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Myocardial Infarction
Myocardial infarction, also known as a heart attack, results from prolonged lack of oxygen supply to heart muscle, causing cell death. It is usually caused by a blockage of a coronary artery from an atherosclerotic plaque rupture. Symptoms include chest pain and shortness of breath. Diagnosis involves evaluating symptoms, electrocardiogram changes, and cardiac enzyme levels. Treatment focuses on restoring blood flow, reducing workload and complications through medications like antiplatelets, anticoagulants, beta blockers, and ACE inhibitors.
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Definition of MI, its causes, and key mechanisms including coronary artery blockage.
Common symptoms are chest pain, tachycardia, and shortness of breath with various other signs.
Includes common risks like high blood pressure, diabetes, and obesity, plus less common factors.
Suggests dietary changes to reduce MI risk focusing on whole grains, fruits, and lean proteins.
Defines different types of MI based on causes and mechanisms, such as primary and secondary causes.
Overview of lifestyle, genetic, environmental factors that increase MI risk.Describes the physiological effects of MI on heart cells including myocardial injury.
Explains the link between atherosclerosis and the development of heart attack through plaque.
Discusses cell death, remodeling, reperfusion injury, and hibernating myocardium post-MI.
Covers diagnostic approaches including ECG findings, physical symptoms, and cardiac markers.
Details on coronary angiography to visualize heart arteries and potential interventions.
Basic aim of pharmacotherapy in managing MI to reduce morbidity & ensure patient comfort.
List and function of antiplatelet medications essential for acute MI management.
Covers possible antithrombotic medications to prevent thrombus formation in MI.
Discusses glycoprotein IIb/IIIa inhibitors that help prevent thrombus during MI treatment.
Describes the role of vasodilators in improving myocardial oxygen supply and comfort.
Defines beta-blockers and their effects on reducing cardiac demand and preventing arrhythmias.
Importance of ACE inhibitors in reducing mortality post-MI and indications for use.
Details on alternative use of angiotensin receptor blockers when patients can't tolerate ACE inhibitors.
Emphasizes the need for analgesics to ensure patient comfort during MI treatment.
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Myocardial Infarction
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- 3. MUHAMMAD ADEEL PHARM-D G.C UNIVERSITYFAISALABAD
- 4. MYOCARDIAL INFARCTION Definition: Myocardial infarction(MI) also called (heart attack) is the irreversible death (necrosis) of heart muscle due to prolonged lack of oxygen supply (Ischemia) when blood flow ( enriched with oxygen ) stops to a part of heart causing damage to heart muscles . Mechanism Of Myocardial Infarction: The mechanism of an MI often involves the complete blockage of a coronary artery caused by a rupture of an atherosclerotic plaque .
- 5. OTHER NAMES OFMYOCARDIAL INFARCTION Also called cardiac Infarction , Coronary attack Infarction of heart , Myocardial Infarct . Signs And Symptoms • Most common sign and symptom is chest pain which travels into shoulders , arms , back , neck and jaws . Often it occurs in the center or left side of the chest and lasts for more than a few minutes . ( 30 – 60 minutes ) . • Patient Blood Pressure(BP) is initially elevated because of peripheral arterial vasoconstriction.
- 6. SIGNS AND SYMPTOMS •Patient heart rate (HR) is often increased (Tachycardia) . • In some patient the symptom is epigastric with a feeling of indigestion , fullness and gas . • Respiratory rate also increased due to pulmonary congestion or Anxiety . • Other Signs And Symptoms are Fatigue , tiredness , Malaise , Coughing , Wheezing , Production of Frothy Sputum , Shortness of Breath , Nausea , Cold sweats , Dizziness , Headache .
- 7. RISK FACTORS OFMYOCARDIAL INFARCTION • Commonly occur due to Coronary artery disease . • High Blood Pressure . • Smoking . • Diabetes . • Lack of Exercise . • High Blood Cholesterol . • Obesity . • Poor diet • Excessive Alcohol Intake .
- 8. LESS COMMON RISKFACTORS OF MYOCARDIAL INFARCTION Coronary artery spasm may occur due to : Cocaine . Emotional Stress . Extreme colds . • Age ( Men are at higher risk of heart attack after age of 45 than women ) . • Family History . • High blood pressure during pregnancy .
- 9. PREVENTION FROM MYOCARDIAL INFARCTION Oneway to lower the risk of heart attack is use of a healthy diet. This diet should largely consist of : • Whole grains • Vegetables • Fruits • Lean protein Reduce the amount of the following in your diet : • Sugar • Saturated fat • Cholesterol
- 10. CLASSIFICATION OF MYOCARDIAL INFARCTION Type1 : Spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion or rupture, fissuring, or dissection . Type 2 : MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia hypertension , or hypotension .
- 11. Type 3 : Suddenunexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by new ST elevation or evidence of fresh thrombus in coronary artery . Type 4 : Associated with coronary angioplasty or stents: • Type 4a – MI associated with Percutaneous Coronary Intervention (PCI) . • Type 4b – MI associated with stent thrombosis as documented by angiography or at Autopsy . Type 5 : MI associated with CABG
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- 13. LIFESTYLE • Smoking (36%) •Obesity (20%) • Lack of exercise (7-12%) • stress-related causes and chronic high stress levels (about 3% ) • Tobacco smoking and short-term exposure to air pollution • Other factors e.g lack of physical activity
- 14. LIFESTYLE • Acute andprolonged intake of high quantities of alcoholic drinks.
- 15. DISEASE • Diabetes mellitus •high blood pressure. • high levels of blood cholesterol • Endometriosis in women under the age of 40 and obesity • A number of acute and chronic infections
- 16. GENETIC • Family history •genes CDKN2A & 2B at 9p21 genomic locus.
- 17. OTHERS • Men aremore at risk than women(before manupause) • Family history of ischemic heart disease • contraceptive pills • Heart attacks appear to occur more commonly in the morning hours(6am to noon) • Old age increases risk of a heart attack.
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- 19. SUB-TYPES 1. Non-ST ElevatedMI 2. ST-Elevated MI
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- 23. PATHOLOGICAL TYPES 1. Subendocardial Myocardial Infarction 2. Transmural Myocardial Infarction
- 24. EFFECT OF MION HEART CELLS 1. Myocardial Cell Death 2. Evolution of MI and Ventricular Remodeling
- 25. EFFECT OF MION HEART CELLS 3. Reperfusion Injury 4. Stunned and Hibernating Myocardium
- 26. DIAGNOSIS OF MYOCARDIAL INFARCTION Adiagnosis of myocardial infarction can be done by: 1. Integrating the history of the presenting illness. 2. Physical examination 3. Electrocardiogram findings 4. Cardiac markers (blood tests for heart muscle cell damage). 5. A coronary angiogram allows visualization of narrowing or obstructions on the heart vessels. • A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department.
- 27. DIAGNOSTIC CRITERIA WHO Criteria2000: According to the WHO criteria as revised in 2000, the diagnostic of Myocardial Infarction are: • A cardiac troponin rise accompanied by • Typical symptoms (shortness of breath, chest pain, back pain, anxiety etc.) • Pathological Q waves • ST elevation or depression • Coronary intervention
- 28. PHYSICAL EXAMINATION The generalappearance of patients may vary according to the experienced symptoms: • The patient may be comfortable, or restless and in severe distress with an increased respiratory rate. • A cool and pale skin is common and points to vasoconstriction. • Some patients have low-grade fever (38–39 °C). • Blood Pressure may be elevated or decreased, and the pulse can become irregular.
- 29. PHYSICAL EXAMINATION If heartfailure occurs, then: • elevated jugular venous pressure and hepatojugular reflux(for right ventricular failure). • Swelling of the legs due to peripheral edema may be found on inspection.
- 30. ELECTROCARDIOGRAM • The primarypurpose of the electrocardiogram is to detect ischemia or acute coronary injury. • A serial ECG may be used to follow rapid changes in time. • The standard 12 lead ECG does not directly examine the right ventricle, and is relatively poor at examining the lateral walls of the left ventricle.
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- 32. ELECTROCARDIOGRAM • A normalECG does not rule out acute myocardial infarction. • Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care.
- 33. CARDIAC MARKERS • Cardiacmarkers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream. • Until the 1980s, the enzymes AST and LDH were used to assess cardiac injury. Now, the markers most widely used in detection of MI are Creatine kinase and Cardiactroponins T and I as they are more specific for myocardial injury. • The cardiac troponins T and I which are released within 4–6 hours of an attack of MI and remain elevated for up to 2 weeks, have nearly complete tissue specificity and are now the preferred markers for assessing myocardial damage.
- 34. CARDIAC MARKERS • Heart-typefatty acid binding protein is another marker, used in some home test kits. • New markers such as glycogen phosphorylase isoenzyme BB are under investigation. • When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24-hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.
- 35. CORONARY INTERVENTION (ANGIOGRAPHY) • Indifficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. • A catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart. • A radio-opaque dye is administered through the catheter and a sequence of x-rays (fluoroscopy) is performed. • Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure.
- 36. PHARMACOTHERAPY Treatment of diseasewith drugs is called pharmacotherapy
- 37. MEDICATION SUMMARY • Thegoals of pharmacotherapy for myocardial infarction are to reduce morbidity and to prevent complications. The main goals of emergency department medical therapy are rapid intravenous thrombolysis, optimization of oxygenation, reduction of cardiac workload, and pain control.
- 38. 1. ANTIPLATELET AGENTS •Antiplatelet agents are member of a class of a pharmaceuticals that decrease platelet aggregation and inhibit the thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect. • It include the drugs: 1. Aspirin 2. Clopidogrel (Plavix) 3. Ticagrelor (Brilinta) 4. Prasugrel (Effient) 5. Vorapaxar (Zontivity)
- 39. 2. ANTITHROMBOTIC AGENTS •Antithrombotic agents prevent the formation of thrombi associated with myocardial infarction and inhibit platelet function by blocking cyclooxygenase and subsequent platelet aggregation. Unfractionated intravenous heparin and fractionated low-molecular- weight subcutaneous heparins are the 2 choices for initial anticoagulation therapy. • It include the drugs: 1. Bivalirudin (Angiomax) 2. Heparin 3. Enoxaparin (Lovenox) 4. Dalteparin (Fragmin)
- 40. 3. GLYCOPROTEIN IIB/IIIA INHIBITORS •They work by preventing platelet aggregation and thrombus formation. They do so by inhibition of GpIIb/IIIA receptors on the surface of platelets. • Glycoprotein IIb/IIIa inhibitors prevent acute cardiac ischemic complications that is unresponsive to conventional therapy. It include the drugs: 1. Tirofiban (Aggrastat) 2. Eptifibatide (Integrilin)
- 41. 4. VASODILATORS • Vasodilatorsrelieve chest discomfort by improving myocardial oxygen supply, which in turn dilates epicardial and collateral vessels, improving blood supply to the ischemic myocardium. • It include the drugs: Nitroglycerine
- 42. 5. BETA-ADRENERGIC BLOCKERS •This category of drugs has the potential to suppress ventricular ectopy due to ischemia or excess catecholamines. In the setting of myocardial ischemia, beta-blockers have antiarrhythmic properties and reduce myocardial oxygen demand. • It include the drugs: 1. Metoprolol 2. Esmolol 3. Atenolol
- 43. 6. ANGIOTENSIN-CONVERTING ENZYME INHIBITORS •ACE inhibitors may prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. ACE inhibitors reduce mortality rates after myocardial infarction. Administer ACE inhibitors as soon as possible as long as the patient has no contraindications and remains in stable condition. ACE inhibitors have the greatest benefit in patients with ventricular dysfunction. • It include the drugs: 1. Captopril 2. Enalapril 3. Quinapril 4. Lisinopril
- 44. 7. ANGIOTENSIN-RECEPTOR BLOCKER • Angiotensin-receptorblockers may be used as an alternative to ACE inhibitors in patients who develop adverse effects, such as a persistent cough. An angiotensin-receptor blocker should be administered to patients who are intolerant of ACE inhibitors. • It include the drugs: 1. Irbesartan 2. Candesartan 3. Valsartan 4. Azilsartan 5. Eprosartan mesylate 6. Losartan
- 45. 8. ANALGESICS Pain controlis essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain. It include the drugs: Morphine sulfate