Hyperemia and infarction
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Hyperemia and congestion both refer to an increase in blood volume within tissues, but have different mechanisms. Hyperemia is an active process of arteriolar dilation that increases blood flow, as seen with inflammation. Congestion is a passive process where impaired venous outflow causes blood to accumulate. Infarction occurs when vascular occlusion causes ischemic necrosis of tissue. It is a major cause of illness and death, with most cardiovascular deaths due to myocardial or cerebral infarction. Arterial thrombosis, embolism, and hypoperfusion underlie most infarctions. The risk depends on vascular anatomy, occlusion rate, and tissue vulnerability to ischemia.
Hyperemia and infarction
- 1. Hyperemia and Infarction Ikram Ullah M.Phil MLSc
- 2. HYPEREMIA AND CONGESTION Hyperemia and congestion both refer to an increase in blood volume within a tissue but they have different underlying mechanisms Hyperemia is an active process resulting from arteriolar dilation and increased blood inflow, as occurs at sites of inflammation or in exercising skeletal muscle. Hyperemic tissues are redder than normal because of engorgement with oxygenated blood Congestion is a passive process resulting from impaired outflow of venous blood from a tissue It can occur systemically, as in cardiac failure, or locally as a consequence of an isolated venous obstruction
- 3. Congested tissues have an abnormal blue-red color (cyanosis) that stems from the accumulation of deoxygenated hemoglobin in the affected area In long-standing chronic congestion, inadequate tissue perfusion and persistent hypoxia may lead to parenchymal cell death secondary tissue fibrosis And the elevated intravascular pressures may cause edema or sometimes rupture capillaries, producing focal hemorrhages
- 5. INFARCTION An infarct is an area of ischemic necrosis caused by occlusion of the vascular supply to the affected tissue The process by which such lesions form termed infarction, is a common and extremely important cause of clinical illness Roughly 40% of all deaths in the United States are a consequence of cardiovascular disease, with most of these deaths stemming from myocardial or cerebral infarction. Pulmonary infarction is a common clinical complication, bowel infarction often is fatal, and ischemic necrosis of distal extremities (gangrene) causes substantial morbidity in the diabetic population
- 6. Arterial thrombosis or arterial embolism underlies the vast majority of infarctions. Less common causes of arterial obstruction include vasospasm, extrinsic compression of a vessel, such as by tumor, a dissecting aortic aneurysm, or edema within a confined space Uncommon causes vessel twisting (e.g., in testicular torsion or bowel volvulus), traumatic vascular rupture, and entrapment in a hernia sac Although venous thrombosis can cause infarction, the more common outcome is simply congestion; typically, bypass channels rapidly open to provide sufficient outflow to restore the arterial inflow. Infarcts caused by venous thrombosis thus usually occur only in organs with a single efferent vein (e.g., testis or ovary).
- 8. Factors That Influence Infarct Development Anatomy of the vascular supply: The presence or absence of an alternative blood supply is the most important factor in determining whether occlusion of an individual vessel causes damage Rate of occlusion: Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies For example, small interarteriolar anastomoses, which normally carry minimal blood flow, interconnect the three major coronary arteries If one coronary artery is slowly occluded flow in this collateral circulation may increase sufficiently to prevent infarction—even if the original artery becomes completely occluded.
- 9. Tissue vulnerability to ischemia. Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. Myocardial cells, although hardier than neurons, still die after only 20 to 30 minutes of ischemia. By contrast, fibroblasts within myocardium remain viable after many hours of ischemia. Hypoxemia. Understandably, abnormally low blood O2 content (regardless of cause) increases both the likelihood and extent of infarction