1. 1. MYOCARDIAL INFARCTION PRESENTED BY- SAM MATHEW STAFF NURSE DH ED
2. 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 MI and what the appropriate interventions are. Understand the treatment options available to treat MI. Nursing responsibilities Follow up care
3. 3. DEFINITION . Myocardial infarction is a disease condition which is caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus .
4. 4. 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.
5. 5. MI Classifications MIs can be subcategorized by anatomy and clinical diagnostic information. Anatomic Transmural - atherosclerosis involving a major coronary artery, it is usually as a result of complete occlusion of the artery in addition on ECG ST elevation and q waves are seen(STEMI)(epicardium,myo,endocardium) Subendocardial - small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. It is particularly susceptible to ischemia,in addition to ST depression is seen on ecg(NSTEMI) Diagnostic ST elevations (STEMI)-ECG must show new ST elevation in two or more adjacent ECG leads or new LBBB , it must be greater than 2 mm in leads V2 and V3 or greater than 1 mm in all other leads. non ST elevations (NSTEMI)-ST segment depression 0.5mm or dynamic T- wave inversion with pain or discomfort , and cardio specific proteinstroponin are rises in blood in NSTEMI.
6. 6. CORONARY ARTERIES OF HEART
7. 7. Tunica Intima T. Adventitia Tunica media plaques Thrombus Atherosclerosis is a narrowing of the arteries caused by a buildup of plaque
8. 8. ETIOLOGY
9. 9. NON-MODIFIABLE RISK FACTORS MODIFIABLE RISK FACTORS ETIOLOGY
10. 10. NON-MODIFIABLE RISK FACTORS FACTOR AGE SEX FAMILY HISTORY
11. 11. AGE: More than 40 years. FAMILY HISTORY: Myocardial infarction can be inherited from parents to children. GENDER: Myocardial infarction is 3 times more in men than women.
12. 12. MODIFIABLE RISK FACTORS FACTOR HIGH BLOOD LIPIDS LEVEL HYPER- TENSION SMOKING PHYSICAL INACTIVITY OBESITY DIABETES MELLITUS STRESS
13. 13. HIGH BLOOD CHOLESTROL LEVEL LOW DENSITY LIPOPROTEIN (LDL) DANGEROUS HIGH DENSITY LIPOPROTEIN (HDL) LIPIDS (LIPOPROTIENS)
14. 14. HYPERTENSION High blood pressure our arteries are designed to pump blood at a certain pressure. If that pressure is exceeded, the walls of the arteries will be damaged . injury to endothelial lining , atherosclerosis narrowed & thickened arterial walls risk of M.I.
15. 15. SMOKING Smoking can damage the walls of your arteries.( toxic substances in cigarette) Atherosclerosis narrowed & thickened arterial walls Risk of M.I.
16. 16. PHYSICAL INACTIVITY Improper lipid metabolism LDL level increases Starts accumulating in blood vessels Risk of M.I.
17. 17. OBESITY More lipids are produced LDL level increases Atherosclerosis Risk of M.I.
18. 18. DIABETES MELLITUS Diabetes increases the risk of MI because it increases the rate of atherosclerotic progression and adversely affects the lipid profile Risk of having M.I.
19. 19. STRESS Release stress hormones like adrenaline, noradrenaline, and cortisol increase in heart rate, and elevated blood pressure its causing damage over time to all your blood vessel That damage increases the risk of plaque buildup in coronary arteries or can even cause a rupture of plaque MI The way you handle stress also matters. If you respond to it in unhealthy ways -- such as smoking, overeating,or not exercising - that makes matters worse.
20. 20. PATHOPHYSIOLOGY
21. 21. How a Heart Attack Happens
22. 22. Cholesterol deposition within the wall of the main artery This deposited cholesterol ultimately forms a plaque in the wall of the artery called atherosclerotic plaque. Atherosclerotic plaque formation is a long term process, required many years to establish. Sometimes this plaque may rupture or erode,it leads to activate clotting mechanism so platelet aggregation and fibrin deposition, which lead to formation of an occlusive thrombus in a coronary artery. This occlusive thrombus completely block a coronary artery and interrupts blood supply to part of the myocardium (heart muscle), It lead to irreversible changes and death of myocardial cells, and ultimately ST-segment elevation myocardial infarction develops. PATHOPHYSIOLOGY
23. 23. CLINICAL MANIFESTATIONS Chest pain due to a lack of blood and oxygen supply of the heart muscle Characteristics: Severe, immobilizing chest pain. Usually prescribed as heaviness, pressure, tightness, burning. Location: Substernal, Retrosternal or Epigastric. Radiation: It may radiate to neck, jaw, arm or back. Duration: Lasts for 20 minutes or more. PAIN
24. 24. Cardiovascular- Initially the BP and pulse may be elevated. Later, BP will drop due to decreased cardiac output. palpitation. Jugular veins may become distended and have obvious pulsations.
25. 25. CONTD.. Respiratory- Respiratory symptoms occur when the damaged the heart muscle limits the pumping action of the left ventricle, causing acute left heart failure and consequent lung congestion. Shortness of breath Dyspnea/Tachypnea Crackles Pulmonary edema
26. 26. Gastrointestinal- Nausea Vomiting Stimulation of vomiting center by severe pain causes nausea & vomiting FEVER It is due to inflammatory process caused by Myocardial cell death.
27. 27. In response to pain and the blood flow abnormalities that result from dysfunction of the heart muscle SYMPATHETIC NERVOUS SYSTEM STIMULATION Increased catecholamine releases.(adrenal medulla) Diaphoresis (perfuse sweating Cold & clammy skin (cold sweat). Integumentary system (Skin) cool, clammy skin Diaphoresis Pallor, Cyanosis Coolness of extremities
28. 28. Genitourinary- Hypoperfusion to the kidneys leads to decrease renal perfusion pressure which is required to maintain glomerular filteration rate in the kidney Decrease GFR leads to decrease urinary output Urine output (Oliguria): 30ml/HR or