<p> SLIME REVISION – ACS HAND OUT</p><p>Definition</p><p> Acute: Comes on quickly  Coronary: Relating to the arteries supply the heart  Syndrome: Group of symptoms</p><p> Acute coronary syndrome: A group of symptoms associated with the heart arteries which come on quickly (Roughly) o Also: . Not relieved by rest/removal of possible trigger . Lasting more than 20 minutes despite GTN </p><p>The 3 Types of ACS  Unstable angina – Coronary chest pain, coming on at rest/unprovoked. WITHOUT TISSUE DAMAGE OR DEATH.  NSTEMI (Non-ST Elevation myocardial infarction) – Coronary chest pain cause by partial occlusion of the coronary arteries leading to some tissue damage and death but not causing ST elevation on ECG. Tissue damage is confirmed by using Cardiac troponin T level in the blood.  STEMI (ST Elevation myocardial infarction) – As above however cause by complete occlusion leading to more extensive death of tissue and ST elevation on ECG</p><p>Pathophysiology Process of atherosclerosis 1. LDL migrates into artery wall activating macrophages 2. Macrophage ingest the oxidised LDL and produce inflammatory cytokines which in turn attracts and activates more inflammatory cells 3. Macrophages develop into foam cells 4. Macrophages present the oxidised LDL as an antigen to T cells 5. T-cells produce more cytokines 6. Cytokines result in smooth muscle cell migration and multiplication – stabilising plaque. See diagram</p><p>Process leading to Angina/ACS: 1. Atherosclerosis leads to narrowing of coronary arteries which can lead to decrease oxygen supply during high cardiac demand (E.G. Exercise) 2. Plaques may rupture, exposing necrotic centre which leads to platelet aggregation and thrombus formation. This may lead to further narrowing (unstable angina) or complete occlusion (MI). 3. Thrombi may also embolise and lead to more distal occlusion Risk factors for atherosclerosis Non Modifiable –  Increasing age  Male gender  Family history of IHD  Ethnicity</p><p>Modifiable (Common and less common) • Hyperlipidaemia • Homocysteinaemia • Smoking • Gout • Hypertension • Drugs: OCP, COX-2 inhibitors, • Diabetes mellitus Cocaine • Lack of exercise • Personality • Obesity • CRP • Heavy alcohol consumption • Soft water • Abnormal coagulation factors– High fibrinogen or Factor VII</p><p>Signs and symptoms of ACS Symptoms • Pain – Crushing/Squeezing/Heaviness – Retrosternal (Epigastric, Back, Neck, Jaw, Shoulder) – Radiation to any of the above • Nausea • Dizziness/Syncope • SOB • Sense of impending doom</p><p>Signs • Tachycardia/Bradycardia • Hypotension/Syncope • Tachypnoea • Vomiting, pallor, sweatiness • Signs of acute heart failure – Crepitations, Raised JVP, Murmur</p><p>Investigations</p><p>Cardiac enzymes</p><p>- Troponins : Most sensitive and specific for myocardial damage. T and I are specific to myocardial damage but can be false + from infection, severe PE, RHF and myocarditis. Released from 2-4 hours, peaks at 12 hours and lasts for 7 days - CKMB : specific if theres not skeletal muscle damage. Peaks at 12 hrs. Normal in 2-3 days - LDH : less specific than troponins. LDH1 is cardiac and LDH2 is serum therefore can do a ratio between them. Peak 72 hours, normal in 10-14 days</p><p>Management</p><p>- For all ACS do MONA first o Morphine (5-10mg slow IV injection) o Oxygen (titrate sats to need) o Nitrates - GTN spray (400mcg = 1 spray) or tablet (1mg) o Aspirin (300mg chewed)</p><p>- Then NSTEMI and UA managed the same o LMWH i.e. Enoxaparin 1mg/kg BD or Fondaparinux 2.5mg OD o Clopidogrel 300mg loading dose o Beta blocker - atenolol 5mg o Nitrates – usually IV o Consider coronary angiography within 72 hr</p><p>- STEMI management o REPERFUSE ASAP!!! 120 minutes call to balloon time for PCI o Thrombolyse if cant get to a 24hr PCI centre within 120 mins (note CIs) o Clopidogrel 600mg loading dose prior to either reperfusion o BB and ACE inhibitor</p><p>- Longer term management of ACS o Continuous ECG monitoring as inpatient/ CCU o Aspirin 75mg OD (lifelong) o Clopidogrel 75mg (1 year) o Beta blocker (1 year - lifelong) o ACE inhibitor o Statin o Modification of risk factors</p><p>Complications of MI</p><p>SPARED mnemonic: </p><p>- sudden death - pericarditis - aneurysm/arrhythmia - ruptured ventricular wall - embolism - Dresslers syndrome</p>