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ANKI Cardiovascular > [3] Acute Myocardial Infarction REDO > Flashcards

[3] Acute Myocardial Infarction REDO Flashcards

1
Q

What happens in a myocardial infarction?

A

A complete occlusion of a coronary vessel, leading to infarct (death) of the myocardium it supplies

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2
Q

What causes a complete occlusion of a coronary vessel?

A

The fibrous cap of the atheromatous plaque undergoes erosion or fissuring, exposing blood to the thrombogenic material in the necrotic core. This results in a platelet ‘clot’ followed by a fibrin thrombus, which can either occlude the entire vessel where it forms, or break off to form an embolism

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3
Q

What are the causes of a myocardial infarction?

A
  • Coronary heart disease
  • Drug misuse, e.g. cocaine, amphetamides, methamphetamies
  • Hypoxia
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4
Q

What are the symptoms of a myocardial infarction?

A
  • Chest pain, which may radiate to the jaw, neck, arms, and back
  • Shortness of breath
  • Feeling weak and/or lightheaded
  • Overwhelming feeling of anxiety
  • Autonomic features, such as sweating, pallor, nausea, and vomiting
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5
Q

What is the chest pain like in a myocardial infarction?

A

Typical ischaemic chest pain, that is very severe, persistent at rest, and often no precipitatnt

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6
Q

Where is ischaemic chest pain felt?

A

It can be central, retrosternal, or left sided. It may radiate to the shoulders and arms, with the left side being more common than the right, as well as the neck, jaw, epigastrum, and back

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7
Q

How is the nature of ischaemic chest pain described?

A

As tightening, crushing, constriction, or pressure

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8
Q

Is the chest pain in myocardial infarction relieved by rest?

A

No

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9
Q

How is a myocardial investigation investigated?

A
  • ECG
  • Blood tests to look for cardiac troponin and creatine kinase
  • Chest x-ray
  • Echocardiogram
  • Coronary angiography
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10
Q

What are the functions of ECG investigations in a patient with a suspected myocardial infarction?

A
  • Confirm diagnosis of MI
  • Determine what type of MI was experienced
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11
Q

Why is it important to determine what kind of MI a patient has experienced?

A

To determine the best treatment

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12
Q

What can MIs be classified into?

A

STEMI or NSTEMI

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13
Q

What is more serious, a STEMI or NSTEMI?

A

STEMI

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14
Q

What happens in a STEMI?

A

There is prolonged interruption to the blood supply, caused by a total blockage of a coronary artery. This can cause extensive damage to a large area of the heart, and the damage extends through the full thickness of the myocardium

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15
Q

How can a STEMI be differentiated from a NSTEMI?

A

ECG

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16
Q

How does a STEMI appear on ECG?

A

It has ST elevation in 2 or more leads facing the same area, of at least 1mm in limb leads, or 2mm in chest leads. There will also be a new left bundle branch block

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17
Q

What happens to the ECG minutes to hours after a STEMI heart attack?

A

ST elevation, with T wave upright

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18
Q

What happens to the ECG hours to a half a day after an STEMI?

A
  • ST elevation
  • Decreasing T wave
  • Decreasing R wave
  • Q wave begins
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19
Q

What happens to the ECG 1-2 days after STEMI?

A

Q wave deepens

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20
Q

What happens to the ECG a few days after a STEMI?

A
  • ST normalises
  • T wave is inverted
  • Q wave persists
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21
Q

What happens to the ECG a few weeks after a STEMI?

A
  • ST and T normal
  • Q waves persist
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22
Q

Why is an NSTEMI less serious than a STEMI?

A

Because the supply of blood to the heart is only partially blocked, and therefore a smaller section of the heart is damaged, and the damage does not extend the full thickness of the myocardium

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23
Q

How is an NSTEMI differentiated from unstable angina?

A

Measurement of blood troponin - troponin is present in the blood with an NSTEMI, but not unstable angina

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24
Q

What are Acute Coronary Syndromes (ACS)?

A

A group of symptoms attributed to the obstruction of the coronary arteries

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25
Q

What are the types of ACS?

A
  • Unstable angina
  • NSTEMI
  • STEMI
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26
Q

What is unstable angina?

A

When there is serious restriction to blood flow to the heart, but no pernament damage

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27
Q

Why is unstable angina considered to be a medical emergency?

A

Due to the possibility of progression to serious heart damage, or a STEMI

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28
Q

What is the goal of treatment of unstable angina?

A

Prevent it from progressing to MI, and limiting muscle loss in MI

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29
Q

How can an ECG be used to localise the vessel that is blocked in an MI?

A

The abnormality will be seen in the lead facing the infarcted, dead myocardium, and so to determine, you should look at the lead in which the abnormality is found

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30
Q

What are cardiac troponin I (cTnI) and T (cTnT)?

A

Both proteins important in actin/myosin interactions

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31
Q

When are cTnI and cTnT released?

A

In myocyte death, as occurs during a myocardial infarction

32
Q

When will cardiac troponins be found in the blood following an MI?

A

They rise 3-4 hours after the first onset of pain, and peak at 18-36 hours. They then decline slowly for 10-14 days

33
Q

What is the advantage of the use of cardiac troponins clinically?

A

They are a very sensitive and specific biomarker

34
Q

What is creatine kinase?

A

An iso-enzyme found in the heart, as well as skeletal muscle and the brain

35
Q

What is the cardiac isoform of creatine kinase?

A

CK-MB

36
Q

What does the presence of CK-MB in the blood indicate?

A

A myocardial infarction has occured

37
Q

When will CK-MB be found in the blood after an MI?

A

First rises 3-8 hours after onset, and peaks at 24 hours

38
Q

Why might a chest x-ray be useful in MI?

A

To rule out other causes of symptoms, and check for complications that might arise as a result of MI, e.g. pulmonary oedema

39
Q

What is an echocardiogram?

A

A sonogram of the heart that uses sound waves to build up a picture of the internals of the heart

40
Q

What information about the heart can an echo provide?

A
  • Size and shape of heart
  • Pumping capacity
  • Location and extent of any tissue damage
41
Q

What is the application of an echocardiogram in a MI?

A

It identifies exactly what area of the heart is damaged, and how that damage has affected the functioning of the heart

42
Q

What is the use of coronary angiography in MIs?

A

It is used to determine if a blockage or narrowing has occured in the coronary arteries, and if so, where

43
Q

What does the coronary angiography procedure involve?

A

Inserting a catheter into a blood vessel in the groin or arm, and then guiding it using x-rays into the coronary arteries. Contrast is then pumped through the catheter, and visualised using an x-ray to see how it flows through the coronary arteries, and determine the site of blockage or narrowing

44
Q

What is involved in the emergency treatment of a STEMI?

A
  1. Attach ECG monitor and record 12 lead ECG
  2. Obtain IV access and take bloods
  3. Perform a brief assessment
  4. Give aspirin and clopidogrel
  5. Morphine and anti-emetic
  6. If PCI is available within 120 minutes, perform primary PCI. If not, fibrinolysis
45
Q

What bloods should be taken during the immediate management of STEMI?

A
  • FBC
  • U&E
  • Glucose
  • Lipids
  • Troponin
46
Q

What should the brief assessment include in the immediate management of STEMI?

A
  • History of CVD disease and risk factors for IHD
  • Examination
  • CXR if it will not delay treatment
  • Information about any contraindications to fibrinoylsis or PCI
47
Q

What should be looked for on examination in STEMI?

A
  • Pulse
  • BP in both arms
  • JVP
  • Murmurs
  • Signs of CCF
  • Upper limb pulses
  • Scars from previous cardiac surgery
48
Q

What dose of aspirin should be given in the immediate management of STEMI?

A

300mg PO

49
Q

What dose of clopidogrel should be given in the immediate management of a STEMI?

A

300mg PO

50
Q

What dose of morphine should be given in the immediate management of a STEMI?

A

5-10mg IV

51
Q

Give an example of an anti-emetic that can be given alongside morphine in the immediate management of a STEMI?

A

Metoclopramide 10mg IV

52
Q

What is aspirin?

A

A weak organic acid

53
Q

How is aspirin unique among the NSAIDs?

A

It irreversibly acetylates, and thus inactivates, cyclooxygenase

54
Q

How do low doses of aspirin prevent platelet aggregation?

A

They irreversibly inhibit thromboxane production via the acetylation of cyclooxygenase, thus stopping thromboxanes action of platelet aggregation

55
Q

How long does decreased platelet aggregation due to aspirin last?

A

3-7 days

56
Q

Why does decreased platelet aggregation due to aspirin last for 5-7 days?

A

Because platelets lack nuclei, and so they cannot synthesise new enzyme, so the lack of thromboxane persists for the lifetime of the platelet

57
Q

What are the most common side effects of aspirin?

A
  • Indigestion and epigastric pain
  • Bleeding and bruising
58
Q

What are the uncommon and rare side effects of aspirin?

A
  • Hives
  • Tinnitus
  • Difficulty breathing
  • Allergic reations
  • Haemorrhage
59
Q

What are the pharmacokinetics of aspirin dependant on?

A

Dose

60
Q

What are the pharmacokinetics of aspirin in low doses (such as in STEMI)?

A

It shows first order kinetics with a half life of 4 hours

61
Q

What is considered to be ‘higher doses’ of aspirin?

A

12x300mg/day

62
Q

What are the pharmacokinetics of aspirin at high doses?

A

Zero order kinetics

63
Q

How is aspirin metabolised at cardiac doses?

A

It is hydrolysed to salicylate and acetic acid by esterases in the tissues and blood

64
Q

What hapepns to salicyate in the body?

A

It is converted by the liver to water soluble conjugates that are rapidly cleared by the kidney

65
Q

Why should aspirin be avoided in patients with gout?

A

Because salicylate is secreted into the urine, and can affect uric acid secretion

66
Q

What is the mechanism of action of clopidogrel?

A

It irreversibly inhibits the binding of ADP to its receptors on platelets, and thereby inhibits the activation of GP IIb/IIIa receptors required for platelets to bind to fibrinogen and each other

67
Q

What are the common side effects of clopidogrel?

A
  • Bleeding
  • Nosebleeds
  • Diarrhoea
  • Abdominal pain
  • Indigestion
  • Increased bleeding from wounds
68
Q

What are the serious side effects of clopidogrel?

A
  • Severe bleeding or pain
  • Haematemesis
  • Haematuria or blood in stool
  • Allergic reaction
69
Q

What are the cautions and contraindications to clopidogrel?

A
  • Active stomach ulcer, or stomach ulcer in past
  • Brain haemorrhage
  • Haemophilia, or other bleeding disorder
  • Liver or kidney problems
  • Previous allergic reactions to medication
  • Pregnant or breastfeeding
70
Q

What is the problem with taking other drugs alongside clopidogrel?

A

It can affect its efficacy, or increase the changes of getting side effects

71
Q

What drugs might interact with clopidogrel?

A
  • Aspirin (may be recommended theyrre together together anyway)
  • NSAIDs
  • Anticoagulants such as warfarin
  • Other types of antiplatelets such as dipyridamole
  • SSRIs
  • PPIs
72
Q

Is clopidogrel bound to plasma proteins?

A

Yes, extensively

73
Q

Describe the metabolism of clopidogrel?

A

It undergoes hepatic metabolism by cytochrome P450 enzymes to active metabolites

74
Q

How long does it take to reach the maximum effect of clopidogrel?

A

3-5 days

75
Q

What happens when clopidogrel is suspended?

A

The platelet system needs time to recover

76
Q

How does elimination of clopidogrel and its metabolites occur?

A

Faecal and renal routes

ANKI Cardiovascular (24 decks)

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