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

Management of Acute Coronary Syndrome Flashcards

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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
What is the use of beta-blockers?
Hypertension, Angina, MI Arrhythmias, Heart failure
26
What are the side effects of beta-blockers?
Bradycardia, Hypotension, Cold extremities, Lethargy, Fatigue, Impotence, Precipitate heart failure if poor left ventricular function
27
What is the role of calcium channel blockers in cardiovascular treatment?
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
28
Who are contra-indicated from beta-blockers?
Asthma Peripheral vascular disease Cardiac conduction problems
29
What do dihydropyridines affect?
Peripheral and coronary vasodilation and act on vascular smooth muscle
30
What are the two types of calcium channel blockers?
Dihydropyridines & Non-hydropyridines
31
What do non-dihydropyridines affect?
Affect cardiac conduction, slow the heart rate and act on myocardial tissue.
32
What are the uses of calcium channel blockers?
Prophylaxis of angina Prophylaxis of hypertension Arrhythmias Used when beta blockers not appropriate
33
What are the side effects to calcium channel blockers?
Swollen ankles Headache Constipation Flushing Bradycardia Oedema
34
Who are contra-indicated from beta blockers?
Severe hypotension Heart failure Sick sinus syndrome
35
How does aspirin act as an antiplatelet?
Aspirin irreversibly inhibits cyclo-oxygenase, preventing thromboxane production and platelet aggregation for 7-10 days.
36
What are the uses for aspirin?
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
37
What are the side effects of aspirin?
Bronchospasms, GI bleeds, GI irritation, Tinnitus
38
What are the doses of aspirin?
Loading dose 300mg Low dose 75mg
39
Who are contra-indicated from aspirin?
Actively bleeding risk Low platelet count Allergy
40
What are P2Y12 receptor antagonists, and how do they work?
Medications like clopidogrel and prasugrel prevent ADP-mediated activation of platelets, often used in combination with aspirin to prevent atherothrombotic events.
41
What is the action of anticoagulants like heparin?
They prevent blood clotting by suppressing clotting factors, used in conditions like unstable angina, STEMI, NSTEMI, and deep vein thrombosis (DVT).
42
What is the role of glycoprotein IIb/IIa antagonists?
Inhibit final common pathway involved in platelet aggregation.
43
What are the uses to glycoprotein IIb/IIa antagonists?
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
What are the side effects of glycoprotein IIb/IIa antagonists?
Bleeding, Back pain, Fever, Headaches, Hypotension, Nausea
45
What are contra-indicated of glycoprotein IIb/IIa antagonists??
Active internal bleeding Hypertensive retinopathy Major surgery within last 2 months
46
What is the action of anticoagulants?
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
What are the uses to anti-coagulants?
Thromboprophylaxis Unstable angina STEMI NSTEMI DVT FE
48
What are the side effects to anti-coagulants?
Bleeding Hyperkalaemia HIT
49
What is contra-indicated for anti-coagulants?
After major surgery Peptic ulcer Severe hypotension
50
What other drugs are used (hypertension)?
ACE/ARB inhibitors
51
What is the role of ACE inhibitors in cardiovascular disease?
They reduce peripheral resistance without increasing heart rate or contractility, improving outcomes in heart failure, hypertension, and post-MI.
52
What is the action of nicorandil?
Potassium channel activator with nitrate component Arterial and venous vasodilating
53
What is the action of nicorandil?
Potassium channel activator with nitrate compound Arterial and venous vasodilating.
54
What is the use of nicorandil?
Prevention & longterm management of angina No acute treatment
55
What are the side effects to nicorandil?
Headache Ulceration Dizziness Flushing
56
Who are contra-indicated from nicorandil?
Severe hypotension Left ventricular failure Hypokalaemia Acute pulmonary oedema
57
What is nicorandil mode of action when it's mode is nitrate-like action?
Dilates epicardial coronary arteries - increase coronary bloodflow Venodilation - decrease preload - decrease myocardial oxygen requirement
58
What is the mode of action for nicorandil when K+ channel opener ATP?
Dilates peripheral arterioles - decreased afterload - decreased myocardial oxygen requirement. Dilates coronary resistance vessels - increase coronary blood flow.
59
What is the mechanism for ranolazine?
Facilitates myocardial relaxation Doesn't affect heart rate / blood pressure Interferes with sodium channel, decrease calcium influx
60
What is the use of ranolazine?
Adjunct in stable angina Oral tablet
61
What are the side effects to ranolazine?
Dizziness Headache Constipation Nausea Vomiting
62
Who is contra-indicated from ranolazine?
Severe renal impairment Caution long GT syndrome
63
What is ivabradine's mechanism?
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
What is the use of ivabradine?
Treatment of angina in patients with normal sinus rhythm Add on for stable patients
65
What are the side effects for ivabradine?
GI Nausea Constipation Diarrhoea
65
Who are contra-indicated from ivabradine?
Heart rate <76 Acute MI Unstable angina Unstable heart failure
66
What is the mechanism of action for statins?
Statins inhibit HMG-CoA reductase, blocking cholesterol synthesis, and are used for primary and secondary prevention of cardiovascular events.
67
What is the use of statins?
Primary or secondary prevention of CV events Hyperlipidemia
68
What are the side effects of statins?
Muscle aches and pains Myopathy - rhabdomolysis Nausea Insomnia
69
Who are contra-indicated from statins?
Liver disease
70
What is the standard dose for statins?
80mg OD
71
What is reperfusion therapy?
Reperfusion restores blood flow.
71
What are the two choices for reperfusion?
Primary percutaneous coronary intervention (PCI) Thrombolysis
72
Who is reperfusion mainly for?
STEMI patients. All suitable candidates.
73
What is the goal for STEMI reperfusion?
Recognise rapidly Time is muscle ECG criteria for urgent reperfusion Posterior MI New LBBB
74
When can PCI be provided?
Can be achieved 90 minutes of arrival to ED Symptom onset within previous 12 hours
75
When are thrombolytics used?
Between 6-12 hours of symptoms Ideally within 60 minutes of primary PCI
76
What is the action of thrombolytics?
Fibrinolytic drug activate plasminogen which turns into plasmin which then degrades the fibrin clot breaking thrombus
77
What is the use of thrombolytics?
Acute MI PE Ischaemic stroke
78
What are the side effects to thrombolysis?
Cerebral bleed
79
What are the benefits of PCI compared to thrombolysis?
Maintains coronary artery patency Less bleeding Lower mortality Lower risk of stroke Lower risk of re-infarction Less-post infarct angina
79
What is the secondary prevention medical management?
6As Aspirin - 75mg Another Antiplatelet Atorvastatin ACE inhibitor Atenolol Aldosterone in those with clinical heart failure
80
What are the secondary prevention for ACS?
Low dose aspirin - decrease risk of death by 25% Statins Smoking Diet & weight modifications DVLA Limit alcohol Increased excercise Controlled diabetes / hypertension
80
What are the aims for therapy in a stable angina - reducing oxygen demand?
Decreasing cardiac work: Beta blockers Rate limiting calcium channel blockers Ivadraline
81
What are the aims for therapy in a stable angina - increase oxygen supply?
Improving coronary blood flow: Nitrates - used to relieve ischaemia rapidly during an attack of taken regularly as prophylaxis Calcium channel blockers Nicorandil
81
What is the line of treatment for acute NSTEMI?
BATMAN Beta blockers Aspirin - 300mg stat Ticagrelor Morphine - pain Anticoagulant Nitrate - relieve coronary artery spasm (oxygen if required)
82
What is the management for NSTEMI / unstable angina?
Sublingual FTM or IV nitrates Morphine - pain Oral beta blockers Aspirin Tricagrelor / clopidogrel ACE inhibitors Statin Fondaparinux
83
What is the main counselling for medications?
What Why Significance Risks How What do they do if they miss a dose Courses How to get supplies
84
What is the initial treatment of ACS?
Morphine Oxygen Nitrates Aspirin
85
What is the mechanism of action for clopidogrel?
Antiplatelet - inhibits ADP binding to its platelet receptor
85
What does DAPT include?
Aspirin & P2Y12 receptor (prasugrel & ticagrelor)
85
What is the mechanism of action for aspirin?
Antiplatelet - inhibits thromboxane a2 (potent platelet aggregator)
86
What would you do if you're prescribing DAPT but patient has high risk of GI bleed?
Gastro-protection
86
What is the mechanism of fondaparinux?
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
86
What is the mechanism of action for enoxaparin?
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
87
What is the mechanism of bivalirudin?
Reversible direct thrombin inhibitor
87
What is the mechanism of abciximab, eptifibatide, tirofiban?
Glycoprotein IIb/IIa receptor antagonists

Week 2 - Acute Coronary Syndrome (3 decks)

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