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Alkalosis is the result of a process reducing hydrogen ion concentration of arterial blood plasma (alkalemia). In contrast to acidemia (serum pH 7.35 or lower), alkalemia occurs when the serum pH is higher than normal (7.45 or higher).
The body normally attempts to compensate for this homeostatically, but if this fails or is overridden, the blood pH will rise, leading to respiratory alkalosis. This increases the affinity of oxygen to hemoglobin and makes it harder for oxygen to be released into body tissues from the blood. The symptoms of respiratory alkalosis include ...
Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate ( HCO − 3 ), or alternatively a direct result of increased bicarbonate concentrations.
Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. [5] The normal range of blood calcium is typically between 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L ), while levels less than 2.1 mmol/L are defined as hypocalcemic.
Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide.
Self-induced hypocapnia through hyperventilation is the basis for the dangerous schoolyard fainting game. [ citation needed ] Deliberate hyperventilation has been used by underwater breath-hold divers for the purpose of extending dive time as it effectively reduces respiratory drive due to low CO 2 levels.
Hypovolemia then leads to metabolic alkalosis (increase in blood pH) by stimulating bicarbonate reabsorption in order to maintain extracellular volume. [5] [10] In summary, the symptoms of alkalosis is the net result of over-consumption of absorbable alkali, hypercalcemia-induced hypovolemia, and impaired glomerular filtration rate. [5]
The effect is an electrolyte imbalance similar to that seen with thiazide diuretic therapy (which causes pharmacological inhibition of NCC activity). [ 4 ] Gitelman syndrome was formerly considered a subset of Bartter syndrome until the distinct genetic and molecular bases of these disorders were identified.