1. S.NO. SPECIFIC OBJECTIVE CONTENT MATTER TEACHING LEARNING ACTIVITIES INTRODUCTION The heart muscle must have adequate blood supply to contract properly. The coronary arteries carry oxygen to the myocardium. When coronary arteries are narrowed or blocked the area of heart muscle supplied by that artery becomes ischemic and injured which gives rise to various disease conditions. EVALUATION MYOCARDIAL INFARCTION Myocardial infarction is leading cause of sudden death in men and women. It is caused by an obstruction in a coronary artery resulting in necrosis to the tissues supplied by the artery. The obstruction is usually due atherosclerotic plaque, a thrombus or an embolism. The area most affected is left ventricle. The student teacher defines MI verbally. What do you mean by Myocardial infarction? 1. 2. 3. Define Myocardial infarction. Enlist the risk factors of Myocardial infarction. RISK FACTORS NON-MODIFIABLE RISK FACTORS:-Family history -Increasing age -Race The student teacher enumerates the risk factors of MI on PPT. What are the various risk factors of MI.

2. -Male gender MODIFIABLE RISK FACTORS:-Blood lipid level abnormalities -Diabetes mellitus -Hypertension -Physical inactivity -Obesity -Cigarette smoking -Alcohol consumption 4. 5. Describe the pathophysiology of MI in detail. PATHOPHYSIOLOGY Enumerate the clinical manifestations of MI CLINICAL MANIFESTATIONS Cardiovascular -Chest pain or discomfort, palpitations. -Increased blood pressure. -pulse deficit In an MI, an area of myocardium is permanently destroyed. MI is usually caused by reduced blood flow in a coronary artery due to rupture of atherosclerotic plaque and subsequent occlusion of artery by the thrombus. Other causes of MI are vasospasm of coronary artery, decreased oxygen supply, and increased demand for oxygen. In each case a profound imbalance exists between myocardial supply and demand. The area of infarction develops over minutes to hour. As the cells are deprived of oxygen, ischemia develops and cellular injury occurs and lack of oxygen results in infarction. The student teacher explains What are the pathophysiology by using pathophysiological ppt. Changes occurring in MI? The student teacher enumerates the clinical manifestations by using ppt. What are the clinical manifestations of MI?

3. -ST segment and T wave changes. Respiratory -Shortness of breath -Dyspnea,tachypnea -crackles -pulmonary edema Gastrointestinal -nausea and vomiting Genitourinary -Decreased urinary output indicates cardiogenic shock. Skin -cool,clammy ,diaphoretic and pale appearance due to sympathetic stimulation may indicate cardiogenic shock Neurologic -Anxiety,restlessness,light headedeness Psychological -Fear with feeling of impending doom. 6. Discuss the assessment and diagnostic findings of MI ASSESSMENT AND DIAGNOSTIC FINDINGS The diagnosis of MI is based on the presenting symptoms and laboratory test results.The prognosis depends on the severity of coronary artery obstruction and extent of myocardial damage. Physical examination is always conducted.but the examination alone does not confirm the diagnosis. Patients history:The patients history has two parts:the description of the presenting symptoms and the history of previous illness and family The student teacher discusses the diagnostic techniques with the help of ppt and lecture cum discussion What are the diagnostics measures used to diagnose MI?

4. history of heart disease.Previous history also include the risk factors for heart disease. Electrocardiogram:The ECG provides the information that assist in diagnosing acute MI. It should be obtained within 10 minutes from the time the patient reports the pain or arrives the emergency department. By monitoring ECG changes over time, the location, evolution and resolution of an MI can be identified and monitored. The classic ECG changes are T wave inversion, ST segment elevation and development of abnormal Q wave .During recovery from MI the ST segment often is the first ECG indicator to return to normal. Echocardiogram:The echocardiogram is used to evaluate ventricular function.It may be used to assist in diagnosing an MI especially when ECG is nondiagnoctic.The echocardiogram can detect hypokinetic and akinetic wall motion and can determine the ejection fraction. Laboratory tests:Creatinine kinase and its isoenzymes:Ck-MB is the cardiac-specific isoenzyme,found in cardiac cells. Elevated CK-MB assessed by mass assay is an indicator of acute MI;its level begins to rise within a few hours and peaks within 24 hours of an MI. Myoglobin: Myoglobin is heme protein helps transport oxygen.It is found in cardiac cells and skeletal

5. muscle.It starts to oncrease within 1-3 hours and peaks within 12 hours after onset of symptoms. Troponin:It is a protein found in the myocardium regulates the contractile process.There are three isomers of troponin C,I and T. Troponin I and T are specific for cardiac muscles and these tests are currently recognised as reliable and critical markers of myocardial injury.An increased level of troponins in serum can be detected within few hours during acute MI. It remains elevated for a long period often as long as 3 weeks and can be used to detect recent myocardial damage. 7. Enlist the complications of MI COMPLICATIONS Acute pulmonary edema Heart failure Cardiogenic shock Dysrhythmias Pericardial effusion Myocardial rupture The student teacher enlists the complications with the help of chart What are the complications of MI? 8. Explain the medical management of the patient with MI. MEDICAL/SURGICAL MANAGEMENT It focuses on reducing the workload of heart,relieving pain,improving tissue perfusion,preventing complications and further tissue damage.Immediately after MI a client is admitted to a coronary unit.The client heart is contantly monitored for dysrhythmias.The clients vital signs are The student teacher describes the medical management with the help of ppt. What can be the medical management of the patient with MI?

6. monitored by arterial line for hemodynamic monitoring or noninvasive B.P monitoring system. Pharmacological therapy:The patient with MI is given aspirin,nitroglycerin,morphine,beta blockers and other medications as indicated.Patients should receive beta blockers initially,throughout the hospitalisation and after discharge.These medications decrease the incidence of future cardiac events. Thrombolytics:These medications are administered I/V , can be given directly into coronary artery in cardiac catheterization lab. The purpose of thrombolytics is to dissolve and luse the thrombus in a coronary artery,causing reperfusion and minimize the size of infarction. Analgesics:The analgesics of choice for acute MI is morphine sulphate administered in I/V boluses to decrease pain and anxiety.It decreases the preload and afterload thus decreasing the workload of heart.It also relax the bronchioles to enhance the oxygenation.The cardiovascular response to morphine is monitored closely,particularly B.P which can decrease and repiratory rate can be depressed. ACE inhibitors:ACE inhibitors prevent the conversion of

7. angiotensin I to angiotensin II.In the absence of angiotensin II B.P will decrease and kidneys excrete sodium and fluid which further decreases the oxygen demand of the heart. Antidysrhythmic agents:Three dysrhythmias may occur following an MI are: ventricular fibrillation, bradycardias, tachycardias. Ventricular fibrillation is treated with defibrillation. Atropine and if needed a temporary pacemaker may be inserted for bradycardias. Two tachycardias that may occur are atrial fibrillation and ventricular tachycardia. Atrial tachycardias is treated with digoxin or amiodrone. Ventricular tachycardias is treated with lidocaine or cardioversion.If the dysrhythmias are continous then magnesium sulphate can be given. Medical treatment guidelines for acute myocardial infarction:-Use rapid transit to the hospital -Obtain 12-lead ECG to read within 10 minutes. -Obtain laboratory blood specimens of cardiac biomarkers, including troponins. -Obtain other diagnostics to clarify diagnosis. Begin routine medical interventions:-Supplemental oxygen -Nitroglycerin -Morphine -Aspirin 162-325mg -Beta blockers

8. -Angiotensin converting enzyme inhibitors within 24 hours. Evaluate for indications for reperfusion therapy:-Percutaneous coronary intervention -Thrombolytic therapy Continue therapy as indicated:-I/V heparin/low molecular weight heparin -Clopidogrel or ticlopidine -Glycoprotein IIb/IIIa inhibitor -Bed rest(12-24 hours) Emergent percutaneous coronary intervention:-The patient in whom an acute MI is suspected may be referred for an immediate 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.Supirior outcomes have been reported with the use of PCI compared to thrombolytics.PCI treats the underlying atherosclerotic lesions.Because the duration of oxygen deprivation is directly related to number of cells that die,the time from the patients arrival in the emergency department to time PCI is performed should be less than 60 minutes.This is frequently referred door to balloon time.Cardiac catheterization lab and staff must be available if an emergent PCI is performed within short time.

9. NURSING MANAGEMENT Elaborate the nursing management of the patient with MI in detail The nursing priorities are 1) To relieve pain, anxiety. 2)To reduce myocardial workload.' 3)To prevent and assist in treatment of life threatening disarrythmias. 4) To promote self care. NURSING DIAGNOSIS, INTERVENTION AND RATIONALE I. Pain related to tissue ischemia secondary.to coronary occlusion manifested by complaints of chest pain, facial grimacing. Intervention: Obtain full description of pain from patient including location, intensity, duration, quality and radiation. Rationale: Pain is a subjective symptom and must be described by the patient. Intervention: .Instruct patient to report pain immediately. Rationale: Delay in reporting pain hinders pain relief. Intervention: Provide calm and quiet The student teacher elaborates the nursing management with the help of ppt. What will the nursing care of the patient with MI?

10. environment and other comfort measures. Rationale: Decreased external stimuli may aggravate anxiety. Intervention: Administer supplementary oxygen. Rationale: Increases the oxygen supply to myocardium thereby relieving discomfort. II. Anxiety / fear related to change in health and socio economic status manifested by apprehension, increased tension, restlessness, uncertainty etc. Interventions: Note presence of hostility withdrawal or denial. Rationale: Ongoing anxiety may be present manifested by depression. Intervention: Encourage patient to communicate with one another, sharing questions. Rationale: Sharing information may relieve tension of unexpressed worries. Intervention: Answer all questions honestly. Rationale: To win the confidence of the patient.

11. III. Altered tissue perfusion related to reduction of blood flow due to vaso constriction manifested by thrombo embolitic formation. Interventions: Inspect for cyanosis, cold and clammy skin. Rationale: Systemic vasoconstriction resulting from decreased cardiac output may be evidenced by decreased skin perfusion. Intervention: Assess for homan's sign, erythema and edema. Rationale: Indicator for deep vein thrombosis. Interventions: Monitor laboratory details eg: ABG' S BUN Indicators of organ perfusion. Prepare the patient for thromboembolytic therapy. Rationale: To dissolve the clot and to restore perfusion of myocardium. IV. Excess fluid volume related to increased sodium and water retention manifested by dependent edema. Interventions: Measure intake output to detect whether there is decrease in output. Rationale: Decreased cardiac output results in impaired kidney perfusion. Na/H2o retention

12. and reduced urine output. Intervention: Weigh daily Rationale: Sudden changes in weight indicate fluid imbalance. Intervention: Provide low sodium diet. Rationale: Sodium will enhance fluid retention. Intervention: Note the development of dependent edema. Rationale: Indicates development of CHF. Intervention: Administer diuretics as prescribed. Rationale: To correct fluid overload. V. Knowledge deficit related to lack of factual information regarding implications of heart disease and future health status manifested by anxiety, worries, gloomy face etc. Interventions: Assess patient's level -of knowledge and ability to learn. Rationale: It is necessary to create individual instruction plan. Intervention: Educate the patient about basic informations regarding M.I., its cause,

13. prevention and management. Rationale: Patient will gain adequate knowledge about his disease and will try to avoid a second attack. Intervention: Emphasize on the importance of avoiding the risk factors of M.I. Rationale: Modifiable risk factors can be prevented if we take adequate precautions. OTHER NURSING MANAGEMENT: Provide semi-fowler's positions to promote chest expansions and comfort. Oxygen administration to treat tissue hypoxia. Check vital signs every 15 minutes. Watch for PVC (Premature Ventricular Contractions) in the ECG. Assess the L.O.C. Morphine is the drug of choice to relieve chest pain. Strict I/O chart. Bed rest. Sedation and hypnotics to relieve unnecessary anxiety. Clear liquid diet for 48 hours and thereafter soft bland diet. Cardiac enzymes should be repeated. Educate the patient to control diet high in fats and cholesterol. Summary: Today we have dealt with: Definition of MI Risk factors Pathophysiology Clinical manifestations

14. Diagnostic findings Medical management Nursing management Conclusion : MI is a life threatening disease caused by many factors. Health education must be given to the patients with predisposing or risk factors to prevent it. Early diagnosis is also very important for saving the life of the patient. BIBLIOGRAPHY: 1)Black M. Joyce ; Medical surgical nursing ; 5th edition ; W.B Saunders Company ; Singapore 1980 ; pg no. 1238. 2)Spring house ; handbook of medical surgical nursing ; 3rd edition ; Judith A. Schilling McCann; Pennsylvania 1998 ; pg. No. 617-618. 3)Suddarths and brunner; Textbook of medical surgical nursing; 11th edition; Lippincott Williams and Wilkins ; United states of America 2009; pg. No.

15. 4)White lois; Medical surgical nursing; Delmar publishers ; india 1998; pg. No. 5)Lewis Mantik shoron; Medical surgical nursing; 6th edition; Mosby Elsevier; United states of America 2004; pg. No. 6) www.findarticles.com 7)Sorensen and luckmann; medical surgical nursing 4th edition; W.B sauders company; pg no.-1150-1164 8)A Reference Manual of Nurses on Coronary Care Nursing by Sister Nancy, Kumar Publishing House, Pg. No. 48-49. 9)www.medscape.com 10)www. jama.ama-assn.org