Acute Coronary Syndrome and Myocardial Infarction, Study notes of History

Download Acute Coronary Syndrome and Myocardial Infarction and more Study notes History in PDF only on Docsity! Sami Mukhlif Al-obaidy INTERVENTIONAL CARDIOLOGIST and SENIOR LECTURERE FIBMS Cardiol , CABM (Med.), FIBMS (Med.), D.M (Med.), D.M (Chest Diseases), MBChB, MESC CORONARY ARTERY DISEASE ACUTE CORONARY SYNDROMES Acute coronary syndrome is a term that encompasses both unstable angina and myocardial infarction. Unstable angina is characterised by new-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest in the absence of myocardial damage. Myocardial infarction differs from unstable angina, since there is evidence of myocardial necrosis. The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Acute coronary syndrome may present as a new phenomenon in patients with no previous history of heart disease or against a background of chronic stable angina. The risk markers that are indicative of an adverse prognosis include recurrent ischaemia, extensive ECG changes at rest or during pain, raised troponin I or T levels, arrhythmias and haemodynamic complications (hypotension, mitral regurgitation) during episodes of ischaemia. Careful assessment and risk stratification are important because these guide the use of more complex pharmacological and interventional treatments Vomiting and sinus bradycardia are often due to vagal stimulation and are particularly common in patients with inferior MI. Nausea and vomiting may also be caused or aggravated by opiates given for pain relief. Sometimes infarction occurs in the absence of physical signs. Sudden death, from ventricular fibrillation or asystole, may occur immediately and often within the first hour. If the patient survives this most critical stage, the liability to dangerous arrhythmias remains, but diminishes as each hour goes by. It is vital that patients know not to delay calling for help if symptoms occur. Complications may occur in all forms of acute coronary syndrome but have become less frequent in the modern era of immediate or early coronary revascularisation Sees Boece eRe ge Rey ed Symptoms * Prolanged cardiac pain: chest, Nawsea and vemiting throat, arms, epigastrium or * Breathlessness . back * Collapse/syncape © Ansiety and fear of impending death Physical signs Signs of sympathetic activation * Pallor * Tachycardia « Sweating Signs of vagal activation * Vomiting * Bradycardia Signs of impaired myocardial function * Hypotension, oliguria, cold * Third heart sound peripheries © Quiet first heart sound © Narrow pulse pressure * Diffuse apical impulse * Raised jugular venous pressure © Lung crepitations Low-orade fever Complications © Mitral regurgitation * Pericarditis Complications: • Arrhythmias • Recurrent angina • Acute heart failure • Pericarditis • Dressler’s syndrome • Papillary muscle rupture • Ventricular septum rupture • Ventricular rupture • Embolism • Ventricular remodelling • Ventricular aneurysm Ul aVF V3 Ve Fig. 16.67 Acute transmural anterior myocardial infarction. This ECG was recorded from a patient who had developed severe chest pain 6 hours earlier. There is ST elevation in leads |, aVL, V2, Vs, Vs, V5 and Vs, and there are Q waves in leads V3, V, and V;. Anterior infarcts with prominent changes in leads V,, V, and V, are sometimes called ‘anteroseptal’ infarcts, as opposed to ‘anterolateral’ infarcts, in which the ECG changes are predominantly found in V,, V5 and V5.  Ml aVF V3 Ve Fig. 16.68 Acute transmural inferolateral myocardial infarction. This ECG was recorded from a patient who had developed severe chest pain 4 hours earlier. There is ST elevation in inferior leads Il, Ill and aVF and lateral leads V., V; and Vs. There is also ‘reciprocal’ ST depression in leads aVL and V>. IS THERE IS A TIMING FOR ECG CHANGES IN STEMI??? Immediate clinical assessment ECG Troponin (Oxygen + cardiac rhythm monitoring Aspirin 300 mg PO Ticagrelar 180 mg PO Metoprolol 5-15 mg IV/50-100 mg PO ‘Transfer to a specialist cardiology unit PCl+ Thrombolysis IV + Medium- GP lib/lila fol inux oF Yes) a antagonists LMW heparin IV aa (No aaa | csi, gens pecan I 16.51 Late management of myocardial infarction Risk stratification and further investigation (see text) Lifestyle modification * Diet (weight control, * Cessation of smoking lipid-lowering, ‘Mediterranean e Regular exercise diet’) Secondary prevention drug therapy © Antiplatelet therapy (aspirin ® Additional therapy for control and/or clopidogrel) of diabetes and hypertension © B-blocker ® Mineralocorticoid receptor © ACE inhibitor/ARB antagonist © Statin Rehabilitation Devices e Implantable cardiac defibrillator (high-risk patients) (ACE = angiotensin-converting enzyme; ARB = angiotensin receptor blocker)