Alkalosis - what is it? Alkalosis: causes, symptoms and treatment. Gas alkalosis (respiratory, respiratory) Alkalosis is characterized by an increase in pH and hypocapnia

Acidosis- a typical form of CBS disorder, characterized by a relative or absolute excess of acids in the body.

In the blood, during acidosis, there is an absolute or relative increase in [Н + ] and a decrease in pH below normal (conditionally, below the “neutral” pH range, taken as 7.39–7.40).

Alkalosis‑‑ a typical form of CBS disorder, characterized by a relative or absolute excess of bases in the body.

In the blood during alkalosis, there is an absolute or relative decrease in [Í + ] or an increase in pH (conditionally, above the “neutral” pH range, taken as 7.39–7.40).

Endogenous and exogenous acidoses and alkaloses

Endogenous causes CBS shifts are the most frequent and significant in clinical practice. This is explained by the fact that in many disorders of the vital functions of various organs and tissues, the functions of both chemical buffer systems and physiological mechanisms for maintaining optimal CBS in the body are disrupted.

Exogenous causes CBS violations - excessive intake of substances of an acidic or alkaline nature into the body:

 Medicines used in violation of the dosage and/or treatment regimen(for example, salicylates; solutions for artificial nutrition, including proteins containing acidic substances: NH 4 Cl, arginine-HCl, lysine-HCl, histidine. Their catabolism produces H +);

 toxic substances used accidentally or knowingly(eg methanol, ethylene glycol, paraldehyde, hydrochloric acid);

 individual food products. Acidosis often develops in people who use synthetic diets (contain amino acids with acidic properties). Consumption of large quantities of alkaline mineral waters and milk can lead to the development of alkalosis.

Compensated and uncompensated acid-base disorders

The determining parameter of the degree of compensation for violations of WWTP is the pH value.

Compensated shifts CBS are considered those at which the blood pH does not deviate beyond the normal range: 7.35–7.45. The “neutral” value is conventionally taken to be 7.39–7.40. pH deviations in the ranges:

 7.38–7.35 - compensated acidosis;

 7.41–7.45 - compensated alkalosis.

With compensated forms of CBS violations, changes in the absolute concentration of the components of the hydrocarbonate buffer system (H 2 CO 3 and NaHCO 3) are possible. However, the [H 2 CO 3 ]/ ratio remains within the normal range (i.e. 20/1).

Uncompensated violations of CBS are called those in which the blood pH is outside the normal range:

 at pH 7.34 and below - uncompensated acidosis;

 at pH 7.46 and above - uncompensated alkalosis.

Uncompensated acidosis and alkalosis are characterized by significant deviations in both the absolute concentrations of H 2 CO 3 and NaHCO 3 and their ratio.

 pH 7.29 - subcompensated acidosis (below 7.29 - uncompensated acidosis);

 pH 7.56 - subcompensated alkalosis (above 7.56 - uncompensated alkalosis).

Gas and non-gas disorders of WWTP

According to the origin of the CBS disorder They are divided into gas, non-gas and mixed (combined).

Gas disorders of acid-base status

Gas(respiratory) CBS disorders (regardless of the development mechanism) are characterized by a primary change in the CO content in the body 2 and, as a consequence, the concentration of carbonic acid in the ratio [HCO 3 – ]/[ H 2 CO 3 ] .

Respiratory and acidosis and alkalosis are usually remain compensated for a long time. This is due to both the activation of physiological compensation mechanisms (mainly due to a mobile decrease in the volume of alveolar ventilation - an increase in gas acidosis and a decrease in gas alkalosis), and the effects of buffer systems.

The reason for the development of gas disorders is CBS(and acidosis and alkalosis) are disturbances of alveolar ventilation. As a result, the volume of ventilation of the lungs ceases to meet the needs (it is either higher or lower than optimal) of gas exchange of the body over a certain time.

General links in the pathogenesis of gas acidosis and alkalosis

Decreased alveolar ventilation leads to respiratory acidosis.

Gas (respiratory) acidosis occurs due to the accumulation of excess CO 2 in blood and a subsequent increase in the concentration of carbonic acid in it.

Most common causes of respiratory acidosis:

 airway obstruction(for bronchial asthma, bronchitis, emphysema, aspiration of foreign bodies);

 impaired compliance of the lungs(for example, with pneumonia or hemothorax, atelectasis, pulmonary infarction, diaphragmatic paresis);

 increasing functional “dead” space(for example, with pneumosclerosis or hypoperfusion of lung tissue);

 disorders of respiratory regulation (for example, with encephalitis, cerebrovascular disorders, poliomyelitis);

 increased production of endogenous CO 2 when catabolic processes are activated in patients with fever, sepsis, prolonged convulsions of various origins, heat stroke, as well as with parenteral administration of large amounts of carbohydrates (for example, glucose);

 excess intakeinto the body of exogenous carbon dioxide in the inhaled air(this can be, for example, in spacesuits, submarines, aircraft) or when there are a large number of people in a confined space (for example, in a mine or a small room).

Increased effective alveolar ventilation (hyperventilation) of the lungs causes respiratory alkalosis.

Hyperventilation of the lungs causes hypocapnia (decreasedpCO 2 in the blood), a decrease in the level of carbonic acid in the blood and the development of gas(respiratory) alkalosis.

Causes of respiratory alkalosis:

 being at high altitude (altitude and mountain sickness);

 neurotic and hysterical states;

 brain damage due to concussion, stroke, neoplasms;

 lung diseases (for example, pneumonia, bronchial asthma);

 hyperthyroidism;

 severe fever;

 various drug intoxications (for example, salicylates, sympathomimetics, progestogens);

 renal failure;

 excessive and prolonged painful or thermal irritation.

In addition, the development of gas alkalosis is possible if the mechanical ventilation regime is violated, leading to hyperventilation.

Non-gas acid-base disorders

Non-gas(non-respiratory) violations of CBS are characterized by a primary change in the content of bicarbonate in the ratio: [ HCO 3 – ]/[ H 2 CO 3 ] .

Reasons for the development of non-gas wastewater treatment plant violations:

 metabolic disorders;

 violation of the excretion of acidic and basic compounds by the kidneys;

 loss of intestinal juice;

 loss of gastric juice;

 introduction of exogenous acids or bases into the body.

Types of non-gas acid-base disorders

Non-gas disorders of CBS are characterized by the development of 3 types of disorders: metabolic, excretory and exogenous acidoses and alkaloses.

General characteristics of non-gas acid-base disorders

N EGAS ACIDOSES

The most characteristic manifestations of non-gas acidoses include following.

 Increased (compensatory) alveolar ventilation. In severe acidosis, deep and noisy breathing may be recorded: periodic Kussmaul breathing. It is often referred to as “acidotic breathing.” Cause of hyperventilation- an increase in the H + content in the blood plasma (and other biological fluids) - a stimulus for the inspiratory neurons of the respiratory center. However, as pCO2 decreases and the degree of damage to the nervous system increases, the excitability of the respiratory center decreases and periodic breathing develops.

 Increasing depression of the nervous system and GNI. This is manifested by drowsiness, lethargy, stupor, coma (for example, with acidosis in patients with diabetes). To the main reasons oppression of GNI include the following.

 Disturbances in the energy supply of brain neurons caused by a decrease in its blood supply.

 Ion imbalance, as well as subsequent changes in the physicochemical and electrophysiological properties of the neurons of the respiratory center, leading to a decrease in their excitability.

 Circulatory failure. Reasons insufficiency of blood supply is considered to be a decrease in vascular tone with the development of arterial hypotension (caused by hypocapnia), up to collapse, and a decrease in cardiac output.

 Decreased blood flow in the brain, myocardium and kidneys. This aggravates dysfunction of the nervous system and heart, and also causes oliguria (decreased diuresis).

 Hyperkalemia. Cause hyperkalemia - transport of excess H + ions into the cell in exchange for K +, released into the intercellular fluid and blood plasma.

 Hyperosmia. With non-gas acidosis, hyperosmolar syndrome develops. Causes his are like that.

 Increased concentration of K+ in the blood due to cell damage.

 An increase in the Na + content in the blood plasma as a result of the “displacement” of sodium ions from their connection with protein molecules by excess H +.

 Edema. Main reasons The following are considered edema.

 Tissue hyperosmia due to increased dissociation under conditions of acidosis of organic and inorganic compounds (electrolytes).

 Hyperoncia of tissues as a result of increased hydrolysis and dispersity of protein molecules with an increase in the content of H + ions in liquids.

 Reduced fluid reabsorption in microvessels due to venous stagnation, characteristic of circulatory failure.

 Increased permeability of the walls of arterioles and precapillaries under conditions of acidosis.

 Loss of Ca 2+ bone tissue with the development of osteodystrophy. The reason for this is the increased use of calcium bicarbonate and phosphate in bone tissue to “neutralize” excess hydrogen ions in the blood and other body fluids. This process is regulated by the BCP. As a result of this, osteoporosis, osteodystrophy develops, and in children - rickets. These changes in calcium metabolism and the state of bone tissue are called the “reckoning phenomenon” for compensation of non-gas acidosis.

Non-gas alkaloses

With all the variety of variants of non-gas alkaloses, they have a number of common, naturally developing features. The main ones include the following.

 Hypoxia. Main reasons Hypoxia in non-gas alkalosis is considered to be hypoventilation of the lungs caused by a decrease in [H + ] in the blood; and an increase in the affinity of Hb for oxygen due to a decrease in the H + content in the blood. This causes a decrease in the dissociation of HbO 2 and the supply of oxygen to tissues.

 Hypokalemia. Basic causes hers are like that.

 Increased urinary excretion of K+ by the kidneys under conditions of aldosteronism.

 Activation of the exchange of Na + for K + in the distal tubules of the kidneys due to an increase in primary urine.

 Loss of K+ (albeit to a limited extent) due to vomiting. The consequences of hypokalemia are as follows.

 Transport of H + into the cell with the development of acidosis in it.

 Metabolic disorders, especially: inhibition of proteosynthesis.

 Deterioration of neuromuscular excitability.

 Insufficiency of central and organ-tissue blood flow. Main reasons for this:

 Decreased tone of arteriolar walls as a result of disruption of energy supply to tissues and ion balance.

 Arterial hypotension, which develops as a result of decreased cardiac output, hypotension of the arteriolar walls and hypovolemia.

 Microcirculation disorders with the development of capillary-trophic insufficiency. Their reasons consist in a violation of the central and organ-tissue blood flow, as well as the aggregate state of the blood due to hemoconcentration (most pronounced with repeated vomiting and polyuria).

 Deterioration of neuromuscular excitability, manifested by muscle weakness and impaired motility of the stomach and intestines. Causes these changes are hypokalemia and changes in the content of other ions in the blood and intercellular fluid, as well as hypoxia of tissue cells.

 Functional disorders of organs and tissues up to their failure. Causes- hypoxia, hypokalemia and disorders of neuromuscular excitability.

Typical forms of acid-base imbalance

Respiratory acidosis

Respiratory acidosis is characterized by a decrease in blood pH and hypercapnia (an increase in blood pCO 2 of more than 40 mm Hg). However, there is no linear relationship between the degree of hypercapnia and clinical signs of respiratory acidosis. The latter are largely determined by the cause of hypercapnia, the characteristics of the underlying disease and the reactivity of the patient’s body.

Causes and signs of respiratory acidosis

Compensated acidosis, as a rule, does not cause significant changes in the body.

Uncompensated acidosis leads to significant disruption of the body’s vital functions and the development of a complex of characteristic changes in it.

Causes and consequences of respiratory acidosis

Cause of respiratory acidosis- increasing hypoventilation of the lungs (for example, with spasm of the bronchioles or obstruction of the respiratory tract). The mechanism of bronchiole spasm includes: increased release of acetylcholine from nerve terminals and increased sensitivity of cholinergic receptors to acetylcholine.

The most dangerous consequence of bronchospasm in conditions of acidosis is the formation of a vicious pathogenetic circle “Bronchospasm  increase in pCO 2  rapid decrease in pH  increased bronchospasm  further increase in pCO 2.”

Important pathogenic consequences respiratory acidosis are:

 dilation of brain arterioles with the development of arterial hyperemia and increased intracranial pressure. The causes of these disorders are prolonged and severe hypercapnia and hyperkalemia. They lead to a decrease in the basal muscle tone of the walls of brain arterioles. These changes manifest themselves as severe headache and psychomotor agitation, followed by drowsiness and lethargy. Compression of the brain also leads to increased activity of vagus nerve neurons, which in turn causes arterial hypotension, bradycardia, and sometimes cardiac arrest;

 spasm of arterioles and ischemia of other (except the brain!) organs. The main causes of ischemia are hypercatecholaminemia, observed in conditions of acidosis, and hypersensitization of α-adrenergic receptors in peripheral arterioles. Ischemia of tissues and organs manifests itself multiple organ dysfunction. However, as a rule, signs of renal ischemia dominate: with a significant increase in pCO 2 is decreasing renal blood flow and glomerular filtration volume and the mass of circulating blood increases. This significantly increases the load on the heart and in chronic respiratory acidosis (for example, in patients with respiratory failure) can lead to a decrease in the contractile function of the heart, i.e. To heart failure;

 disruption of blood and lymph flow in the microvasculature due to spasm of arterioles in tissues and organs (except for the brain!) and heart failure, leading to a decrease in blood perfusion pressure in the arterioles and disruption of its outflow through the venules;

 hypoxemia and hypoxia due to pulmonary hypoventilation; impaired pulmonary perfusion due to heart failure; decrease in the affinity of Hb for oxygen (as a consequence of hypercapnia); disturbances of biological oxidation processes in tissues (due to impaired microhemocirculation, hypoxemia, decreased activity of tissue respiration enzymes, and in case of acidosis, glycolysis); Thank you to the author! explain! Y

 ion imbalance- increased content of K + ions in the intercellular fluid, hyperkalemia, hyperphosphatemia, hypochloremia. Causes ionic imbalance are hypoxia, disruption of the energy supply of cells and an increase in the concentration of H + in the extracellular fluid. In this case, the entry of H + into the cells is accompanied by the release of K + from them. Consequence hyperkalemia is a decrease in the threshold of cell excitability, incl. cardiomyocytes. This often leads to cardiac arrhythmias, including fibrillation.

Mechanisms of compensation for respiratory acidosis

The body has developed immediate and long-term mechanisms to compensate for respiratory acidosis. Both groups of mechanisms are aimed at neutralizing excess H + formed during the dissociation of carbonic acid (Fig. 14-3).

Urgent compensation of respiratory acidosis

The mechanism of urgent compensation for respiratory acidosis (Fig. 14-3) is realized with the participation of the body’s chemical buffer systems, as well as the Cl – ÷ HCO 3 – exchange mechanism (antiport) of erythrocytes. The most significant include:

 Red blood cell hemoglobin buffer. It is the most capacious. Excess H+ binds to non-oxygenated Hb of erythrocytes.

 Protein buffer system of cells. It decreases in extracellular fluid as a result of exchange for intracellular K +.

 Protein and phosphate buffers of bone tissue. They are also activated when the pH drops significantly.

 Blood plasma protein buffer. Proteins accept H + ions with anionic ligands, releasing Na + into the blood plasma.

 AnionsHCO 3 – . They leave erythrocytes in exchange for Cl - plasma, replenish its bicarbonate buffer, thereby helping to eliminate acidosis.

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Rice. 14-3. Mechanisms of compensation for respiratory acidosis.

Long-term compensation of respiratory acidosis

The mechanisms of long-term compensation for prolonged respiratory acidosis are realized mainly by the kidneys. It takes 3–4 days to achieve the effect. With respiratory acidosis, the following are activated in the kidneys:

 acidogenesis;

 ammoniogenesis;

 secretion of NaH 2 PO 4;

 K + – Na + exchange.

These mechanisms simultaneously ensure reabsorption of bicarbonate and Na + into the blood, which replenishes the consumption of the bicarbonate buffer system.

Typical changes in CBS parameters in respiratory acidosis

gas acidosis - increase in pCO 2 blood.

With gas acidosis (capillary blood) are as follows.

A patient has an attack of bronchial asthma.

Respiratory alkalosis

Respiratory alkalosis characterized increased pH and hypocapnia(a decrease in blood pCO 2 to 35 mm Hg or more).

Cause and main signs of respiratory alkalosis

Cause of gas alkalosis- hyperventilation of the lungs. In this case, the volume of alveolar ventilation is higher than that required to remove the amount of CO 2 that is formed in the metabolic process over a certain period of time.

Main signs of gas alkalosis

 Disturbances of central and organ-tissue circulation due to increased tone of the walls of cerebral arterioles, leading to its ischemia; and a decrease in the tone of the walls of arterioles in organs and tissues (except the brain!). This, in turn, leads to the following consequences.

 Arterial hypotension.

 Deposition of blood in dilated vessels.

 Decrease in BCC.

 Decrease in venous pressure.

 Decreased blood flow to the heart.

 Decrease in stroke and cardiac output.

This chain of changes in blood circulation reduces the blood supply to tissues and organs, including the heart. This further aggravates systemic circulatory disorders, which closes the hemodynamic vicious circle in gas alkalosis.

 Hypoxia, arising as a result of the following processes.

 Circulatory failure.

 Increases the affinity of Hb for oxygen, reducing the dissociation of HbO 2 in tissues.

 Violation (under conditions of respiratory alkalosis) of carboxylation of pyruvic acid and its conversion into oxaloacetate, as well as the reduction of the latter into malate. In addition to aggravating energy deficiency, the described disorders create conditions for the development of metabolic acidosis.

 Inhibition of glycolysis under hypoxic conditions: reduction of pCO 2 to 15–18 mm Hg. Art. accompanied by inhibition of the activity of many glycolytic enzymes.

 Hypokalemia. Develops significantly due with the transport of K + from the intercellular fluid into cells in exchange for H +.

 Muscle weakness, which is manifested by physical inactivity, intestinal paresis, and paralysis of skeletal muscles. These disorders are mainly the result of hypokalemia.

 Heart rhythm disturbances(paroxysms of tachycardia, extrasystole) are caused by hypokalemia. When the K + content in the blood plasma decreases to 2 mmol/l, hyperpolarization of the plasmalemma of cardiomyocytes develops, often leading to cardiac arrest in systole.

 Hyperventilation tetany, which is a consequence of the following processes.

 Decreased in interstitial fluid due to increased binding of K+ by albumin.

 Decrease in H+ concentration in the intercellular fluid. Blood plasma pH is an important factor regulating the binding of Ca 2+ by albumins: a decrease (with alkalosis) activates the fixation of Ca 2+ by proteins.

Mechanisms of compensation for respiratory alkalosis

Elimination of respiratory alkalosis is achieved with the participation of 2 groups of mechanisms: urgent and long-term. Both provide:

 reduction in the concentration of HCO 3 – in blood plasma and other biological fluids;

 increase in pCO 2 and, as a consequence, the concentration of H 2 CO 3 (Fig. 14-4).

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Rice. 14-4. Mechanisms of compensation for respiratory alkalosis.

Urgent mechanisms for compensation of respiratory alkalosis

 due to the suppression of the activity of inspiratory neurons with a decrease in blood pCO 2 and restoration of carbon dioxide levels.

 Action of intracellular buffer systems: hydrocarbonate, protein, hemoglobin, phosphate. This ensures the release of H + from the cell into the interstitium and further into the blood in exchange for K + and Na +.

 Activation of glycolysis with the formation of lactate and pyruvate, which leads to a decrease in blood pH + and an increase in HCO 3.

 Intracellular outputCl – into interstitial fluid in exchange for HCO 3 – . This reduces its concentration both in the interstitium and in the blood plasma and, as a result, reduces the pH.

Activation of extracellular buffer systems does not have a significant role in eliminating gas alkalosis due to their low capacity for H + generation.

Long-term mechanisms of compensation for respiratory alkalosis

They are implemented mainly, kidneys due to:

 inhibition of acidogenesis due to the increased concentration of HCO 3 - in the epithelium of the distal parts of the nephron;

 activation of kaliuresis;

 increased excretion from blood into urineNa 2 HPO 4 ;

 inhibition of ammoniogenesis.

The latter occurs when glutaminase activity is inhibited under conditions of alkalosis and the content of glutamate entering the mitochondria is reduced.

Typical changes in CBS indicators in respiratory alkalosis

Main pathogenetic factor with respiratory alkalosis - decrease in pCO 2 in blood.

Typical changes in CBS indicators(capillary blood) in gas alkalosis are as follows.

Blood was taken from a patient after an attack of hysteria.

Metabolic acidosis

Metabolic acidosis is one of the most common and dangerous forms of CBS disorders. Such acidosis is observed with cardiac, renal and hepatic, many types of hypoxia, depletion of buffer systems (for example, with blood loss or hypoproteinemia).

Causes of metabolic acidosis

 Metabolic disorders. They lead to the accumulation of excess non-volatile acids (lactate, pyruvate and other substances with acidic properties) under the following conditions.

 Various types of hypoxia or heavy physical work.

 Development of forms of pathology affecting large areas of tissue and organs (extensive burns and/or tissue inflammation).

 Prolonged fever, alcohol intoxication, development of diabetes mellitus with the accumulation of ketone compounds: acetone, acetoacetic or -hydroxybutyric acids.

 Insufficiency of buffer systems and physiological mechanisms for neutralizing and removing excess non-volatile acids from the body.

Typical changes in CBS indicators in metabolic acidosis

The main pathogenetic factor is the depletion of HCO 3 – (hydrocarbonate buffer) due to the accumulation of non-volatile compounds (lactate, CT).

Typical directions of changes in ACR (capillary blood) indicators for all non-gas acidoses are as follows.

The patient was admitted to the clinic with a preliminary diagnosis of diabetes mellitus.

Mechanisms of compensation for metabolic acidosis

Mechanisms for compensating metabolic acidosis are divided into urgent and long-term (Fig. 14-5).

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Rice. 14-5. Mechanisms of compensation for metabolic acidosis.

Urgent mechanisms for eliminating metabolic acidosis

Urgent mechanisms eliminating or reducing the degree of metabolic acidosis are to activate:

 bicarbonate buffer system of intercellular fluid and blood plasma. This system is capable of eliminating even significant acidosis (due to its large buffer capacity);

 bicarbonate buffer of erythrocytes and other cells. Observed with significant acidosis;

 cell protein buffer system various fabrics. It is observed when excess non-volatile acids accumulate in the body;

 bicarbonate and hydrophosphate buffers of bone tissue;

 d breathing center. This ensures an increase in the volume of alveolar ventilation, rapid removal of CO 2 from the body and often Y to the author! explain! Normalization of pH. It is significant that the “buffer power” of the external respiration system under conditions of metabolic acidosis is approximately 2 times greater than that of all chemical buffers. However, the functioning of this system alone is absolutely insufficient to normalize pH without the participation of chemical buffers.

Long-term mechanisms of compensation for metabolic acidosis

Long-term compensation of metabolic acidosis is realized mainly by the kidneys with the participation (to a significantly lesser extent) of bone tissue, liver and stomach buffers. Compensatory mechanisms include:

 renal mechanisms. With the development of metabolic acidosis in the kidneys, the mechanisms of ammoniogenesis (the main mechanism), acidogenesis, secretion of monosubstituted phosphates (NaH 2 PO 4) and Na + , K + -exchange are activated. Collectively, renal mechanisms promote increased H + secretion in the distal renal tubules and bicarbonate reabsorption in the proximal nephron;

 bone buffers(hydrocarbonate and phosphate). They play an essential role in chronic acidosis;

 hepatic compensation mechanisms. They are implemented by intensifying the formation of ammonia and gluconeogenesis, detoxification of substances with the participation of glucuronic and sulfuric acids, followed by their removal from the body;

 increased production of hydrochloric acid by the parietal cells of the stomach. Observed with long-term acidosis.

Metabolic alkalosis

Metabolic alkalosis is characterized by an increase in blood pH and an increase in the concentration of bicarbonate in it.

The concept of metabolic alkalosis is the most controversial in the pathophysiology of CBS. This is due to the fact that:

 one part of the conditions with an increase in blood pH is the result of the accumulation of alkaline valencies due to impaired renal function. Therefore, these states should be classified as excretory-renal adcalosis(see below);

 another part of CBS disorders with elevated pH is caused by the body’s loss of acidic compounds of gastric contents (due to its HCl) through vomiting or through a gastric fistula. The described variant of alkalosis should be designated as excretory gastric alkalosis(see below);

Consequently, in clinical practice, true metabolic alkaloses are observed only in conditions resulting from disorders of the exchange of “alkaline” ions Na +, Ca 2+ and K +. They are discussed below.

Main causes of metabolic alkalosis

 Primary hyperaldosteronism. This is the result of pathological processes that primarily affect the zona glomerulosa of the adrenal cortex: its tumor (adenoma, carcinoma) or hyperplasia. These conditions are accompanied by hyperproduction of aldosterone.

 Secondary hyperaldosteronism. It develops as a result of stimulation of aldosterone production by the zona glomerulosa of the adrenal cortex by influences of extra-adrenal origin, i.e. secondary. The main ones among the latter include the following.

 Increased levels of angiotensin-II in the blood (for example, in patients with chronic arterial hypertension or hypovolemia).

 Blockade or decrease in the synthesis of glucocorticoids and androgens in the adrenal gland, which is accompanied by a compensatory increase in aldosterone production.

 Hyperplasia of the juxtaglomerular apparatus (for example, in Bartter's syndrome).

 An increase in the blood level of ACTH, which stimulates the synthesis of glucocorticoids.

 Hypofunction of the parathyroid glands. This is accompanied by a decrease in the content of Ca 2+ ions in the blood (hypocalcemia) and an increase in the concentration of Na 2 HPO 4 (hyperphosphatemia).

Mechanisms of development of metabolic alkalosis

The pathogenesis of metabolic alkalosis includes several links. The main ones include redundant:

 secretion of ionsH + AndK + renal tubular epithelium into primary urine;

 reabsorptionNa + from primary urine into the blood;

 accumulation in cellsH + with the development of intracellular acidosis;

 delay in cellsNa + ;

 cell hyperhydration due to an increase in osmotic pressure caused by excess Na +.

These mechanisms are realized through a cascade of metabolic reactions, incl. through a change in the activity of Na +, K + -ATPase and, as a consequence, the metabolism of substances containing Na + and K + ions. A number of these metabolic processes are directly controlled by aldosterone. That is why this type of CBS impairment is rightly called metabolic alkalosis.

Mechanisms of compensation for metabolic alkalosis

Mechanisms for compensating for metabolic alkalosis are aimed at reducing the concentration of bicarbonate in the blood plasma and other extracellular fluids. However, the body practically does not have sufficiently effective mechanisms for eliminating alkalosis.

Depending on the time (speed) of activation, the mechanisms of compensation for metabolic alkalosis are divided into urgent and long-term (Fig. 14-6).

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Rice. 14-6. Mechanisms of compensation for metabolic alkalosis.

Urgent mechanisms for eliminating metabolic alkalosis

The mechanisms for urgent elimination of metabolic alkalosis are as follows.

 Cellular compensation mechanisms. These include the following.

 Activation of glycolysis processes, tricarboxylic acid cycle and others. They provide the formation of non-volatile organic acids (lactic, pyruvic, ketoglutaric and others). Acids increase the H + content in cells, diffuse into the extracellular fluid (where they reduce the concentration of HCO 3 –), and also enter the blood plasma (where they also eliminate excess HCO 3 – anion).

 The action of a protein buffer that releases the H + ion into the cytosol and further into the interstitial fluid in exchange for Na +.

 Transport of excess HCO 3 – ions from the intercellular fluid into the cytoplasm in exchange for an equivalent amount of Cl –. This mechanism operates mainly in red blood cells.

The role of these and other cellular mechanisms in reducing the degree of metabolic alkalosis is quite significant: they are able to buffer about 30% of alkali.

 Extracellular buffer systems. They are not essential in eliminating alkalosis. This is due to the fact that the main buffer of blood plasma and extracellular fluid is protein. However, the dissociation of H+ from protein molecules is small. This mechanism neutralizes only about 1% of bases.

 Decreased alveolar ventilation volume. This is observed with an increase in the content of bicarbonate in the liquid media of the body. In this regard, pCO 2, the concentration of carbonic acid and the H + ions formed during its dissociation increase. As a result, the pH decreases.

Long-term mechanisms of compensation for metabolic alkalosis

Long-term compensation of metabolic alkalosis is carried out with the participation of the kidneys. They ensure effective removal of excess HCO 3 – from the body. However, the significance of this mechanism is progressively limited as the degree of alkalosis increases (due to an increase in the threshold for bicarbonate reabsorption).

Typical changes in CBS indicators in non-gas alkaloses

The main pathological factors in non-gas alkalosis are an increase in HCO 3 and hypokalemia.

Typical directions of changes in COS (capillary blood) indicators for all non-gas alkaloses are as follows.

Results of additional studies: increased aldosterone levels in the blood, hypokalemia, signs of Itsenko-Cushing's disease.

Excretory acid-base disorders

Excretory disorders of CBS are the result of impaired excretion from the body (excessive loss or, on the contrary, retention in it) of acids or bases with the development, respectively, of acidosis or alkalosis.

Excretory acidoses

Types, causes of development and examples of excretory acidoses are shown in Figure 14-7.

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Rice. 14-7. Types of excretory acidosis.

Mechanisms of compensation for excretory acidosis(Fig. 14-8) are similar to those in metabolic acidosis. These include immediate (cellular and non-cellular buffers) and long-term responses.

It is important that with renal excretory acidosis, real mechanisms for eliminating excess non-volatile acids from the body are ineffective. This significantly complicates the patient’s condition, since other mechanisms of long-term compensation for excretory acidosis (activation of hepatic metabolic and excretory processes, bicarbonate and phosphate buffers of bone tissue, increased synthesis of HCl in the parietal cells of the stomach) are not always able to eliminate excess H + in the body.

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Rice. 14-8. Mechanisms of compensation for excretory acidosis. *In renal excretory acidosis they are ineffective.

Examples of typical changes in CBC (capillary blood) parameters during excretory acidosis

Uncompensated renal excretory acidosis

The patient is being treated with a diagnosis of Chronic diffuse glomerulonephritis.

The main pathogenetic factor is a violation of the excretion of acidic valencies from the body by the kidneys.

Compensated intestinal excretory acidosis

The patient has a fistula of the small intestine with prolonged loss of intestinal juice.

The main pathogenetic factor is the excretion of bases from the body with intestinal juice.

Excretory alkaloses

Types, causes of development and examples of excretory alkalosis are shown in Figure 14-9.

Y layout! insert picture “fig-14-9”

Rice. 14-09. Types of excretory alkalosis.

General causes and mechanisms of development of excretory alkalosis

 Loss by the bodyHClstomach. The reason for this is vomiting of gastric contents (for example, with toxicosis of pregnancy, pylorospasm, pyloric stenosis, intestinal obstruction) or suction through a tube. This variant of excretory alkalosis is designated as gastric (gastric).

 Increased excretion from the body by the kidneysNa + , which is combined with hydrogen carbonate retention. The most common reasons for these changes are as follows.

 Taking diuretics(mercury-containing, furosemide, ethacrynic acid). Diuretics cause at least 3 effects.

 Inhibition of reabsorption of Na + and water in the kidneys. As a result, Na + is excreted from the body in increased quantities, and the content of alkaline bicarbonate anions in the blood plasma increases.

 Release of Cl – ion along with Na +, which causes hypochloremia. The described variant of excretory renal alkalosis is also referred to as hypochloremic.

 Development of hypovolemia and hypokalemia, aggravating the patient’s condition. For example, hypokalemia causes the transport of H + into the cell from the intercellular fluid, which potentiates alkalosis.

 The presence in the glomerular filtrate of the kidneys is so-called. poorly absorbed anions. These include anions of nitrate, sulfate, metabolic products of some antibiotics (penicillins), which are poorly reabsorbed in the proximal nephron tubules. These anions enter the body with food or drugs. The accumulation of poorly reabsorbed anions in primary urine is accompanied by increased excretion of K + by the kidneys and the development of hypokalemia, activation of H + transport into cells from the intercellular fluid, as well as the release of H + into primary urine and the reabsorption of HCO 3 – .

 Hypovolemia(developing, for example, with repeated blood loss, vomiting, diarrhea, increased sweating). A decrease in blood volume activates the renin‑angiotensin‑aldosterone system. In this regard, secondary aldosteronism develops. Aldosterone is known to increase the excretion of K + and Na + and the reabsorption of HCO 3 . The latter aggravates the degree of alkalosis. All of the above variants of excretory alkalosis are called renal (renal).

 Increased excretion from the bodyK + intestines. The most common cause of this is the abuse of laxatives and/or frequent enemas, which in turn causes the following phenomena.

 Excessive excretion of K + with intestinal contents and the development of hypokalemia; hypokalemia stimulates the transport of Na + ions from the intercellular fluid into cells with the development of alkalosis, both intracellular and in the blood plasma. This type of CBS disorder is designated as excretory intestinal (enteral) alkalosis.

 In this case, the loss of K + is combined with increased excretion of fluid from the body and the development of hypovolemia.

 Hypovolemia is accompanied by secondary hyperaldosteronism and subsequent increased excretion of H + and K + ions from the body in urine; excretory renal alkalosis develops. In other words, the excretory intestinal alkalosis that forms initially is later potentiated by the development of renal excretory alkalosis.

General mechanisms of compensation for excretory alkalosis

The compensatory mechanisms of excretory alkalosis are similar to those in metabolic alkalosis. They are aimed at reducing the content of hydrocaryuonate in the blood plasma (see Fig. 14-6).

Examples of typical changes in CBS (capillary blood) indicators during excretory alkalosis

Compensated excretory gastric alkalosis

The patient has a concussion and repeated vomiting with a sour smell.

Main pathogenetic factor for excretory alkalosis - loss of hydrochloric acid by the body with gastric contents as a result of repeated vomiting.

Compensated excretory renal alkalosis

The patient receives a diuretic drug (ethacrynic acid).

Main pathogenetic factor in this case - an increase in the reabsorption of HCO 3 - and an increase in the content of this anion in the blood plasma.

Exogenous acid-base balance disorders

These CBS disorders develop as a result of the ingestion of exogenous agents with acidic or basic properties.

Exogenous acidosis

Causes of exogenous acidosis

 Taking acid solutions(for example, hydrochloric, sulfuric, nitrogen) by mistake or for the purpose of poisoning.

 Prolonged consumption of foods and drinks containing acids(for example, lemon, apple, salicylic).

 Taking drugs containing acids and/or their salts (for example, salicylic acid (aspirin), calcium chloride, arginine-HCl  , To the author! This drug is not in the register of medicines registered in the Russian Federation, there is a drug “arginine” and lysine-HCl  ) Y to the author! This drug is not in the register of medicines registered in the Russian Federation, there is a drug “lysine” Y.

 Transfusion of donor blood products preserved with sodium citrate.

General mechanisms of the formation of exogenous acidosis

 Increased concentrationH + in organism due to excess intake of acid solutions. This leads to rapid depletion of buffer systems.

 Release of excessH + due to the dissociation of acid salts (for example, NaH 2 CO 3, NaH 2 PO 4 and CaHCO 3, sodium citrate).

 Secondary metabolic disorders in tissues and organs under the influence of exogenous acids. This is accompanied by the simultaneous accumulation of both exogenous and endogenous acid valencies. For example, when salicylates are ingested, acidosis is the result of the formation of salicylic acid (exogenous) in the body and at the same time the accumulation of endogenous lactic acid. In this case, the origin of acidosis is twofold (mixed): exogenous (due to the intake of salicylates) and metabolic (due to metabolic disorders under the influence of excess exogenous acid).

 Liver and kidney damage with a significant increase in the concentration of H + in the blood and other biological fluids. The development of renal and liver failure potentiates the degree of acidosis.

Mechanisms of compensation for exogenous acidosis

The mechanisms for compensating for exogenous acidosis are the same as for metabolic acidosis (see Fig. 14-5).

Examples of typical changes in CBS (capillary blood) parameters during exogenous acidosis

Exogenous uncompensated acidosis

The patient undergoes surgery using a heart-lung machine (a large amount of blood preserved with sodium citrate is used).

The main pathogenetic factor of acidosis in this case, an excess of exogenous citric acid in the body.

Exogenous acidosis compensated

The patient has been taking salicylic acid medications for a long time.

Main pathogenetic factor- accumulation of excess H + in the body (formed during the dissociation of salicylic acid).

Exogenous alkalosis

Exogenous alkalosis is a relatively rare violation of CBS; as a rule, this is a consequence of ingestion of either excess bicarbonate used in buffer solutions or alkalis in food and drink.

The most common causes of exogenous alkalosis

 Administration for a short time of excessHCO 3 – -containing buffer solutions. This is most often observed in the treatment of conditions accompanied by acidosis (for example, lactic acidosis or ketoacidosis in patients with diabetes). The rapid administration of alkaline buffer solutions to patients with a reduced renal excretion process is especially dangerous (in the clinic, a similar situation can arise in patients suffering from renal failure that has developed as a result of diabetes).

 Prolonged use of food and drink containing large amounts of alkalis. It is observed in patients with gastric ulcers who take large quantities of alkaline solutions and milk. This syndrome is called milk-alkali syndrome.

Mechanism of development of exogenous alkalosis

The mechanism of development of exogenous alkalosis usually includes 2 links:

 main (primary) - increase in the concentration of HCO 3 – introduced into the body.

 additional (secondary) - increased formation and/or impaired excretion of endogenous bicarbonate.

The latter is usually observed in renal failure.

Mechanisms of compensation for exogenous alkalosis

The mechanisms of compensation for exogenous alkalosis are identical to those in metabolic alkalosis (see Fig. 14-6).

Typical changes in CBS indicators (capillary blood)

Exogenous alkalosis compensated

A patient with diabetes is injected intravenously with a buffer solution containing sodium bicarbonate.

Main pathogenetic factor- excess HCO 3 – in blood plasma.

Mixed acid-base balance disorders

In clinical practice, signs of mixed (combined) forms of impairment of CBS in the same patient are often observed, i.e. gas and non-gas acidosis or alkalosis at the same time.

Examples of mixed CBS disorders

 Heart failure. The patient may develop mixed acidosis: gas (due to impaired alveolar perfusion and pulmonary edema) and non-gas- metabolic (as a result of circulatory hypoxia) and excretory renal (due to renal hypoperfusion).

 Brain injury or pregnancy. Observed mixed alkalosis: gas(caused by hyperventilation) and non-gas- gastric excretory (due to repeated vomiting of gastric contents).

Other combinations of disorders are also possible, incl. multidirectional in changes in CBS indicators. They are often called combined.

Examples of combined CBS disorders

 Chronic broncho-obstructive pulmonary diseases. With them it develops respiratory acidosis, and in connection with the use of glucocorticoids (for the purpose of treating lung disease), at the same time it is formed excretory chloride-dependent alkalosis. The resulting change in pH depends on the dominance of metabolic disorders, lung and kidney functions.

 Severe chronic gastroenteritis. Accompanied by vomiting (with loss of acidic gastric contents) and development of excretory alkalosis, combined with diarrhea (with loss of alkaline intestinal juice) and the development excretory acidosis. In these and other similar cases, frequent re-examination of all (main and additional) indicators of CBS and flexible, adequate treatment are necessary.

Principles for eliminating acid-base imbalance disorders

Respiratory acidosis

The main goal of treatment for respiratory acidosis is- reduction in the degree or elimination of respiratory failure.

Elimination methods respiratory acidosis different in acute and chronic forms of respiratory failure.

For acute respiratory failure carry out a set of urgent (!) measures aimed at ensuring the optimal volume of alveolar ventilation:

 restore airway patency (remove foreign bodies, suck out fluid, mucus or vomit, eliminate tongue retraction, etc.);

 stop the intake of excess carbon dioxide into the body (for example, normalize the gas composition of the air in spacesuits, aircraft, rooms, when performing mechanical ventilation);

 transfer the patient to mechanical ventilation in the absence or insufficiency of spontaneous breathing (after restoration of airway patency);

 when ventilating the lungs, atmospheric air or gas mixtures enriched with oxygen are used. In this case, the concentration of O 2 in the gas mixture should not be higher than the level that ensures optimal pO 2 in a given patient: hyperoxygenation of the body is accompanied by increased formation of pathogenic reactive oxygen species: 1 O – 2, O – 2,  OH, H 2 O 2 and subsequent activation of lipid peroxide processes. It is also important to remember that the use of hypoxic gas mixtures and mixtures with the addition of CO 2 in cases of severe respiratory failure is inadmissible. Their use potentiates hypercapnia and aggravates the patient's condition.

For chronic respiratory failure carry out a set of measures based on etiotropic, pathogenetic and symptomatic principles.

Etiotropic principle respiratory acidosis is aimed at eliminating the causes of acidosis: hypoventilation and/or hypoperfusion of the lungs, as well as reduced diffusion capacity of the airborne barrier. The etiotropic principle of eliminating gas acidosis is implemented using a number of methods:

 restoration of airway patency(for example, with the help of bronchodilators, expectorants, bronchial drainage, sputum suction) and normalization of pulmonary ventilation. In case of decompensated gas acidosis, mechanical ventilation is performed. This is done under pH control to prevent hyperventilation and the development of post-hypercapnic gas alkalosis;

 improving pulmonary blood perfusion(with the help of cardiotropic drugs; drugs that regulate vascular tone and the aggregate state of the blood);

 regulation of the activity of the respiratory center(limiting the intake of drugs that reduce its excitability, for example, sedatives or narcotic analgesics, and prescribing stimulants of its function);

 restrictions on the patient's physical activity(in order to reduce the volume of alveolar ventilation).

Pathogenetic principle of treatment of respiratory acidosis aims to eliminate the main pathogenic factor of respiratory acidosis: increased CO 2 content in the blood (hypercapnia) and other biological fluids of the body. This goal is achieved carrying out measures to eliminate the cause causing disruption of gas exchange in the lungs(i.e. - etiotropic therapy) since the introduction of buffer solutions containing bicarbonate to eliminate chronic respiratory acidosis is ineffective. This is explained by the fact that exogenous HCO 3 is quickly removed from the body by the kidneys, and if their excretory function is impaired (with renal failure), exogenous alkalosis can develop.

Symptomatic treatment at respiratory acidosis aims to eliminate unpleasant and painful sensations that aggravate the patient’s condition: severe headache, severe and prolonged tachy- or bradycardia, psychomotor agitation, excessive sweating and others.

Respiratory alkalosis

Goal of treatment for respiratory alkalosis- elimination of CO 2 deficiency in the body. Therapeutic measures are based on etiotropic, pathogenetic and symptomatic principles.

Etiotropic principle of treatment of respiratory alkalosis carried out by eliminating the cause of hyperventilation:

 inadequate (excessive) ventilation of the lungs during anesthesia or in other situations with the use of mechanical ventilation (in these cases, repeated determination of blood pH and CO 2 is required);

 liver failure;

 drug intoxication (for example, salicylates, adrenergic agonists, progestogens);

 hyperthyroidism;

 anemia;

 hyperpyretic fever.

 pulmonary embolism.

 stressful condition.

 brain injuries and others.

Pathogenetic treatment respiratory alkalosis aimed at normalizing the carbon dioxide content in the body. To this end, a number of activities are carried out:

 breathing gas mixtures with a high partial content of CO 2. For this use:

 carbogen (a mixture including 95% O 2 and 5% CO 2);

 “rebreathing” method - inhalation of air exhaled by the patient into the bag. In hospitals, a special “rebreathing breathing” device is used, which allows dosing the CO 2 content in the inhaled air;

 Ventilation. This method is used for severe metabolic disorders and vital functions of the body that develop as a result of chronic gas alkalosis;

 correction of water and electrolyte metabolism using buffer solutions, the composition of which depends on the specific disorders of ion and water metabolism in a given patient.

Symptomatic principle of therapy for respiratory alkalosis aims to prevent and/or eliminate symptoms aggravating the patient's condition. For this purpose, anticonvulsants, cardiotropic, vasoactive and other drugs are used (depending on the symptoms of each individual patient).

Non-gas acidoses

The main goal of treatment of non-gas acidoses- elimination of excess acids (H +) from the body and restoration of normal HCO 3 – content. Therapeutic measures are also based on etiotropic, pathogenetic and symptomatic principles.

Etiotropic treatment of non-gas acidosis implies the elimination of a disease, pathological process or condition that causes the development of non-gas acidosis. This principle is implemented by carrying out specialized therapy for the corresponding disease or condition (for example, diabetes, alcoholism, shock, heart, liver, kidney failure, poisoning); and parenteral introduction into the body of fluids containing acidic substances (in particular, citrated blood).

Pathogenetic treatment non-gas acidoses aimed at normalizing the content of HCO 3 – in body fluids. Often, eliminating the cause itself provides such a result. This is possible due to the ability of normally functioning kidneys to restore HCO 3 reserves in the body within 2–3 days. However, if the cause of acidosis is not quickly eliminated or this is impossible (for example, with chronic renal or heart failure), then measures are taken to long-term complex therapy. It includes:

 restoration of the bicarbonate buffer by parenteral infusion of solutions containing bicarbonate;

 correction of water and electrolyte metabolism. This is especially necessary with significant hyperkalemia, and in some cases with hypocalcemia, hyperchloremia. Solutions containing cations and anions are administered in the volumes necessary to correct their shifts in each individual patient;

 normalization of the functions of the kidneys, lungs, liver, circulatory system, including microcirculation. This promotes the activation of physiological mechanisms for eliminating shifts in CBS;

 increasing the efficiency of metabolism in tissues. This ensures, on the one hand, the elimination of excess acid metabolites, and on the other, the normalization of organ functions. Use solutions containing glucose, insulin, vitamins, proteins, and coenzymes.

Symptomatic treatment for non-gas acidosis aims to eliminate symptoms that complicate the course of the underlying pathology. Treatment is aimed at eliminating severe headaches, disorders of neuromuscular tone (for example, hyporeflexia, muscle weakness, physical inactivity), cardiac arrhythmias, gastrointestinal functions, paresthesias, encephalopathy and other symptoms.

Non-gas alkaloses

The main goal of treating non-gas alkalosis- restoration of the normal content of buffer bases, primarily bicarbonate.

Therapeutic measures at non-gas alkaloses are based on etiotropic, pathogenetic and symptomatic principles.

Etiotropic principle of non-gas alkaloses involves eliminating the cause that caused alkalosis: loss of acidic stomach contents, increased excretion of H + by the kidneys, increased excretion of Na + and K + ions from the body in the urine when taking diuretics, excessive intravenous administration of bases.

Pathogenetic treatment non-gas alkaloses is aimed at blocking the key links in the pathogenesis of non-gas alkalosis. It must be taken into account that the body does not have effective mechanisms to prevent and/or eliminate them. In this regard, an emergency complex of therapeutic effects is required:

 restoration of the content of acidic valences in the body, for which the calculated amount of hydrochloric acid solution is administered intravenously;

 elimination of electrolyte balance disorders and hypovolemia. Achieved by parenteral administration of solutions containing the necessary ions: sodium chloride, potassium chloride, calcium salts. Due to hypokalemia that naturally develops in non-gas alkalosis, patients are prescribed potassium-sparing drugs (for example, spironolactone), as well as complex solutions including potassium chloride and glucose, administered simultaneously with insulin. This promotes the transport of K+ into cells;

 stimulation of excretion of excess HCO 3 – from the body. For this purpose, carbonic anhydrase inhibitors are used [for example, acetazolamide (diacarb )], which increases the excretion of bicarbonate by the kidneys. In patients with renal failure, hemodialysis is used;

 eliminating the deficiency of ATP and creatine phosphate in cells and reducing the degree of disruption of their energy supply. This is achieved by introducing a complex solution of “glucose + insulin”. Additionally, preparations of vitamins of group B, as well as A, C, E, are used, many of which are coenzymes of biological oxidation reactions.

Symptomatic treatment at non-gas alkaloses is aimed at eliminating complications of both the underlying disease and the alkalosis itself, as well as eliminating or reducing the severity of symptoms that aggravate the patient’s condition. To this end:

 correct protein metabolism. It is disrupted due to a deficiency of K +, which acts as a cofactor for proteosynthesis enzymes. To the greatest extent, protein metabolism disorders are detected in the myocardium, nervous system, and striated muscles (this is what causes the development of heart failure, decreased neuromuscular excitability, intestinal motility, hypotonicity and physical inactivity). To eliminate protein metabolism disorders, patients are administered (in addition to potassium solutions) preparations of amino acids and vitamins;

 use ​​cardiotropic and vasoactive drugs that help restore the contractile function of the heart and vascular tone. This ensures the normalization of central and organ-tissue hemodynamics, as well as blood microcirculation;

 eliminate disorders of the gastrointestinal tract function (manifested by slowing of its peristalsis, constipation, disruption of cavity and membrane digestion). Enzyme preparations, components of gastric and intestinal juice, and cholinomimetics are also used.

Chapter 15

Typical vitamin metabolism disorders

In 1880, Russian doctor N.I. Lunin proved that food products contain substances that are not proteins, fats, carbohydrates or mineral salts, but are vital for the normal development and functioning of the body.

In 1895, Professor V.V. Pashutin found out that scurvy, widespread at that time, develops due to a lack of food of a factor formed by plants, but not synthesized in the human body.

In 1911, the Polish scientist K. Funk isolated the first vitamin in crystalline form - thiamine (vitamin B 1). The term “vitamin” was also proposed by Funk in connection with the presence of an amino group in thiamine. Although it later became clear that many vitamins do not contain an amino group or even a nitrogen atom, the term itself has been preserved.

Vitamins are not plastic material and do not serve as a source of energy.

Types of vitamins

Vitamins, vitamers and their functions are given in Table 15-1. There are currently 13 groups, or families, of vitamins. Almost every family consists of several vitamins, which are proposed to be called vitamers.

Layout Table 14‑1 should be placed on one page

Y Layout There is a note to Table 14‑1, DO NOT TEAR AWAY from the table

Table 15-1. Classification of vitamins

• What is Alkalosis
• What causes alkalosis
• Alkalosis symptoms
• Treatment of Alkalosis
• Which doctors should you contact if you have Alkalosis?

What is Alkalosis

Alkalosis- increasing the pH of the blood (and other tissues of the body) due to the accumulation of alkaline substances.

Alkalosis(Late Lat. alcali alkali, from Arabic al-quali) - a violation of the acid-base balance of the body, characterized by an absolute or relative excess of bases.

What causes alkalosis

Based on the origin of alkolosis, the following groups are distinguished.

Gas alkalosis

It occurs as a result of hyperventilation of the lungs, leading to excessive removal of CO 2 from the body and a drop in the partial tension of carbon dioxide in the arterial blood below 35 mm Hg. Art., that is, to hypocapnia. Hyperventilation of the lungs can be observed with organic lesions of the brain (encephalitis, tumors, etc.), the effect on the respiratory center of various toxic and pharmacological agents (for example, some microbial toxins, caffeine, corazol), with elevated body temperature, acute blood loss, etc.

Non-gas alkalosis

The main forms of non-gas alkalosis are: excretory, exogenous and metabolic. Excretory alkalosis can occur, for example, due to large losses of acidic gastric juice due to gastric fistulas, uncontrollable vomiting, etc. Excretory alkalosis can develop with long-term use of diuretics, certain kidney diseases, as well as endocrine disorders leading to excessive sodium retention in the body. In some cases, excretory alkalosis is associated with increased sweating.

Exogenous alkalosis is most often observed with excessive administration of sodium bicarbonate to correct metabolic acidosis or neutralize increased gastric acidity. Moderate compensated alkalosis can be caused by prolonged consumption of food containing many bases.

Metabolic alkalosis occurs in some pathol. conditions accompanied by disturbances in electrolyte metabolism. Thus, it is observed during hemolysis, in the postoperative period after some extensive surgical interventions, in children suffering from rickets, hereditary disorders of the regulation of electrolyte metabolism.

Mixed alkalosis

Mixed alkalosis - (a combination of gas and non-gas alkalosis) can be observed, for example, with brain injuries accompanied by shortness of breath, hypocapnia and vomiting of acidic gastric juice.

Pathogenesis (what happens?) during Alkalosis

With alkalosis (especially associated with hypocapnia), general and regional hemodynamic disturbances occur: cerebral and coronary blood flow decreases, blood pressure and cardiac output decrease. Neuromuscular excitability increases, muscle hypertonicity occurs, up to the development of convulsions and tetany. Suppression of intestinal motility and the development of constipation are often observed; the activity of the respiratory center decreases. Gas alkalosis is characterized by decreased mental performance, dizziness, and fainting may occur.

Alkalosis symptoms

Symptoms of gas alkalosis reflect the main disorders caused by hypocapnia - hypertension of the cerebral arteries, hypotension of the peripheral veins with a secondary decrease in cardiac output and blood pressure, loss of cations and water in the urine. The earliest and leading signs are diffuse cerebral ischemia - patients are often excited, anxious, may complain of dizziness, paresthesia on the face and limbs, quickly get tired of contact with others, concentration and memory are weakened. In some cases, fainting occurs. The skin is pale, gray diffuse cyanosis is possible (with concomitant hypoxemia). Upon examination, the cause of gas alkalosis is usually determined - hyperventilation due to rapid breathing (up to 40-60 respiratory cycles per 1 min), for example: with thromboembolism of the pulmonary arteries; lung pathology, hysterical shortness of breath (so-called dog breathing) or due to a mode of artificial ventilation of the lungs above 10 l/min. As a rule, there is tachycardia, sometimes a pendulum-like rhythm of heart sounds; pulse is small. Systolic and pulse blood pressure are slightly reduced when the patient is in a horizontal position; when he is transferred to a sitting position, orthostatic collapse is possible. Diuresis is increased. With prolonged and severe gas alkalosis (pCO2 less than 25 mmHg st.) dehydration and seizures may occur as a result of developing hypocalcemia. In patients with organic pathology of the central nervous system and “epileptic readiness,” gas alkalosis can provoke an epileptic seizure. The EEG reveals an increase in amplitude and a decrease in the frequency of the main rhythm, bilateral synchronous discharges of slow waves. ECG often reveals diffuse changes in myocardial repolarization.

Metabolic alkalosis, which often appears with the use of mercury diuretics and with massive infusions of alkaline solutions or nitrate blood into the patient, is usually compensated, is transient in nature and does not have pronounced clinical manifestations (some respiratory depression and the appearance of swelling are possible). Decompensated metabolic alkalosis usually develops as a result of primary (with prolonged vomiting) or secondary (from potassium loss during massive hemolysis, diarrhea) loss of chlorine by the body, as well as in terminal conditions, especially accompanied by dehydration. Progressive weakness, fatigue, thirst are noted, anorexia, headache, and minor hyperkinesis of the muscles of the face and limbs appear. Convulsions due to hypocalcemia are possible. The skin is usually dry, tissue turgor is reduced (swelling is possible with excessive fluid infusion). Breathing is shallow, rare (unless pneumonia or heart failure is associated). As a rule, tachycardia, sometimes embryocardia, is detected. Patients first become apathetic, then lethargic, drowsy; subsequently, disorders of consciousness worsen until the development of coma. The ECG often reveals low T wave voltage and signs of hypokalemia. Hypochloremia, hypokalemia, and hypocalcemia are detected in the blood. The reaction of urine in most cases is alkaline (in A., due to primary losses of potassium, it is acidic).

Chronic metabolic alkalosis, which develops in patients with peptic ulcers due to long-term intake of large quantities of alkalis and milk, is known as Burnett's syndrome, or milk-alkali syndrome. It is manifested by general weakness, loss of appetite with aversion to dairy foods, nausea and vomiting, lethargy, apathy, itching, in severe cases - ataxia, deposition of calcium salts in tissues (often in the conjunctiva and cornea), as well as in the kidney tubules, which leads to the gradual development of renal failure.

Treatment of Alkalosis

Therapy for gas alkalosis consists of eliminating the cause that caused hyperventilation, as well as directly normalizing the gas composition of the blood by inhaling mixtures containing carbon dioxide (for example, carbogen). Therapy for non-gas alkalosis depends on its type. Solutions of ammonium, potassium, calcium chlorides, insulin, and agents that inhibit carbonic anhydrase and promote the excretion of sodium and bicarbonate ions by the kidneys are used.

Patients with metabolic alkalosis, as well as with gas alkalosis that developed against the background of serious diseases, such as pulmonary embolism, are hospitalized. Gas alkalosis due to neurogenic hyperventilation can in most cases be eliminated at the point of care for the patient. With significant hypocapnia, inhalation of carbogen is indicated - a mixture of oxygen (92-95%) and carbon dioxide (8-5%). For convulsions, calcium chloride is administered intravenously. If possible, eliminate hyperventilation, for example, by administering seduxen, morphine, and if the mode of artificial ventilation is incorrect, by correcting it.

In case of decompensated metabolic alkalosis, solutions of sodium chloride and calcium chloride are administered intravenously to the patient. For hypokalemia, intravenous potassium preparations are prescribed - panangin, potassium chloride solution (preferably simultaneous administration of glucose with insulin), as well as potassium-sparing drugs (spironolactone). In all cases, ammonium chloride can be prescribed internally, and for alkalosis caused by excessive administration of alkalis, diacarb can be prescribed. Treatment of the underlying disease is carried out, aimed at eliminating the cause of alkalosis (vomiting, diarrhea, hemolysis, etc.).

Metabolic alkalosis is a disorder of the acid-base state, manifested by a decrease in hydrogen and chlorine ions in the extracellular fluid, high blood pH values ​​and high concentrations of bicarbonate in the blood. To maintain alkalosis, there must be a disturbance in the renal excretion of HCO3~. Symptoms and signs in severe cases include headache, lethargy and tetany. Diagnosis is based on clinical data and determination of arterial blood gas composition and plasma electrolyte levels. Correction of the underlying cause is necessary; intravenous or oral administration of acetazolamide or HCI is sometimes indicated.

ICD-10 code

E87.3 Alkalosis

Causes of metabolic alkalosis

The main reasons for the development of metabolic alkalosis are the loss of H + by the body and the load of exogenous bicarbonate.

Loss of H+ by the body with the development of metabolic alkalosis is observed, as a rule, with damage to the gastrointestinal tract and kidney pathology. In these situations, along with the loss of hydrogen ions, chlorides are also lost. The body's response aimed at replenishing chloride losses depends on the type of pathology, which is reflected in the classification of metabolic alkalosis.

Loss of H+ through the gastrointestinal tract

This is the most common cause of the development of metabolic alkalosis in the clinic of internal diseases.

Classification and causes of metabolic alkalosis

Gastric juice contains sodium chloride and hydrochloric acid in high concentrations, and potassium chloride in lower concentrations. Secretion of 1 mmol/l H + into the gastric lumen is accompanied by the formation of 1 mmol/l bicarbonates in the extracellular fluid. Therefore, the loss of hydrogen and chlorine ions during vomiting or suction of gastric juice through a tube is compensated by an increase in the concentration of bicarbonates in the blood. At the same time, potassium loss occurs, which leads to the release of K+ from the cell with its replacement by H+ ions (development of intracellular acidosis) and stimulation of bicarbonate reabsorption. Developed intracellular acidosis is an additional factor contributing to the loss of hydrogen ions due to a compensatory reaction, manifested in increased secretion by cells, including the renal tubules, which leads to acidification of urine. This complex mechanism explains the so-called “paradoxical acidic urine” (low urine pH values ​​in conditions of metabolic alkalosis) with prolonged vomiting.

Thus, the development of metabolic alkalosis caused by the loss of gastric juice is due to the accumulation of bicarbonates in the blood in response to several factors: the direct loss of H + with the contents of the stomach, the development of intracellular acidosis in response to hypokalemia, as well as the loss of hydrogen ions by the kidneys as a compensatory reaction for intracellular acidosis. For this reason, to correct alkalosis, it is necessary to administer solutions of sodium chloride, potassium chloride or HCL.

Loss of H+ through the kidneys

In this case, alkalosis usually develops with the use of powerful diuretics (thiazide and loop), which remove sodium and potassium in chlorine-bound form. In this case, a large amount of fluid is lost and hypovolemia develops, a sharp increase in the total excretion of acids and chlorine, resulting in the development of metabolic alkalosis.

However, with long-term use of diuretics against the background of developed hypovolemia and persistent metabolic alkalosis, compensatory retention of sodium and chlorides occurs, and their excretion in urine decreases to values ​​​​less than 10 mmol/l. This indicator is important in the differential diagnosis of chloride-sensitive and chloride-resistant variants of metabolic alkalosis. When the chloride concentration is less than 10 mmol/l, alkalosis is regarded as hypovolemic, chloride-sensitive, and it can be corrected by the administration of sodium chloride solutions.

Symptoms of metabolic alkalosis

Symptoms and signs of mild alkalosis are usually associated with an etiological factor. More severe metabolic alkalosis increases the binding of ionized calcium to proteins, leading to hypocalcemia and the development of symptoms of headache, lethargy, and neuromuscular irritability, sometimes with delirium, tetany, and seizures. Alkalemia also lowers the threshold for symptoms of angina and arrhythmias. Associated hypokalemia may cause weakness.

Forms

Posthypercapnic alkalosis

Posthypercapnic alkalosis usually develops after respiratory failure has resolved. The development of posthypercapnic alkalosis is associated with the restoration of the acid-base state after respiratory acidosis. In the genesis of posthypercapnic alkalosis, the main role is played by increased renal reabsorption of bicarbonates against the background of respiratory acidosis. The rapid restoration of PaCO2 to normal using artificial ventilation does not reduce the reabsorption of bicarbonates and is replaced by the development of alkalosis. This mechanism for the development of acid-base disorders requires a careful and slow decrease in P a CO2 in the blood in patients with chronic hypercapnia.

Chloride-resistant alkalosis

The main reason for the development of chloride-resistant alkalosis is an excess of mineralocorticoids, which stimulate the reabsorption of potassium and H + in the distal nephron and maximum reabsorption of bicarbonates by the kidneys.

These variants of alkalosis may be accompanied by an increase in blood pressure due to increased production of primary aldosterone (Conn's syndrome) or due to activation of the renin RAAS (renovascular hypertension), increased production (or content) of cortisol or its precursors (Cushing's syndrome, treatment with corticosteroids, administration of drugs with mineralocorticoids). properties: carbenoxolone, licorice root).

Normal blood pressure levels are detected in diseases such as Bartter's syndrome and severe hypokalemia. In Bartter's syndrome, hyperaldosteronism also develops in response to activation of the RAAS, but the extremely high production of prostaglandins that occurs with this syndrome prevents the development of arterial hypertension.

The cause of metabolic alkalosis is a violation of the reabsorption of chlorides in the ascending limb of the loop of Henle, which leads to an increase in the excretion of chlorides associated with H +, sodium, and potassium in the urine. Chloride-resistant variants of metabolic alkalosis are characterized by a high concentration of chlorides in the urine (more than 20 mmol/l) and resistance of alkalosis to the administration of chlorides and replenishment of circulating blood volume.

Another reason for the development of metabolic alkalosis may be bicarbonate load, which occurs with constant administration of bicarbonates, massive blood transfusion and treatment with alkaline exchange resins, when the alkali load exceeds the ability of the kidneys to excrete them.

Diagnosis of metabolic alkalosis

To recognize metabolic alkalosis and the adequacy of respiratory compensation, it is necessary to determine the gas composition of arterial blood and plasma electrolyte levels (including calcium and magnesium).

Often the cause can be determined by history and physical examination. If the cause is unknown and renal function is normal, urinary K and Cl~ concentrations should be measured (values ​​are not diagnostic of renal failure). A urine chloride level of less than 20 mEq/L indicates significant renal reabsorption and suggests a Cl-dependent cause. A urine chlorine level greater than 20 mEq/L suggests a Cl-independent form.

Urinary potassium levels and the presence or absence of hypertension help differentiate Cl-independent metabolic alkalosis.

A urine potassium level of less than 30 mEq/day indicates hypokalemia or laxative misuse. Urinary potassium levels greater than 30 mEq/day without hypertension suggest diuretic overuse or Barter or Gitelman syndromes. Potassium levels greater than 30 mEq/day in the presence of hypertension require an assessment of the likelihood of hyperaldosteronism, mineralocorticoid excess, and renovascular disease; studies usually include plasma renin activity and aldosterone and cortisol levels.

Everything in the human body is balanced. If this balance is disturbed, then diseases occur. Blood has its own special composition. Alkalosis is an imbalance in the composition of the blood that exhibits its own symptoms. It is divided into respiratory and metabolic alkaloses. The article will also discuss the causes and methods of treating the disease.

Alkalosis and acidosis

What is alkalosis? This is an imbalance in the composition of the blood, where the pH level increases due to the accumulation of an alkaline substance. An imbalance occurs at the level of acids and alkalis, where more hydrogen is added to substances compared to their release of acid. The opposite state of alkalosis is acidosis - when the amount of acids in the blood is greater than normal.

The disease can be compensated or decompensated, depending on the pH level.

• Compensated alkalosis indicates fluctuations in hydrogen levels within normal limits; only minor deviations may be observed.
• Uncompensated alkalosis is accompanied by an abnormal level of hydrogen, which is facilitated by an imbalance of acid and alkali, as well as an excess of bases.

Abnormalities in the composition of the blood become quite natural during infectious diseases or in extreme situations. In this situation, the respiratory system also changes, which adapts to the existing circumstances. Depending on which substance becomes abundant, alkalosis or acidosis develops.

There are such types of alkalosis and acidosis, which depend on the causes of their occurrence:

1. Respiratory alkalosis (or acidosis) – the cause is impaired ventilation of the lungs, which reduces CO2 tension.
2. Metabolic alkalosis (or acidosis) is a metabolic disorder. There is an increase or decrease in the amount of volatile substances, which provokes a particular disease.
3. Non-respiratory alkalosis (or acidosis) – observed in the absence of respiratory causes.

Other types of alkalosis are:

• Gas - the cause is hyperventilation of the lungs.
• Non-gas is divided into three types:

1. Excretory – develops against the background of uncontrollable vomiting, loss of gastric juice as a result of gastric fistulas, endocrine disorders, long-term use of diuretics.
2. Exogenous - the reasons for its development are the intake of food, which contains a lot of bases, and the administration of sodium bicarbonate.
3. Metabolic - develops after surgery, against the background of rickets or a hereditary disorder of electrolyte metabolism in children.

• Mixed - a combination of gas and non-gas alkalosis.

Metabolic alkalosis

A decrease in the amount of chlorine and hydrogen in the extracellular space leads to the development of metabolic alkalosis. It is diagnosed by the presence of a large amount of bicarbonate and elevated pH. Severe cases are accompanied by the following symptoms:

• Strong headache.
• Tetany.
• Lethargy.

Treatment will consist of addressing the root cause of metabolic alkalosis. They are:

1. Loss of positively charged hydrogen.

The reasons for their occurrence are:

• Pathological changes in the gastrointestinal tract and kidneys.
• Repeated vomiting.
• Gastric drainage.
• Therapy with diuretics.
• Conn's syndrome.
• Potassium starvation.
• Barter syndrome.
• Itsenko-Cushing syndrome.
• Blood transfusion.

When the body loses potassium, calcium is also excreted, which affects the functioning of the heart. Convulsive syndromes develop and neuromuscular excitability increases. A complication of the disease can be failures in enzymatic systems.

Respiratory alkalosis

The appearance of respiratory alkalosis is facilitated by hyperventilation, which can be chronic or acute, which is why the disease also has such types. This significantly reduces the CO2 pressure.

1. Moderate hypercapnia is the cause of the development of chronic respiratory alkalosis.
2. Severe hypercapnia is the cause of the development of acute respiratory alkalosis.

Symptoms of respiratory alkalosis include convulsions, lightheadedness, and a state of stupor due to the low amount of blood entering the brain. Arrhythmia appears in those who have heart disease. The disease often occurs in seriously ill people who spend all their time in a supine position.

The first symptoms can be detected when there are disturbances in the cardiovascular or respiratory system. To monitor the condition, you need to be diagnosed by a doctor.

Damage to the nervous system leads to a persistent form of respiratory alkalosis. Another cause of the disease may be mechanical ventilation. Here are the signs:

• Numb lips.
• Nausea.
• The appearance of paresthesia.
• Feeling of tightness in the chest.

Respiratory alkalosis may signal the onset of sepsis even before obvious signs appear.

Symptoms of alkalosis

How can you recognize the onset of alkalosis? According to the symptoms he exhibits. They are:

1. Brain ischemia. Because of this, the patient becomes anxious, excited, dizzy, quickly gets tired of communication, paresthesia of the limbs appears, attention and memory deteriorate.
2. Pallor of the skin, appearance of gray cyanosis.
3. Rare breathing - 40-60 breaths per minute.
4. Tachycardia, pendulum-like rhythm of tones, small pulse.
5. , the appearance of orthostatic collapse when taking a vertical position.
6. Diuresis and dehydration.
7. The appearance of seizures.
8. Epilepsy is possible due to disorders of the nervous system.

Metabolic alkalosis rarely shows clear symptoms. They are often blurred and are as follows:

• Edema.
• Respiratory depression.
• Pasty.

Decompensated alkalosis can be recognized by the following symptoms:

1. Thirst.
2. Minor hyperkinesis.
3. Weakness.
4. Headache.
5. Lack of appetite.
6. Dry skin and decreased turgor.
7. Rare and shallow breathing.
8. Apathy.
9. Drowsiness.
10. Retardation of consciousness.

Metabolic alkalosis in Barter syndrome can be identified by the following signs:

• Decreased appetite.
• Aversion to dairy products.
• Scratching on the skin.
• Weakness and apathy.
• Accumulation of salts in the conjunctiva, kidney tubules, cornea.

Alkalosis in children

The appearance of alkalosis in children is not news to doctors. The lability of metabolic processes in a small organism often leads to this disease, as the site notes.

Metabolic alkalosis often develops after birth trauma, with intestinal obstruction and pyloric stenosis.

Heredity plays an important role in whether a child will have alkalosis. Often, children are genetically transmitted to a disorder in the transport of chlorine in the gastrointestinal tract. In this case, an analysis is made of stool, which contains a lot of chlorine, and urine, where it may be completely absent.

Gas alkalosis develops against the background of toxic syndrome and viral respiratory diseases, fever, meningitis, brain tumors, encephalitis, pneumonia, and head injuries.

Gas alkalosis of the compensated type often develops after mechanical ventilation during resuscitation. However, over time the disease goes away. It is also observed after poisoning with various drugs. Parents are advised here to remove all medications from the child's sight.

An acute calcium deficiency will result in the following symptoms:

• In children - sweating, trembling limbs, convulsions.
• In older children - tinnitus, tingling and numbness in the hands. Neuropsychotic signs appear at a late stage of the disease.

Causes of alkalosis

The types of alkalosis have already been discussed above, which are divided depending on the causes of the disease. That’s right: alkalosis develops for several reasons:

• Metabolic alkalosis develops against the background of the body losing a large number of hydrogen ions. This can be facilitated by drug treatment, repeated vomiting, and drainage in the stomach. We should also not forget about metabolic diseases such as Barter syndrome, Itsenko-Cushing syndrome, adrenogenital syndrome and Conn syndrome. Often observed in the postoperative period and in children with rickets.
• Exogenous alkalosis develops after large doses of sodium bicarbonate. This may be done accidentally or after long-term treatment of the disease. It can also be caused by a poor, uniform diet, when a large amount of bases enters the body.
• Decompensated alkalosis develops against the background of loss of chlorine by the body. This can be caused by high temperature and lack of fluid in the body.
• Mixed alkalosis is observed with brain injuries. Here there is a mixture of symptoms of gas and non-gas alkalosis:

1. Dyspnea.
2. Vomit.
3. Increased neuromuscular excitation.
4. Blood pressure drop.
5. Decreased heart rate.
6. The appearance of hypertonicity, which leads to convulsions.
7. Constipation.
8. Deterioration of breathing.
9. Decreased performance.
10. Weakness up to confusion and even loss of consciousness.

Treatment of alkalosis

The occurrence of alkalosis prompts immediate hospitalization of the patient. No treatment with folk remedies is carried out here. Only with neurogenic hyperventilation, which occurs against the background of a hysterical state or nervous shock, can hospital treatment be excluded.

Already right on the spot, the patient must be calmed by eliminating the traumatic situation and creating a favorable environment. For severe heart palpitations, medications are given (Corvalol or Validol). They help to calm down, come to one’s senses and normalize the state.

Treatment is based on eliminating the disorders that have occurred in the body. In case of high hypocapnia, carbogen inhalation is prescribed. For convulsions, an injection of calcium chloride into a vein is necessary. During the administration of the drug, the patient will feel fever, which should be reported to him.

For hyperventilation, Seduxen is given. This drug is not given to older people or those with severe illness. Also, it is not taken by children under 6 months, and at older ages it is given in minimal quantities.

If there are signs of hypokalemia, Panangin is injected into a vein, followed by a solution of potassium chloride. Also shown are a solution of insulin and glucose, Spironolactone. For liver pathologies, amino acids are prescribed.

For any type of disease, ammonium chloride is administered. Diacarb is prescribed if too many alkalis were introduced during treatment.

In addition to the main treatment of alkalosis, the symptoms that developed as a result of the disease (diarrhea, nausea, etc.) are eliminated. Here physiological solutions (for example, saline) are prescribed. The chlorine content is increased by introducing potassium chloride solution and HCI solution.

Treatment of alkalosis in premature babies is carried out by administering ascorbic acid orally. Other drugs are not used, which is not necessary.

Lifespan

Alkalosis is a fatal disease because it is an imbalance of substances within the body that respond and participate in the processes of various organs. If the balance of substances is disturbed, the functioning of individual organs is disrupted, which provokes various diseases. Life expectancy here becomes insignificant due to the development of serious pathologies and serious diseases.

The doctors' prognosis is comforting if the patient turns to them for help. There are many effective drugs that help eliminate alkalosis. The result is complete recovery, if the disease is not hereditary or congenital.

It is almost impossible to prevent the development of alkalosis. Only a nutritious and varied diet, timely treatment of all diseases and staying in environmentally friendly places can protect against the development of diseases. However, alkalosis cannot be avoided if the cause is genetic inheritance or congenital diseases.

It is a consequence of alveolar hyperventilation and hypocapnia (decrease in pCO 2 below 35 mm Hg). Causes acute respiratory alkalosis: 1) hyperventilation during hypoxia (pneumonia, severe anemia, congestive heart failure, pulmonary embolism, asthma), stay at high altitudes; 2) stimulation of the respiratory center (diseases of the central nervous system - stroke, tumor; poisoning with salicylates, carbon monoxide); 3) hyperventilation during mechanical ventilation.

A decrease in pCO 2 during gas alkalosis reflexively leads to a drop in blood pressure, as well as to a spasm of the cerebral arteries, up to an ischemic stroke. With prolonged hyperventilation, collapse phenomena may occur. Hypocalcemia developing under conditions of alkalosis causes an increase in neuromuscular excitability and can lead to convulsive phenomena (tetany). Patients often experience anxiety, dizziness, paresthesia, cardiac arrhythmias (the result of hypokalemia); in severe cases, confusion and fainting are observed.

Chronic respiratory alkalosis - This is a state of chronic hypocapnia that stimulates a compensatory renal response, resulting in a significant decrease in plasma (maximum renal response takes several days to manifest).

Scheme 2. Mechanisms of compensation for respiratory alkalosis

The most important mechanism for compensating for hypocapnia is a decrease in the excitability of the respiratory center, leading to CO 2 retention in the body.

Compensation is carried out mainly due to the release of protons from tissue non-hydrocarbonate buffers. Hydrogen ions move from cells to the extracellular space in exchange for potassium ions (hypokalemia may develop) and form carbonic acid when interacting with HCO 3. The release of protons from cells can cause the development of intracellular alkalosis. The consequence of hypoxia with established hyperventilation is the development of metabolic acidosis, compensating for the pH shift.

Long-term compensation for developed alkalosis is associated with the renal compensation mechanism: the secretion of protons decreases, which is expressed by a decrease in the excretion of organic acids and ammonia. Along with this, reabsorption is inhibited and the secretion of bicarbonate is stimulated, which helps to reduce its level in the blood plasma and return the pH to normal (Scheme 2).

BB and SB indicators decrease with compensation of gas alkalosis. BE is usually within normal limits or may be reduced.

Principles of correction of respiratory alkalosis: elimination of hyperventilation. In compensated and subcompensated conditions, no additional interventions are required. In case of decompensation, additional measures are necessary to eliminate metabolic disorders in tissues.

Non-gas acidosis

The most dangerous and most common form of CBS violations. Most often it develops with the accumulation of non-volatile metabolic products in the blood and a primary decrease in bicarbonates due to excessive formation of non-volatile organic acids, which leads to a decrease in the pH of the intracellular environment of the body. BB, SB, BE indicators are reduced.

Metabolic acidosis. Causes : a) lactic acidosis and increased levels of PVK in tissues (various types of hypoxia), liver damage, increased physical activity, infections, etc.); b) acidosis due to the accumulation of other organic and inorganic acids (extensive inflammatory processes, burns, infections, injuries, etc.); c) ketoacidosis (type 1 diabetes mellitus, complicated by ketosis; fasting, liver dysfunction, fever, alcohol intoxication, etc.).

Excretory acidosis.Causes : a) renal (delay of organic acids in renal failure - diffuse nephritis, uremia, hypoxia of kidney tissue, sulfonamide intoxication); b) intestinal, gastroenteral (loss of bases) - diarrhea, small intestinal fistulas; c) hypersalivation (loss of bases) - stomatitis, nicotine poisoning, toxicosis of pregnant women, helminthiases; d) potassium-sparing diuretics.

Exogenous acidosis.Causes : a) long-term consumption of food and drink containing large amounts of acids (for example, malic, citric, hydrochloric, salicylic); b) taking drugs containing acids and their salts (for example, aspirin, calcium chloride, lysine, HCl, etc.); c) poisoning with methanol, ethylene glycol, toluene; d) transfusion of large quantities of blood replacement solutions and liquids for parenteral nutrition, the pH of which is usually below 7.0.

Scheme 3. Mechanisms of compensation for non-gas acidosis

* In case of excretory acidosis, they are ineffective.

Clinical manifestations of non-gas acidosis depend on the underlying pathological process and the severity of the impairment of CBS and may be sharp And chronic. In acute non-gas acidosis, a decrease in blood pCO 2 due to hyperventilation leads to a decrease in the excitability of the respiratory center, and Kussmaul respiration, characteristic of diabetic, hepatic or uremic coma, may appear. There is a decrease in blood pressure, arrhythmias, confusion and the onset of coma. With a significant increase in the concentration of potassium ions in the blood (hyperkalemia) and with a low content in the myocardium, ventricular fibrillation of the heart may develop, which is facilitated by increased secretion of catecholamines by the adrenal glands, stimulated by ↓ pH.

Most often chronic non-gas acidosis observed in chronic renal failure, when the kidneys are unable to excrete acids with an increase in their production or consumption, [HCO - 3] in patients in the final stage of the disease is usually reduced to 12–20 mmol/l.

Chronic non-gas acidosis may present with weakness, malaise, and anorexia associated with the underlying disease.

The principles of correction of non-gas acidosis: depend on the cause that caused it and are aimed at restoring the bicarbonate reserve and potassium homeostasis. At acute non-gas acidosis: introduction of trisamine or Na + bicarbonate with a decrease in pH to 7.12 and below; replenishment of K+ deficiency when it decreases; mechanical ventilation; treatment of the underlying disease: a) for diabetic ketoacidosis - insulin and fluid; b) for alcoholism - glucose, salts; c) for diarrhea - correction of water and electrolyte metabolism; d) in case of acute renal failure - hemodialysis or peritoneal dialysis, etc.

At chronic non-gas acidosis: treatment of the underlying disease (DM, alcoholism, heart, liver, kidney failure, poisoning); administration of bases when the level of bicarbonate in the blood plasma is less than 12 mmol/l or pH 7.2 or lower ( per os NaHCO 3 tablets); correction of water-electrolyte metabolism; hemodialysis or peritoneal dialysis; improvement of microcirculation in tissues ( per os glucose, vitamins, proteins); in case of renal failure, administration of hydrocarbonate buffer solutions under pH control (if less than 7.2); improvement of microcirculation in tissues ( rer os glucose, insulin, vitamins, proteins); symptomatic treatment. With oliguria and parenteral administration of Na + bicarbonate, pulmonary edema may develop.