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ACS Acute Coronary Syndrome = unstable angina or NSTEMI or STEMIPathophysiology • Atheromatous plaque rupture in coronary artery → thrombosis → vessel occlusion • Myocardial infarction (MI) = Myocardial cell death that causes release in troponinRISK FACTORS • Age • Diabetes • Male • Hyperlipidaemia • FHx • Obesity • Smoking • Cocaine • HypertensionSigns • Distress • Hyper or hypotension th • Anxiety • 4 HS • Pallor • HF signs • Sweatiness • Pansystolic murmur – papillary muscle dysfunction • Tachy or Brady • Low grade feverSymptoms • Acute central crushing chest pain lasting > 20 minutes • Radiating down left arm and jaw • Nausea • Sweatiness • Clamminess – due to autonomic/vagal symptoms • Dyspnoea • PalpitationsDIFFERENTIALS • Stable angina • GORD • Pericarditis • MSK pain • Myocarditis • Pancreatitis • PE INVESTIGA TIONS • ECG • CXR o STEMI • Cardiomegaly • Pulmonary oedema ▪ Hyperacute (tall) T waves – occurs first ▪ ST elevation • Widened mediastinum ▪ >1mm (1small square) in limb leads • Bloods ▪ >2mm (2small squares) in precordial leads (V1-6) ▪ T wave inversion • FBC ▪ Pathological Q waves • U+Es o NSTEMI • Glucose • ST depression • Lipids • T wave inversion • Cardiac enzymes – Troponin • Non-specific changes • Notdiseasespecific • Lag tim– repeat after 3 hoursECG Lateral = LCx Inferior = RCA or LCx Anterior/septal = LADAnterior STEMI • ST elevation and hyperacute T waves in V2-4 • ST elevation in I and aVL with reciprocal ST depression in lead III • Q waves are present in the septal leads V1-2 • These features indicate a hyperacute anteroseptal STEMIMANAGEMENT • A → E assessment • Morphine – pain relief • Oxygen – improve oxygenation of ischaemic myocardiumand treatment of pulmonary oedema (not if COPD) • GTN spray/infusion • Aspirin – antiplatelet • Anti-emetic – metoclopramide or ondansetron • Clopidogrel – give once confirmed ACS • Unfractioned heparinPrimary PCI • Reperfusion therapy • Invasive procedure to open the blocked artery and treat the underlying atheromatous plaque by balloon angioplasty and stent placement • Restore the coronary blood supply, minimise cardiac damage and improve outcome • Aim to receive < 90 minutes • After PCI change clopidogrel to ticagrelorSecondary prevention • Medications • Rehabilitation • Statin • Smoking cessation • Ticagrelor – preventsre-infarction • Exercise • Eplerenone • Diet • ACEi • Driving • Beta blocker • Returning to work • Aspirin – preventsre-infarctionComplications • Arrhythmias (AF, VF, heart block) • HF • LVD and HF, can occur acutely and cause pulmonaryoedema, indicator of poor prognosis • Cardiogenic Shock • treat with revascularisation and urgent angioplasty • Myocardial rupture • Papillarymuscle rupture – mitral regurgitation → HF • Inter ventricular septum rupture – VSD • Pericarditis • central pleuritic chest pain relieved by sitting forward, pericardial rub on auscultation,saddle shaped ST elevation • Dressler’s syndrome • recurrent pericarditis, pleural affusions, fever, anaemia and increased ESR, treat with NSAIDS (aspirin/ibuprofen) and steroids if severe • 2-3 weeks after MI by localised immune response • May need pericardiocentesis to remove fluid from around heart • Psychological • DeathTypes of MI • Type 1 • Spontaneous MI related to ischaemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring or dissection • Typ• Secondary to ischaemia due to either increased oxygen demand or decreased supply ( infection) • Type 2 management – not ACS treatment as problem is not a blocked artery – treat underlying cause, - will often have underlying CAD • Type 3 • biomarker valuesd cardiac death often with symptoms suggestive of myocardial ischaemiabefore • Type 4 • MI associated with PCI or stent thrombosis (iatrogenic) • Type 5 • MI assoc with cardiac surgery (CABG)