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Myocardial Infarction Flashcards

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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
When does Q wave formation and T wave inversion occur?
first day
26
How do you know if someone has had an MI?
q waves AND/OR inverted T waves
27
On which leads will an inferior MI be shown?
II, III, AVF
28
On which leads will an anterior MI be shown?
V1-6
29
which are the anterior leads?
V1 and V2
30
Which are the septal leads?
V3 and V4
31
Which are the lateral leads?
V5 and V6, lead I and AVL
32
What are other tests that could be carried out to diagnose STEMI?
- cardiac enzymes | - protein markers
33
What are the disadvantages of these other tests?
- may be normal at presentation | - may not have time to wait for test results in a STEMI
34
What protein do we measure?
Troponin as it is highly specific for cardiac muscle damage and it can detect tiny amounts of myocardial necrosis
35
Why is early treatment key?
To avoid muscle damage caused by heart failure in the long term
36
What is the mode of action of STEMI drugs?
- clopidogrel blocks the ADP receptors | - cyclooxygenase is also blocked by aspirin to stop its conversion to thromboxane A2
37
How soon does clopidogrel start to work?
Within 2 hours
38
How should ACS be treated?
300mg aspirin
39
How should ACS with ECG changes or elevation of cardiac markers be treated?
300mg of aspirin | 300mg of clopidogrel
40
What at the indications for thrombolysis?
- 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
What are the risk of thrombolysis?
- failure to re-perfuse - haemorrhage - hypersensitivity
42
What is the probability that thrombolysis will work and open the artery?
50%
43
What affect does failed thrombolysis of acute reocculsion have on the body?
long term mortality risk doubled
44
What does primary angioplasty involve?
- 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
What is the importance of age and time in deciding whether to carry out thrombolysis or angioplasty ?
- younger patients (under 65) have less time before a delay in angioplasty outweighs the risk of thrombolysis - older patients have more time
46
What is the optimal time frame for angioplasty?
angioplasty inserted within 90 minutes of diagnosis
47
What is the treatment plan for STEMI?
- analgesia - anti-emetic - aspirin (300mg) clopidogrel (300mg) - GTN - oxygen (if hypoxic) - primary angioplasty - thrombolysis (if beyond 90 mins away from hospital)
48
What are the complications of an Acute MI?
- death - Arrhythmic complications - structural complications - functional complications
49
What is an example of an arrhythmic complication?
VF
50
What is VF?
chaotic, rapid, disordered electrical activity which results in a loss of cardiac output.
51
Infarction will cause VF true or false?
true
52
What is the only treatment for VF?
defibrillation - shock delivered in an attempt to repolarise the heart to get the sa node to re set the rhythm
53
What are the main structural complications caused by STEMI?
- cardiac rupture - ventricular septal defect - mitral valve regurgitation (if papillary muscles are damaged)
54
What other structural complications can arise from a STEMI?
-Left ventricular aneurysm formation -mural thrombus -inflammation resulting in acute pericarditis -dressler's syndrome (rare autoimmune condition - chronic pain following an MI)
55
What are functional complications of a STEMI?
- LVF, RVF, biventricular failure - chronic cardiac failure - cardiogenic shock
56
What is killip classification in hospital mortality
measure of mortality stage 4 is most severe ie most likely chance of mortality
57
Name the components of killip classification
I- no signs of heart failure II- crepitation but little heart failure III- crepitation and a lot of heart failure IV- cardiogenic chock
58
What are routine observations in the CCU?
- cardiac monitor - pulse and BP - heart sounds - crepitation - fluid balance
59
Why don't we get acute occlusion of coronary arteries in NSTEMI?
due to intravascular thrombolysis, our own body breaks up the clot.
60
How does intravascular thrombolysis occur?
- tissue plasminogen activator combines with plasminogen to form plasmin. - plasmin breaks up clot and results in fibrin degradation products being formed
61
What is the outcome from NSTEMI?
- short term - good outcome | - long term - poor outcome
62
What are the long term outcomes in relation to STEMI and NSTEMI?
ST depression have a poorer outcome long term than ST elevation
63
What are the incidence rate comparison between STEMI and unstable angina/NSTEMI
More people who arrive at hospital with chest pain are unstable angina/NSTEMI than STEMI Could also be non- cardiac related
64
The ECG will always be abnormal in NSTEMI. True/False?
False, the ECG may be normal
65
What may we see on ECG is NSTEMI?
- ST depression | - T wave inversion
66
What is the outcome likelihood if there are ECG changes in NSTEMI?
ECG changes in NSTEMI indicate bad outcome
67
What is troponin?
-a protein on actin and myosin chain which aids in muscle contraction
68
How can troponin be used?
- to identify MI - nearly absolute myocardial specificity - show any cardiac damage even microscopic
69
What do we measure with troponin?
-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
What other conditions can cause troponin increase?
- CCF - Hypertensive crisis - renal failure - PE - sepsis - Stroke/TIA - pericarditis/myocarditis - post arrhythmia
71
What is a type 1 MI?
spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection
72
What is a type 2 MI?
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
What is a type 3 MI?
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
How to treat NSTEMI?
- inhibition of coagulation cascade (factor Xa) | - to prevent NSTEMI from becoming a STEMI
75
What drugs for acute NSTEMI?
- warfarin - LMW warfarin - aspirin - clopidogrel
76
What drugs long term for NSTEMI?
- long term aspirin | - 3 months of clopidogrel
77
What are IIb/IIIa inhibitors?
- last and most potent form of dealing with platelet aggregation and activation - this protein which slows fibrinogen to activate platelets
78
What are the indications for angioplasty in NSTEMI?
- patients with NSTEMI who have troponin detected should receive early coronary angiography and revascularisation - not as an emergency but ASAP
79
What are you looking for in a coronary angiography in a NSTEMI?
Looing for patient with a vulnerable or high grade stenosis
80
What is coronary revascularisation?
- 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
What are the advantages of a Stent?
- improve flow - less chances of clot - improve appearance of vasculature
82
What are the indications for longer term clopidogrel use?
- 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
What is PCI?
percutaneous coronary intervention (stenting)
84
What are examples of secondary preventions?
- healthy lifestyle - smoking cessation - good BP - normal cholesterol - diabetes control
85
What are the four phases of cardiac rehabilitation?
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

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