

measure of mortality stage 4 is most severe ie most likely chance of mortality

57
Q

Name the components of killip classification

A

I- no signs of heart failure
II- crepitation but little heart failure
III- crepitation and a lot of heart failure
IV- cardiogenic chock

58
Q

What are routine observations in the CCU?

A
  • cardiac monitor
  • pulse and BP
  • heart sounds
  • crepitation
  • fluid balance
59
Q

Why don’t we get acute occlusion of coronary arteries in NSTEMI?

A

due to intravascular thrombolysis, our own body breaks up the clot.

60
Q

How does intravascular thrombolysis occur?

A
  • tissue plasminogen activator combines with plasminogen to form plasmin.
  • plasmin breaks up clot and results in fibrin degradation products being formed
61
Q

What is the outcome from NSTEMI?

A
  • short term - good outcome

- long term - poor outcome

62
Q

What are the long term outcomes in relation to STEMI and NSTEMI?

A

ST depression have a poorer outcome long term than ST elevation

63
Q

What are the incidence rate comparison between STEMI and unstable angina/NSTEMI

A

More people who arrive at hospital with chest pain are unstable angina/NSTEMI than STEMI
Could also be non- cardiac related

64
Q

The ECG will always be abnormal in NSTEMI. True/False?

A

False, the ECG may be normal

65
Q

What may we see on ECG is NSTEMI?

A
  • ST depression

- T wave inversion

66
Q

What is the outcome likelihood if there are ECG changes in NSTEMI?

A

ECG changes in NSTEMI indicate bad outcome

67
Q

What is troponin?

A

-a protein on actin and myosin chain which aids in muscle contraction

68
Q

How can troponin be used?

A
  • to identify MI
  • nearly absolute myocardial specificity
  • show any cardiac damage even microscopic
69
Q

What do we measure with troponin?

A

-when clots are broken down and platelet emboli are sent to clog up our microvascular circulation and nip off small and isolated pockets of myocytes.

70
Q

What other conditions can cause troponin increase?

A
  • CCF
  • Hypertensive crisis
  • renal failure
  • PE
  • sepsis
  • Stroke/TIA
  • pericarditis/myocarditis
  • post arrhythmia
71
Q

What is a type 1 MI?

A

spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection

72
Q

What is a type 2 MI?

A

MI secondary to ischemia due to an imbalance of O2 supply and demand, as from coronary spasm or embolism, anemia, arrhythmias, hypertension or hypotension

73
Q

What is a type 3 MI?

A

sudden unexpected cardiac death including P1A, often with symptoms suggesting ischemia with new St segment elevation; new ;left bundle branch block; or pathological or angiographic evidence of fresh coronary thrombus - in the absence of reliable biomarker findings

74
Q

How to treat NSTEMI?

A
  • inhibition of coagulation cascade (factor Xa)

- to prevent NSTEMI from becoming a STEMI

75
Q

What drugs for acute NSTEMI?

A
  • warfarin
  • LMW warfarin
  • aspirin
  • clopidogrel
76
Q

What drugs long term for NSTEMI?

A
  • long term aspirin

- 3 months of clopidogrel

77
Q

What are IIb/IIIa inhibitors?

A
  • last and most potent form of dealing with platelet aggregation and activation
  • this protein which slows fibrinogen to activate platelets
78
Q

What are the indications for angioplasty in NSTEMI?

A
  • patients with NSTEMI who have troponin detected should receive early coronary angiography and revascularisation
  • not as an emergency but ASAP
79
Q

What are you looking for in a coronary angiography in a NSTEMI?

A

Looing for patient with a vulnerable or high grade stenosis

80
Q

What is coronary revascularisation?

A
  • balloon catheter inserted into obstructed artery
  • when balloon is inflated it breaks up the atherosclerotic plaque
  • when lumen is widened, balloon catheter with deflated balloon is removed
81
Q

What are the advantages of a Stent?

A
  • improve flow
  • less chances of clot
  • improve appearance of vasculature
82
Q

What are the indications for longer term clopidogrel use?

A
  • any drug eluting stent- 1 year
  • ACS medical treatment - 3 months
  • ACS bare metal stent - 3 months
  • Elective PCI - 3 months
  • STEMI and no PCI - 4 weeks
  • Aspirin intolerant - indefinitely
83
Q

What is PCI?

A

percutaneous coronary intervention (stenting)

84
Q

What are examples of secondary preventions?

A
  • healthy lifestyle
  • smoking cessation
  • good BP
  • normal cholesterol
  • diabetes control
85
Q

What are the four phases of cardiac rehabilitation?

A

I- in patient
II- early post discharge period
III- structured exercise programme - usually hospitals based
IV- long term maintained physical activity and lifestyle change - community based

Cardiology (32 decks)

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