Alkalosis

ALKALOSIS, alkalosis, increased alkalinity of blood and tissues of the organism. In the normal state, the reaction of the blood is slightly alkaline. The concentration of H-ions in it at 18° is equal to 0.29.10^-7 normality and at 37° - 0.45.10^-7, which corresponds to 2.3.10^-7 and 5.8.10^-7 concentration of hydroxyl ions (see Active reaction); the hydrogen exponent (pH) of the blood at 18° will be 7.56 and at 37° - 7.35. If the alkalinity of the blood is determined by titration, entirely different values are obtained; this depends on the fact that along with the actual alkalinity (concentration of hydroxyl ions) in the blood there is also undissociated alkali, mainly in the form of carbonates (the latter represents the so-called reserve alkalinity). In case of an increase in acids in the blood, the latter are bound by the reserve alkalinity, as a result of which the latter decreases, while the actual reaction of the blood remains unchanged. Alkalosis can be of two types: 1) associated with an increase in the concentration of hydroxyl ions and 2) depending on an increase in reserve alkalinity. Alkalosis of the first type occurs much less frequently and is called decompensated alkalosis, since in the normal state the organism usually copes with an increase in the concentration of hydroxyl (as well as hydrogen) ions with the help of its regulatory apparatus, namely, the buffer system (lungs, kidneys, partly liver). If alkali is introduced into the blood of an animal, it is impossible to achieve a sharp change in the actual reaction, because the introduced alkali is bound by the buffer system (a series of salts, as well as NH3, partly protein, but mainly bicarbonates and carbonates, which maintain the constant actual reaction of the blood; when alkalis are introduced, bicarbonates turn into carbonates, when acids are introduced, the reverse transition is observed). A slight increase in actual alkalinity can be obtained in humans by introducing bicarbonates or sodium citrate (Kohler), and in normal people these deviations pass within 24-48 hours, in pathological cases they persist for a long time. Also, small fluctuations in pH in the alkaline direction are observed in various febrile processes, for example, pneumonia, sepsis (Michaelis and Davidoff), during convulsive phenomena. Alkalosis of the second type - compensated, associated with an increase in reserve alkalinity, is more common; this is called hypercapnia (in the normal state, reserve alkalinity is equal to 77-53 volume percent CO₂). This is observed also as a physiological phenomenon, for example, during gastric secretion. HCl, apparently, is formed from NaCl as a result of combination with carbonic acid, which gives HCl and carbonates. The actual reaction of the blood does not change in this case, because the formed alkali is excreted by the kidneys in the form of carbonates, as a result of which not only the potential alkalinity of the urine increases, but also the pH; in the blood, only the reserve alkalinity increases from 53.0-59.6% to 63% (Hermanns, Saks). The tension of carbonic acid in the alveolar air increases, since between the latter and the stable alkalinity there is a direct dependence regulated by respiration. This dependence is so close that, by measuring the pressure of carbonic acid in the alveolar air, one can judge the stable alkalinity of the blood without resorting to analysis of the latter. As a result, disorders of respiration, associated with an increase in the tension of carbonic acid in the alveolar air compared to the blood, lead to an increase in reserve alkalinity (mountain sickness, hyperventilation of the lungs). Conversely, an increase in the latter enhances gas exchange and can even cause tetany of respiration (Grant and Goldmann, Gyorgy and Vollmer, Gollwitzer-Meyer). The same tetany can be obtained experimentally by introducing secondary phosphate. Lehmann and Löwy, by introducing carbonates into the organism, obtained enhanced gas exchange. A sharply expressed alkalosis is observed in tetania parathyreopriva and its idiopathic form, much weaker in hyperthyroidism and hyperinsulinemia; constantly in epilepsy (Jarlow, Bisgaard, Noerwig), less frequently in tetany, laryngospasm, increased neuromuscular excitability. To explain this type of alkalosis, it should be noted (as established by Freundenberg and Gyorgy) that this alkalosis is associated with a decrease in calcium and an increase in potassium. According to the works of Spiro and Mond, calcium chloride, due to complex compounds, changes the reaction of amino acid and protein solutions in the acidic direction, potassium chloride - in the alkaline direction. In connection with the doctrine of the antagonism of calcium and potassium and their relation to sympathicotonia and vagotonia, alkalosis associated with the nervous system was interpreted as a vagotonic constitution. However, the existence of such constitutions as well as their connection with the potassium and calcium content in the blood is problematic. This is aggravated by the fact that the relationship of calcium content to alkalosis is not fully established, since in some cases alkalosis is observed without its decrease; more constant is such a relationship with ionized calcium, which is subject to ultrafiltration.