2- nursing care for Myocardial Infarction.pptx

MI for nurses

1. Coronary Artery Disease (CAD) Angina Pectoris

2. Learning objectives

3. Learning objectives

4. Introduction Cardiovascular disease are the leading cause of death for woman and men. An understanding of the pathology of cardiovascular disease processes and clinical management allows the critical care nurse to accurately anticipate and plan interventions. The lecture focus on cardiac disorders commonly seen in critical care environment

5. Coronary Artery Disease (CAD) DESCRIRTION: Is an insidious, progressive disease that result in coronary arterial narrowing or complete occlusion. ETIOLOGY - Atherosclerosis - Thrombosis - Spasm - Coronary dissection - Aneurysm formation

6. Nonmodifiable CAD Risk Factors Age Gender Family history Race

7. Modifiable CAD Risk Factors Elevated serum lipids Hypertension Cigarette smoking Impaired glucose tolerance Oral contraceptives Obesity Physical inactivity Stress/anxiety Hyperhomocystinemia (inborn error of metabolism) Diet high in saturated fat cholesterol and calories

8. Pathophysiology Atherosclerotic plaque narrows lumen of artery Angina: discrepancy between oxygen supply and demand causes hypoxia Plaque rupture and coronary thrombosis Plaque regression is possible with change in risk factors

9. PATHOPHYSIOLOGY

10. Acute Coronary Syndrome is used to describe the array of clinical presentation of CAD that range from unstable angina to acute myocardial infarction ANGINA: Is a blockage or spasm of a coronary artery leading to diminished blood supply to the myocardium. ( coronary ischemia) Acute Coronary Syndrome (ACS)

11. Type Of Angina Pectoris: Stable Angina Unstable Angina Variant Angina Angina Pectoris

12. Stable Angina Is predictable and caused by similar precipitating factors each time such as exercise, emotional upset and tachycardia; is the result of fixed lesions Pain control is achieved by rest and sublingual or intravenous administration of the coronary artery vasodilator nitroglycerin

13. More intense, different from stable angina. May awaken the person from sleep or may necessitate more than nitrate for pain relief, and the change in the level or frequency of symptom. PREINFARCTION OR CRESCENDO ANGINA : Severe angina that persists for more than 15 minutes and is not relieved by three nitroglycerin tablets Unstable Angina

14. Caused by coronary artery spasm with or without atherosclerotic lesions. It commonly occurs when the individual is at rest and also can be cyclic occurring at the same time every day. Smoking, alcohol and cocaine use may also precipitate spasm. Drug of choice for variant angina are agents that vasodilate the coronary arteries such as nitroglycerin or calcium channel blockers. Variant Angina ( Prinzmetal Angina)

15. Objective ECG evidence of myocardial ischemia (ST-segment changes) without the patient experiencing any symptoms of angina. Individual with co-existing CAD and diabetes mellitus are particularly susceptible to silent ischemia and silent myocardial infarction (MI). Silent Ischemia

16. Location : *beneath sternum , radiating to neck and jaw upper chest.*beneath sternum , radiating down left arm.*upper chest*neck and jaw* epigastric *epigastric radiating to neck, jaw and arm*left shoulder and intrascapular Duration : * 0.5 to 15 minutes (stable).* Duration longer than 15 min without relief from rest or medication indicates unstable angina or preinfarction symptoms. Quality: *sensation of pressure or heavy weight on the chest. *Burning sensation * shortness of breath , with feeling of suffocation*feeling of tightness.*most severe pain ever experienced Characteristics Of Angina Pectoris

17. Radiation: * jaw * left shoulder * right arm * medial aspect of left arm. Precipitating factors: * Exertion/exercise* cold weather* exercising after a large heavy meal *emotional upset* fright, anger* walking against the wind* coitus. Medication relief: Usually within 45 seconds to 5 minutes of sublingual nitroglycerin administration Characteristics Of Angina Pectoris

18. The major goals of medical therapy for angina as an acute coronary syndrome are: Increase coronary artery perfusion to the myocardium Prevent myocardial infarction disability or death Actively intervene in acute coronary syndromes Medical Management

19. The pharmacologic treatment of choice are vasodilation by nitroglycerin intravenous antiplatelet agents such as the glycoprotein IIb / IIIa inhibitors, aspirin ,and IV heparin Another option is to take the patient directly to the cardiac catheterization laboratory for direct visualization of the coronary arteries and recanalization by the cardiologist. Medical Management

20. Nursing intervention focus on : Assessment of chest pain : location, duration, quality, radiation, medication relief and precipitating Relief of pain: in the critical care unit control of angina pain is achieved by a combination of supplemental oxygen, nitrates, analgesia (morphine) and surveillance of the angina and of the effects of pharmacologic therapy. Nursing Management

21. Maintain a calm environment : ensuring that the elements of a calm environment that will alleviate the patient’s fear and anxiety are maintained Coronary precautions : PATIENT BED REST Nursing Management

22. Doing ECG when ever the patient have chest pain Doing cardiac enzymes (CPK, CK-MB,T.I) Patient education : points to cover include risk factor modification, signs and symptoms of angina, when to call the physician, medications, and dealing with emotions and stress. Nursing Management

23. MYOCARDIAL INFARCTION (MI)

24. DESCRIRTION: Irreversible myocardial necrosis due to an abrupt decrease or total cessation of coronary blood flow to a specific area of the myocardium The three mechanism that are primarily responsible for the acute reduction in oxygen delivery to the myocardium are: Plaque rupture New coronary artery thrombosis Coronary artery spasm Myocardial Infarction (MI)

25. Zone of Ischemia: The outer region of the myocardium and is composed of viable cells . (T-wave inversion) Zone of Injury: The area surround the infarcted zone but still potentially viable tissue . (elevated ST segments) Pathophysiology

26. Zone of Infarction: The area of cellular death and muscle necrosis in the myocardium . ( development of pathologic Q waves) Pathophysiology

27. MI are classified according to their location on the myocardial surface and the muscle layers affected: Transmural MI (Pathologic Q-wave MI): involves all three muscle layers the endocardium, myocardium, and epicardium Classification of MI

28. Nontransmural MI (Non-Q-wave MI): are classified as either Subendocardial : involving the endocardium Subepicardial : involving the epicardium Some Myocardium may be involved in nontransmural MI but it is not a full thickness MI. Generally abnormal Q wave are not seen. Classification of MI

29. It begins with the end of QRS complex, and extends to the beginning of T wave S-T segment

30. If depressed or elevated, indicates physiological or organic changes S-T segment

31. Anatomic Groups (Summary)

32. ST SEGMENT NORMAL ST SEGMENT ST segment < 2-3 small square (80 to 120 ms) ST segment is isoelectric and at the same level as subsequent PR-interval

33. Variable Shapes Of ST Segment Elevations in AMI Goldberger AL. Goldberger: Clinical Electrocardiography: A Simplified Approach. 7th ed: Mosby Elsevier; 2006.

34. The ECG manifestation that are used to diagnose an MI and pinpoint the area of damaged ventricle include inverted T waves, ST-segment elevation, and pathologic Q wave. Surface of left ventricle ECG leads coronary artery usually involved Inferior II,III,aVf Right coronary artery (RCA) Lateral V5,V6,I,aVL Left Circumflex (LCX) Anterior V2,V3,V4 Left Anterior Descending (LAD) Septal V1,V2 Left Anterior Descending (LAD) Posterior V1,V2 (indirect) Left circumflex or RCA V7,V8,V9(direct) Myocardial Infarction Location

35. Myocardial Infarction Location

36. Myocardial Infarction Location

37. Myocardial Infarction Location

38. The definitive diagnosis of MI is based on a combination of Clinical symptoms: The most common is prolonged severe chest pain (last 30 min or more), which often associated with nausea, vomiting, and diaphoresis. Pain is located in the substernal or left precordial area like an elephant sitting on my chest. The pain may be radiate to the back, neck, jaw or left arm. Neither rest nor nitrates relieve the pain Assessment and Diagnosis

39. 12-lead ECG changes : The ECG manifestation that are used to diagnose an MI and pinpoint the area of damaged ventricle include inverted T waves, ST-segment elevation, and pathologic Q waves Cardiac enzyme levels: To confirm the diagnosis of acute MI, serum CK-MB isoenzymes , and Troponin I or Troponin T Assessment and Diagnosis

40. Bradycardias Bundle branch block Varying degrees of heart block Atrial and ventricular dysrhythmias Dysrhythmias and Acute MI

41. Tissue ischemia Hypoxemia Autonomic nervous system influences Metabolic derangement Acid-base imbalances Hemodynamic abnormalities Drugs, especially digoxin toxicity Electrolyte imbalances (K+ and Mg++) Fiber stretch (dilation and cardiomyopathy) Etiology of Dysrhythmias in MI

42. Dysrhythmias Ventricular aneurysm (see picture) Ventricular septal defect (see picture) Papillary muscle rupture Pericarditis Cardiac rupture Sudden death Heart failure Pulmonary edema Cardiogenic shock Complications of MI

43. Medical Management

44. Clinical Guideline Address the issue of Recanalization of the coronary artery : the essential immediate interventions are fibrinolytic therapy or PCI to open occluded artery for the patient with an acute STEMI Anticoagulation : in acute phase after STEMI, HEPARIN is administered in combination with fibrinolytic therapy to open the coronary artery. Dysrhythmia Interventions: the antidysrhytmic with the best safety Medical Management

45. record after STEMI is amiodarone. Beta-blockers also are recommended for all patients after STEMI. Tight Glucose Control: control Glucose during acute phase and after MI improves survival Prevention of Ventricular Remodeling: Many patient are risk for development Heart Failure (HF) after STEMI. Vasodilators drugs as ACEIs or ARBs can stop or limit the ventricular remodeling that leads to HF Medical Management

46. Nursing intervention focus on : Patient assessment : monitoring the patient for dysrhythmia ; evaluating vital signs for hemodynamic deterioration ; auscultating breath sounds for signs of pulmonary congestion ; listening to heart sounds for abnormalities ; evaluating side effects from the medication Control of angina pain : continued ischemic pain represents myocardium at risk; pain can be controlled by nitroglycerin and morphine. If the patient is within 12 hour window in which the Nursing Management

47. myocardium can be salvaged. PTCA or stent is the intervention of choice. If cardiac catheterization is not available thrombolytic therapy is used. Balance myocardial oxygen supply and demand and optimize cardiac output: Myocardial oxygen supply increased by the use of positive inotropic drugs such as dopamine and dobutamine Avoiding negative inotropic drugs such as beta blockers ; Nursing Management

48. Give supplemental oxygen To decrease cardiac work and myocardial oxygen consumption bed rest with commode privileges is usually supplied during the first 24-48 hrs. Prevent Complications: Put the patient in upright position to foster better lung expansion and also decreases venous return which lower preload and decrease cardiac work ; Nursing Management

49. Deep breathing decreases the risk of atelectasis ; Avoid increasing intraabdominal pressure ( Valsalva maneuver) and give stool softeners to lessen the risk of constipation from analgesics and bed rest ; Controls the critical care environment by decreasing noise , diminishing sensory overload , and allowing adequate rest periods ; Because appetite is poor in such patients in first 24 hrs , Give a light diet. Nursing Management

50. Patient education: if the person arrives at the hospital after the window of time has passed when the myocardium can be saved, the patient is educated to clarify the reason for admission to the critical care unit and the important of avoiding straining when coughing, moving, or using the commode or bathroom. Nursing Management

51. Thank you