Myocardial infarction

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A presentation on Acute Myocardial Infarctions for the nursing student

A presentation on Acute Myocardial Infarctions for the nursing student

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  • 1. Acute Myocardial Infarction Sarah Priore RN BSN
  • 2. Objectives
      • Define and understand the epidemiology of MI’s and how they are classified
      • Will be able to identify the risk factors associated with MI’s
      • Will be able to recognize signs and symptoms of acute MI and what the appropriate interventions are.
      • Understand the treatment options available to treat acute MI.
  • 3. Definition
    • Otherwise know as heart attack
    • An MI occurs when there is a diminished blood supply to the heart which leads to myocardial cell damage and ischemia.
    • Contractile function stops in the necrotic areas of the heart.
    • Ischemia usually occurs due to blockage of the coronary vessels.
  • 4. Definition cont.
    • This blockage is often the result of thrombus that is superimposed on an ulcerated or unstable atherosclerotic plaque formation in the coronary artery.
    • MI’s are described by the area of occurrence.
    • Anterior, Inferior, Lateral or Posterior.
  • 5. Coronary Artery Anatomy
  • 6. Coronary artery events
    • Ischemia – Outer most area, source of arrhythmias, viable if no further infarction.
    • Injury – Viable tissue found between ischemic and infarcted areas.
    • Infarction/necrosis – Center area, dead not viable tissue that turn into scar.
  • 7.  
  • 8.  
  • 9. MI Classifications
    • MI’s can be subcategorized by anatomy and clinical diagnostic information.
    • Anatomic
    • Transmural and Subendocardial
    • Diagnostic
    • ST elevations (STEMI) and non ST elevations (NSTEMI).
  • 10. Epidemiology
    • MI’s are the leading cause of death in the United States, affecting one in five men and one in six women.
    • 450,000 people in the US die from coronary disease each year.
    • Incidence rates increase with age as do mortality rates due to infarction.
  • 11. Epidemiology
    • The survival rate for those hospitalized due to MI has reached approximately 95%.
    • This is the result of the advancements made in modern medical technology.
  • 12. Risk Factors
    • The presence of any risk factor is associated with doubling the risk of an MI.
    • Non Modifiable
    • Age
    • Gender
    • Family history
  • 13. Risk Factors
    • Modifiable
    • Smoking
    • Diabetes Control
    • Hypertension
    • Hyperlipidemia
    • Obesity
    • Physical Inactivity
  • 14. Smoking
    • Tobacco use increases the risk of coronary artery disease two to six times more than non smokers.
    • Nicotine increases platelet thrombus adhesion and vessel
    • inflammation.
  • 15. Diabetes & Hypertension
    • Diabetes not only increases the rate of atherosclerotic formation in vascular vessels but also at an earlier age.
    • The constant stress of high blood pressure has been associated with the increased rate of plaque formation.
    • Shearing Stress and inflammation of endothelial lining begins the process.
  • 16. Hyperlipidemia
    • Elevated levels of cholesterol, LDL’s or triglycerides are associated with the increased risk of coronary plaque formation and MI.
    • Almost 50% of the U.S.
    • population has some
    • form of dyslipidemia.
  • 17. Obesity and Physical Inactivity
    • Mortality rate from CAD is higher in those who are obese.
    • Some evidence shows that those who carry their weight in their abdomen have a higher incidence of CAD
    • Physically inactive people have lower HDL levels with higher LDL levels and an increase in clot formation.
  • 18. Pathophysiology
    • Ischemia develops when there is an increased demand for oxygen or a decreased supply of oxygen.
    • Ischemia can develop within 10 seconds and if it lasts longer than 20 minutes, irreversible cell and tissue death occurs.
    • Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supply.
  • 19. Pathophysiology
    • As vessel occlusion continues cell death spreads to the myocardium and eventually to the epicardium.
    • Severity of the MI depends on three factors.
      • Level of occlusion
      • Length of time of occlusion
      • Presence or absence of collateral circulation
  • 20. Signs and Symptoms
    • Signs and symptoms are unique to each individual patient.
    • Ranging from no symptoms to sudden cardiac arrest.
  • 21. Chest Pain
    • The most common initial manifestation is chest pain or discomfort.
    • This is not relieved by rest, position change or nitrate administration.
    • Pain is described by heaviness, pressure, fullness and crushing sensation.
    • Not everyone experiences this sensation.
  • 22. Chest Pain
    • PQRST assessment for chest pain
    • P- Precipitating events
    • Q- Quality of pain
    • R- Radiation of pain
    • S- Severity of pain
    • T- Timing
  • 23. Nausea and Vomiting
    • Not everyone will experience this.
    • Vomiting results as a reflex from severe pain.
    • Vasovagal reflexes initiated from area of ischemia.
  • 24. Sympathetic Nervous System Stimulation
    • During an MI increased catecholamines are released.
    • This results in diaphoresis and vasoconstriction of peripheral blood vessels.
    • “ Cool Sweat” with a temperature increase during the first 24 hours.
  • 25. Cardiovascular Changes
    • Initially the BP and pulse may be elevated.
    • Later, BP will drop due to decreased cardiac output.
    • Urine output will decrease
    • Lung sounds will change to crackles
    • Jugular veins may become distended and have obvious pulsations.
  • 26. Video
    • Watch your own heart attack…This is a little graphic!
    • http://www.youtube.com/watch?v=LUt1xXASm_s
  • 27. Within the first 10 minutes upon arrival to the hospital:
    • Check vital signs and evaluate oxygen saturation
    • Establish IV access
    • Obtain and review 12-lead ECG
    • Take a brief focused history and perform a physical exam
    • Obtain blood samples to evaluate initial cardiac markers, electrolytes and coagulation
  • 28. Diagnostics
    • After collecting patient health history, a series of EKG’s should be taken to rule out or confirm MI.
    • 12 lead EKG’s can help to distinguish between ST-elevation MI’s and Non-ST-elevation MI’s.
  • 29. Normal Sinus Rhythm
  • 30. Angina
    • Stable
    • Chest pain caused by the build up of lactic acid and irritation to the myocardial nerve fibers.
    • Chest pain caused by the 4 E’s.
    • Pain is usually relieved with rest, pain meds and nitrates.
  • 31. Variable/Prinzmetal/Spasm
    • Transient ischemia that occurs unpredictably and almost always at rest.
    • Pain is caused by vasospasm of the arteries.
    • ST segment elevations will be noted.
  • 32. Unstable
    • Chest pain at rest or with exercise and tends to last greater than 15 minutes.
    • This results in reversible myocardial ischemia but is a sign that an infarct is soon to come.
    • EKG will reveal ST segment depression and T wave inversion.
  • 33. STEMI
    • ST segment elevations
    • T wave changes
    • Q wave development
    • Enzyme elevations
    • Reciprocals
  • 34. NSTEMI
    • ST segment depressions
    • T wave changes
    • No Q wave development
    • Mild enzyme elevations
    • No reciprocals
  • 35. STEMI vs. NSTEMI
  • 36. Phases of a STEMI
    • Hyperacute Phase
      • Occurs within the first few hours of MI onset.
      • Leads facing the infarcted surface: ST segment elevation.
      • Leads facing the uninjured surface: ST segment depression (reciprocals)
      • T waves become tall, widened and might be taller than the R wave.
  • 37. Phases of a STEMI
    • Fully Evolved Phase
      • Q wave development
      • ST elevation
      • T waves start to become inverted in leads facing the injury.
  • 38. Phases of a STEMI
    • Resolution phase
      • Weeks after there will be a gradual return of ST segments to baseline.
      • T waves will gradually return to normal but are the last to change back.
  • 39. Serum Cardiac Markers
    • Myocardial cells produce certain proteins and enzymes associated with cellular functions.
    • When cell death occurs, these cellular enzymes are released into the blood stream.
    • CPK and troponin
  • 40. CPK
    • Creatine Phosphokinase
    • Begin to rise 3 to 12 hours after acute MI.
    • Peak in 24 hours
    • Return to normal in 2 to 3 days
  • 41. Troponin
    • Myocardial muscle protein released into circulation after injury.
    • These are highly specific indicators of MI.
    • Troponin rises quickly like CK but will continue to stay elevated for 2 weeks.
    • Myoglobin-lacks cardiac specificity.
  • 42. Serum Cardiac Markers
  • 43. Treatment Options
    • The immediate goal for any acute MI is to restore normal coronary blood flow to vessels and salvage myocardium.
    • There are a variety of medical and medicinal therapies to treat an MI.
  • 44. General Treatment for the MI patient
    • MONA
    • Morphine
    • Oxygen
    • Nitroglycerin
    • Aspirin
  • 45. Fibrinolytic Therapy
    • Indicated for patients with STEMI MI’s.
    • Should be given within 12 hours of symptom onset.
    • Fibrinolytics will break down clots found within the vessles
    • Contraindications: post op surgical patients, history of hemorrhagic stroke, ulcer disease, pregnancy, ect.
  • 46. Cardiac Catheterization
    • A diagnostic angiography which includes angioplasty and possible stenting.
    • Performed by an interventional cardiologist with a cardiac surgeon on stand by.
    • Percutaneous procedure through the femoral or brachial artery.
  • 47. Cardiac Catheterization
    • Upon arrival to the cath lab all actue MI patients will receive:
      • A bolus dose of plavix
      • IV Integrelin
      • Heparin dose either subcu or IV drip
      • Angiomax : a DTI may be substituted for heparin and integrelin.
  • 48.  
  • 49. Cardiac Catheterization while undergoing an MI
    • http://www.youtube.com/watch?v=TS0Je1m9Q8A&feature=related
    • Angioplasty and Stenting
    • http://www.youtube.com/watch?v=9FPapBbbS4o&feature=related
  • 50. Coronary artery bypass graft
    • Surgical treatment where saphenous vein is harvested from the lower leg and used to bypass the occluded vessels.
  • 51.  
  • 52. Long Term Care
    • Smoking Cessation and lifestyle modifications.
    • Aspirin, Beta Blockers and Clopidogrel will be indefinite.
    • Lipid lowering medication along with diet modifications.
  • 53. References
    • Bolooki, H.M.& Askari, A. (Published August 8 2010). Acute Myocardial Infarction. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/acute-myocardial-infarction/#s0050
    • Lewis, S., Heitkemper, M., & Dirksen, S. (2004). Medical surgical nursing assessment and management of clinical problems. St. Louis, MO: Mosby.
    • McCance, K.L., Huether, S.E., Brashers, V.L.& Rote, N.S. (2010). Pathophysiology the biological basis for disease in adults and children. Maryland Heights, MO: Mosby Elsevier.