Myocardial Infarction Pathophysiology

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Myocardial Infarction Pathophysiology

Myocardial Infarction Pathophysiology


Myocardial infarction refers to the process of destruction of heart tissue due to inadequate blood supply, so that coronary blood flow is reduced. Causes of decreased blood supply may be due to a critical narrowing of coronary arteries due to atherosclerosis or total blockage of an artery by embolism or thrombus. Decrease in coronary blood flow can also be caused by shock or bleeding. In each case it is always an imbalance between supply and oxygen demand of the heart.

30 minutes after the occlusion, metabolic bleeding, occurs as a result of ischemia. Glycosis anaerobes play a role in providing energy to produce lactase. The changes in electrical membrane potential, after 20 minutes of cellular changes include rupture lisotum and structural defects sarkolema which becomes irreversible at the central infarct zone. Ischemia zone around infarct area may be made ​​up by the cells of normal or abnormal cells. Areas of ischemia can be flipped if the circulation adequately met. The goal of therapy is to improve the area of ischemia and prevent the expansion of the central zone of necrosis.

Interfere with the function of ventricular myocardial infarction and predisposes to hemodynamic changes that include: The decline of contraction, decreased stroke volume, abnormal wall motion, decreased ejection fraction, increased left ventricular volume at end systole and end diastole, and increased ventricular end-diastolic pressure. Compensation mechanism cardial output and perfusion which may include reflex sympathetic stimulation to increase heart rate, vasoconstriction, ventricular hypertrophy, as well as water retention with myocardial demands. But it is planned to make ends meet with and reduce the demands for oxygen.

Myocardial infarction healing process may take several weeks. Occur within 24 hours of cellular edema and leukocyte infiltration. Cardiac enzymes released into the cell. Tissue degradation and necrosis occurred on the second or third. Scar tissue formation begins in the third week as fibrous connective tissue replaces necrotic tissue, scar tissue formed settled in 6 weeks to 3 months.

Myocardial infarction is most common in the left ventricle and can be expressed according to the affected area of ​​myocardium. If the three divider wall transmural myocardial infarction, it is called and if only a part of the myocardium is called subendocardial infarction. Myocardial infarction can also be expressed according to location in the heart, which in general can occur in the posterior, anterior, septal anterior, anterolateral, and apical posteroinferior. The location and extent of the lesion determine the extent of the decline occurred function, complications and healing.

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