Myocardial infarction

Myocardial infarction

1. MYOCARDIAL INFARCTION

2. Definition Acute myocardial infarction (MI) is a clinical syndrome that results from occlusion of a coronary artery, with resultant death of cardiac myocytes in the region supplied by that artery. Defined by “Current diagnosis and treatment in Cardiology - 2013”

3. The degree of altered function depends on the area of heart involved and the size of infarction In acute MI cardiac cells can withstand ischemic conditions for approximately 20 minutes before cellular death begins It takes 4-6 hours for the entire thickness of the heart to become necrosed

4. CLASSIFICATION

5. CLASSIFICATION AWMI IWMI PWMI LWMI RVMI

6. ETIOLOGY AND PATHOPHYSIOLOGY

7. CLINICAL MANIFESTATIONS CHEST PAIN

8. SYMPATHETIC NERVOUS SYSTEM STIMULATION CATECHOLAMINE RELEASE DIAPHORESIS COOL AND CLAMMY EXTRIMITIES DUE TO VASOCONSTRICTION

9. CARDIOVASCULAR MANIFESTATIONS TACHYCARDIA ELEVATED BP INITIALLY CRACKLES ON AUSCULTATION

10. NAUSEA VOMITING AS A RESULT OF VASOVAGAL REFLEX BY SEVERE PAIN FEVER- 100.4 F AS A RESULT OF INFLAMATION

11. Diagnostics History collection, physical exmn 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.

12. NORMAL SINUS RHYTHM

13. STEMI ST segment elevations T wave changes Q wave development Enzyme elevations Reciprocals

14. 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.

15. NSTEMI ST segment depressions T wave changes No Q wave development Mild enzyme elevations No reciprocals

16. STEMI vs. NSTEMI

17. 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

18. 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

19. 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.

20. Cardiac catheterization echocardiography

21. COMPLICATIONS DYSRHYTHMIAS Most common present 80% patients HEART FAILURE occur when the pumping power of heart diminished CARDIOGENIC SHOCK Inadequate oxygen and nutrients are supplied to the tissues because of severe LV dysfunction

22. PAPILLARY MUSCLE DYSFUNCTION valvular dysfuction , causes- MR,TR VENTRICULAR ANEURYSM Myocardial wall thinned and bulges out during contraction PERICARDITIS DRESSLER SYNDROME pericarditis with effusion and fever develops 4-6 weeks after MI

23. MANAGEMENT preserve cardiac muscle fibers Vital signs Iv assess ECG Biomarkers

24. MANAGEMENT INITIAL MANAGEMENT M- Morphine O- oxygen N-Nitrates A- Antiplatelets

25. EMERGENT PERCUTANEOUS CORONARY INTERVENTION (PCI ) PCI may be used to open the occluded coronary artery in an acute MI and promote reperfusion to the area that has been deprived of oxygen . PCI is performed should be less than 90 minutes.

26. Usually PCI with the placement of stent will be performed Complications- dissection of ccoronary artery Cardiac tamponade Restenosis Hematoma formation at the site

27. Thrombolytic therapy/ fibrinolytic therapy The purpose of thrombolytics is to dissolve and lyse the thrombus in a coronary artery (thrombolysis), allowing blood to flow through the coronary artery again (reperfusion), minimizing the size of the infarction, and preserving ventricular function

28. Indications Chest pain for longer than 20 minutes, unrelieved by nitroglycerin ST-segment elevation in at least two leads that face the same area of the heart Less than 24 hours from onset of pain

29. Absolute Contraindications Active bleeding Known bleeding disorder History of hemorrhagic stroke History of intracranial vessel malformation Recent major surgery or trauma

30. Relative contraindications Active peptic ulcer disease Pregnancy Stroke more than 3 months back Uncontrolled hypertension

31. Start within 30 minutes( door-to-needle time)

32. Common thrombolytics 1 st generation Streptokinase Urokinase 2 nd generation alteplase ( tPA ) reteplase Anistreplase

33. Nursing considerations Minimize the number of times the patient’s skin is punctured. Avoid intramuscular injections. Draw blood for laboratory tests when starting the IV line. Monitor for acute dysrhythmias, hypotension, and allergic reaction . Monitor for reperfusion: resolution of angina or acute ST-segment changes . Check for signs and symptoms of bleeding:

34. Pharmacologic management Analgesics morphine sulphate decreases preload and afterload reduce anxitey Nitrates IV nitroglycerin

35. ACE inhibitors increases the left ventricular function prevent ventricular remodelling Beta-adrenergic blockers decreases the contractility and myocardial oxygen demand Cholesterol lowering agents Stool softeners

36. SURGICAL MANAGEMENT CORONARY ARTERY BYPASS GRAFT(CABG) Construction of new conduits between aorta or other major arteries with help of CPB machine Indications Triple vessel disease 60% occlusion of LAD Fails medical management

37. Grafts used Internal mammary artery Great saphenous vein Inferior epigastric artery Radial artery

38. Nursing Management Assessment subjective data objective data

39. Diagnosis Ineffective cardiopulmonary tissue perfusion related to reduced coronary blood flow from coronary thrombus and atherosclerotic plaque Acute pain related to myocardial ischemia as evidenced by severe chest pain and tightness, radiation of pain to the neck and arms Anxiety related to perceived threat of death, possible lifestyle changes as evidenced by fearful attitudes, frequent questioning

40. Cardiac rehabilitation phase 1- hospital pahse 11- early recovery- 2-12 wk phase 111- late recovery- long term maintanece programme