ACIDOSIS

From Big Medical Encyclopedia

ACIDOSIS (acidosis; lat. acidus acid + osis) — the disturbance of acid-base balance in an organism which is characterized by the excess content of anions of volatile and nonvolatile acids.

And. can be compensated (partially or completely) and noncompensated (dekompensirovanny).

At completely compensated And. accumulation of anions of acids thanks to existence of buffer systems and physiological mechanisms of compensation does not cause the shift of pH for limits of physiological norm (7,35 — 7,45). For partially compensated And. it is characteristic, despite decrease in pH, preservation physiological and physical. - chemical mechanisms of compensation. However if accumulation of anions of acids is considerable, and the effect of compensation is not expressed, concentration of hydrogen ions increases, the size pH decreases — develops noncompensated And.

On origins distinguish: 1) And. exchange (metabolic, not gas), connected with excess accumulation in an organism of anions of nonvolatile acids or considerable loss of cations of alkalis; 2) And. gas or respiratory (respiratory), connected with insufficient removal of carbonic acid lungs.

A metabolic acidosis

the Metabolic acidosis — the most often found form of disturbance of acid-base equilibrium of blood. The reasons leading to development exchange And. owing to excess accumulation of acids in an organism, are numerous. One of them — ketoacidosis — partial oxidation of fats and excess accumulation of acetone bodies (acetoacetic, beta and hydroxy-butyric acids), napr, at the complicated current of a diabetes mellitus or at starvation. In these conditions the formed ketone bodies do not manage to be oxidized in fabrics and are allocated in a significant amount with kidneys. At the same time the organism loses at the same time large number of Na + and To + , since their allocation happens in the form of sodium and potassium salts. However ability of kidneys to allocate the last is limited therefore gradually there is their excess accumulation in blood and fabrics in this connection pH of blood decreases.

Exchange And. it can be observed also at partial oxidation of carbohydrates in connection with accumulation in fabrics milk to - you. Development And. similar character it is observed at the strengthened physical activity, at hypoxemic conditions of various character (see. Hypoxia ), at an acute heart failure (cardiogenic shock), at severe damages of a liver (cirrhoses, toxic dystrophy), at long feverish states etc.

At diseases of kidneys (renal failure) arises azotemic And., connected with excess accumulation in blood and fabrics of phosphates, sulfates, anions of organic acids. The renal failure leads to reduction of removal of the last at not changed or increased removal of cations. This state, as a rule, arises at uraemia. Reason exchange And. there can be also excess exogenous administration of acids in an organism, in particular at poisoning acetic to - that, long or uncontrolled reception of salicylates, ammonium muriate, salt to - you etc.

The second group of the reasons is represented by the factors leading to excess loss of HCO anions 3 - in an organism either through kidneys, or through went. - kish. a path as it takes place at long ponosa, fistulas of intestines, bilious and pancreatic channels when the organism loses a significant amount of sodium bicarbonate and potassium with juice of a pancreas and intestines, and also with bile. For exchange And. a renal origin, at Krom the canalicular reabsorption of sodium bicarbonate is broken, allocation of a large amount of bicarbonates with urine is characteristic. An example of a metabolic acidosis of a renal origin is And., arising at late toxicoses of pregnancy (see. Nephropathy of pregnant women ).

Compensation exchange And. it is carried out by means of buffer systems of blood and physiological mechanisms of compensation (lungs, kidneys). Action of buffer systems, and hl. obr. the bicarbonate buffer, comes down first of all to neutralization of excess of acids. Reaction happens according to the scheme H + + AH + + NaHCO 3 = H 2 CO 3 + NaAH.

As a result of this reaction are formed of strong nonvolatile acid weak coal to - that and salt of nonvolatile acid. Buffer capacity of blood gradually decreases, and the content of sodium bicarbonate decreases to 2,9 — 10 mekv/l (at norm 20 — 26 mekv/l).

Formed at the same time many CO 2 it is removed through lungs that is promoted by so-called compensatory short wind — the hyperventilation resulting from immediate effect of the increased concentration of hydrogen ions and surplus of CO 2 on a respiratory center (the pulmonary mechanism of compensation). Removal of acids and recovery of concentration of sodium bicarbonate in plasma at normal function of kidneys happens due to increase in filtering of some organic acids (pyroracemic, ß - hydroxy-butyric, acetoacetic) and changes of metabolism in an epithelium of renal tubules that leads finally to increase in maintenance of hydrogen ions in urine and to increase in a reabsorption of bicarbonate. Both of these mechanisms of renal compensation finally lead to increase in titratable acidity of urine. The shift towards dominance in urine of hydrophosphates causes characteristic for exchange And. decrease in pH of urine. At a long current exchange And. in a canalicular epithelium process of education and receipt in urine of ammonium where it connects a hydrogen ion and chlorine, forming ammonium muriate (NH amplifies 3 + H + + NaCl = NH 4 Cl + Na + ). By means of this mechanism of binding of a hydrogen ion the last is brought in a large number without further decrease in pH of urine.

A gaseous acidosis

the Gaseous acidosis — increase in concentration of carbonic acid and increase in partial pressure of CO 2 (pCO 2 ) in blood (see. Hypercapnia ) — develops at reduction of lung ventilation (respiratory insufficiency, hypoventilation), and also at inhalation of air with high concentration of CO 2 .

Can be the reasons of respiratory insufficiency: 1) oppression of function of a respiratory center (shock, increase in intracranial pressure, overdose of morfinopodobny drugs and barbiturates); 2) the disturbances of breath connected with defeat of the neuromuscular device of respiratory muscles (poliomyelitis, botulism, paralysis of a phrenic nerve, a myasthenia, the period of recovery of spontaneous breath after use of relaxants); with restriction of mobility of a thorax at an injury and a number of diseases (a kyphoscoliosis, high standing of a diaphragm, ossification of costal cartilages, deformation of edges); 3) hypoventilation owing to insufficient passability of pneumatic ways (a foreign body in respiratory tracts, a bronchospasm) or owing to reduction of respiratory lung volume (pneumonia, a heart attack of a lung, a pneumosclerosis, a scleroderma, bronchiectasias, etc.). At heavy respiratory insufficiency the size pCO 2 blood about 70 — 120 mm of mercury can increase. above (norm of 35 — 42 mm of mercury.).

Gas And. can arise at inhalation of air or gas mixtures with high concentration of CO 2 at long stay indoors without updating of air or during the use of the narcotic device with the exhausted absorber. Hypoventilation can be observed also at the wrong carrying out artificial respiration (see).

Compensation gas And. it is carried out first of all with participation of the gemoglobinovy buffer, thanks to Krom the hydrogen ions which are formed at dissociation of carbonic acid are kept by the recovered hemoglobin in erythrocytes, and the HCO anions which are emitted in exchange for ions of chlorine from erythrocytes in plasma 3 - promote education in it additional amounts of sodium bicarbonate (NaHCO 3 ). Thus, at a gaseous acidosis primary increase in H 2 CO 3 it is compensated by secondary increase in NaHCO 3 , thanks to what essential changes in the ratio of concentration of components of the bicarbonate buffer of plasma can not occur, and pH of plasma will remain within physiological borders. The second stage of compensation of a gaseous acidosis is the increase in a reabsorption of sodium in kidneys providing a gain of NaHCO 3 in plasma. The bigger reabsorption of sodium in kidneys at a gaseous acidosis is promoted by increase in pCO 2 in blood, and also the increased turning into to urine of the main phosphates (Na 2 HPO 4 ) in acid (NaH 2 PO 4 ). The last causes a nek-swarm increase in titratable acidity of urine at gas And. See also Alkalosis .

Physiological acidosis

Physiological And. it is accepted to call a state And., a cut arises at the full-term newborn children and comes to light from first minutes after the birth and for several days of the post-natal period of life. On the mechanism of the development physiological And. represents the mixed form A., in a cut a component metabolic And. it is shown by increase in content in blood of hl. obr. milk to - you, and a component of a gaseous acidosis — a hypercapnia. Exchange shifts at the same time meet more often and are expressed more clearly.

On extent of disturbance of acid-base balance this type of Ampere-second of the beginning should be carried to noncompensated since the first minutes after the birth of pH of blood at children it is reduced.

Mechanism of development physiological And. connect with development of a hypoxia in a fruit, the cut it is exposed in the course of childbirth, and also with reorganization of a hemodynamics at the newborn in connection with inclusion at them in the general circulation of pulmonary and portal blood circulation. The Nek-ry role in development And. plays excess receipt of acid products from blood of mother during childbirth before switching off of placental blood supply.

The factors promoting development physiological And. at newborn children, are: functional immaturity of a respiratory center and in this regard imperfection of respiratory compensation, and also lack of compensation from kidneys which regulatory role is shown only to 3 — to the 5th day after the birth but also during this period their compensatory function is limited.

To bigger education milk to - you at newborns promote the increased activation of enzymes of glycolysis at a hypoxia at a fruit and newborns. As a rule, special treatment is not required.

A clinical picture of acidosis

the Most characteristic sign expressed And. oppression of function of c is. N of page, expressed in drowsiness, a sopor (see. Devocalization ) and to a coma (see). At And. pH of blood can decrease to 7,1, in certain cases exchange And. even to 6,8 that is the lowest indicator compatible to life. Coma arises during the falling of pH lower than 7,2.

One of the most expressed clinical signs And. disturbances of breath are. At exchange And. at early stages of its development increase in minute volume of breath (polypnea), a cut as a result of compensatory decrease in pCO is observed further 2 blood and decreases in excitability of a respiratory center can become noisy, superficial (see. Kussmaulya breath ). Increase in pCO 2 blood at gas And. causes a spasm of bronchioles.

Changes of pCO 2 blood at And. cause corresponding changes of the central and peripheral hemodynamics (see. Hypercapnia , Hypocapny ). So, decrease in pCO 2 (at exchange And.) causes falling of a tone of vessels owing to what arterial pressure falls and the minute volume of heart decreases, the brain and coronary blood stream decreases. On the contrary, increase of pCO 2 leads blood to a spasm of arterioles, including renal, increases arterial pressure, complicates cardiac performance. Big surplus of CO 2 can cause increase in a tone of a vagus nerve and a cardiac standstill. Vessels of a brain under the influence of increase in pCO 2 extend that increases formation of cerebrospinal fluid and promotes increase in intracranial pressure. At the same time it is noted that intravenous administration of the substances increasing osmotic pressure (solutions of glucose, etc.) » usually does not reduce intracranial pressure at such patients.

Influence And. on function of kidneys it is shown in reduction of mocheobrazovatelny function: coming in the conditions of gas And. narrowing of renal vessels limits a blood stream on vessels of kidneys, reduces pressure in afferent vessels of renal balls and reduces the volume of the removed urine. At exchange And. falling of the central arterial pressure leads first of all to reduction of formation of urine.

Exchange And. significantly influences a water salt metabolism: potassium concentration in plasma increases, the osmotic pressure of extracellular liquid increases (in connection with strengthening of potassium ions, sodium, chlorine) that causes increase in volume of extracellular liquid. Disturbances of a rhythm of cordial reductions (atrial tachycardia, atrial and ventricular premature ventricular contraction), deterioration in sokratitelny ability of a myocardium, development of hypostases of fabrics are a consequence of these changes. At gas And. potassium concentration in plasma also increases.

Recognition and assessment of weight And. are facilitated by definition of the main indicators of an acid-base state by means of Astrup's express method (see. Express methods ).

Treatment

In hard cases exchange And. (pH = 7,25 and below) 8,4% enter solution of sodium bicarbonate of 100 — 200 ml. In other cases it is recommended to enter 4,2; 2,1 and 1,05% solutions of sodium bicarbonate.

Necessary for correction exchange And. doses of sodium bicarbonate are calculated, proceeding from the deficit of buffer systems (DBS). For this purpose use Mellemgard's formula — Astrupa:

The DBC = 0, Z × SBO × W,

where the DBC — deficit of buffer systems (in mekv/l), SBO — shift of the buffer bases (in mekv/l), W — the weight of the patient (in kg).

At it is long existing exchange And., followed by the expressed disturbances of electrolytic balance, elimination And. shall pass within 2 — 3 days to give the chance to an organism to make a regrouping of electrolytes in the conditions of the carried-out correction. Administration of sodium bicarbonate is surely controlled by definition of pH of blood.

The patient with a renal failure at dehydration of an organism enter intravenously also normal saline solution, 5% solution of glucose (to 200 — 500 ml). At treatment gas And., observed most often at patients with respiratory insufficiency, the means improving first of all lung ventilation (bronchial spasmolytics, steroid hormones, antibiotics and streptocides are applied at an aggravation of inflammatory process, and also cardiac glycosides and diuretics). Due to the oppression of a respiratory center under the influence of a heavy hypercapnia apply stimulators of breath: Cordiaminum on 1 ml to 5 — 10 times a day intramusculary or intravenously. Reasonablly drop introduction of 10 ml of 2,4% of solution of an Euphyllinum for 200 — 300 ml of normal saline solution. Apply to stimulation of a respiratory center remeflin in a daily dose up to 8 — 16 mg inside or intravenously. The important place in therapy both exchange, and gas And. occupy inhalations of oxygen (see. Oxygen therapy ).

As acute management at respiratory insufficiency apply auxiliary or artificial ventilation of the lungs (see. Artificial respiration).

Acidosis at children

Acid-base equilibrium at healthy children remains on a fixed level and pH of blood fluctuates in the same limits, as at adults (7,35 — 7,45).

Development And. at children it is noted at many diseases: rheumatism and collagenoses, sepsis, dystrophy, rickets and rakhitopodobny diseases, bronchial asthma, diffusion glomerulonephritis, diseases of a liver and biliary tract, scarlet fever, whooping cough, measles, etc. In hard and medium-weight cases of the specified diseases there is always a decrease in pH of blood, a cut clinically is not shown and does not demand treatment.

At a diabetes mellitus (see. diabetes mellitus ), uraemias (see), intestinal toxicosis with eksikozy at children of chest age, a syndrome of respiratory frustration at newborns (see. Distress syndrome ) And. can reach dangerous borders (pH = 7,1 — 7,2) when there are its clinical signs (disturbances of consciousness, Kussmaul's breath) for which elimination the directed therapy is necessary. Besides, the acid-base imbalance is the leading etiology at such diseases as infantile renal acidosis and acidosis lactic family.

Intestinal toxicosis with eksikozy (toxic dyspepsia according to the old nomenclature) develops at children of the first year of life, most often at intestinal infection (dysentery, salmonellosis, a colienteritis). The diarrhea and vomiting which are constantly observed from the first hours of a disease quickly lead to dehydration of an organism of the child. Further in a clinical picture of a disease signs of defeat of c prevail. N of page: the adynamia accrues, the child falls in soporous, and then into coma. During this period of a disease are noted sharp angidremiya (see) and heavy exchange And.; pH of blood can decrease to 7,2, and deficit of the bases to reach 10 — 12 mekv/l.

Than more considerably And. at toxicosis, that the forecast is more adverse.

The syndrome of respiratory frustration of newborns is shown by the adynamia, cyanosis, short wind, disturbances of breath demanding acute management. And. in these cases of hl. obr. respiratory, but also metabolic disturbances join: collects milk to - that, ability of hemoglobin to connect oxygen decreases, the expressed hyperpotassemia takes place.

Resuscitation actions (release of respiratory tracts from slime, an artificial respiration, introduction of cardiotonic means, caustic solutions, cocarboxylase, oxygen, etc.) achieve the goal only in case of efficiency of correction of disturbances of acid-base equilibrium.

Acidosis is infantile renal call also renal canalicular And. or Butler's syndrome — Laytvuda — Albright; other synonyms — giperkhloremicheskiya, hron, idiopathic tubular Ampere-second a hypercalcuria and a gipotsitraturiya — are used less often.

This type of pathology is caused by inability of renal tubules to removal from an organism of hydrogen ions. Reaction of urine alkaline, titratable acidity and release of ammonia are reduced, allocation with urine of sodium, potassium, calcium and bicarbonates is increased. As a result of the specified biochemical disturbances at patients giperkhloremichesky A.

Zabolevaniye constantly is defined can begin in the period of a neonatality and is shown in the form of cyanosis, frustration of depth and a respiratory rhythm. In blood concentration of lactic and pyruvic acid is increased, their allocation with urine increases. These facts speak about dominance of glycolytic splitting of carbohydrates over oxidizing. Family inheritance of this disease is revealed, as formed the basis to call it acidosis lactic family (see. Lactacidemia ).

In recent years in connection with studying of the mechanism of effect of the enzyme of a lactate dehydrogenase catalyzing reaction of transformation milk to - you in pyroracemic, are suggested that lactic family And. represents only some biochemical option A. infantile renal. Possibly, in these cases, except the main enzymatic defect breaking processes of secretion of hydrogen ions also defect of action of a lactate dehydrogenase joins. Believe that it is genetically caused enzymatic defect, but quantitative and high-quality damages of the enzymes participating in development of this type of pathology are not specified yet.

Pathogeny of this form And. remains not clear.

If renal infantile And. it is found at chest age, it is called Laytvud's syndrome. At children of advanced age symptoms from outside went. - kish. a path are expressed poorly, but rakhitopodobny changes of a skeleton gradually accrue, delay of growth, a nephrocalcinosis, symptoms of a hypopotassemia is distinct. And. it is constant. This symptom complex at children of advanced age is called Albright's syndrome (see. Laytvuda-Albright syndrome ).

Treatment consists in purpose of sodium bicarbonate or potassium bicarbonate. The dose necessary for normalization of level of bicarbonates of plasma is individual, it fluctuates depending on age and intensity of metabolic frustration from 2,5 to 12 g of soda a day.

Considering losses of potassium, it is useful to give a half of necessary bicarbonates in the form of potassium bicarbonate. Big loading does by sodium necessary restriction in food of sodium chloride.

At early diagnosis, timely begun and systematically carried out treatment it is possible to provide normal development of the child. In parallel with disappearance And. the general condition, a condition of bones improves, growth is resumed. The termination of treatment leads to return of all symptoms of a disease.

See also Acid-base equilibrium .


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H. H. Lapteva; A. A. Valentinovich (ped.), H. M. Mukharlyamov (rubbed.).

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