Acute Coronary Syndromes

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  • Created by: LBCW0502
  • Created on: 17-01-19 10:52
What is Ischaemia Heart Disease?
Narrowing of the lumen of the coronary arteries resulting in an imbalance between the supply of oxygen (and other essential nutrients) and the myocardial demand resulting in myocardial ischaemia and chest pain
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What is stable angina? (1)
Chest pain (tightness, heavy pressure, squeezing or crushing). Begins slowly, get worse over next few minutes (myocardial oxygen demand increases slowly), lasts 15 mins (relieved with rest/GTN), can be picked up late. Often predictable, may spread
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What is stable angina? (2)
May feel like indigestion/heartburn. Different symptoms (back/arm/neck pain, fatigue, SOB, weakness). Comes on at same intensity at same exertion. Disguise chest pain e.g. walking up the stairs. Central crushing pain
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What are the factors considered in myocardial oxygen demand?
Work rate (HR) and work load (TPR)
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What are the factors considered in myocardial oxygen supply?
Thrombus, atheroma, vasoconstriction
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What tests are carried out to diagnose angina?
Cardiac enzyme, troponin (cardiac specific – only released when heart muscle dies/breaks down, doesn’t appear in any other area of the body). Positive treadmill test – used to determine when angina takes place, measure myocardial oxygen demand/supply
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What are the treatments to control symptoms of stable angina?
Medicines to reduce myocardial oxygen demand. Lifestyle advice (stop smoking)
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What are the treatments to control symptoms of stable angina (e.g. bisoprolol, atenolol)?
Beta blockers - blocks beta receptor of sympathetic response (b1-b2). Reduces myocardial oxygen demand by reducing HR/BP. Side effects - bronchospasm, peripheral vasoconstriction, impotence, fatigue
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What is the significance of controlling HR?
Heart doesn’t need to beat so hard, don’t want muscle to be over-exerted, want cardiac muscle to rest as much as possible. Should not consider reduction in exercise due to fatigue
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What are the treatments to control symptoms of stable angina (e.g. dihydropyridines, amlodipine, felodipine)?
Calcium channel blockers - revent Ca influx into smooth muscle cells. Reduces myocardial oxygen demand by reducing afterload and preload. Side effects - flushing, headache, dizziness, ankle swelling
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What are the treatments to control symptoms of stable angina (e.g. isosorbide mononitrate)?
Nitrates - stimulation of soluble guanylate cyclase by NO derived from organic nitrate ester molecule. Venodilation (decrease preload, decrease myocardial oxygen demand). Side effects - flushing, hypotension
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What are the treatments to reduce the risk of stable angina?
Lifestyle advice (stop smoking/salt reduction/exercise)
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What are the treatments to reduce the risk of stable angina (e.g. aspirin, clopidogrel)?
Anti-platelet agents - inhibits platelet reaction to stimuli by blocking TxA2/P2Y12 receptor respectively. Reduces change of clot formation. Side effects - GI disturbance, bleeding, bronchoconstriction
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What are the treatments to reduce the risk of stable angina (e.g. atorvastatin, simvastatin)?
Cholesterol lowering agents - blocks cholesterol synthesis in liver, blocks HMG-CoA reductase. Reduces serum cholesterol atherosclerotic plaque formation. Side effects - nasopharyngitis/headache/constipation/flatulence/dyspepsia/nausea, arthralgia
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What needs to be considered during patient education?
Titration of dose, ensure patient is aware of signs e.g. bleeding and what action to take, use of GTN spray (replacement/GP surgery/hospital)
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Describe features of stable and vulnerable plaques (1)
Atheroma (reduced lipid core with thick fibrous cap reinforced with increased smooth muscle cells/covering, unlikely to burst) and labile clot (large lipid core with thin fibrous cap, macrophages interact with thrombus)
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Describe features of stable and vulnerable plaques (2)
(if it ruptures, it starts a blocking cascade, clot occurs in artery with lack of oxygen supply to the heart)
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What is an acute coronary syndrome?
Rupture of atheromatous plaque resulting in sudden/critical reduction in blood flow in coronary artery by platelet aggregation and/or thrombus formation causing injury or infarction of myocardial tissue precipitating chest pain, rest/minimal exertion
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Outline the process for diagnosis of acute coronary syndromes
Admission (chest pain). Working diagnosis (acute coronary syndrome). ECG (persistent ST-elevation/ST/T abnormalities/normal or undermined ECG). Biochemistry (ECG/troponin rise or fall/troponin normal). Diagnosis (STEMI/NSTEMI/unstable angina)
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Outline the treatment of ACS (STEMI)
Initial treatment of ACS. STEMI - anti-platelet, anti-ischaemic or anti-coagulant therapy - thrombolytics or primary PCI/CABG - rescue PCI/CABG or angiography - long term management
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Outline the treatment of ACS (UA/NSTEMI)
Initial treatment of ACS. UA/NSTEMI - anti-platelet, anti-ischaemic or anti-coagulant therapy - angiography - PCI/CABG - long term management
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What does a cardiac centre do?
Reduce clot in artery at cardiac centre – PAMI call
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What are the effects of myocardial ischaemia, injury and infarction on ECG? (1)
Myocardial ischaemia causes ST segment depression with/without T wave inversion as result of altered repolarisation. Myocardial injury causes ST segment elevation with/without loss of R wave
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What are the effects of myocardial ischaemia, injury and infarction on ECG? (2)
Myocardial infarction causes deep Q waves due to absence of depolarisation current from dead tissue and receding currents from opposite side of heart
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What are the effects of myocardial ischaemia, injury and infarction on ECG? (3)
Myocardial tissue is dead – cannot recover dead tissue (no oxygen/nutrients supplied to tissue area) – zone of infarction. Zone of injury – could be saved if nutrients/oxygen is supplied (aim to reduce area of necrosis).
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What are the effects of myocardial ischaemia, injury and infarction on ECG? (4)
Zone of ischaemia – cells start to shut down, still experience chest pain
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Describe features of coronary angioplasty and stenting
A blood tipped tube is inserted in coronary artery. Balloon is expanded several times. Opens artery, could collapse if left alone (add stent to keep artery open)
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Give examples of drug therapy for patients with STEMI undergoing PCI
Aspirin, clopidogrel, prasurgrel, ticagrelor, UFH, enoxaparin/long acting, glycoprotein IIb/lIIIa inhibitors (abciximab/eptifibatide), intra-coronary vasodilators
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Describe features for inhibition of platelet activation in ACS (1)
Aspirin (TxA2, Tp alpha), clopidogrel (ADP, P2Y12), heparin (short acting)/LMWH/DTi/rivaroxaban (thrombin/PAR1/4), statins, GPIs, NO, PgI2, fibrinolysis etc. (diagram)
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Describe features for inhibition of platelet activation in ACS (2)
60 receptors identified in platelets. r-tPA – breaks down clots and is absorbed into the blood
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What are the absolute contraindications for thrombolytics?
Recent head trauma/cranial tumor, previous haemorrhagic shock, stroke/cerebro-vascular events <1 year old, active internal bleeding, major surgery within 2 weeks
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What are the relative contraindications for thrombolytics?
Active peptic ulcer, diabetic retinopathy, pregnancy, uncontrolled HTN
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Describe features of thrombolytics (e.g. r-tPA, streptokinase, urokinase)
Enhances endogenous effect of tPA in cleaving plasminogen to produce plasmin which breaks down fibrin. Reduce clot burden and allows for myocardial tissue oxygenation. Side effects - anaphylactic reaction, chills, CNS haemorrhage, stroke, hypotension
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What is fibrinolysis?
The enzymatic breakdown of the fibrin in blood clots (diagrams)
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Give examples of drug therapy for patients with NSTEMI
Aspirin, clopidogrel, prasugrel, ticagrelor, UFH, enoxaparin, fondaparinux, oral isosorbide mononitrate, IV GTN infusion, beta blockers, rate limiting Ca channel blockers, high dose statin (atorvastatin, anti-inflammatory properties)
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What are the main blood vessels to the heart?
Right coronary artery (right atrium/ventricle), left main and left anterior coronary arteries (left atrium/ventricle)
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Where do clots in the heart usually take place?
Clots usually occur in blood vessels near the apex of the heart. Clots higher up blood vessels – more at risk of damage after MI, more at risk of death (stents not usually put in coronary arteries)
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Describe features of coronary artery bypass graft
Single/double/triple/quadruple (no. of surgeries). Take blood vessels, arteries or veins (mammary) in different parts of the body, re-plant opposite atheroma. Sedation, heart stopped, arteries 3 mm diameter of lumen. Long term benefits (not for life)
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What is a bypass machine?
Allows blood to flow through the body whilst heart is stopped (longer time heart is stopped, more risk of damage)
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Describe the drug management after CABG (1)
Lifestyle advice. Anti-platelet agents (aspirin/clopidogrel), cholesterol lowering agents (atorvastatin, simvastatin), analgesia at lower doses (paracetamol/dihydrocodeine), diuretics (furosemide)
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Describe the drug management after CABG (2)
Continue secondary preventative meds (ACE/beta blocker), opportunity to discontinue anti-angina meds (e.g. amlodipine)
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Other cards in this set

Card 2

Front

What is stable angina? (1)

Back

Chest pain (tightness, heavy pressure, squeezing or crushing). Begins slowly, get worse over next few minutes (myocardial oxygen demand increases slowly), lasts 15 mins (relieved with rest/GTN), can be picked up late. Often predictable, may spread

Card 3

Front

What is stable angina? (2)

Back

Preview of the front of card 3

Card 4

Front

What are the factors considered in myocardial oxygen demand?

Back

Preview of the front of card 4

Card 5

Front

What are the factors considered in myocardial oxygen supply?

Back

Preview of the front of card 5
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