myocardial infarction

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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 MIs and how they are classified
    • Will be able to identify the risk factors associated with MIs
    • 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.
  • MIs 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

  • MIs can be subcategorized by anatomy and clinical diagnostic information.
  • Anatomic
  • Transmural and Subendocardial
  • Diagnostic
  • ST elevations (STEMI) and non STelevations (NSTEMI).

10. Epidemiology

  • MIs 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, LDLs 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 itlasts 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 attackThis 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 EKGs should be taken to rule out or confirm MI.
  • 12 lead EKGs can help to distinguish between ST-elevation MIs and Non-ST-elevation MIs.

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 Es.
  • 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.