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Acute Myocardial Infarction

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.

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Acute Myocardial Infarction

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  1. Acute Myocardial Infarction Dr. Meg-angela Christi Amores

  2. 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

  3. 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

  4. Pathogenesis • Atherosclerotic plaque disruption • Thrombogenesis • Platelet activation • Platelet aggregation, cross-linking • Coagulation cascade activated

  5. 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.

  6. 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

  7. 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

  8. 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

  9. Lab Findings • Electrocardiogram (ECG) • ST-segment elevation • Serum Cardiac Biomarkers • Proteins released from necrotic heart muscle • Troponin I • CKMB • Cardiac imaging

  10. 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

  11. Intervention • Primary percutaneous coronary intervention • Angioplasty • Fibrinolysis • Within 30 mins of presentation • tPA • Streptokinase • rPA (reteplase)

  12. 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)

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