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Week 2 - Acute Coronary Syndrome > Management of Acute Coronary Syndrome > Flashcards

Management of Acute Coronary Syndrome Flashcards

1
Q

What is Angina?

A

A clinical syndrome caused by insufficient oxygen delivery to the heart muscle, leading to ischemia. It results from an imbalance between increased demand and decreased supply, often due to atherosclerotic plaques in coronary arteries.

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2
Q

What is ischemia?

A

Restriction of blood flow

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3
Q

What does decreased supply cause?

A

Coronary plaque perfusion
Decrease perfusion pressure
Decrease arterial oxygen content

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4
Q

What is the most common symptom of an angina?

A

Constricting discomfort in the front chest; radiating to neck, jaw and left arm.

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5
Q

What does an increase demand cause?

A

Increase heart rate
Increase pre-load
Increase after-load
Increase contractility

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6
Q

What are the aims of treating angina?

A

Relieve symptoms,
Prevent or slow disease progression,
Prevent further cardiac events, and improve survival and quality of life.

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7
Q

What are the characteristics of stable angina?

A

Precipitated by exertion or extreme temperatures, relieved by rest or nitrates, with a set pattern of triggers. It involves long-term management to prevent attacks and reduce the risk of coronary artery disease.

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8
Q

What defines unstable angina?

A

An acute coronary syndrome characterized by sudden worsening of symptoms, no/minor ECG changes or troponin rise, and less responsiveness to treatment. It can progress to myocardial infarction (MI).

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9
Q

What are Acute Coronary Syndromes (ACS)?

A

A spectrum of conditions including unstable angina, Non-ST Segment Elevation Myocardial Infarction (NSTEMI), and ST-Segment Elevation Myocardial Infarction (STEMI).

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10
Q

What is the role of troponin in diagnosing myocardial infarction?

A

Troponin levels rise 4-8 hours after MI onset, peak at 18-24 hours, and remain elevated for up to 10 days, allowing late diagnosis and detecting re-infarctions.

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11
Q

Why do troponin levels rise?

A

Infarction to the myocardiocytes. Necrosis causes troponin to be released into the bloodstream.

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12
Q

What characterizes a STEMI?

A

A plaque rupture leading to thrombosis, causing irreversible necrosis of heart muscle due to a long interruption in blood supply.

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13
Q

What changes do you see on an ECG for a STEMI?

A

ST segment elevation.

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14
Q

What distinguishes a Non-STEMI?

A

Myocardial necrosis with risk of progression to a STEMI, but with blood flow still present. Treatment focuses on relieving ischemia and preventing further MI or death.
Partial occlusion.

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15
Q

What changes do you see on an ECG for NSTEMI?

A

ST segment drop.

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16
Q

What is subendocardial ischemia?

A

Myocardial damage which is often confined to the deep (subendocardial) layer of left ventricular muscle - only subendocardial is affected.

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17
Q

What happens to the wall when a coronary artery is occluded?

A

Entire wall thickness from endocardium to epicardium is affected.

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18
Q

What are the key medications used in cardiovascular disease?

A

Antiplatelets, anticoagulants, fibrinolytics, beta-blockers, ACE inhibitors, calcium channel blockers, statins, and others like nicorandil and ivabradine.

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19
Q

How do nitrates work in angina treatment?

A

They vasodilate arteries and veins, improving coronary blood flow, reducing myocardial workload, and decreasing oxygen demand.

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20
Q

What are the uses of nitrates?

A

They are used for prophylaxis of angina and acute heart failure.

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21
Q

What are the side effects of nitrates?

A

Headache,
Flushing,
Hypotension,
Syncope,
Facial flushing,
Postural hypotension

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22
Q

Who are contra-indicated from nitrates?

A

Acute circulatory failure,
Shock,
Head trauma,
Severe hypotension,
Aortic stenosis

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23
Q

Why is GTN used and how is it administrated?

A

Short acting
2 x sublingual and every 5 minutes

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24
Q

What is the action of beta-blockers?

A

They block beta-1 adrenoreceptors, reducing heart rate, force of contraction, and cardiac workload, which lowers myocardial oxygen demand.

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25
Q

What is the use of beta-blockers?

A

Hypertension,
Angina,
MI
Arrhythmias,
Heart failure

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26
Q

What are the side effects of beta-blockers?

A

Bradycardia,
Hypotension,
Cold extremities,
Lethargy,
Fatigue,
Impotence,
Precipitate heart failure if poor left ventricular function

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27
Q

What is the role of calcium channel blockers in cardiovascular treatment?

A

They block calcium access to cells, causing vasodilation and reducing the rate and force of heart contractions. They are used to prevent angina, hypertension, and arrhythmias.
Peripheral vasodilation
Coronary vasodilation
Reduced rate & force of contraction

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28
Q

Who are contra-indicated from beta-blockers?

A

Asthma
Peripheral vascular disease
Cardiac conduction problems

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29
Q

What do dihydropyridines affect?

A

Peripheral and coronary vasodilation and act on vascular smooth muscle

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30
Q

What are the two types of calcium channel blockers?

A

Dihydropyridines & Non-hydropyridines

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31
Q

What do non-dihydropyridines affect?

A

Affect cardiac conduction, slow the heart rate and act on myocardial tissue.

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32
Q

What are the uses of calcium channel blockers?

A

Prophylaxis of angina
Prophylaxis of hypertension
Arrhythmias
Used when beta blockers not appropriate

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33
Q

What are the side effects to calcium channel blockers?

A

Swollen ankles
Headache
Constipation
Flushing
Bradycardia
Oedema

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34
Q

Who are contra-indicated from beta blockers?

A

Severe hypotension
Heart failure
Sick sinus syndrome

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35
Q

How does aspirin act as an antiplatelet?

A

Aspirin irreversibly inhibits cyclo-oxygenase, preventing thromboxane production and platelet aggregation for 7-10 days.

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36
Q

What are the uses for aspirin?

A

Revascularisation to restore sufficient blood flow to affected vessel (reperfusion)
Inhibit clot formation - stop the plaque from getting bigger
Support plaque stabilisation
Secondary prevention of CV disease, TIA, stroke

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37
Q

What are the side effects of aspirin?

A

Bronchospasms,
GI bleeds,
GI irritation,
Tinnitus

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38
Q

What are the doses of aspirin?

A

Loading dose 300mg
Low dose 75mg

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39
Q

Who are contra-indicated from aspirin?

A

Actively bleeding risk
Low platelet count
Allergy

40
Q

What are P2Y12 receptor antagonists, and how do they work?

A

Medications like clopidogrel and prasugrel prevent ADP-mediated activation of platelets, often used in combination with aspirin to prevent atherothrombotic events.

41
Q

What is the action of anticoagulants like heparin?

A

They prevent blood clotting by suppressing clotting factors, used in conditions like unstable angina, STEMI, NSTEMI, and deep vein thrombosis (DVT).

42
Q

What is the role of glycoprotein IIb/IIa antagonists?

A

Inhibit final common pathway involved in platelet aggregation.

43
Q

What are the uses to glycoprotein IIb/IIa antagonists?

A

Prevention of ischemic cardiac complications to patients undergoing PCI.
Short term prevention of MI in patient with unstable angina not responding to conventional treatment and scheduled for PCI

44
Q

What are the side effects of glycoprotein IIb/IIa antagonists?

A

Bleeding,
Back pain,
Fever,
Headaches,
Hypotension,
Nausea

45
Q

What are contra-indicated of glycoprotein IIb/IIa antagonists??

A

Active internal bleeding
Hypertensive retinopathy
Major surgery within last 2 months

46
Q

What is the action of anticoagulants?

A

Prevents blood from clotting.
Doesn’t thin blood.
Suppressing the synthesis or function of various clotting factors - so it takes longer to clot
Anti-thrombotic

47
Q

What are the uses to anti-coagulants?

A

Thromboprophylaxis
Unstable angina
STEMI
NSTEMI
DVT
FE

48
Q

What are the side effects to anti-coagulants?

A

Bleeding
Hyperkalaemia
HIT

49
Q

What is contra-indicated for anti-coagulants?

A

After major surgery
Peptic ulcer
Severe hypotension

50
Q

What other drugs are used (hypertension)?

A

ACE/ARB inhibitors

51
Q

What is the role of ACE inhibitors in cardiovascular disease?

A

They reduce peripheral resistance without increasing heart rate or contractility, improving outcomes in heart failure, hypertension, and post-MI.

52
Q

What is the action of nicorandil?

A

Potassium channel activator with nitrate component
Arterial and venous vasodilating

53
Q

What is the action of nicorandil?

A

Potassium channel activator with nitrate compound
Arterial and venous vasodilating.

54
Q

What is the use of nicorandil?

A

Prevention & longterm management of angina
No acute treatment

55
Q

What are the side effects to nicorandil?

A

Headache
Ulceration
Dizziness
Flushing

56
Q

Who are contra-indicated from nicorandil?

A

Severe hypotension
Left ventricular failure
Hypokalaemia
Acute pulmonary oedema

57
Q

What is nicorandil mode of action when it’s mode is nitrate-like action?

A

Dilates epicardial coronary arteries - increase coronary bloodflow

Venodilation - decrease preload - decrease myocardial oxygen requirement

58
Q

What is the mode of action for nicorandil when K+ channel opener ATP?

A

Dilates peripheral arterioles - decreased afterload - decreased myocardial oxygen requirement.

Dilates coronary resistance vessels - increase coronary blood flow.

59
Q

What is the mechanism for ranolazine?

A

Facilitates myocardial relaxation
Doesn’t affect heart rate / blood pressure
Interferes with sodium channel, decrease calcium influx

60
Q

What is the use of ranolazine?

A

Adjunct in stable angina
Oral tablet

61
Q

What are the side effects to ranolazine?

A

Dizziness
Headache
Constipation
Nausea
Vomiting

62
Q

Who is contra-indicated from ranolazine?

A

Severe renal impairment
Caution long GT syndrome

63
Q

What is ivabradine’s mechanism?

A

Lowers heart rate - selectively and specfically inhibting the cardiac pacemaker (sodium-potassium inward current) - controls spontaneous diastolic depolarisation in SA node
Decreased myocardial oxygen demand
No effect on BP or contraction
Acting directly on sinus node
Most atrial fibrillation originates from left atrium therefore ineffective in AF
Decreased myocardial oxygen demands
No effects on blood pressure or contraction

64
Q

What is the use of ivabradine?

A

Treatment of angina in patients with normal sinus rhythm
Add on for stable patients

65
Q

What are the side effects for ivabradine?

A

GI
Nausea
Constipation
Diarrhoea

65
Q

Who are contra-indicated from ivabradine?

A

Heart rate <76
Acute MI
Unstable angina
Unstable heart failure

66
Q

What is the mechanism of action for statins?

A

Statins inhibit HMG-CoA reductase, blocking cholesterol synthesis, and are used for primary and secondary prevention of cardiovascular events.

67
Q

What is the use of statins?

A

Primary or secondary prevention of CV events
Hyperlipidemia

68
Q

What are the side effects of statins?

A

Muscle aches and pains
Myopathy - rhabdomolysis
Nausea
Insomnia

69
Q

Who are contra-indicated from statins?

A

Liver disease

70
Q

What is the standard dose for statins?

A

80mg OD

71
Q

What is reperfusion therapy?

A

Reperfusion restores blood flow.

71
Q

What are the two choices for reperfusion?

A

Primary percutaneous coronary intervention (PCI) Thrombolysis

72
Q

Who is reperfusion mainly for?

A

STEMI patients.
All suitable candidates.

73
Q

What is the goal for STEMI reperfusion?

A

Recognise rapidly
Time is muscle
ECG criteria for urgent reperfusion
Posterior MI
New LBBB

74
Q

When can PCI be provided?

A

Can be achieved 90 minutes of arrival to ED
Symptom onset within previous 12 hours

75
Q

When are thrombolytics used?

A

Between 6-12 hours of symptoms
Ideally within 60 minutes of primary PCI

76
Q

What is the action of thrombolytics?

A

Fibrinolytic drug activate plasminogen which turns into plasmin which then degrades the fibrin clot breaking thrombus

77
Q

What is the use of thrombolytics?

A

Acute MI
PE
Ischaemic stroke

78
Q

What are the side effects to thrombolysis?

A

Cerebral bleed

79
Q

What are the benefits of PCI compared to thrombolysis?

A

Maintains coronary artery patency
Less bleeding
Lower mortality
Lower risk of stroke
Lower risk of re-infarction
Less-post infarct angina

79
Q

What is the secondary prevention medical management?

A

6As

Aspirin - 75mg
Another Antiplatelet
Atorvastatin
ACE inhibitor
Atenolol
Aldosterone in those with clinical heart failure

80
Q

What are the secondary prevention for ACS?

A

Low dose aspirin - decrease risk of death by 25%
Statins
Smoking
Diet & weight modifications
DVLA
Limit alcohol
Increased excercise
Controlled diabetes / hypertension

80
Q

What are the aims for therapy in a stable angina - reducing oxygen demand?

A

Decreasing cardiac work:
Beta blockers
Rate limiting calcium channel blockers
Ivadraline

81
Q

What are the aims for therapy in a stable angina - increase oxygen supply?

A

Improving coronary blood flow:
Nitrates - used to relieve ischaemia rapidly during an attack of taken regularly as prophylaxis
Calcium channel blockers
Nicorandil

81
Q

What is the line of treatment for acute NSTEMI?

A

BATMAN
Beta blockers
Aspirin - 300mg stat
Ticagrelor
Morphine - pain
Anticoagulant
Nitrate - relieve coronary artery spasm
(oxygen if required)

82
Q

What is the management for NSTEMI / unstable angina?

A

Sublingual FTM or IV nitrates
Morphine - pain
Oral beta blockers
Aspirin
Tricagrelor / clopidogrel
ACE inhibitors
Statin
Fondaparinux

83
Q

What is the main counselling for medications?

A

What
Why
Significance
Risks
How
What do they do if they miss a dose
Courses
How to get supplies

84
Q

What is the initial treatment of ACS?

A

Morphine
Oxygen
Nitrates
Aspirin

85
Q

What is the mechanism of action for clopidogrel?

A

Antiplatelet - inhibits ADP binding to its platelet receptor

85
Q

What does DAPT include?

A

Aspirin & P2Y12 receptor (prasugrel & ticagrelor)

85
Q

What is the mechanism of action for aspirin?

A

Antiplatelet - inhibits thromboxane a2 (potent platelet aggregator)

86
Q

What would you do if you’re prescribing DAPT but patient has high risk of GI bleed?

A

Gastro-protection

86
Q

What is the mechanism of fondaparinux?

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

86
Q

What is the mechanism of action for enoxaparin?

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

87
Q

What is the mechanism of bivalirudin?

A

Reversible direct thrombin inhibitor

87
Q

What is the mechanism of abciximab, eptifibatide, tirofiban?

A

Glycoprotein IIb/IIa receptor antagonists

Week 2 - Acute Coronary Syndrome (3 decks)

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