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Cardiovascular Medicine > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What is acute coronary syndrome?

A

Sudden cardiac death, NSTEMI, STEMI and unstable angina are all acute coronary syndromes

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2
Q

What is used to differentiate between all of the different acute coronary syndromes?

A

Troponin levels

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3
Q

What does an acute coronary syndrome cause?

A

Myocardial ischaemia

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4
Q

What is myocardial infarction?

A

Death of the cardiac myocytes caused by a lack of oxygen

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5
Q

How do stable and unstable angina present?

A

Stable= only occurs on exertion, relieved by rest

Unstable= occurs at rest

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6
Q

What is the diagnostic criteria for an myocardial infarction?

A

ECG changes + one of the following;

  • Symptoms of ischaemia
  • New ECG changes
  • Evidence of a coronary problem on coronary angiogram or autopsy
  • Evidence of new cardiac damage on another test
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7
Q

What does troponin indicate?

A

Myocardial injury (it is not exclusive to MI)

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8
Q

What other cardia condition may cause a +ve troponin?

A
  1. Arrhythmias
  2. Pulmonary embolism
  3. Cardiac contusion
  4. Sepsis
  5. Anaemia
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9
Q

What are the definitions for the two different types of MI?

A

Type 1= spontaneous MI assocaited with ischaemia and due to a primary cardiac event such as plaque erosion, rupture, fissuring or dissection

Type 2= Due to an imbalance in the supply and demand of oxygen. It is a result of ischaemia but not ischaemia from thrombosis of a coronary artery

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10
Q

What red flags might be mentioned when taking a history that are associated with acute coronary syndrome

A

Ischaemic sounding chest pain (radiating to arm/jaw, discomfort rather than pain/tightening/weight, nausea, sweating & breathlessness)

Risk factors (male, older age, known heart disease, hypertensive, high cholesterol, diabetes, smoker, FHX)

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11
Q

What would you expect to see when examining a patient suffering from an acute coronary syndrome?`

A

The patient may look very unwell if having a STEMI but they may also look completely fine
Often there are no specific examination features to find

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12
Q

What should you ensure to check during the examination of a patient with suspected acute coronary syndrome?

A
  • Heart rate and blood pressure in both arms.

* Listen for murmurs and for crackles in the chest

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13
Q

What is the acute management of a patient with an coronary syndrome?

A
  1. Admit to hospital
  2. Serial ECG
  3. Attach to a cardiac monitor
  4. Gain IV access
  5. Give O2 only if levels low
  6. Blood tests- check troponin
  7. GTN & pain medication
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14
Q

When is GTN / nitrates contraindicated and why?

A

In hypotensive patients- it causes arterial dilation and so will drop BP even further

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15
Q

In which type of acute coronary syndrome will GTN have no effect?

A

In cases where the artery is completely blocked

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16
Q

Which two methodologies can be used to reopen a blocked coronary artery (reperfusion therapy)

A
  1. Mechanical (Primary Percutaneous Coronary Intervention (PCI))
  2. Pharmacologically (anti-thrombolytics + anti-fibrinolytics + beta blockers, statins & ACE inhibitors
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17
Q

What is the guidance regarding thrombolysing patients in the community?

A

If the patient is more than 2 hours away from the cath lab, they should be thrombolysed then transferred

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18
Q

What is the risk associated with thrombolysis?

A

The patient is at risk of bleeding

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19
Q

What are the risks associated with coronary angiography and Percutaneous Coronary Intervention (PCI)? (6)

A
  • Bleeding from arterial access site (usually go from radial artery nowadays rather than the traditional femoral route)
  • Myocardial infarction
  • Coronary perforation
  • Emergency CABG
  • Stroke
  • Dye can affect kidney function (“contrast nephropathy”)
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20
Q

What is the goal of pharamacological management of acute coronary syndrome?

A
  1. Increase myocardial oxygen supply?

2. Decrease myocardial oxygen demand

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21
Q

What is the optimum window for thrombolysing a stemi?

A

2 hours

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22
Q

If primary PCI cannot be delivered within 2 hours what should happen?

A

Thrombolyse the patient and give fibrinolytics

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23
Q

What is the most common type of thrombolytic agent given today and how does it work?

A

serine proteases convert plasminogen to the natural fibrinolytic agent plasmin- Plasmin lyses clot by breaking down the fibrinogen and fibrin contained in a clot

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24
Q

What are the two different categories of fibrinolytics used to thrombolyse?

A
  1. Fibrin specific agents

2. Non-fibrin specific agents

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25
Q

How do the fibrin specific agents work?

A

catalyse the conversion of plasminogen to plasmin in the absence of fibrin

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26
Q

Name 3 fibrin specific fibrinolytics used to thrombolyse

A

Alteplase
Reteplase
Tenecteplase

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27
Q

How do non-fibrin specific agents work?

A

catalyse systemic fibrinolysis.

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28
Q

Name a non-fibrin specific fibrinolytic

A

Streptokinase

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29
Q

What are the 7 contraindications of thrombolysis with fibrinolytics?

A
  • Prior intracranial haemorrhage (ICH)
  • Known structural cerebral vascular lesion
  • Known malignant intracranial neoplasm
  • Ischaemic stroke within 3 months
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (excluding menses)
  • Significant closed-head trauma or facial trauma within 3 months
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30
Q

Explain the dual antiplatelet therapy that should be administered to any patient with an acute coronary syndrome

A

aspirin (300 mg loading dose) and ticagrelor (180 mg loading dose).

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31
Q

How should a coronary syndrome be managed initially?

A

ECG & Troponin

MOANA

  1. Morphine
  2. Oxygen
  3. Aspirin loading dose (300mg)
  4. Nitrates (GTN)
  5. Antiplatelet (ticagrelor)
32
Q

When should a STEMI patient be offered
A) PCI
B) Thrombolysis

A

A) If the patient has presented to hospital within 12 hours of symptom onset and they can be seen in PCI within 120 minutes.

B) If the patient has presented to hospital within 12 hours of symptom onset and they cannot be seen in PCI within 120 minutes

33
Q

How should an NSTEMI be managed (after the initial acute coronary syndrome management)?

A
  1. Ensure they have recieved the dual antiplatelet (aspirin and ticagrelor)
  2. Give an anticoagulant (fondapainux or unfractionated heparin if the PT has renal impairment)
  3. Tirofiban
  4. Nitrates for pain management
  5. Risk assess using GRACE score
  6. If GRACE is 3 or less carry out coronary angiography immediately. If GRACE is 3 or more carry out angiography within 72 hours
  7. Cardiac rehab and secondary prevention
34
Q

How should unstable angina be managed after the initial acute coronary syndrome management?

A
  1. Dual antiplatelet medication: aspirin and ticagrelor
  2. Anticoagulant- Fondapainux or unfractionated heparin in renal impairment
  3. Nitrates- pain management
  4. Statin
  5. ACEi
  6. Beta blocker
  7. PCI or CABG when stable
35
Q

What are the drugs given as secondary prevention following an acute coronary syndrome?

A

6 As

  1. Aspirin
  2. Antiplatelet (continued for 12 months)
  3. Atorvastatin
  4. ACEi
  5. Atenolol
  6. Aldosterone antagonist- for patients with clinical heart failure
36
Q

What is the Killip classification used for?

A

Used to identify features of heart failure (it also provides the 30 day mortality of each classification)

37
Q

Describe each Killip classification

A

I - No clinical signs of heart failure (30 day mortality 6%)

II- Lung crackles (30 day mortality 17%)

III- Frank pulmonary oedema (30 day mortality 38%)

IV- Cardiogenic shock (30 day mortality 81%)

38
Q

Name some of the poor prognostic factors associated with acute coronary syndrome

A
  • Age
  • Development of heart failure
  • Peripheral vascular disease
  • Reduced systolic blood pressure
  • Killip class (see table)
  • Initial serum creatinine concentration
  • Elevated initial cardiac markers
  • Cardiac arrest on admission
  • ST segment deviation
39
Q

List the complications associated with acute coronary syndrome

A
  1. Cardiac arrest
  2. Cardiogenic shock
  3. Heart failure
  4. Arrythmias
  5. Rupture of myocardial structures
  6. Left ventricular thrombus ‘
  7. Pericarditis
  8. Dressler’s syndrome
  9. Ventricular septal defect
  10. Acute mitral regurgitation
40
Q

What are the two classes of antithrombotic agent?

A
  1. Anti-platelets

2. Anticoagulants

41
Q

What is the difference between an antiplatelet and an anticoagulant?

A

Antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing. Anticoagulants slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing.

42
Q

Name the 3 different types of antiplatelet

A
  1. Aspirin
  2. P2Y12 ADP Receptor antagonists
  3. GP IIb/IIIa receptor antagonists
43
Q

Explain the mechanism of action of aspirin

A

Inhibits thromboxane A2 (which normally stimulates platelet aggregation and vasoconstriction)

44
Q

Name the study which found that there was no significant differences between patient outcomes when they were given low dose aspirin VS high dose aspirin

A

CURRENT-OASIS 7

45
Q

Why is aspirin given in acute MI?

A

Reduces cardiovascular death, non-fatal MI and no-fatal stroke

46
Q

Why is aspirin given in unstable angina?

A

Reduces the rate of vascular events (cardiovascular death, non-fatal MI and non-fatal stroke) by 50%

47
Q

Why is aspirin given in secondary prevention?

A

Reduces reinfarction and reduces combined vascular events

48
Q

Name the two P2Y12 ADP receptor antagonist drugs

A

Ticagrelor and Clopidogrel

49
Q

What is the mechanism of action of P2Y12 ADP recepor antagonists?

A

Prevent platelet activation by inhibiting the step in the platelet activation cascade in which ADP activates P2Y12

50
Q

Name the trial that found that Clopidogrel + aspirin was more effective than aspirin alone

A

CURE trial

51
Q

Explain the mechanisms behind Clopidogrel resistance

A
  • Clopidogrel is a prodrug activated by Cyp 2C19 (this is slow and variable metabolism)
  • 14% of population have low CYP2C19 levels and demonstrate resistance to clopidogrel
52
Q

Which drug more effectively reduces vascular death, MI & stroke more effectively; clopidogrel or ticagrelor?

A

Ticagrelor

53
Q

Name a GP IIb/IIIa receptor antagonist drug

A

Tirofibin

54
Q

Explain how tirofibin works

A

Works in a similar way to P2Y12 ADP Receptor Antagonists except it antagonises GP IIb/IIIa which is further down the platelet activation cascade

55
Q

Name the two different types of anticoagulants

A
  1. P2Y12 inhibitors

2. Heparin

56
Q

Name 2 P2Y12 inhibitor drugs

A

Prasugrel & Fondaparinux

57
Q

What must P2Y12 inhibitor drugs be used in combination with?

A

Aspirin

58
Q

Compare prasugel (a P2Y12 inhibitor) with ticagrelor (a P2Y12 receptor antagonist)

A

Both inhibit ADP receptors and prevent the ctivation of P2Y12 in the platelet activation cascade however, compared to clopidogrel, prasugrel inhibits ADP–induced platelet aggregation more rapidly & more consistently.

59
Q

Explain the mechanism of action of Fondaparinux

A

Selectively inhibits factor Xa

60
Q

Briefly explain the mechanism of action of heparin?

A

Inactivates thrombin and factor X

61
Q

Name three beta blockers

A

Atenolol, propranolol, bisoprolol

62
Q

What is the purpose of beta blockers in acute coronary management?

A

Improve the symptoms and prognosis of acute coronary syndrome

63
Q

Explain the mechanism of action of beta blockers

A

They reduce the force of contraction and the speed of conduction in the heart by prolonging the refractory period in the SA node.

64
Q

Name the study that found beta blockage had no effect on on mortality or the end points of death, reinfarction or cardiac arrest. but it reduced reinfarction & arrhythmic death by 0.5%

A

COMMIT/CCS Trial

65
Q

Name the two types of nitrate drug

A 
Glyceryl Trinitrate (short acting)
Isosorbide mononitrate (long acting)
66
Q

Breifly explain the mechanism of action of nitrate drugs

A

Converted to nitric oxide which increases cyclic guanosine monophosphate synthesis which reduces intracellular Ca2+ causing vessels to relax (mainly causing venous dilation)

67
Q

Explain how nitrates are useful in acute coronary syndrome

A

Relaxing the venous capacitance vessels reduces cardiac preload and left ventricular filling which in turn reduces cardiac work and myocardial oxygen demand. This relieves angina and cardiac failure.

68
Q

Why are statins used in secondary prevention following an acute coronary syndrome?

A

They reduce the liklihood of a further coronary event by reducing serum cholesterol

69
Q

Briefly explain the mechanism of action of statins

A

Statins competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, an enzyme involved in cholesterol synthesis, especially in the liver.

70
Q

Name a statin drug

A

Atorvastatin

71
Q

List three ACE inhibitor drugs

A

Ramapril, lisinopril & perindopril

72
Q

Why would you given an acute coronary syndrome patient an ACE inhibitor?

A

In secondary prevention to reduce the risk of subsequent cardiovascular events such as MI and stroke

73
Q

Explain the mechanism of action of ACE inhibitors

A

ACE cleaves angiotensin I into angiotensin II. Ace inhibitors therefore prevent this from happening and therefore prevent hypertension by preventing arteriolar constriction, preventing water retention and preventing sympathetic activation.

74
Q

What are 2 significant side effects associated with ACE inhibitors?

A

Dry cough

Hyperkalaemia

75
Q

When would you given an acute coronary syndrome patient an Aldosterone antagonist?

A

You would prescribe this for patients ho develop chronic heart failure as a result of ACS

76
Q

Name an aldosterone antagonist drug

A

Spirinolactone

77
Q

Breifly explain the pathophysiology of aldosterone receptor antagonists

A

Decreases the reabsorption of salt and water by competitively binding to the aldosterone receptor

Cardiovascular Medicine (24 decks)

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