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myocardial infarction .pptxurhdbdjdjdjdnfnn
- 1. MYOCARDIAL INFARCTION Presented by, Шубхамядав Джакал джаянт Сарсар прутхьирадж
- 2. CONTENTS: 1. Definition 2. Typesof infarcts 3. Epidemiology 4. Etiology 5. Etiopathogenesis 6. Pathophysiology 7. Clinical manifestations 8. Diagnosis 9. Management: Non-pharmacological Pharmacological
- 3. MYOCARDIAL INFARCTION MI isdefined as a diseased condition which is caused by reduced blood flow in a coronary artery due to atherosclerosis & occlusion of an artery by an embolus or thrombus. MI or heart attack is the irreversible damage of myocardial tissue caused by prolonged ischaemia & hypoxia.
- 5. TYPES OF INFARCTS 1.According to anatomic region of left ventricle invoved: Anterior Posterior Lateral Septal Circumferential Combinations- Anterolateral, Posterolateral, Anteroseptal 2. According to degree of thickness of ventricular wall involved: Transmural (full thickness) Laminar (subendocardial) 3. According to age of infarcts: Newly formed (acute, recent, fresh) Advanced infarcts (old, healed, organised)
- 6. EPIDEMIOLOGY: In industrial countriesMI accounts for 10-25% of all deaths. Incidence is higher in elderly people, about 5% occurs at people under age 40. Males have higher risk. Women during reproductive period have low risk. In 2006, studies revealed a prediction that India would account for 40-60% of cardiovascular diseases burden within next 10-15 years. Over last 30 years, the rate of diseases increased from 2- 6% in rural population and 4-12% in urban population.
- 7. Tobacco smoking Hypertension Drug abuse Obesity Stress Alcohol ETIOLOGY
- 8. Age Gender Diabetes Hyperlipoproteinaemia Family history of Ischaemic Heart Disease Hyperhomocysteinemia Chronic kidney disease
- 9. ETIOPATHOGENESIS: 1. Mechanism of myocardialischaemia. 2. Role of platelets. 3. Acute plaque rupture. 4. Non-atherosclerotic causes. 5. Transmural versus subendocardial infarcts.
- 10. PATHOPHYSIOLOGY Atherosclerosis Arterial spasmAtherosclerosis+Plaque split+Thrombus gradual sudden not usually reversible Obstruction sudden reversible occlusion obstruction ISCHAEMIA Hypoxia Reduced oxygen demand Angina Thrombolysis Unstable angina Permanent thrombus Necrosis MYOCARDIAL INFARCTION
- 11. CLINICAL MANIFESTATIONS: • Chestpain / chest discomfort • Dyspnea • Fatigue • Other symptoms include: Increased sweating Weakness Nausea Vomiting Light-headedness Palpitation • Anxiety, sleeplessness, hypertension or hypotension, arrhythmia. • Chest pain is less in women, their common symptoms are weakness, fatigue & dyspnea.
- 12. Complications include: Arrhythmia Cardiogenic shock (10%) Congestive heart failure Thromboembolism Rupture (5%) Cardiac aneurism (5%) Pericarditis
- 13. DIAGNOSIS: 1.Clinical features: Pain Indigestion Apprehension Shock Low gradefever 2.Serum cardiac markers: Creatinine phosphokinase (CK) Lactic dehydrogenase (LDH) Cardiac specific troponins (cTn)
- 14. 3.ECG changes: STsegment elevation T wave inversion appearance of wide deep Q waves.
- 15. MAGNETIC RESONANCE IMAGING (MRI) CHESTX- RAY ANGIOGRAPHY POSITRON EMISSION TOMOGRAPHY (PET scan):
- 16. MANAGEMENT: 1.NON-PHARMACOLOGICAL: Counselling and educationof patients Life style measures Smoking cessation Avoid Alcohol intake Diet and nutrition Salt restriction
- 17. 2.PHARMACOLOGICAL: Thrombolytic agents Anticoagulants Antiplatelet agents Antihypertensiveagents Lipid lowering drugs Vasodialators Others i) Analgesics ii) Antiulcer drugs iii) Antidepressants
- 18. TREATMENT ALGORITHM FORMI: Myocardial Infarction Pre-hospital or on arrival GTN spray, Oxygen, Pain relief, Admission to hospital, Aspirin, Thrombolytics During hospital admission Add: beta blocker, ACE inhibitor, insulin Consider: Revascularization (Angioplasty, Stenting, Arterial bypass) Long term Rehabilitation classes: Aspirin, beta blocker, ACE inhibitor, Statins
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