Myocardial Infarction

1. Myocardial Infarction Reynel Dan Galicinao Angelia Galinato Fiona Samantha Ajoc

2. Myocardial Infarction Formation of localized necrotic areas within the myocardium Usually follows sudden coronary occlusion and abrupt cessation of blood and oxygen flow to the heart muscle Prolonged ischemia (>35-45min) produces irreversible damage and necrosis of the myocardium

3. Risk Factors

4. Modifiable: Atherosclerosis CAD, HPN Impaired glucose tolerance Obesity Elevated serum triglyceride, LDL, and cholesterol levels Decreased serum HDL levels Smoking Excessive intake of saturated fats, carbohydrates, salt Sedentary lifestyle Use of drugs (amphetamines [shabu], cocaine) Stress Type A personality (aggressive, competitive attitude, addiction to work, chronic impatience)

5. Non-modifiable Age: >45yo Genetic Predisposition: family hx of CAD, early coronary disease Race: American, African, Hispanic/Latino Sex: Men are more susceptible than premenopausal women, although incidence is rising among women who smoke and take hormonal contraceptive The incidence in postmenopausal women is equal in men Women have higher morbidity and mortality rates than men, (older and have more preexisting diseases when MI occurs, women delay seeking treatment longer than men do)

6. Causes

7. MI results from occlusion of one of the coronary arteries which can stem from: Atherosclerosis Coronary Thrombosis / Embolism Platelet aggregation Coronary artery stenosis/spasm Decreased blood flow with shock and/or hemorrhage Direct trauma

8. Pathophysiology

10. MI almost always occurs in the left ventricle due to occlusion of left anterior descending artery (LADA) & often significantly depresses left ventricular fcn (anterior wall infarction) Alterations in fcn depend on size and location of an infarct

11. Contractile fcn in the necrotic area cease permanently Healing requires formation of scar tissues that replace the necrotic myocardial muscle Scar tissue inhibits contractility

12. 3 Areas which Develop in MI Zone of Infarction – records pathologic Q wave in the ECG Zone of Injury – gives rise to elevated ST segment Zone of Ischemia – produces inversion of T wave

13. Classification of MI Transmural infarct – extends from endocardium to epicardium Subendocardial infarct – affects the endocardial muscles Intramural infarction – seen in patchy areas of the myocardium; equally associated with angina pectoris

14. Complications of MI Dysrhythmias Cardiogenic Shock Pericarditis Rapture of myocardium Ventricular aneurysm CHF Dressler’s Syndrome

15. Assessment Findings

17. Cardinal symptom of MI:persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, and shoulder blades

18. Unrelieved by rest or nitroglycerine

19. Anxiety and Apprehension

20. Feeling of “doom”, restlessness

21. Shock

23. Total Creatine Kinase Level Rises within 3h after onset of chest pain Peaks within 24h after damage and death of cardiac tissue CK-MB isoenzyme Peak elevation: 18-24h after onset of chest pain Returns to N° 48-72h later Troponin level Rises within 3h Remains elevated up to 3wks

24. Myoglobin Rises within 1h after cell death Peaks in 6h Returns to N° within 24-36h or less LDH level Rises 24h after MI Peaks 48-72h Falls to N° in 7days WBC Elevated WBC (10,000-20,000 cells/mm3) on 2nd day following MI lasts up to 1wk

26. Hours to days after MI, ST and T wave changes will return to N°

28. Thallium scan – assess ischemia or necrotic muscle tissue Multigated cardiac pool imaging scans – evaluate left ventricular fcn Cardiac catheterization – determine the extent and location of obstructions of the coronary arteries

29. Collaborative Management

30. Medications Analgesic Relief of pain This is a priority; pain may cause shock Administer IV Morphine sulfate, Lidocaine, or Nitroglycerine

31. Thrombolytic Therapy Disintegrate dlood clot by activating fibrinolytic processes Streptokinase, Urokinase, Tissue Plasminogen Activator (TPA) Administration is most crucial between 3-6h after initial infarction has occurred Detect for occult bleeding during and after thromolytic therapy Assess neurologic status changes (may indicate GI bleeeding or cardiac tamponade)

32. Anticoagulant and antiplatelet medications - administered after thrombolytic therapy to maintain arterial patency. Other meds: Beta-adrenergic blocking agents; Diazepam (Valium)

33. Treatment

34. Goals Prevention of further tissue injury and limitation of infarct size Maximize myocardial tissue perfusion and reduce myocardial tissue demands

35. Supplemental O2 by nasal cannula – increase myocardial oxygen supply; relieves pain Cardiac monitoring – detect occurrence of dysrhythmias Percutaneous transluminal coronary angioplasty – reopen occluded artery

36. Nursing Diagnoses Acute pain Decreased cardiac output Ineffective tissue perfusion: Cardiopulmonary Excess fluid volume Imbalanced nutrition: Less than body requirements

37. Fatigue Activity intolerance Ineffective sexuality patterns Anxiety Ineffective coping Ineffective denial

38. Nursing Management

39. Promoting Oxygenation and Tissue Perfusion Instruct pt to avoid over fatigue; stop activity immediately in the presence of chest pain, dyspnea, light-headedness, faintness O2 therapy for first 24-48h or longer if pain, hypotension, dyspnea, dysrhythmia persist Monitor VS changes Position pt to Semi-Fowler’s

40. Promoting Adequate CO Monitor: Dysrhythmias, ECG tracings VS Effects of ADLs on cardiac status Rate and rhythm of pulse Administer pharmacotherapy as prescribed Promote rest, minimize unnecessary disturbances

41. Promoting Comfort Relieve pain Admin morphine sulfate as ordered To decrease sympathetic stimulation, which increases myocardial oxygen demand Prevent shock from severe pain

42. Providing Rest CBR with TP for 34-48h Admin diazepam (Valium) as ordered Explain purpose of CCU For continuous monitoring and safety during early recovery period Provide psychosocial to pt and SO Calmness and competency are extremely reassuring

43. Promoting Activity Gradual increase in activity after first 24-48h May be allowed to sit on a chair for increasing periods of time May begin ambulation on 4th or 5th day Monitor for signs of dysrhythmia, chest pain, changes in VS during activity

44. Promoting Nutrition and Elimination Small frequent feedings Low-calorie, low-cholesterol, low-sodium diet Avoid stimulants Avoid very hot or very cold beverages and gas-forming foods Avoid use of Valsalva Maneuver Use bedside commode Administer stool softener as ordered

45. Promoting Relief of Anxiety and Feeling of Well-Being Provide opportunity for pt and SO to explore concerns and identify alternative coping methods Facilitate Learning Start teaching when pt is free of pain and excessive anxiety Promote positive attitude and active participation of pt and SO