The critical value for hemoglobin (HGB) that is mentioned in this document is not specified. The document states that the partial pressure of oxygen in blood determines the outcome of vascular occlusion, and that partial flow obstruction may lead to infarction in an anemic or cyanotic patient, where oxygen tension would be lower, whereas the same obstruction may have no effect under normal oxygen tension conditions. However, it does not provide a specific critical HGB value.
The critical value for hemoglobin (HGB) that is mentioned in this document is not specified. The document states that the partial pressure of oxygen in blood determines the outcome of vascular occlusion, and that partial flow obstruction may lead to infarction in an anemic or cyanotic patient, where oxygen tension would be lower, whereas the same obstruction may have no effect under normal oxygen tension conditions. However, it does not provide a specific critical HGB value.
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My lecture presentation on "Infarction" for third professional mbbs
The critical value for hemoglobin (HGB) that is mentioned in this document is not specified. The document states that the partial pressure of oxygen in blood determines the outcome of vascular occlusion, and that partial flow obstruction may lead to infarction in an anemic or cyanotic patient, where oxygen tension would be lower, whereas the same obstruction may have no effect under normal oxygen tension conditions. However, it does not provide a specific critical HGB value.
The critical value for hemoglobin (HGB) that is mentioned in this document is not specified. The document states that the partial pressure of oxygen in blood determines the outcome of vascular occlusion, and that partial flow obstruction may lead to infarction in an anemic or cyanotic patient, where oxygen tension would be lower, whereas the same obstruction may have no effect under normal oxygen tension conditions. However, it does not provide a specific critical HGB value.
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Dr.
Farheen Zehra Definition An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue Clinical examples of infarction: Myocardial infarction Cerebral infarction Pulmonary infarction Gangrene of limbs Atrial fibrillation with mural thrombi Basis of infarction:
Vascular compromise Obstruction to arterial supply Impeded venous drainage Common causes: Arterial occlusion: 99% result from arterial occlusion (thrombotic or embolic events) Other causes: • Local vasospasm • Expansion of an atheroma (haemorrhage within a plaque) • Extrinsic compression of a vessel (e.g. by tumor) • Twisting of the vessels (e.g. in testicular torsion or bowel volvulus) • Compression of the blood supply by edema or by entrapment in a hernia sac • Traumatic rupture of the blood vessel Venous occlusion: (organs with single venous out flow) • Thrombosis Classification Based on the colour & presence or absence of infection Morphology Red (haemorrhagic) infarcts occur
1) With venous occlusions (such as in ovarian torsion)
2) In loose tissues (such as lung), which allow blood to
collect in the infarcted zone 3) In tissues with dual circulations (e.g., lung and small intestine), permitting flow of blood from the unobstructed vessel into the necrotic zone (obviously such perfusion is not sufficient to rescue the ischemic tissues) 4) In tissues that were previously congested because of sluggish venous outflow 5) When flow is re-established to a site of previous arterial occlusion and necrosis (e.g., following fragmentation of an occlusive embolus or angioplasty of a thrombotic lesion) Morphology White (anaemic) infarcts occur With arterial occlusions in solid organs with end-arterial circulation (such as heart, spleen, and kidney), where the solidity of the tissue limits the amount of haemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds Most of the infarcts are wedge shaped With the occluded vessel at the apex and the periphery of the organ forming the base When the base is a serosal surface, there is often an overlying fibrinous exudate. The lateral margins may be irregular, reflecting the pattern of vascular supply from adjacent vessels. Margins become hyperaemic Initially: all infarcts are poorly defined and slightly haemorrhagic Later: margins tend to become better defined by a narrow rim of hyperaemia attributable to inflammation at the edge of the lesion. Examples of infarcts: A, Hemorrhagic roughly wedge- shaped pulmonary infarct. B, Sharply demarcated white infarct in the spleen. Splenic infarction Histology of infarction Changes depends on time Ischemic coagulative necrosis Inflammation Liquefactive necrosis Abscess formation Scar tissue Factors Influence Development of Infarct The major determinants include: 1) The nature of the vascular supply 2) The rate of development of the occlusion 3) The vulnerability of a given tissue to hypoxia 4) The blood oxygen content. Factors That Influence Development of an Infarct The major determinants: (1) Nature of the vascular supply (double or single blood supply) The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage. Lungs, for example, have a dual pulmonary and bronchial artery blood supply; thus, obstruction of a small pulmonary arteriole does not cause infarction in an otherwise healthy individual with an intact bronchial circulation. Similarly, the liver, with its dual hepatic artery and portal vein circulation, and the hand and forearm, with their dual radial and ulnar arterial supply, are all relatively insensitive to infarction. In contrast, renal and splenic circulations are end-arterial, and obstruction of such vessels generally causes infarction. Factors That Influence Development of an Infarct
The major determinants:
(2) Rate of development of occlusion. Slowly developing occlusions are less likely to cause infarction because they provide time for the development of alternative perfusion pathways. For example, small inter- arteriolar anastomoses —normally with minimal functional flow—interconnect the three major coronary arteries in the heart. If one of the coronaries is only slowly occluded (i.e., by an encroaching atherosclerotic plaque), flow within this collateral circulation may increase sufficiently to prevent infarction, even though the major coronary artery is eventually occluded. Factors That Influence Development of an Infarct The major determinants: 3) Vulnerability to hypoxia. The susceptibility of a tissue to hypoxia influences the likelihood of infarction. • Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. • Myocardial cells, although hardier than neurons, are also quite sensitive and die after only 20 to 30 minutes of ischemia. • In contrast, fibroblasts within myocardium remain viable even after many hours of ischemia Factors That Influence Development of an Infarct The major determinants: 4) Oxygen content of blood. The partial pressure of oxygen in blood also determines the outcome of vascular occlusion. Partial flow obstruction of a small vessel in an anaemic or cyanotic patient might lead to tissue infarction, whereas it would be without effect under conditions of normal oxygen tension. In this way, congestive heart failure, with compromised flow and ventilation, could cause infarction in the setting of an otherwise inconsequential blockage. Factors That Influence Development of an Infarct
