An EKG is performed, looking for changes that are characteristic of a myocardial infarction. In the absence of these characteristic markers, heart damage is detected by cardiac markers in the blood that identify heart muscle damage. Depending on the risk assessment, stress testing or angiography may be used to identify coronary artery disease in these patients. In patients with heart failure, stress testing or coronary angiography may be performed to identify and treat underlying coronary artery disease.
The disease process underlying most ischemic heart disease is atherosclerosis of the coronary arteries, which decreases blood flow to the heart muscle. Atherosclerosis is the thickening of the artery wall as a result of plaque formation, which is the accumulation of fatty materials such as cholesterol.
Atherosclerosis reduces blood flow to the heart muscle, causing ischemia. When these plaques weaken, they can develops a tear, which forms blood clot that obstructs blood flow, causing a myocardial infarction.
Treatment of ischemic heart disease is dependent on the underlying disease process. Accessed Jan. Deedwania P, et al. Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis. Jameson JL, et al. Chest discomfort. In: Harrison's Principles of Internal Medicine. New York, N. Hall J, et al. Myocardial ischemia. In: Principles of Critical Care. McKean SC, et al. Chest pain. State of oxygenation of blood- it is in respect of arterial partial oxygen and haemoglobin level.
Efficiency of heart 4. Nature of affected tissue- brain and heart are more vulnerable to ischaemia. Degeneration atrophy and replacement fibrosis- Gradual obstruction of blood supply Gangrene- sudden or gradual but complete deprivation of blood supply Infarction- Sudden and complete deprivation of blood supply 36 Generally, symptoms depend on the location of the ischemia.
Regular medical care allows a health care professional to provide early screening tests and to promptly evaluate symptoms and your risks for developing ischemia. Surgery may be needed to remove dead tissue or repair injured areas. Once the initial event is managed, treatment turns to prevention of future ischemia. The red cells entering the effected area escape through damaged capillaries and lie free on the dead tissues.
Also, a great deal of fibrin derived from blood lie on the dead tissue. Until necrosis is visible the ischaemic area cannot be called infarct. Initially neutrophils predominate ,later macrophages and fibroblasts appear. Eventually, necrotic area is replaced by fibrous scar tissue, may show dystrophic calcification. In cerebral infarcts, the liquefactive necrosis is followed by gliosis i.
Regeneration of cells and organization of granulation tissue. Cut surface : dark purple Shows blocked vessel near the apex of the infarcted area. Old organized and healed pulmonary infarcts appear as retracted fibrous scars.
The margin of the infarct shows inflammatory reaction — initially acute but later macrophages and fibrous tissue predominate. Most common cause : thromboemboli arising in heart eg. A hemorrhagic infarct has some phagocytes containing haemosiderin. Small cavitary infarcts are called lacunar infarcts and are commonly found as a complication of systemic hypertension.
Mechanism of myocardial ischemia 2. Role of platelets 3. Complicated plaques 4. Non — atherosclerotic causes Infusion of fibrinolysins in the first few hours of development of acute MI in such cases restores blood flow in the blocked vessel in majority of cases. Intramural hemorrhage — is found in about one third of cases of acute MI.
Hemorrhage and thrombosis may occur together in some cases. There is ischemic coagulative necrosis of the myocardium which eventually heals by fibrosis. However, sequential microscopic changes are observed. Glucose—insulin—potassium in acute myocardial infarction.
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