Diseases List

ID 71
Name MYOCARDIAL INFARCTION
Cause Causes: 1. Commonly- occlusion of coronary artery by thrombus formation at the site of rupture of a pre-existing atheromatous plaque or atherosclerotic stensis. prolonged myocardial ischaemia precipitated in most cases by an occlusive coronary thrombus at the site of a preexisting atherosclerotic stenosis. 2. Rarely- i. prolonged coronary vasospasm, ii. hypotension causing inadequate myocardial blood flow, or iii. excessive metabolic demand. 3. Very rarely- i. embolic occlusion of coronary vessel, ii. vasculitis, iii. aortic root or coronary artery dissection, or iv. aortits. 4. Cocaine- may be a cause, specially in young individual.
Signs Symptoms
Diagnosis
Investigations Investigations: 1. Blood- leukocytosis & high ESR. 2. Urine- shows albumin & sugar. 3. Change in plasma enzymes- Name Start Peak Fall to normal CK 4-6 hours 12 hours 48-72 hours AST 12 hours 1st or 2nd day 4th day LD 12 hours 2-3 days Elevated for about a week The most sensitive markers of myocardial cell damage are the cardiac troponins T & I, which are released with 4-6 hours and remain elevated for upto 2 weeks. The American College of Cardilogy and the European Society of Cardiology have redefined MI as ‘a typical rise in cardiac troponin T or I or CK-MB above the 99th centile for normal, with at least one of the following: ischemic symptoms, development of pathological Q waves on the ECG, ischemic ECG changes (ST depression or elevation) or coronary artery intervention (e.g PCI)2 4. E.C.G- Abnormal Q wave is diagnostic. ST segment elevated or depressed, T wave inverted. 5. Chest X-ray- may show pulmonary oedema, or pericardial effusion; heart may be normal in size or occasionally cardiomegaly. 6. Echocardiography- should be done at bedside if possible. It is very helpful in assessing ventricular function & detecting cardiac complications, such as cardiac rupture, VSD, MR & pericardial effusion. 7. Radionuclide ventricular scanning- to assess left ventricular function.
Management Management:1.2 Early management of acute myocardial infarction- 1. Immediate hospitalization- if approachable (where defibrillator is available). 2. Rest- absolute bed rest. 3. Oxygen supplement- high-flow oxygen 2-3 litre/minute by nasal catheter should be started immediately. 4. a. Intravenous access should be opened immediately for rapid i.v medication, b. ECG monitoring. 5. Relief of pain- Inj. morphine 10mg or diamorphine 5mg initially i.v slowly is given immediately. In severe cases it may be repeated in smaller doses in every 3-4 hours interval. 6. Antiemetic- Inj. cyclizine 50mg or prochlorperazine (stemetil) 12.5mg i.v stat to prevent vomiting. 7. Oral aspirin 300mg stat (soluble or chewable) and then 75-150mg daily for at least 4 weeks- it improves survival (30% reduction in short-term mortality) & enhances the effect of thrombolytic therapy. 8. L Thrombolytic therapy: Appropriate use of thrombolytic drugs may bring great benefit to the patient, if it can be initiated within first 1-3 hours; 25-50% or greater reduction in mortality rate can be achieved. Even if it can be given within 12 hours of onset of symptoms, there may be a significant reduction in short-term mortality. Inj. Sterptokinase 1.5 million units in 100ml of saline given as an i.v infusion over 60 minutes (half in 20 minutes & rest in 40 minutes). Or, Inj. Alteplase2 (a genetically engineered i.e recombinant tissue plasminogen activator or tPA; it is not antigenic and rarely causes hypotension)- a bolus dose of 15mg given in i.v drip over 90 minutes, followed by 0.75mg/kg (max. 50mg) over 30 minutes, & then 0.5mg/kg (max. 35mg) over 60 minutes. Many hospitals or clinics only use Alteplase where Streptokinase is supposed to be contraindicated. Recently, other two genetically engineered plasminogen activator products are also available, which can be used as alternative of Alteplase viz, Reteplase (rPA), Tenecteplase (INK) N.B: Streptokinase is an antigenic drug, if once it is used, neutralizing antibodies are formed in the circulation, which may persist for 5 years or more. So that, subsequent use of this drug may be ineffective or occasionally may cause serious allergic reaction. Therefore, if it is necessary to use any thrombolytic drug further, it is better to use another drug in the next few years
Introduction Myocardial infarction is defined as the myocardial tissue damage due to ischaemic necrosis, occuring as a result of occlusion of coronary artery blood supply, commonly by thrombus formation & rarely by other causes
History
Etiology
Clinical Features Clinical features: 1. Onset- acute, and usually at rest. 2. Symptoms due to ischaemia- pain, which starts at rest & located in the mid or upper sternal region, constricting or pressing or crushing in character, radiates along the shoulders & usually not relieved by glyceryl trinitrate. 3. Symptoms of heart failure- breathlessness, cough & frothy (sometimes bloody) sputum. Patient cannot lie down flat in bed because of pulmonary oedema. 4. Symptoms due to cardiogenic shock-limbs are cold, severe sweating, restlessness, confusion & oliguria. 5. Symptoms due to muscle necrosis-fever (100-103°F), leukocytosis, high ESR. 6. On examination- patient is anxious restless, propped up in position, blood pressure is low & declines, pulse is high, pulsus alternance, central cyanosis, hurried respiration etc. 7. Heart sounds are faint and indistinguishable, soft systolic murmur, pericardial friction sound.
Preventions
Treatment
Complications Complications: 1. Cardiac arrhythmias. 2. Shock & peripheral circulatory failure. 3. Left & right ventricular failure. 4. Pulmonary or systemic embolism. 5. Post myocardial infarction syndrome. Arrhythmias in myocardial infarction2- 1. Ventricular fibrillation 2. Ventricular tachycardia 3. Accelerated idioventricular rhythm 4. Ventricular ectopics 5. Atrial fibrillation 6. Atrial tachycardia 7. Sinus bradycardia 8. Heart block
Prognosis
Types
Classification
Observation
Pathology
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