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Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
Afshan ali myocardial infarction
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Afshan ali myocardial infarction

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BEMS UNIVERSITY OF POONCH AJK

BEMS UNIVERSITY OF POONCH AJK

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  • 1. Myocardial Infarction• Myocardial infarction or “heart attack” is an irreversible injury to and eventual death of myocardial tissue that results from ischemia and hypoxia.• Myocardial infarction is the leading killer of both men and women in the United States.
  • 2. • Critical myocardial ischemia can occur as a result of increased myocardial metabolic demand, decreased delivery of oxygen and nutrients to the myocardium via the coronary circulation, or both. An interruption in the supply of myocardial oxygen and nutrients occurs when a thrombus is superimposed on an ulcerated or unstable atherosclerotic plaque and results in coronary occlusion.
  • 3. • A high-grade (>75%) fixed coronary artery stenosis caused by atherosclerosis or a dynamic stenosis associated with coronary vasospasm can also limit the supply of oxygen and nutrients and precipitate an MI.• Conditions associated with increased myocardial metabolic demand include extremes of physical exertion, severe hypertension (including forms of hypertrophic obstructive cardiomyopathy), and severe aortic valve stenosis.• Other cardiac valvular pathologies and low cardiac output states associated with a decreased mean aortic pressure, which is the prime component of coronary perfusion pressure, can also precipitate
  • 4. Causes• Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation• Coronary artery vasospasm• Ventricular hypertrophy• Hypoxia• Coronary artery emboli
  • 5. Causes• Cocaine• Arteries• Coronary anomalies• Aortic dissection• Pediatrics Kawasaki disease, Takayasu arteritis• Increased afterload which increases myocardial demand
  • 6. Risk factors for atherosclerosis• Age• Male gender• Smoking• Hypercholesterolemia and triglyceridemia• Diabetes Mellitus• Poorly controlled hypertension• Type A personality
  • 7. Risk factors for atherosclerosis• Family History• Sedentary lifestyle
  • 8. Mechanisms of Myocardial damageThe severity of an MI is dependent of three factors• The level of the occlusion in the coronary• The length of time of the occlusion• The presence or absence of collateral circulation
  • 9. • The death of myocardial cells first occurs in the area of myocardium most distal to the arterial blood supply: the endocardium.• As the duration of the occlusion increases, the area of myocardial cell death enlarges, extending from the endocardium to the myocardium and ultimately to the epicardium.• The area of myocardial cell death then spreads laterally to areas of watershed or collateral perfusion. Generally, after a 6- to 8-hour period of coronary occlusion, most of the distal myocardium has died. The extent of myocardial cell death defines the magnitude of the MI. If blood flow can be restored to at-risk myocardium, more heart muscle can be saved from irreversible damage or death
  • 10. Myocardial InfarctionCoronary blood flow and myocardial infarction The location of a myocardial infarction will be largely determined by which coronary blood vessel is occluded.The two main coronary arteries supplying the myocardium are:a) the left coronary artery (which subdivides into the left anterior descending and circumflex branches) andb) the right coronary artery
  • 11. Coronary Arteries for the heartThe two main coronary arteries supplying the myocardium are:1. the left coronary artery (which subdivides into the left anterior descending and circumflex branches) and2. the right coronary artery
  • 12. Myocardial Infarction• The left anterior descending artery supplies blood to the bulk of the anterior left ventricular wall, while the left circumflex artery provides blood to the left atrium and the posterior and lateral walls of the left ventricle.• The right coronary artery provides blood mainly to the right atria and right ventricles.• Nearly 50% of all myocardial infarctions involve the left anterior descending artery that supplies blood to the main pumping mass of the left ventricle.• The next most common site for myocardial infarction is the right coronary artery, followed by the left
  • 13. Myocardial Infarction MorphologyA myocardial infarction may be:a) transmural, meaning it involves the full thickness of the ventricular wall, orb) subendocardial, in which the inner one third to one half of the ventricular wall is involved.Transmural infarcts tend to have a greater effect on cardiac function and pumping ability since a greater mass of ventricular muscle is involved.
  • 14. Signs and symptoms• Acute MI can have unique manifestations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. An asymptomatic MI is not necessarily less severe than a symptomatic event, but patients who experience asymptomatic MIs are more likely to be diabetic. Despite the diversity of manifesting symptoms of MI, there are some characteristic symptoms.
  • 15. Signs and symptoms Contd.• Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax• Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back• Associated dyspnea or shortness of breath• Associated epigastric discomfort with or without nausea and vomiting• Associated diaphoresis or sweating• Syncope or near syncope without other cause
  • 16. Signs and symptoms Contd.• An MI can occur at any time of the day, but most appear to be clustered around the early hours of the morning or are associated with demanding physical activity, or both. Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) before the infarct.
  • 17. Investigation / Cardiac Biomarkers• Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle• Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury• These biomarkers have a characteristic rise and fall pattern
  • 18. Troponin T and I• These isoforms are very specific for cardiac injury• Preferred markers for detecting myocardial cell injury• Rise 2-6 hours after injury Peak in 12-16 hours Stay elevated for 5-14 days
  • 19. Creatinine Kinase ( CK-MB)• Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB)• Increased in over 90% of myocardial infraction• However, it can be increased in muscle trauma, physical exertion, post- op, convulsions, and other conditions
  • 20. Creatine Kinase (MB)• Time sequence after myocardial infarction Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days• MB2 released from heart muscle and converted to MB1.• A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicates myocardial injury
  • 21. Myoglobin• Damage to skeletal or cardiac muscle release myoglobin into circulation• Time sequence after infarction Rises fast 2hours Peaks at 6-8 hours Returns to normal in 20-36 hours• Have false positives with skeletal muscle injury and renal failure
  • 22. Renal Failure and Renal Transplantation• Diagnostic accuracy of serum markers of cardiac injury are altered in patients with renal failure• Cardiac troponins decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy• Current data show levels of troponin I are unaltered while levels of troponin T may be elevated
  • 23. CBC• CBC is indicated if anemia is suspected as precipitant• Leukocytosis may be observed within several hours after myocardial injury and returns returns to levels within the reference range within one week
  • 24. Chemistry Profile• Potassium and magnesium levels should be monitored and corrected• Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization
  • 25. C-reactive Protein (CRP)• C- reactive protein is a marker of acute inflammation• Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event
  • 26. Chest X-Ray• Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax)• Chest radiography also reveals complications of myocardial infarction such as heart failure
  • 27. Echocardiography• Use 2-dimentional and M mode echocardiography when evaluating overall ventricular function and wall motion abnormalities• Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)
  • 28. Electrocardiogram• A normal ECG does not exclude ACS• High probability include ST segment elevation in two contiguous leads or presence of q waves• Intermediate probability ST depression• T wave inversions are less specific
  • 29. Myocardial InfarctionCompensatory mechanisms of myocardial infarctionAs a result of the hypotension and hemodynamic changes that accompany a myocardial infarction, the cardiovascular system initiates a number of reflex compensatory mechanisms designed to maintain cardiac output and adequate tissue perfusion:1.Catecholamine release : Increases heart rate, force of contraction and peripheral resistance.2. Sodium and water retention.3. Activation of renin–angiotensin system leading to peripheral vasoconstriction.4. Ventricular hypertrophy.Unfortunately, these compensatory changes may increase oxygen demand and workload on the infarcted heart and worsen overall cardiac function.
  • 30. Myocardial Infarction Complications of myocardial infarctionDepending on the extent of the area involved in a myocardial infarction, a number of complications might arise, including:1. Rupture of weakened myocardial wall. Bleeding into pericardium may cause cardiac tamponade and further impair cardiac pumping function. This is most likely to occur with a transmural infarction. Rupture of the septum between the ventricles might also occur if the septal wall is involved in the infarction.2. Formation of a thromboembolism from pooling of blood in the ventricles.3. Pericarditis : Inflammation due to pericardial friction rub. Often occurs 1 to 2 days after the infarction.4. Arrhythmia : Common as a result of hypoxia, acidosis and altered electrical conduction through damaged and necrotic areas of the myocardium. May be life-threatening and lead to fibrillation.
  • 31. Myocardial Infarction Complications of myocardial infarction5. Reduced cardiac function : Typically presents with reduced myocardial contractility, reduced wall compliance, decreased stroke volume and increased left ventricular end diastolic volume.6. Congestive heart failure may result if a large enough area of the myocardium has been damaged such that the heart no longer pumps effectively.7. Cardiogenic shock : Marked hypotension that can result from extensive damage to the left ventricle. The resulting hypotension will trigger cardiovascular compensatory mechanisms that will further tax the damaged myocardium and exacerbate impaired function. Cardiogenic shock is associated with a mortality rate of 80% or greater.
  • 32. Myocardial Infarction Rationale for therapy A main goal of intervention for myocardial infarction is to limit the size of the infarcted area and thus preserve cardiac function. Early recognition and intervention in a myocardial infarction have been shown to significantly improve the outcome and reduce mortality in patients. If employed in the early stages of myocardial infarction, antiplatelet- aggregating drugs such as aspirin and clot-dissolving agents such as streptokinase and tissue plasminogen activator may be very effective at improving myocardial blood flow and limiting damage to the heart muscle.
  • 33. Myocardial Infarction Rationale for therapy Other drugs such as vasodilators, β -adrenergic blockers and ACE inhibitors can also improve blood flow and reduce workload on the injured myocardium and thus reduce the extent of myocardial damage. The development of potentially life-threatening arrhythmias is also common during myocardial infarction as a consequence of hypoxia, acidosis and enhanced autonomic activity and must be treated with appropriate antiarrhythmic drugs. Supportive therapies such as oxygen, sedatives and analgesics are also utilized.
  • 34. Myocardial Infarction Treatment for myocardial infarction1. Oxygen : Used to maintain blood oxygenation as well as tissue and cardiac O2 levels.2. Aspirin : If administered when myocardial infarction is detected, the antiplatelet properties of aspirin may reduce the overall size of the infarction.3. Thrombolytic therapy :If employed in the first 1 to 4 hours following the onset of a myocardial infarction, these drugs may dissolve clots in coronary blood vessels and re-establish blood flow.4. Vasodilator drugs : Intravenous nitroglycerin can increase blood flow to the myocardium and reduce myocardial work.
  • 35. Myocardial Infarction Treatment for myocardial infarction5.β -Blockers : Blunt the effect of catecholamine release on the myocardium, reduce heart rate and myocardial work.6. Pain management : Sublingual nitroglycerin, morphine if necessary7. Antiarrhythmic drugs : To treat and prevent a number of potentially life-threatening arrhythmias that might arise following a myocardial infarction.8. ACE inhibitors : the negative effects of vasoconstriction and salt and water retention on the myocardium.
  • 36. Myocardial Infarction Thrombolytic Agents Used Clinicallya. Streptokinase : Derived from β -hemolytic streptococcus bacteria; involved in the activation of plasminb. Anistreplase (APSAC) : Complex of human lys-plasminogen and streptokinase; Administered as a prodrugc. Alteplase (TPA): Recombinant tissue plasminogen activatord. Urokinase : Endogenous human enzyme that converts plasminogen to active plasmine. Routes of administration : Intravenous. for all of the abovef. Major unwanted effects : Internal bleeding, gastrointestinal bleeding, stroke, allergic reactions
  • 37. Myocardial Infarction Pain Management in Myocardial Infarctiona. Sublingual nitroglycerin : Potent vasodilator of coronary arteries, also dilatesb. peripheral arteries and veins to reduce preload and afterload on the heartc. Morphine sulfate : Powerful opioid analgesic that also provides a degree ofd. sedation and vasodilatation; although the opioid analgesics have little effect one. the myocardium, they are powerful respiratory depressants
  • 38. Myocardial Infarction Aspirin• Inhibits the cyclo-oxygenase pathway for the synthesis of prostaglandins, prostacyclins and thromboxanes. • Inhibits aggregation of platelets and is effective in reducing myocardial infarction, stroke and mortality in high-risk patients.
  • 39. Myocardial InfarctionKey terms• Cardiac tamponade : Excessive pressure that develops from the accumulation of fluid in the pericardium.• Pericarditis : Inflammation of the pericardium.• Stroke volume : Volume of blood ejected from each ventricle per beat.• End-diastolic volume : Volume of blood remaining in the ventricle at the end of systole (contraction).

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