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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood has a number of rheological properties which partially determine flow, especially at capillary level, and its capacity to deliver oxygen. It is non-Newtonian, pseudoplastic, thixotropic and viscoelastic. Viscosity can be studied with different types of viscosimeters (coaxial cylinder or capillary viscosimeters). It can be defined by the ratio of stress of deformation to rate of deformation. Viscosity depends on macrorheological parameters: hematocrit, serum proteins, especially fibrinogen and globulins, and also on microrheological parameters: degree of aggregation and red blood cell deformability. Viscosity rises when the temperature falls and decreases with the radius of the tube through which the blood flows (Fahraeus-Linqvist effects). Blood viscosity is studied clinically at different temperatures, and, above all, at different rates of deformation by carefully recording the hematocrit. Plasma viscosity, fibrinogen, albumia and immunoglobulin levels, the viscosity of blood cell suspensions in normal saline must also be taken into consideration. Special investigations (rheoscopy, filtrability) provide information about red cell aggregation and deformability. Hyperviscosity syndromes are observed with: --raised hematocrit (polycythemia and pseudopolycythemia), --conditions with raised serum proteins or changes in their composition (especially hyperfibrinogenemia, raised immunoglobulins, low albumin levels); inflammatory syndromes, dysglobulinemias (Fahey's syndrome of plasma hyperviscosity), --low temperature (hypothermia), --increased red cell aggregability (shock, fat embolism), --reduced red cell deformability due to various congenital and acquired conditions (sickle cell anemia, renal failure, hyperlipoproteinemia, thrombosis, diabetes). Conversely, hypoviscosity may occur with a low hematocrit, hypoproteinemia, hypofibrinogenemia, and hyperthermia. Increased viscosity results in a slowing of blood flow, stagnation of its constituents and in ischemia. Therapeutic interventions may be considered on the different components of the hyperviscosity syndrome: hemodilation, plasmapheresis, dispersion of aggregants, agents acting on red cell deformability.
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PMID:[Blood hyperviscosity syndromes. Classification and physiopathological understanding. Therapeutic deductions]. 636 7

Blood has particular rheological properties which partly condition its flow, especially in capillary vessels, and its ability to deliver oxygen. It is not subject to gravitation, pseudoplastic, thixotropic and visco-elastic. Blood viscosity depends upon macroscopic factors, such as erythrocyte aggregation and deformability. Hyperviscosity is observed in cases of increased haematocrit (polycythaemia and relative polycythaemia), increased serum proteins and changes in protein balance (e.g. rise in fibrinogen and immunoglobulins, fall in albumin) as seen in inflammation and dysglobulinaemia, drop in temperature (hypothermia), increased erythrocyte aggregation (shock, fat embolism) or imparied deformability due to various acquired or inherited disorders of red cell membrane or cytoplasma (e.g. sickle cell anaemia, renal failure, hyperlipoproteinaemias, thrombosis, diabetes). The various factors may be combined, as in diabetes. Conversely, hypoviscosity may result from decreased haematocrite, fall in blood proteins and fibrinogen, or hyperthermia. Hyperviscosity can be corrected by acting on its various constituents. Treatments include haemodilution, plasmapheresis, anti-aggregants and drugs improving red cell deformability.
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PMID:[Blood viscosity. Measurement and applications (hyper--and hypoviscosity syndromes) (author's transl)]. 723 52

With complex and extensive pharmacological effects, corticosteroids are widely used in many clinical situations. A survey conducted to define the role of corticosteroids in various settings of peri-operative and critical care gave strong evidence to support that the use of corticosteroid is absolutely indicated in patients with adrenal insufficiency, asthma, anaphylaxis, acute spinal cord injury, and increased ICP resulting from brain tumors. As the benefits of corticosteroids are much in evidence, their uses are recommended to extend to postoperative antiemesis, acute respiratory failure (such as ARDS, COPD, and fat embolism), increased ICP associated with brain abscess, thyroid storm, and refractory hypothermia. Beneficial effect could be expected in septic shock with high-dose corticosteroids. Despite extensive reports on their versatile usefulness, evidence-based review did not recommend the use of corticosteroids in increased ICP associated with traumatic head injury and cerebral infarct, cardiac arrest, post-extubation airway edema, and aspiration pneumonia due to poor effectiveness let alone further worsening of the conditions. Great caution must be taken in clinical situations where administration of corticosteroids is considered contraindicated such as systemic fungal infection, hypersensitivity to the drug, intramuscular injection in idiopathic thrombocytopenia purpura, vaccination with live virus.
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PMID:An evidence-based review on the use of corticosteroids in peri-operative and critical care. 1219 90

Little is known about the physiology of large-volume liposuction. Patients are exposed to prolonged procedures, general anesthesia, fluid shifts, and infusion of high doses of epinephrine and lidocaine. Consequently, the authors examined the thermoregulatory and cardiovascular responses to liposuction by assessing multiple physiologic factors. The aims of their study were to serially determine hemodynamic parameters perioperatively, to quantify perioperative and postoperative plasma epinephrine levels, and to chronologically document fluctuations in core body temperature. Five female volunteers with American Society of Anesthesiologists' physical status I and II underwent moderate- to large-volume liposuction. Heart rate, blood pressure, mean pulmonary arterial pressure, cardiac index, and central venous pressure were monitored. Serum epinephrine levels and core body temperature were assessed perioperatively. The hemodynamic responses to liposuction were characterized by an increase in cardiac index (57 percent), heart rate (47 percent), and mean pulmonary arterial pressure (44 percent) (p < 0.05). Central venous pressure was not significantly altered. Maximum epinephrine levels were observed 5 to 6 hours after induction. Significant correlations between cardiac index and epinephrine concentrations were shown intraoperatively (r = 0.75). All patients developed intraoperative low body temperatures (mean 35.5 degrees C). An overall enhanced cardiac function was observed in patients subsequent to large-volume liposuction. The etiology of the altered cardiac parameters was multifactorial but may have been attributable in part to the administration of epinephrine, which counters the effects of general anesthesia and operative hypothermia. Additional explanations for raised cardiac output may be hemodilution or emergence from general anesthesia. Elevated mean pulmonary arterial pressure may be a result of subclinical fat embolism demonstrated in previous porcine studies, although fat was not observed in urine. The unchanged central venous pressure levels indicate that young healthy patients with compliant right ventricles can accommodate the fluid loads of large-volume liposuction. Overall hemodynamic parameters remained within safe limits. Within these surgical parameters, patients should be clinically screened for cardiovascular and blood pressure disorders before liposuction is undertaken, and preventative measures should be taken to limit intraoperative hypothermia.
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PMID:Hemodynamic physiology and thermoregulation in liposuction. 2836 30