myocardial infarction (redirected from Myocaridal infarction)

infarction /in·farc·tion/ (in-fahrk´shun)

1. the formation of an infarct.

2. infarct.

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acute myocardial infarction  (AMI) that occurring during the period when circulation to a region of the heart is obstructed and necrosis is occurring.

cardiac infarction  myocardial i.

cerebral infarction  an ischemic condition of the brain, causing a persistent focal neurologic deficit in the area affected.

mesenteric infarction  coagulation necrosis of the intestines due to a decrease in blood flow in the mesenteric vasculature.

migrainous infarction  a focal neurologic defect that constituted part of a migrainous aura but that has persisted for a long period and may be permanent.

myocardial infarction  (MI) gross necrosis of the myocardium, due to interruption of the blood supply to the area.

Myocardial infarction shown in cross-section of heart (ventricles only).

non–Q wave infarction  myocardial infarction not characterized by abnormal Q waves.

pulmonary infarction  localized necrosis of lung tissue, due to obstruction of the arterial blood supply.

Q wave infarction  myocardial infarction characterized by Q waves that are abnormal either in character or number or both.

silent myocardial infarction  myocardial infarction occurring without pain or other symptoms; often detected only by electrographic or postmortem examination.

watershed infarction  cerebral infarction in a watershed area during a time of prolonged systemic hypotension.

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myocardial infarction

n. Abbr. MI

Necrosis of a region of the myocardium caused by an interruption in the supply of blood to the heart, usually as a result of occlusion of a coronary artery. Also called cardiac infarction.

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Myocardial infarction

Commonly known as a heart attack, a myocardial infarction is an episode in which some of the heart's blood supply is severely cut off or restricted, causing the heart muscle to suffer and die from lack of oxygen.

Mentioned in: Angina, Antimyocardial Antibody Test, Aspartate Aminotransferase Test, Heart Attack, Troponins Test, Ventricular Aneurysm

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myocardial infarction (MI)

[mī′ōkär′dē·əl]

Etymology: Gk, mys, muscle, kardia, heart; L, infarcire, to stuff

necrosis of a portion of cardiac muscle caused by an obstruction in a coronary artery resulting from atherosclerosis, a thrombus, or a spasm. Also called heart attack. See also acute myocardial infarction.

observations The onset of MI is characterized by a crushing, viselike chest pain that may radiate to the left arm, neck, jaw, or epigastrium and sometimes stimulates the sensation of acute indigestion or a gallbladder attack. The patient usually becomes ashen, clammy, short of breath, nauseated, faint, and anxious and often feels that death is imminent. Typical signs are tachycardia, a barely palpable pulse, low blood pressure, mildly elevated temperature, cardiac arrhythmia, and elevation of the S-T segment and Q wave on the electrocardiogram. Laboratory studies usually show an increased sedimentation rate, leukocytosis, and elevated serum levels of creatine kinase and its isoenzyme MB, lactic dehydrogenase and its isoenzymes, and glutamic-oxaloacetic transaminase. Potential complications in MI are pulmonary or systemic embolism, pulmonary edema, acute congestive heart failure, shock, ventricular tachycardia, ventricular fibrillation, and cardiac arrest.

interventions Emergency treatment of MI may require cardiopulmonary resuscitation before the patient reaches the hospital emergency department. Early IV administration of thrombolytic drugs and heparin improves left ventricular function, limits damage, and increases survival rates. Primary percutaneous transvenous coronary angioplasty (PTCA) is being used with increasing frequency and can achieve prompt reperfusion and help prevent the hemorrhagic risks of thrombolysis. Primary PTCA requires a well-staffed, well-equipped cardiac catheterization laboratory that can mobilize within 1 hour and achieve reperfusion within 2 hours.

nursing considerations The patient is admitted to an intensive care unit with continual electrocardiographic monitoring at the acute onset. Blood pressure, temperature, respiration, and apical pulse are checked frequently. Parenteral fluids may be administered, and the patient is usually served a low-sodium, low-cholesterol, low-fat diet. Stool softeners and laxatives may be indicated to prevent straining. The nurse's role in helping the patient and family understand the nature and treatment of the disease is extremely important. Before discharge the nurse usually discusses the need to adhere to the prescribed diet and medication, to limit activities, to rest at regular periods, and to avoid caffeine, nicotine, large meals, and emotional stress.

Locations of pain from myocardial infarction

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myocardial infarction (mīˈ·ō·kärˑ·dē·l in·färkˑ·shn),

n necrosis of cardiac muscle tissue caused by a coronary artery obstruction linked to a spasm, thrombosis, or atherosclerosis. Also called
heart attack.

Myocardial infarction.

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myoblastoma (mī´ōblastō´m),

n a benign neoplasm characterized by large polyhedral cells resembling young muscle cells. Occurs most frequently in the tongue.

myoblastoma, granular cell,

n See tumor, granular cell.

myocardial infarction (heart attack),

n an occlusion or blockage of arteries supplying the muscles of the heart, resulting in injury or necrosis of the heart muscle.

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infarction

1. the formation of an infarct.

2. an infarct.

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cardiac infarction

see myocardial infarction (below) and also myocardial infarction.

cerebral infarction

an ischemic condition of the brain, causing a persistent focal neurological deficit in the area affected.

infarction fever

an aseptic fever caused by liberation of pyrogens from damaged tissue.

intestinal infarction

a common occurrence in horses due to occlusion of arteries by larvae of Strongylus vulgaris. Sections of intestine, sometimes very large ones, become devitalized leading to peritonitis and death.

May also result from torsion or strangulation. See also thromboembolic colic.

myocardial infarction

gross necrosis of the myocardium, due to interruption of the blood supply to the area. See also myocardial infarction.

pulmonary infarction

localized necrosis of lung tissue, due to obstruction of the arterial blood supply.

renal infarction

is usually conical, anemic and multiple and may heal leaving a narrow scar. It is usually clinically inapparent unless the obstructing material is infected. This leads to the development of renal abscess or embolic nephritis, also usually without clinical signs unless the abscesses are large or numerous.

spinal cord infarction

caused sometimes by fibrocartilaginous emboli of prolapsed disk material, causing sudden loss of function of large sections of the spinal cord, leading to flaccid paralysis of the hindlimbs or of all four, depending on the site of the infarct.

splenic infarction

usually hemorrhagic; may be difficult to differentiate from subcapsular hematoma.

venous infarction

a thrombus in a vein may cause infarction, e.g. in the thigh muscles of downer cow, recumbent for long periods, or in the gastric mucosa of pigs, where it is a common finding in acute septicemia.

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myocardial infarction

Acute necrosis of myocardial tissue; in the early post-MI period, there may be a need to rely on 'soft' data, especially if troponin I or CK-MB have yet to ↑, or there is a loss of sensation to the pain characteristic of MI, as occurs in circa 10% Pts with DM; older ♀ may have normal levels of CK after an MI Risk factors for MI ASHD, ↑ cholesterol, HTN, smoking, DM, low selenium, etc Lab Cardiac enzymes, 'flipped' LD, troponins increase to normal size. Pathology Chronology of myocardial changes Fatal complications of MI Shock, arrhythmias, rupture of ventricular aneurysms or papillary muscle, acute CHF, mural thromboembolism Risks ↑ risk with ↑ TGs, ↑ small LDL particle diameter, ↓ HDL-C

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Patient discussion about Myocaridal infarction.

Q. what should I do to prevent heart attack?

A. The American Heart Association recommends that heart attack prevention begin by age 20. This means assessing your risk factors and working to keep them low. For those over 40, or those with multiple risk factors, it’s important to calculate the risk of developing cardiovascular disease in the next 10 years. Many first-ever heart attacks or strokes are fatal or disabling, so prevention is critical. The sooner you begin comprehensive risk reduction, the longer and stronger your heart will beat. For the full article and a quiz to test your heart health: http://www.americanheart.org/presenter.jhtml?identifier=3035379
the abc's of preventing a heart attack:
http://americanheart.org/presenter.jhtml?identifier=3035374 Hope this helps.

Q. What causes Cardiomegaly? My Husband has had a physical checkup and has found to have Cardiomegaly. What does it mean and what causes it?

A. Cardiomegaly means an enlarged heart and it is a sign of an underlying problem. It can have many causes, including:

High blood pressure
Heart valve disorders
Weakness of the heart muscle (cardiomyopathy)
Severe anemia
Thyroid disorders
Excessive iron in the body (hemochromatosis)
Abnormal protein buildup in an organ (amyloidosis)

Q. What causes blood clots? My father had a heart attack which was caused by a blood clot. Am I at risk for developing blood clots too? How do I prevent it from happening?

A. I found a website that checks your risks for inheriting your family's illness, including blood clots. They have a test you can do which is called "Free Risk Assessment for Thrombophilia":
http://www.dnadirect.com/patients/tests/blood_clotting/more_about/GH_Thr_Risk.jsp