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Yr 3 Cardiovascular > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

1
Q

What is myocardial infarction?

A

the death of heart cells due to ischaemia typically caused by the occlusion of arteries.

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2
Q

Describe the causative mechanism of myocardial infarctions:

A

a coronary artery plaque’s fibrous cap ruptures, stimulating platelet aggregation and eventually embolization of a thrombus, blocking blood flow

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3
Q

What two molecules do platelets release that cause vasoconstriction when a plaque ruptures?

A
  1. Thromboxane A2
  2. serotonin
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4
Q

What is a spontaneous MI?

A

an MI due to plaque rupture

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5
Q

What does it mean for an MI to be secondary to ischaemia?

A

the MI is due to increased oxygen demand/ decreased supply e.g.
1) anaemia
2) arrhythmias
3) coronary spasm

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6
Q

Name the five types of myocardial infarction:

A

1) spontaneous MI with ischaemia
2) MI secondary to ischaemia
3) MI in sudden cardiac death
4) MI related to percutaneous coronary intervention/ stent thrombosis
5) MI related to coronary artery bypass (CABG)

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7
Q

What does PCI stand for? (type of vascular surgery)

A

percutaneous coronary intervention

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8
Q

What does CABG stand for?

A

coronary artery bypass graft

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9
Q

What is the key presenting symptom of a myocardial infarction?

A

central crushing chest pain, lasting >20 mins that may radiate to jaw and neck

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10
Q

In which two patient demographics are ‘silent’ MIs seen?

A

1) elderly
2) diabetic

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11
Q

What is a silent MI?

A

reduced oxygen-rich blood flow to the heart that occurs in the absence of chest discomfort or other symptoms of angina

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12
Q

Give 3 presenting features of a ‘silent’ MI:

A
  1. Syncope
  2. Dyspnoea
  3. Fatigue
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13
Q

Other than central crushing chest pain, give 4 other presenting symptoms of an MI:

A
  1. Sweating
  2. Palpitations
  3. Dyspnoea
  4. Signs of heart failure (leg swelling, tachypnoea)
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14
Q

What does STEMI stand for?

A

ST elevation myocardial infarction

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15
Q

What does NSTEMI stand for?

A

non-ST segment elevation myocardial infarction

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16
Q

What is the difference between an NSTEMI and a STEMI?

A

STEMIs are caused by full coronary obstruction, whereas NSTEMIs are caused by partial obstruction

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17
Q

What is the textbook presentation of an MI?

A

A textbook presentation is an acute onset central or left sided chest pain, which often comes at rest, in the morning, gradually increasing in intensity over a period of minutes, with radiates down the left arm, associated with diaphoresis (sweating), and pre-syncopal or syncopal symptoms. However, about 30% of patients present without pain.

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18
Q

Give 5 risk factors for acute coronary syndrome according to the TIMI/ GRACE risk scores:

A

1) age >65
2) severe angina
3) >3 coronary artery disease associated disorders such as hypertension, diabetes and hyperlipidaemia
4) known coronary artery disease
5) recent aspirin use

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19
Q

Give 5 SIGNS of an MI:

A

1) high/ low pulse
2) high/ low blood pressure
3) distress, pallor and sweatiness
4) signs of heart failure (raised JVP, basal crepitations)
5) pan-systolic murmur

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20
Q

What are basal crepitations?

A

Crackling sound at the base of lungs

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21
Q

What other symptoms can be experienced in an MI?

A
  1. Breathlessness
  2. Tachycardia
  3. Vomiting and sinus bradycardia
  4. Distress - impending doom
  5. Sudden death
  6. MI more common in the morning
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22
Q

What sign would indicate ACS over other causes of chest pain?

A
  1. Pain for more than 15 mins
  2. Pain that radiates to arm or the jaw
  3. Diaphoresis (cold sweats)
  4. Vomiting
  5. Exertional chest pain
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23
Q

What would indicate away from ASC?

A
  1. Reproducible chest pain
  2. Pleuritic chest pain
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24
Q

What are 8 signs of impaired myocardial function?

A
  1. 3rd/4th heart sounds
  2. Pan systolic murmur
  3. Pericardial rub
  4. Pulmonary oedema
  5. Hypotension
  6. Quiet first heart sound
  7. Narrow pulse pressure
  8. Raised JVP
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25
Q

What are 4 cardiac differentials for an MI?

A
  1. Angina
  2. Pericarditis
  3. Myocarditis
  4. Aortic dissection
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26
Q

What are 2 pulmonary differential diagnoses for MI?

A
  1. PE
  2. Pneumothorax
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27
Q

Name 5 blood tests that may be used to request a potential myocardial infarction:

A
  1. Troponin
  2. CK-MB
  3. FBC
  4. U&E
  5. Lipids
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28
Q

Other than bloods, give 4 other investigations that may be used to investigate a potential MI:

A

1) echocardiogram
2) angiography
3) ECG (check ST status)
4) chest x-ray (check for heart failure)

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29
Q

What investigation can be used to work out left ventricular ejection fraction?

A

echocardiogram

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30
Q

Describe the MONARCH treatment plan for MIs:

A
  1. Morphine
  2. Oxygen
  3. Nitrates
  4. Aspirin
  5. Re-perfusion (PCl or thrombolysis)
  6. Clopidogrel
  7. Heparin
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31
Q

Describe how thrombolysis drugs work:

A

they enhance thrombus breakdown by activating plasminogen to form plasmin

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32
Q

Give 4 contraindications for thrombolytic drugs:

A
  1. Recent stroke
  2. CNS damage
  3. Recent major trauma/ internal bleed
  4. Bleeding disorder
33
Q

What is the pathology behind an MI?

A

MI is almost always due to occlusive thrombus formation at the site of rupture or erosion of an atheromatous plaque. The pain experienced is usually the same as angina, but lasts longer and may be more severe.
Patients should call an ambulance if they experience ‘angina type pain’, which, after using GTN spray does not subside within 15 minutes.
The pain is often excruciating – look at the patients face / expression / pallor to determine the seriousness of the pain

34
Q

What are the 2 different mechanisms for MI?

A
  1. The fibrous cap of the plaque itself gets a superficial injury, and a thrombus forms on it
  2. In more advanced cases, unstable plaques, the fibrous cap completely ruptures, and not only does the contents escape, but blood can also enter the plaques forming a thrombus within the remaining cap of the plaque

Platelets then release serotonin and thromboxane A2 and this causes vasoconstriction in the area resulting in reduced blood flow to the myocardium, and ischaemic injury

35
Q

What is a transmural MI?

A

this is an infarct that causes necrosis of tissue through the full thickness of the myocardium

36
Q

What is a nontransmural MI?

A

this is an MI that does not cause necrosis through the full thickness of the myocardium

37
Q

What are the ECG findings within the early hours of an MI?

A
  1. Peaked T wave (Very tall wave)
  2. Raised ST-segment
38
Q

What are the ECG findings within 24 hours of an MI?

A

Inverted T waves – this may or may not persist
ST segment returns to normal. Raised ST segments may persist if a left ventricular aneurysm develops

39
Q

What are the ECG findings within days of a MI?

A

Pathological Q waves form – these may resolve in 10% of cases
We say the Q wave is pathological if it is >25% of the height of the R wave, and/or it is greater than 0.04s width (1 small squares) and/or greater than 2mm height (2 small squares)
Q waves are also a sign of a previous MI – the changes in Q waves are generally permanent. The changes in T waves may or may not revert. The ST segment can return to normal within hours.
Non-q-wave infarcts are infarcts that occur without the changes seen in the Q waves, but still with the ST and T changes.

40
Q

What is acute coronary syndrome and the 3 subtypes?

A

a mixture of symptoms and clinical findings due to impaired cardiac perfusion at rest

3 sub types:

  • Unstable angina
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI)
41
Q

What are the risk factors for ACS/MI?

A

Modifiable risk factors:

​High cholesterol

Hypertension

Smoking

Diabetes

Obesity

Non-modifiable risk factors:

​Age

Family history

Male sex

Premature menopause

42
Q

What is GRACE score used for?

A

to give a 6 month probability of death post NSTEMI or unstable angina

<3% = low risk

> 3% = medium-high risk

43
Q

What are the atypical presentations of MI?

A
  • SILENT MI = NO PAIN common in elderly and diabetics
  • epigastric pain
  • palpitations
  • acute confusion
  • syncope
  • diabetic hyperglycaemic crises
44
Q

How is a STEMI diagnosed?

A
  • ST segment elevation >2mm in adjacent chest leads
  • ST segment elevation >1mm in adjacent limb leads
  • New left bundle branch block (LBBB) with chest pain or suspicion of MI
45
Q

How is an NSTEMI diagnosed?

A

Requires two of the following:

  • Cardiac chest pain
  • Newly abnormal ECG which is NOT ST-elevation
  • t wave inversion
  • Raised troponin (with no other reasonable explanation)
46
Q

What is the immediate management of MI/ACS?

A

CPAIN

  • call an ambulance
  • perform an ECG and aim for O2 >90%
  • aspirin 300mg
  • IV morphine for pain relief if required (with an antiemetic)
  • nitrate (GTN)
47
Q

when are GTN and isosorbide mononitrate used?

A

chest pain - angina - to vasodilator blood vessels, preventing MI

  • GTN = short acting vasodilator
  • isosorbide mononitrate = long acting vasodilator (used when beta blocker and Ca channel blocker are contraindicated for angina treatment)
48
Q

management of STEMI?

A
  1. PCI- Percutaneous coronary intervention if available within 2 hours of presenting and 12 hours since onset of pain
  • prasugrel if not on anti-coagulant
  • clopidogrel if on oral anti-coagulant
  1. Thrombolysis if PCI is not available within 2 hours
49
Q

management of NSTEMI?

A

1) PCI - percutaneous coronary intervention if available within 2 hours of presenting and 12 hours since onset of pain

  • prasugrel if not on anti-coagulant
  • clodiodogrel if on oral anti-coagulant

2) thrombolysis if PCI is NOT available within 2 hours

+ start antithrombin therapy eg low dose LMWH or fondaparindux

50
Q

What is the management post-MI?

A
  1. Aspirin 75mg once daily indefinitely
  2. Another antiplatelet

eg (clopidogrel or ticagrelor once daily for 12 months)

  1. Beta blocker (normally bisoprolol)
  2. ACE-inhibitor (normally ramipril)
  3. High dose statin (e.g. Atorvastatin once daily)
  4. Aldosterone antagonist for those with HF
  • ECHO (when stable to assess functional damage to the heart)
  • cardiac rehabilitation
51
Q

what should be closely monitored in patients taking ACEi and aldosterone antagonists?

A

RENAL FUNCTION
- Risk of fatal hyperkalaemia

52
Q

What are complications of an MI?

A
  • arrhythmias
  • congestive cardiac failure
  • thromboembolism (stroke)
  • pericarditis
  • ventricular aneurysm
  • cardiac tamponade
  • cardiogenic shock
  • Dressler’s syndrome
  • death
53
Q

What is Dressler’s syndrome?

A

Post-MI fibrinous pericarditis

54
Q

Give 5 event-reducing drugs for MIs:

A

1) aspirin
2) ADP-receptor blocker (antiplatelet)
3) beta blocker
4) ACE inhibitor
5) statins

55
Q

How many weeks after an MI does Dressler’s syndrome manifest?

A

2-3

56
Q

Give 3 presentations associated with Dressler’s syndrome:

A

1) pleuritic chest pain
2) low grade fever
3) pericardial rub on auscultation

57
Q

Give two potential pericardial manifestations of Dressler’s syndrome:

A

1) pericardial effusion
2) pericardial tamponade

58
Q

What is pericardial tamponade?

A

Bleeding into the pericardial sac compresses the heart preventing it to fill and pump

59
Q

Give 3 investigational findings that confirm a diagnosis of Dressler’s syndrome:

A

1) raised inflammatory markers (CRP and ESR)
2) echocardiogram shows pericardial effusion
3) ECG elevation shows ST elevation and T wave inversion

60
Q

Describe how Dressler’s syndrome is treated:

A

NSAID such as aspirin or ibuprofen and in more severe cases, steroids

61
Q

What major vessel do the coronary arteries branch from?

A

aorta

62
Q

What two coronary vessels branch off the left coronary artery?

A

1) circumflex artery
2) left anterior descending (LAD) artery

63
Q

Describe the course of the right coronary artery?

A

Wraps around the right side and under the heart

64
Q

Give 4 cardiac regions supplied by the right coronary artery:

A

1) right atrium
2) right ventricle
3) inferior aspect of the left ventricle
4) posterior septal area

65
Q

Occlusion of the right coronary artery will affect which aspect of the heart?

A

inferior

66
Q

Describe the course of the circumflex artery:

A

curves around the top, left and back of the heart

67
Q

Give 2 cardiac regions supplied by the circumflex artery:

A

1) left atrium
2) posterior aspect of the left ventricle

68
Q

Occlusion of the circumflex artery will affect which aspect of the heart?

A

lateral

69
Q

Describe the course of the left anterior descending artery:

A

travels down the middle of the heart

70
Q

Give 2 cardiac regions supplied by the left anterior descending artery (LAD):

A

1) anterior aspect of the left ventricle
2) anterior aspect of the septum

71
Q

Occlusion of the left anterior descending artery (LAD) will affect which aspect of the heart?

A

anterior

72
Q

What are the criteria used to identify an ST elevation in patients with previously known LBBB?

A

Sgarbosa criteria

73
Q

What is the Sgarbosa criteria?

A

Concordant (going in same direction as QRS spike) ST elevation >1mm in any lead
ST depression >1mm in V1, V2 or V3
Discordant (going in opposite direction to QRS) ST elevation of >5mm in any lead

74
Q

What leads are represent different areas for a STEMI?

A

Anterior: V1-V4
Inferior: II, III, aVF
High lateral: I, aVL
Low lateral: V5, V6
Posterior: a dominant R wave in V1-3 with ST depression in V1-3 (the mirror image of an anterior MI)

75
Q

What is the gold standard of managing STEMI?

A

Primary percutaneous intervention

76
Q

What is primary percutaneous intervention?

A

Primary percutaneous coronary intervention (PCI) refers to the strategy of taking a patient who presents with STEMI directly to the cardiac catheterization laboratory to undergo mechanical revascularization using balloon angioplasty, coronary stents, aspiration thrombectomy, and other measures.

77
Q

What is unstable angina?

A

Unstable angina is an acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage. It is characterised by specific clinical findings of: 6

prolonged (>20 minutes) angina at rest
new onset of severe angina
angina that is increasing in frequency, longer in duration, or lower in threshold
angina that occurs after a recent episode of myocardial infarction

78
Q

What is the management of unstable angina?

A

Beta blockade (or alternative rate-limiting agent if contraindicated – aim HR of 50-60 bpm)
ACE inhibitor (unless contraindicated – aim for a systolic blood pressure of 120 mmHg or less)
Atorvastatin 80mg OD

Yr 3 Cardiovascular (28 decks)

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