infarction /in·farc·tion/ (in-fahrk´shun)
Myocardial infarction
myocardial infarction (MI) 
infarction [in-fark´ shun]
myocardial [mi″o-kahr´de-al]
1. the formation of an infarct.
2. infarct.
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.
| 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. |
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
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
infarction [in-fark´ shun]
1. infarct.
2. formation of an infarct.
cardiac infarction myocardial infarction.
cerebral infarction an ischemic condition of the brain, causing a persistent focal neurologic deficit in the area affected.
myocardial infarction see myocardial infarction.
pulmonary infarction localized necrosis of lung tissue caused by obstruction of the arterial blood supply, most often due to pulmonary embolism. Clinical manifestations range from the subclinical to pleuritic chest pain, dyspnea, hemoptysis, and tachycardia.
myocardial [mi″o-kahr´de-al]
pertaining to the muscular tissue of the heart (the myocardium).
myocardial infarction (MI) death of the cells of an area of the heart muscle (myocardium) as a result of oxygen deprivation, which in turn is caused by obstruction of the blood supply; commonly referred to as a “heart attack.”
The myocardium receives its blood supply from the two large coronary arteries and their branches. Occlusion of one or more of these blood vessels (coronary occlusion) is one of the major causes of myocardial infarction. The occlusion may result from the formation of a clot that develops suddenly when an atheromatous plaque ruptures through the sublayers of a blood vessel, or when the narrow, roughened inner lining of a sclerosed artery leads to complete thrombosis. Coronary artery disease is the most common type of heart disease in the United States and many other countries. The risk rises rapidly with age, women tending to develop the disease 15 to 20 years later than men.
Other causes of MI may be attributed to a sudden increased unmet need for blood supply to the heart, as in shock, hemorrhage, and severe physical exertion, and to restriction of blood flow through the aorta, as in aortic stenosis.
The myocardium receives its blood supply from the two large coronary arteries and their branches. Occlusion of one or more of these blood vessels (coronary occlusion) is one of the major causes of myocardial infarction. The occlusion may result from the formation of a clot that develops suddenly when an atheromatous plaque ruptures through the sublayers of a blood vessel, or when the narrow, roughened inner lining of a sclerosed artery leads to complete thrombosis. Coronary artery disease is the most common type of heart disease in the United States and many other countries. The risk rises rapidly with age, women tending to develop the disease 15 to 20 years later than men.
Other causes of MI may be attributed to a sudden increased unmet need for blood supply to the heart, as in shock, hemorrhage, and severe physical exertion, and to restriction of blood flow through the aorta, as in aortic stenosis.
Pathology. The most common sites of myocardial infarction are in the left ventricle, that chamber of the heart which has the greatest workload. Tissue changes that occur in the myocardium are related to the extent to which the cells have been deprived of oxygen. Total deprivation results in an area of infarction, in which the cells die and the tissue becomes necrotic. Necrosis in this area is evident within 5 to 6 hours after the occlusion. In response to this necrosis the body increases its production of leukocytes, which aid in removal of the dead cells. As collateral circulation enlarges, it brings fibroblasts, which form a connective tissue scar within the area of infarction. Usually, the formation of fibrous scar tissue is complete within 2 to 3 months.
Immediately surrounding the area of infarction is a less seriously damaged area of injury. It may deteriorate and thus extend the area of infarction or, with adequate collateral circulation, it may regain its function within 2 to 3 weeks.
The outermost area of damage is the zone of ischemia, which borders the area of injury. The cells in this area are weakened by decreased oxygen supply, but function can return usually within two to three weeks after the onset of occlusion.
All of the pathological changes described above can be identified by electrocardiography. The information thus obtained is used to prescribe the varying degrees of physical activity allowed the patient during convalescence.
Immediately surrounding the area of infarction is a less seriously damaged area of injury. It may deteriorate and thus extend the area of infarction or, with adequate collateral circulation, it may regain its function within 2 to 3 weeks.
The outermost area of damage is the zone of ischemia, which borders the area of injury. The cells in this area are weakened by decreased oxygen supply, but function can return usually within two to three weeks after the onset of occlusion.
All of the pathological changes described above can be identified by electrocardiography. The information thus obtained is used to prescribe the varying degrees of physical activity allowed the patient during convalescence.
Risk Factors. Unavoidable traits that increase a person's chances for coronary artery disease include genetic susceptibility, sex, increasing age, and diabetes mellitus. Factors that can be controlled to some extent in order to ameliorate the risk include hypertension, cigarette smoking, and elevated serum lipids. Almost half of the persons who have suffered heart attacks have a history of one or more of these latter three risk factors. Minimizing or eliminating these avoidable factors can reduce the incidence and severity of ischemic heart disease. Preventive measures are discussed more fully under heart.
Symptoms. The most outstanding symptom of acute myocardial infarction is a sudden painful sensation of pressure, often described as a “crushing pain” in the chest, occasionally radiating to the arms, throat, and back, and persisting for hours. Pallor, profuse perspiration, and other signs of shock are present. There may be nausea and vomiting, leading to the mistaken impression that the victim is suffering from acute indigestion. In almost all cases of severe MI the patient is extremely apprehensive and has a sense of impending death.
Severity of symptoms may depend on the size of the artery at the point of occlusion and the amount of myocardial tissue served by the artery. In some instances the artery may be small and the symptoms mild. In other cases the extent of damage is quite large and the attack is fatal.
Within 24 hours of the initial attack there is an elevated temperature and increased white cell count in response to the inflammatory process arising from necrosis of myocardial tissue. Death of the cells also brings about the release of certain enzymes that enter the general circulation. The levels of these enzymes in the blood can be determined by clinical laboratory tests. Within 2 to 4 hours after infarction the level of creatine kinase (CK) is increased; it reaches its peak within 24 hours and subsides to normal level within 48 hours. The level of serum aspartate transaminase (AST) increases rapidly in 4 to 6 hours, reaches its peak in 24 to 48 hours, and returns to normal in five days. In contrast to the rapid rise and decline of these two enzyme levels, lactate dehydrogenase (LD) levels begin to increase the first day after attack and persist at high levels for 10 to 20 days. troponin is another enzyme that is a sensitive marker of myocardial infarction. Tests can be made more specific by measuring the LD1 and CK2 isoenzymes, which are found in the heart. Diagnosis of MI is based on the presenting symptoms and evidence of impaired heart function found by physical examination and electrocardiography and on abnormal serum enzyme levels.
Severity of symptoms may depend on the size of the artery at the point of occlusion and the amount of myocardial tissue served by the artery. In some instances the artery may be small and the symptoms mild. In other cases the extent of damage is quite large and the attack is fatal.
Within 24 hours of the initial attack there is an elevated temperature and increased white cell count in response to the inflammatory process arising from necrosis of myocardial tissue. Death of the cells also brings about the release of certain enzymes that enter the general circulation. The levels of these enzymes in the blood can be determined by clinical laboratory tests. Within 2 to 4 hours after infarction the level of creatine kinase (CK) is increased; it reaches its peak within 24 hours and subsides to normal level within 48 hours. The level of serum aspartate transaminase (AST) increases rapidly in 4 to 6 hours, reaches its peak in 24 to 48 hours, and returns to normal in five days. In contrast to the rapid rise and decline of these two enzyme levels, lactate dehydrogenase (LD) levels begin to increase the first day after attack and persist at high levels for 10 to 20 days. troponin is another enzyme that is a sensitive marker of myocardial infarction. Tests can be made more specific by measuring the LD1 and CK2 isoenzymes, which are found in the heart. Diagnosis of MI is based on the presenting symptoms and evidence of impaired heart function found by physical examination and electrocardiography and on abnormal serum enzyme levels.
Treatment and Patient Care. Immediate care of acute myocardial infarction is concerned with combatting shock, relieving respiratory difficulty, and preventing further circulatory collapse. The victim should be kept lying down, and all tight clothing should be loosened to relieve dyspnea and promote comfort. Supplemental oxygen should be supplied, and oxygen consumption should be reduced by relieving anxiety and pain and supporting respiration. Without delay, but in a calm manner, the patient is transported to a medical care facility. If the victim shows signs of cardiac arrest, efforts at cardiopulmonary resuscitation are begun immediately.
Medical treatment includes administration of thrombolytic therapy and an analgesic such as morphine sulfate or meperidine (Demerol). On occasion the physician may order atropine sulfate with morphine to counteract serious bradycardia. In almost all cases oxygen is administered for at least the first 24 hours.
Intravenous thrombolytic therapy using tissue plasminogen activator or streptokinase should be considered for all patients presenting within 12 hours of onset of pain. Maximum potential benefit occurs when these drugs are administered within 4 to 6 hours. Nursing considerations include the early accurate assessment of potential candidates for thrombolytic therapy, prompt administration of medication, and careful monitoring of complications such as arrhythmias, hypotension, allergic reactions, reocclusion, and hemorrhage. Early catheterization and angioplasty with a stent may also be done and may be superior to intravenous thrombolytic therapy.
Rest is essential for repair of damaged myocardial cells, but that does not necessarily mean absolute bed rest. Whether the patient is placed on bed rest or allowed up in a chair depends on symptoms and nursing judgments. During the acute stage some physicians may prefer that the patient rest in a chair at the bedside. The patient is permitted to get out of bed with assistance and sit in the chair until he begins to feel fatigued. The amount of time the patient is allowed to sit up and become more physically active is gradually increased.
Adequate rest can be achieved more easily if mental anxiety is reduced; a restful environment is thought to enhance the ability to rest. The amount of rest needed and the degree of physical activity allowed depends on how extensive the area of infarction is thought to be, whether cardiac arrhythmias and other complications develop, and the response of the patient to increased physical activity. Careful monitoring of the pulse rate and blood pressure before and after each activity can provide information with which to evaluate the patient's tolerance for exercise and self-care activities.
Most patients with a myocardial infarction are cared for in a coronary care unit during the acute stage. It is important that the patient and family be given a brief explanation of the various kinds of monitoring equipment in use and that they be reassured of each staff member's concern for the patient's welfare.
As the patient's status improves he or she is gradually weaned away from intensive care and encouraged to participate more in self-care. For some, this is a traumatic experience and they become very apprehensive about leaving the security of the monitors and the attention of the staff. Cardiac rehabilitation is also an important aspect of care. In some hospitals the transition from coronary care unit to home is made easier by transfer to a “step-down” or intermediate care unit where the patient's response to activities is monitored and instructions are given regarding care for himself or herself after discharge. Information about local coronary clubs, assistance in patient education, and availability of a Cardiac Work Evaluation Unit to determine the patient's readiness to return to work can be obtained by contacting the local unit of the American Heart Association.
Medical treatment includes administration of thrombolytic therapy and an analgesic such as morphine sulfate or meperidine (Demerol). On occasion the physician may order atropine sulfate with morphine to counteract serious bradycardia. In almost all cases oxygen is administered for at least the first 24 hours.
Intravenous thrombolytic therapy using tissue plasminogen activator or streptokinase should be considered for all patients presenting within 12 hours of onset of pain. Maximum potential benefit occurs when these drugs are administered within 4 to 6 hours. Nursing considerations include the early accurate assessment of potential candidates for thrombolytic therapy, prompt administration of medication, and careful monitoring of complications such as arrhythmias, hypotension, allergic reactions, reocclusion, and hemorrhage. Early catheterization and angioplasty with a stent may also be done and may be superior to intravenous thrombolytic therapy.
Rest is essential for repair of damaged myocardial cells, but that does not necessarily mean absolute bed rest. Whether the patient is placed on bed rest or allowed up in a chair depends on symptoms and nursing judgments. During the acute stage some physicians may prefer that the patient rest in a chair at the bedside. The patient is permitted to get out of bed with assistance and sit in the chair until he begins to feel fatigued. The amount of time the patient is allowed to sit up and become more physically active is gradually increased.
Adequate rest can be achieved more easily if mental anxiety is reduced; a restful environment is thought to enhance the ability to rest. The amount of rest needed and the degree of physical activity allowed depends on how extensive the area of infarction is thought to be, whether cardiac arrhythmias and other complications develop, and the response of the patient to increased physical activity. Careful monitoring of the pulse rate and blood pressure before and after each activity can provide information with which to evaluate the patient's tolerance for exercise and self-care activities.
Most patients with a myocardial infarction are cared for in a coronary care unit during the acute stage. It is important that the patient and family be given a brief explanation of the various kinds of monitoring equipment in use and that they be reassured of each staff member's concern for the patient's welfare.
As the patient's status improves he or she is gradually weaned away from intensive care and encouraged to participate more in self-care. For some, this is a traumatic experience and they become very apprehensive about leaving the security of the monitors and the attention of the staff. Cardiac rehabilitation is also an important aspect of care. In some hospitals the transition from coronary care unit to home is made easier by transfer to a “step-down” or intermediate care unit where the patient's response to activities is monitored and instructions are given regarding care for himself or herself after discharge. Information about local coronary clubs, assistance in patient education, and availability of a Cardiac Work Evaluation Unit to determine the patient's readiness to return to work can be obtained by contacting the local unit of the American Heart Association.
Myocardial infarction. From Frazier et al., 2000.
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.
heart attack.
)
Myocardial infarction.
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.
infarction
1. the formation of an infarct.
2. an infarct.
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.
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
Patient discussion about myocardial 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.
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)
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
Read more or ask a question about myocardial infarctionhttp://www.dnadirect.com/patients/tests/blood_clotting/more_about/GH_Thr_Risk.jsp
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