Post on 07-May-2015
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DESCRIPTIONA presentation on Acute Myocardial Infarctions for the nursing student
- 1.Acute Myocardial Infarction Sarah Priore RN BSN
- 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.
- 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.
- Transmural and Subendocardial
- ST elevations (STEMI) and non STelevations (NSTEMI).
- 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.
- 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
- Family history
13. Risk Factors
- Diabetes Control
- Physical Inactivity
- Tobacco use increases the risk of coronary artery disease two to six times more than non smokers.
- Nicotine increases platelet thrombus adhesion and vessel
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.
- 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.
- 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.
- 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.
- Watch your own heart attackThis is a little graphic!
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
- 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
- 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.
- Transient ischemia that occurs unpredictably and almost always at rest.
- Pain is caused by vasospasm of the arteries.
- ST segment elevations will be noted.
- 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.
- ST segment elevations
- T wave changes
- Q wave development
- Enzyme elevations
- 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.