Acidosis

ACIDOSIS, a state in which there is an excessive amount of acids in the body's tissues compared to the norm, as a result of which the active reaction of the tissue deviates to the acidic side. Under physiological conditions, in the body's tissues, just as in the blood, there exists a strictly defined ratio between acidic and alkaline ions, thanks to which the concentration of hydrogen ions (pH) of the tissues is a constant value for a given tissue. According to data by Graff, the pH of the liver is 7.2, the spleen 7.2, the thyroid gland 7.4, the adrenal glands 7.1, muscles 6.1, the right heart 6.7, the left heart 6.1, and the kidneys 7.0. For subcutaneous tissue, Schade found pH values between 7.01–7.29. As can be seen from the cited figures, the majority of organs have a weakly alkaline reaction (deviating only slightly to the acidic side compared to the reaction of the blood). Only muscle tissue stands apart, which even under physiological conditions has an acidic reaction. Since the buffer system of the tissues, i.e., the system preventing a change in reaction, is a small value, especially compared to the buffer system of the blood, a shift in the pH of the tissues under various pathological conditions occurs easily and sometimes reaches a fairly large magnitude. A comparatively small amount of acid, which has no effect on the pH of the blood, is sufficient for the pH of the tissues to take on a value of less than 6.8, i.e., for true acidosis to appear in the tissues—a state which we almost never observe in the blood.

An example of acidosis resulting from an increase in the amount of acids normally present in tissues is the acidosis of muscle tissue that occurs after intense muscle work, due to the accumulation of a large amount of lactic acid in the muscles (a normal product of carbohydrate metabolism in the muscles). An example of tissue acidosis resulting from the appearance of new acids, which are not normally present and are a product of pathological metabolism in the tissues, is acidosis during inflammation. In this case, acidosis is the result of the accumulation in the inflamed tissue of acidic products of cell decay, which are not normally formed in the body.

The degree of acidosis of inflamed tissue depends on the strength and character of the inflammation. Thus, in the case of acute purulent inflammation of the subcutaneous tissue, Schade found the pH in the center of the affected area to be 5.96, while on the periphery of the affected part the pH was 6.47. In the case of chronic inflammatory processes, the pH of the affected area fluctuates between 6.45–6.80. Closely related to acidosis during inflammation is so-called wound acidosis, which is also a consequence of the accumulation of acidic products of the decay of dead cells.

As for the influence of true blood acidosis, which is sometimes encountered (e.g., in diabetic coma), on the concentration of hydrogen ions in the tissues, this question remains open due to the impossibility of performing direct determinations of the pH of the corresponding tissues. It should only be noted that Schade did not find any changes in the reaction of the subcutaneous tissue in several cases of diabetic coma.

For the determination of tissue pH at the present time, two methods are predominantly used. One of them, proposed by Graff, consists of dousing small pieces of the tissue under investigation with a few drops of specially selected indicators, by the change in color of which one can judge the reaction of the investigated areas. By this method, one can determine only comparatively gross changes in tissue pH. Another method, proposed by Schade, Neukirch, and Halpert—the electrometric method—possesses the advantage that it allows for the determination of the pH of certain tissues in vivo, as well as monitoring the dynamics of pH changes. The determination itself, according to the method of these authors, is performed by the usual electrometric way; only the shape of the electrode is changed. The Schade 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 inserted under the skin or into the tissue of another organ. Due to the capillarity of the tube, a certain amount of tissue fluid is collected in it, the pH of which can be determined without removing the electrode from the tissues.

S. Kashgansky. Blood Acidosis. The reaction of the blood in the norm is weakly alkaline; its pH, the so-called hydrogen exponent (see Hydrogen ions), is on average equal to 7.35 and fluctuates within narrow limits from 7.30 to 7.40. The preservation of the constancy of the blood reaction is ensured by the presence in the blood of buffer systems (see Buffer properties), bicarbonates and CO₂, phosphates, and proteins. Even upon the entry into the blood of comparatively significant amounts of acids, the active reaction (see) of the blood does not go beyond the limits indicated above. This depends on the fact that the acid, in the first place, is bound by the alkali of bicarbonates and alkaline phosphates, displacing carbon dioxide from the former and converting the latter into corresponding acidic salts. Due to the excitation of the respiratory center, increased ventilation of the lungs begins simultaneously, the excess CO₂ is removed, and the previous ratio of H₂CO₃/NaHCO₃, which determines the active reaction of the blood, is restored; on the other hand, the excess of acidic salts is excreted by the kidneys. In this case, there is a 'compensated acidosis,' characterized, mainly, by a decrease in the so-called reserve alkalinity of the blood. Further regulatory adaptation consists in the fact that part of the ammonia, which is split off during the breakdown of amino acids and usually turns into urea, is used to neutralize the excess of acids, whereby the formed salts are excreted through the kidneys. Upon the exhaustion of the regulatory adaptations of the body, the pH of the blood falls and so-called uncompensated acidosis can occur (the reaction falls almost to the neutral point), which is incompatible with life if it lasts for any significant time. The accumulation of acids in the body can take place under various pathological and physiological states, whereby the mechanism of acid formation and the method of regulation in individual forms of acidosis present differences, some of which are not yet sufficiently studied. The most severe disturbances of the acid-base balance are encountered in severe cases of diabetes. Due to the disturbance of carbohydrate utilization, the oxidation of fatty acids suffers; they do not burn, as in the norm, to end products, but remain at the intermediate stage of acetoacetic and oxybutyric acids. Circulating in the blood, these substances tend to change the pH of the blood toward acidity, whereby in severe coma it comes to uncompensated acidosis, and the pH of the blood begins to fall. Temporary improvement of diabetic acidosis can occur upon the transition of bases—magnesium and calcium—from the bones into the blood, as well as upon the therapeutic administration of bicarbonates of Na, Mg, and Ca. It is better to fight diabetic acidosis dietetically—by undernutrition and a diet poor in fat, by which the danger of the accumulation of fatty acids is reduced (the Allen-Joslin method). It is even better to increase the oxidation of glucose with insulin, which quickly eliminates blood acidosis. At the expense of the same acids, acidosis develops in starving people and in febrile patients on a meager diet. During heavy muscular work, a temporary state of acidosis develops at the expense of 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, sports competitions), reduce the degree of such acidosis. Uremic acidosis arises not as a result of excessive acid formation, but as a result of the loss by the kidneys of the ability to excrete acids and acidic salts and thereby preserve the alkaline reserve of the body (the pH of normal urine fluctuates from 5.0–7.0). Acidosis is compensated by the pulmonary regulator until decompensation occurs with clinical symptoms of uremic coma: asthma uraemicum, etc. Finally, in case of insufficiency of the pulmonary regulator (pneumonia, emphysema, slowed blood circulation in heart failure), acidosis can arise as a result of the accumulation of volatile CO₂ in the blood. The therapy of the last two types of acidosis coincides with the therapy of the underlying disease; in renal acidosis, the intake of acids in food is also reduced. Calcium chloride and ammonium are also used in humans for the purpose of fighting pathological states of blood alkalosis (epilepsy, tetany) or as urine acidifiers (in the treatment, for example, of pyelitis by changing the reaction of the 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."