Blood oxygenators hemolysis

This causes the red blood ceU to have less distensibiUty and thus to sickle, leading to rupture of the red blood ceU (hemolysis) and blockage in small capillaries. The sludging in smaU capiUaries leads to poor oxygen delivery, ischemia, and pain. 

No. 276 Disposable blood oxygenator set 1. Extractive substances i. Transparency and appearance ii> Foam teat ill. pH (The difference to the blank solution) iv. Potassium permanganate-reducing substances V. Residue on evaporation Vi. Zink vii. Lead 2. Hemolysis test 3. Pyrogen test... 

With arsine exposure, there may be potential severe hemolysis (the breakdown of red blood cells and the release of hemoglobin). Ensure adequate oxygenation by arterial blood measurement or pulse oxygenation monitoring. Use diuretics to maintain urinary flow. 

It has been found that vitamin K analogues possess an ability to insert themselves into the oxygen-binding cleft of hemoglobin. This may result m hemolysis (dissolution of red blood corpuscles with liberation of their hemoglobin),... 

Equation 13 correlates a mixed set of compounds which produce an abnormal type of mitosis resembling that caused by colchicine. The role of hydrophobic forces causing this kind of mitotic activity is closely related to that causing hemolysis (Equation 18), inhibiting quinea pig ileum (Equation 17), I50 red blood cell oxygen consumption, etc. The results of Table II indicate that Equation 18 can be used as a model for nonspecific membrane perturbation in various systems. 

Oxygen toxicity in red blood cells can cause hemolysis (SED-12, 242) (9). 

In acute exposure prompt medical attention is critical. The victim should be immediately removed to fresh air and away from the source of exposure. Oxygen should be provided if there is a respiratory distress. Initial therapy should be directed at stopping the ongoing hemolysis by performing exchange transfusion. Currently there is no other treatment to decrease arsine hemolysis however, studies in vitro have shown that some dithiol chelators (meso-2,3-dimercaptosuccinic acid, DMSA 2,3-dimercapto-l-propanesulfonic acid, DMPS and 2,3-butanedithiol) are effective (see Further Reading). This should be followed by aims to restore renal function or compensate for lost renal function (hemodialysis). This process does not remove any formed arsenic from the exposed body. Administration of dimercaprol (British Anti-Lewisite, BAL) has no effect on arsine hemolysis, but it lowers blood arsenic levels resulting from arsine exposure. The use of chelators must be... 

The clinical manifestations of serum phosphate depletion depend on the length and degree of the deficiency. Moderate hypophosphatemia of 1.5 to 2,4 mg/dL (0.48 to 0.77 mmol/L) is usually not associated with clinical signs and symptoms (unless chronic, when osteomalacia or rickets develops). Plasma concentrations less than 1.5 mg/dL (0.48 mmol/L) may produce clinical manifestations. Because phosphate is necessary for the formation of ATP, glycolysis and cellular function are impaired by low intracellular phosphate concentrations. Muscle wealmess, acute respiratory failure, and decreased cardiac output may occur in phosphate depletion. At very low serum phosphate (<1 mg/dL or <0.32 mmol/L), rhabdomyolysis may occur. Phosphate depletion in erythrocytes decreases erythrocyte 2,3-diphosphoglycerate, which causes tissue hypoxia because of increased affinity of hemoglobin for oxygen. Severe hypophosphatemia (serum phosphate concentration <0.5 mg/dL [<0.16 mmol/L]) may result in hemolysis of the red blood cells. Mental confusion and frank coma also may be secondary to the low ATP and tissue hypoxia. If hypophosphatemia is chronic, impaired mineralization of bone produces rickets in children and osteomalacia in adults. 

Anemia of rapid onset is most likely to present with cardiorespiratory symptoms snch as tachycardia, palpitations, angina, hypotension, fight-headedness, and breathlessness dne to decreased oxygen delivery to tissues or from hypovolemia in those with acnte bleeding. With severe intravascnlar blood volnme loss, peripheral vasoconstriction and central vasodilation preserve blood flow to vital organs. Over time systemic small vessel dilation increases tissne oxygenation. Vascular compensation resnlts in decreased systemic vascnlar resistance, increased cardiac ontpnt, and tachycardia. With acnte hemolysis and fall in RBC mass, there is some decrease in blood volnme, bnt not in plasma volume. 

The tendency for deoxy HbS to precipitate is why clinical manifestations of sickle cell anemia are brought on by exertion and why treatment includes administration of oxygen. The stiff fibrous precipitate causes the red blood cell to deform into the characteristic sickle shape and makes the normally malleable cell susceptible to hemolysis. 

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