Acidosis

Acidosis, a condition in which there is an excessive, compared to normal, amount of acid in the body tissues, as a result of which the active reaction of the tissue shows a deviation toward the acid side. Under physiological conditions in the body tissues, as well as in the blood, there exists a strictly defined ratio between acid and alkaline ions, thanks to which the concentration of hydrogen ions (pH) of tissues is a constant value for a given tissue. According to Graff's data, pH of the liver is 7.2, spleen - 7.2, thyroid gland - 7.4, adrenal glands - 7.1, muscles - 6.1, right heart - 6.7, left heart - 6.1, kidneys - 7.0. For subcutaneous tissue, Schade found pH values between 7.01-7.29. As can be seen from the given figures, most organs have a slightly alkaline reaction (only slightly deviating toward the acid side compared to the reaction of the blood). Only muscle tissue stands apart, which even under physiological conditions has an acid reaction. Since the buffer system of tissues, i.e., the system preventing changes in reaction, is a small value, especially compared to the buffer system of blood, a shift in tissue pH under various pathological conditions occurs easily and sometimes reaches quite a significant magnitude. A relatively small amount of acid, which has no effect on blood pH, is sufficient for tissue pH to take a value less than 6.8, i.e., for true acidosis to appear in the tissues—a condition that we almost never observe in the blood. An example of A. resulting from an increase in the amount of acids normally present in tissues is acidosis of muscle tissue, occurring after intense muscle work, due to the accumulation in the muscles of a large amount of lactic acid (a normal product of carbohydrate metabolism in muscles). An example of A. of tissues as a result of the appearance of acids not normally present and being products of pathological metabolism in tissues, is A. in inflammation. In this case, A. is the result of accumulation in the inflamed tissue of ACIDIC PRODUCTS of cell breakdown, which in the normal organism do not form. The degree of A. of inflamed tissue depends on the strength and character of inflammation. Thus, in the case of acute purulent inflammation of subcutaneous tissue, Schade found pH in the center of the affected area to be 5.96, while in the periphery of the affected part pH was equal to 6.47. In the case of chronic inflammatory processes, pH of the affected area fluctuates between 6.45-6.80. A. in inflammation is closely related to the so-called wound A., which is also the result of accumulation of acidic products of breakdown of dead cells. As for the effect of true blood A., which sometimes occurs (e.g., in diabetic coma), on the concentration of hydrogen ions in tissues, this question remains open due to the impossibility of making direct determinations of pH of the corresponding tissues. It should only be noted that Schade found no changes in the reaction of subcutaneous tissue in several cases of diabetic coma.- For determining pH of tissues at present time, two methods are used, predominantly. One of them, proposed by Graff, consists in that small pieces of the tissue being studied are poured with several drops of specially selected indicators, according to the change in color of which one can judge the reaction of the areas being studied. With this method, only relatively rough changes in tissue pH can be determined. The other method, proposed by Schade, Neukirch, Halpert - electrometric - has the advantage that it allows determinations of pH of some tissues in vivo, as well as to follow the dynamics of pH changes. The determination itself, according to the method of these authors, is carried out in the usual electrometric way; only the form of the electrode is changed. Schade's electrode is a glass tube, the end of which is drawn out into a capillary 2-3 cm long. This tube can be relatively easily introduced under the skin or into the tissue of another organ. Due to the capillarity of the tube, a certain amount of tissue fluid is drawn into it, the pH of which can be determined without removing the electrode from the tissues.

S. Kashgansky. Blood Acidosis.The reaction of blood in normal conditions is slightly alkaline, its pH, the so-called hydrogen indicator (see Hydrogen ions), on average, is equal to 7.35 and fluctuates within narrow limits from 7.30 to 7.40. The maintenance of constant blood reaction is ensured by the presence in the blood of buffer systems (see Buffer properties), bicarbonates and CO₂, phosphates and proteins. Even when relatively large amounts of acids enter the blood, the active reaction (see) of blood does not go beyond the limits indicated above. This depends on the fact that the acid, first of all, combines with the alkali of bicarbonates and alkaline phosphates, displacing carbon dioxide from the former and converting the latter into corresponding acid salts. As a result of excitation of the respiratory center, simultaneously intensified ventilation of the lungs begins, excess CO₂ is removed, and the previous ratio determining the active reaction of blood is restored; on the other hand, excess acid salts are excreted by the kidneys. In this case, there is "compensated A.", characterized mainly by a decrease in the so-called reserve alkalinity of the blood. The next regulatory adaptation consists in that part of the ammonia, split off during the breakdown of amino acids and usually converted into urea, is used to neutralize excess acids, with the resulting salts being excreted through the kidneys. When the body's regulatory adaptations are exhausted, blood pH falls and so-called uncompensated A. (reaction falls almost to the neutral point) may occur, which is incompatible with life for any considerable length of time. Accumulation of acids in the body can occur in various pathological and physiological conditions, with the mechanism of acid formation and the method of regulation in individual forms of A. differing, partly still insufficiently studied. The most severe disturbances of acid-base balance occur in severe cases of diabetes. Due to the disturbance of carbohydrate utilization, oxidation of fatty acids is impaired, which do not burn, as in normal conditions, to final products, but remain at the intermediate stage of acetoacetic and oxymalic acids. Circulating in the blood, these substances tend to change blood pH toward acidity, and in severe coma it reaches uncompensated A., and blood pH begins to fall. Temporary improvement of diabetic A. can occur when bases - magnesium and calcium - pass from bones into the blood, as well as with therapeutic administration of bicarbonates of Na, Mg and Ca. Diabetic A. is better fought dietetically - by undereating and a fat-poor diet, which reduces the danger of accumulation of fatty acids (Allen-Joslin's method). Even better is to raise glucose oxidation with insulin, which quickly eliminates blood acidosis. A. develops in starving individuals, in febrile patients on a poor diet, due to the same acids. During intense muscular work, a temporary state of A. develops due to lactic acid, which is released during the breakdown of glucose in the process of normal muscle contraction. Carbohydrates, especially sugar, taken during significant physical exertion (for example, athletic competitions), reduce the degree of such A. Uremic A. occurs not due to excessive formation of acids, but due to the loss by the kidneys of the ability to excrete acids and acid salts and thereby preserve the alkaline reserve of the organism (pH of normal urine fluctuates from 5.0-7.0). A. is compensated by the pulmonary regulator until decompensation occurs with clinical symptoms of uremic coma: asthma uraemicum and others. Finally, with insufficiency of the pulmonary regulator (pneumonia, emphysema, slowed circulation in heart failure), A. can occur due to accumulation of volatile CO₂ in the blood. Therapy of the last two types of A. coincides with the therapy of the underlying disease; in renal A., the delivery of acids in food is also reduced. Calcium chloride and ammonium are also used in humans for the purpose of combating pathological conditions of blood alkalosis (epilepsy, tetany) or as acidifiers of urine (in treatment, for example, of pyelitis by changing the reaction of urine).

E. Tareev. Postoperative acidosis, develops after operations as a result of various factors that disrupt the proper course of oxidative processes. According to data from various authors, such factors causing postoperative acidosis include: bleeding, insufficient kidney and liver function, the presence of preoperative acidosis, prolonged fasting, repeated administration of laxatives, cooling of patients, and finally, the duration of the operation, particularly prolonged manipulation in the abdominal cavity. Some authors attribute a special role to general anesthesia. The nature of the organic acids that appear in excess in the blood in the state of postoperative A. has not been finally clarified; however, so-called acetone bodies play a significant role here; particularly characteristic and frequent symptom of postoperative A. is postoperative acetonuria. Parallel studies of various symptoms characterizing A. in the postoperative period and their comparison with changes in carbohydrate metabolism lead to the assumption that postoperative A., both in depth and frequency of occurrence, depends on the degree of disruption of carbohydrate metabolism in the postoperative period. Surgical trauma causes a decrease in oxidative processes in the body, which manifests as a delay in sugar utilization and the formation of products of incomplete oxidation (organic acids) in the blood, including acetone bodies. In most cases, postoperative A. is a rather harmless phenomenon; however, a whole series of severe cases of A. with fatal outcomes has already been described in the literature. This circumstance requires serious attention to postoperative A. Various methods of prevention and therapy have been proposed. Treatment by the introduction of alkalis aims to neutralize acids already circulating in excess. However, this treatment, in which it is not possible to influence the pathological exchange processes themselves, but only their manifestation, is of little value, and in severe A. is almost hopeless. The introduction of glucose solutions aims to give the body readily assimilable sugar in a ready form. However, experimentally, it is not possible to prevent the occurrence of postoperative A. with glucose alone. The best, rational method for both prevention and therapy of postoperative A. is the use of insulin in combination with glucose. Insulin, by influencing the pathological exchange processes, eliminates the source of acid formation. The combined method of administering glucose solutions (intravenously) with subcutaneous insulin injections was proposed in 1923 in America (Thalhimer). Many cases of brilliant application of insulin-glucose therapy in cases of postoperative acidosis of moderate and severe degree, as well as in shock, have been described. Insulin-glucose prevention and therapy acquire special importance in severe operations on depleted cancer patients, in whom oxidation processes are generally sharply reduced. In these cases, the development of postoperative acidosis is particularly severe and is fatal for patients.

E. «Srezov."