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Download Acute Myocardial Infarction
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Acute Myocardial Infarction Dr. Meg-angela Christi Amores • one of the most common diagnoses in hospitalized patients • mortality rate from AMI is ~30% • more than half of these deaths occurring before the stricken individual reaches the hospital Acute MI • usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis • occurs when a coronary artery thrombus develops rapidly at a site of vascular injury • Injury facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation Pathogenesis • • • • • Atherosclerotic plaque disruption Thrombogenesis Platelet activation Platelet aggregation, cross-linking Coagulation cascade activated The amount of myocardial damage depends on: • • • • the territory supplied by the affected vessel whether or not the vessel becomes totally occluded the duration of coronary occlusion the quantity of blood supplied by collateral vessels to the affected tissue • the demand for oxygen of the myocardium whose blood supply has been suddenly limited • native factors that can produce early spontaneous lysis of the occlusive thrombus • the adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery. Risk factors • • • • • • Persons with multiple coronary risk factors Persons with unstable angina Hypercoagulability collagen vascular disease cocaine abuse intracardiac thrombi or masses that can produce coronary emboli Clinical presentation • Usually soon after awakening • PAIN – most common presenting complaint • • • • • • Deep, visceral Heavy, squeezing, crushing, stabbing, burning Similar to angina pectoris but occurs at rest More severe, lasts longer Central portion of chest/ epigastrium/ radiates to arm weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom PE Findings • anxious and restless • Pallor, perspiration • physical signs of ventricular dysfunction – fourth and third heart sounds, decreased intensity of the first heart sound, and paradoxical splitting of the second heart sound Lab Findings • Electrocardiogram (ECG) – ST-segment elevation • Serum Cardiac Biomarkers – Proteins released from necrotic heart muscle – Troponin I – CKMB • Cardiac imaging Management • Prehospital care • • • • Recognition of symptoms Repid deployment of medical team Expeditious transportation Implementation of reperfusion therapy • ER management • Control of discomfort • Limitation of infarct size • O2 Intervention • Primary percutaneous coronary intervention – Angioplasty • Fibrinolysis – Within 30 mins of presentation – tPA – Streptokinase – rPA (reteplase) Hospital care • Should be admitted in the CCU or ICU • Bed rest for first 12 hours • Resume upright position with dangling feet within 24 hours • NPO in first 4-12 hours • 50-55% CHO, <30% fats • Bedside commode, laxative • Sedation (diazepam)