Myocardial Infarction

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A heart attack, also known as a myocardial infarction, usually occurs when a blood clot forms inside a coronary artery at the site of an atherosclerotic plaque. The blood clot severely limits or completely cuts off blood flow to part of the heart. In a small percentage of cases, blood flow is cut off when the muscles in the artery wall contract suddenly, constricting the artery. This constriction, called vasospasm, can occur in an artery that is only slightly narrowed by atherosclerosis or even in a healthy artery. Regardless of the cause of a heart attack, the oxygen deprivation is so severe and prolonged that heart muscle cells begin to die for lack of oxygen. About 1.1 million people in the United States have a heart attack every year; the heart attacks prove fatal for about 40 percent of these people (Microsoft Encarta, 2004).

ETIOLOGY

The most common cause of acute myocardial infarction (AMI) is complete or nearly complete occlusion of a coronary artery usually precipitated by rupture of the vulnerable atherosclerotic plaque and subsequent thrombus formation. Plaque rupture can be precipitated by both internal and external factors.

Internal factors include plaque characteristics, such as the size and consistency of the lipid core and the thickness of the fibrous cap, as well ac conditions to which it is exposed, such as coagulation status and degree of arterial vasoconstriction. Vulnerable plaques most frequently occur in areas with less than 70% stenosis and are characterized by an eccentric shape with an irregular border, a large, thin lipid core, and a thin, fibrous cap.

External factors result from actions of the client or from external conditions that affect the client. Strenuous physical activity and severe emotional stress, such as anger, increased sympathetic activity, which in turn, increases hemodynamic stress that may lead to plaque rupture. At the same time, sympathetic activity increases myocardial oxygen demand. Scientists have reported that external factors, such as exposure to cold and time of day, also affect plaque rupture. Acute coronary events occur more frequently with exposure to cold and during the morning hours. Researchers hypothesize that the sudden increases in sympathetic activity associated with these factors may contribute to plaque rupture. The role of inflammation in triggering plaque rupture is currently being studied.

Regardless of the cause, rupture of the atherosclerotic plaque results in •Exposure of the plaque’s lipid-rich core to flowing blood. •Seepage of blood into the plaque, casing it to expand.
Triggering of thrombus formation.
Partial or complete occlusion of the coronary artery. Unstable angina is associated with short term partial occlusion of a coronary artery. Whereas AMA results from significant or complete occlusion of a coronary artery that last more than one hour. When blood flow ceases abruptly, the myocardial tissue supplies by that artery dies. Coronary artery spasm can also cause acute occlusion (Black & Hawks, 2004).

CLINICAL MANIFESTATIONS

The clinical manifestation result from ischemia of the heart muscle and the decrease in function and acidosis associated with it. The major clinical manifestation is chest pain, which is similar to angina pectoris but more severe and unrelieved by nitroglycerin. The pain may radiate to the neck, jaw, shoulder, back or left arm. The pain also may present near the epigastrium, stimulating indigestion. AMI may also be associated with less common clinical manifestation including the following: •Atypical chest, stomach, back or abdominal pain.

Nausea and dizziness
Shortness of breath and difficulty breathing.
Unexplained anxiety, weakness or fatigue.
Palpitations, cold sweat or paleness (Black & Hawks, 2004).

PATHOPHYSIOLOGY

Myocardial infarction, or ischemic necrosis of the myocardium, results from prolong ischemia to the myocardium with irreversible cell damage and...
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