1. MYOCARDIAL INFARCTION PRESENTED BY Mr. VIJAY DHANESHA Mr. VIJAY DHANESHA NURSING TUTOR NURSING TUTOR SCHOOL OF NURSING SCHOOL OF NURSING MUNI SEVA ASHRAM MUNI SEVA ASHRAM

3. MYOCARDIAL INFARCTION CONTENTSDefinitionPathophysiology Clinical Manifestation Assessment & Diagnostic findings Medical Management Cardiac Rehabilitation

4. DEFINITION An infarct is an area of tissue that has died because of lack of oxygenated blood. The myocardium is affected when a branch of a coronary artery is occluded. The commonest cause is an atheromatous plaque complicated by thrombosis. The extent of myocardial damage depends on the size of the blood vessels & site of the infarct.

6. Pathophysiology 1. Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial wall. 2. Although they are thought to be the precursors of atherosclerosis, fatty streaks are common, even in childhood.not all develop into more advanced lesions. 3. The reason why some fatty streaks continue to develop is unknown, although genetic & environmental factors are involved. 4. The continued development of atherosclerosis involves an inflammatory response. T lymphocytes & monocytes infiltrate the area to ingest the lipids & then die.

8. 5 This causes smooth muscle cells within the vessels to proliferate & form a fibrous cap over the dead fatty core. 6 This deposits, called atheromas or plaques, protrude into the lumen of the vessel, narrowing it & obstructing blood flow. 7 If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from the blood flow & vessel movement. 8 If the cap is thin, the lipid core may grow, causing it to ruptureand haemorrhage into the plaque, allowing a thrombus to develop. 9 The thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction,which is the death of heart tissue.

10. CLINICAL MANIFESTATION CARDIO VASCULAR 1. Chest pain or discomfort 2. Palpitations 3. Heart sounds may include S3, S4 & new onset of murmur, 4. Increased jugular venous distention. 5. B.P.may be elevated b/o sympathetic stimulation or decreased b/o decreased contractility. 6. Pulse deficit may indicate atrial fibrillation. 7. In addition to ST segment & T wave changes, E.C.G. may show tachycardia, bradycardia & disrhythmias.

12. RESPIRATORY 1. Shortness of breath 2. Dyspnea 3. Tachypnea 4. Cracles if M.I. has caused pulmonary congestion. 5. Pulmonary edema may be present.

13. GASTRO INTESTINAL Nausea & vomiting Nausea & vomiting GENITO URINARY Decreased urinary output may indicate cardiogenic shock. Decreased urinary output may indicate cardiogenic shock.PSYCHOLOGICAL Fear with feeling of impending doom. Fear with feeling of impending doom.

14. SKIN 1. Cool, clammy, diaphoretic & pale appearance due to sympathetic stimulation from loss of contractility may indicate cardiogenic shock. 2. Dependent edema may also be present due to poor contractility. NEUROLOGIC 1. Anxiety 2. Restlessness 3. Light headedness 4. Headache 5. Visual disturbances 6. Altered apeech 7. Altered motor function

15. ASSESSMENT & DIAGNOSTIC FINDINGS Dagnosis of M.I. is generally based on the presenting symptoms, the E.C.G.,& laboratory test results. Dagnosis of M.I. is generally based on the presenting symptoms, the E.C.G.,& laboratory test results. The prognosis depends on the severity of coronary artery obstruction the extent of myocardial damage. The prognosis depends on the severity of coronary artery obstruction the extent of myocardial damage.

17. PATIENT HISTORY ELECTROCARDIOGRAMECHOCARDIOGRAM LABORATORY TESTS 1.Creatine kinase & its isoenzymes. 2.Myoglobin 3.Trophin

19. MEDICAL MANAGEMENT The goal of the medical management is to minimize myocardial damage, preserve myocardial function,& prevent complications. This goals are achieved by perfusing the area with the emergency use of thrombolytic medications or P.T.C.A. Minimizing myocardial damage is also accompanied by reducing myocardial oxygen demand & increasing O 2 supply with medications, O 2 administration, and bed rest.

20. PHARMACOLOGICAL THERAPY 1. Trombolytics 2. Analgesics 3. Angiotensin – converting enzyme inhibitors (ACE – I) 4. EMERGENT PERCUTANEOUS CORONARY INTERVENTION (PCI)

23. CARDIAC REHABILITATION After the M.I. patient is free of symptoms, an active rehabilitation program is initiated. Cardiac rehabilitation is a program that target risk reduction by means of education, individual & group support, & physical activity. Cardiac rehabilitation is a program that target risk reduction by means of education, individual & group support, & physical activity.

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