Principles of correction of metabolic acidosis. What is acidosis and how is it treated? What happens if acidosis of the blood

Depending on the presence or absence of unmeasured anions in plasma, metabolic acidosis is distinguished with a large and normal anion gap. Causes of metabolic acidosis include accumulation of ketone bodies, kidney failure or consumption of drugs or toxins (large anion gap), and loss of HCO 3 through the gastrointestinal tract or kidneys (normal anion gap).

This condition occurs either with excessive production of acids by the body, or with insufficient elimination by the kidneys.

Causes of metabolic acidosis

Large anion gap:

Normal anion gap (hyperchloremic acidosis):

Metabolic acidosis is the accumulation of acids due to their increased formation or consumption, reduced excretion from the body, or loss of HCO 3 - through the gastrointestinal tract or kidneys. When the acid load exceeds the capacity of respiratory compensation, acidemia develops. The causes of metabolic acidosis are classified by their effect on the anion gap.

Acidosis with a large anion gap. The most common causes of large anion gap acidosis are:

• ketoacidosis;
• lactic acidosis;
• kidney failure;
• poisoning with toxins.

Ketoacidosis is a common complication of type 1 diabetes, but it also develops with chronic alcoholism, malnutrition, and (less commonly) starvation. Under these conditions, the body uses free fatty acids (FFA) instead of glucose. In the liver, FFAs are converted into keto acids - acetoacetic and β-hydroxybutyric (immeasurable anions). Ketoacidosis is sometimes observed in congenital isovalerian and matilmalonic acidemia.

Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulates as a result of its increased formation in combination with reduced utilization. Excess lactate production occurs during anaerobic metabolism. The most severe forms of lactic acidosis are observed in various types of shock. Reduced lactate utilization is characteristic of liver dysfunction due to a local decrease in its perfusion or due to generalized shock.

Renal failure contributes to the development of acidosis with a large anion gap due to a decrease in acid excretion and impaired reabsorption of HCO 3 - . The large anion gap is due to the accumulation of sulfates, phosphates, urate and hippurate.

Toxins can be metabolized to form acidic products or induce lactic acidosis. A rare cause of metabolic acidosis is rhabdomyolysis; it is believed that the muscles at the same time directly release protons and anions.

Acidosis with normal anion gap. The most common causes of normal anion gap acidosis are:

• loss of HCO3- through the gastrointestinal tract or kidneys;
• violation of renal excretion of acids.

Metabolic acidosis with a normal anion gap is also called hyperchloremic acidosis, since Cl - is reabsorbed in the kidneys instead of HCO 3 - .

In many secrets of the gastrointestinal tract (for example, in bile, pancreatic juice and intestinal fluid) there is a large amount of HCO 3 -. Loss of this ion through diarrhea, gastric drainage, or fistulas can cause acidosis. During ureterosigmoidostomy (implantation of the ureters into the sigmoid colon during their obstruction or removal of the bladder), the intestine secretes and loses T 3 - in exchange for Cl present in the urine - and absorbs ammonium from the urine, which dissociates into ammonia. In rare cases, the loss of HCO 3 - causes the intake of ion exchange resins that bind this anion.

In different types of renal tubular acidosis, either the secretion of H + 3 - (types 1 and 4) or the absorption of HCO 3 - (type 2) is impaired. Impaired acid excretion and a normal anion gap have also been reported in early renal failure, tubulointerstitial nephritis, and carbonic anhydrase inhibitors (eg, acetazolamide).

Symptoms and signs of metabolic acidosis

Symptoms and signs are mainly due to the cause of metabolic acidosis. Mild acidemia itself is asymptomatic. With more severe acidemia, nausea, vomiting, and general malaise can occur.

Severe acute acidemia is a predisposing factor for cardiac dysfunction with a fall in blood pressure and the development of shock, ventricular arrhythmias, and coma.

Symptoms are usually non-specific, and, therefore, differential diagnosis of this condition is necessary in patients who underwent intestinal plastic surgery of the urinary tract. Symptoms develop over time and may include anorexia, weight loss, polydipsia, lethargy, and fatigue. There may also be pain behind the sternum, increased and rapid heartbeat, headache, changes in mental status, such as severe anxiety (due to hypoxia), changes in appetite, muscle weakness and bone pain.

Diagnosis of metabolic acidosis

• Determination of HAC and serum electrolytes.
• Calculation of the anion gap and its delta.
• Application of Winter's formula to calculate compensatory changes.
• Finding out the reason.

Finding out the cause of metabolic acidosis begins with the calculation of the anion gap.

The reason for the large anion gap is obvious; otherwise, a blood test is needed to determine glucose, urea nitrogen, creatinine, lactate, and probable toxins. Most laboratories measure salicylates, but not methanol or ethylene glycol. The presence of the latter is indicated by the osmolar gap. The calculated serum osmolarity is subtracted from the measured osmolarity. Although an osmolar gap and mild acidosis may be due to ethanol, the latter is never the cause of severe metabolic acidosis.

If the anion gap is normal, and there is no obvious cause of acidosis (eg, diarrhea), then determine the electrolytes in the urine and calculate the anion gap of the urine: + [K] - . Normally (including patients with GI losses), the anion gap of urine is 30–50 meq/L. Its increase indicates a renal loss of HCO 3 - . In addition, in metabolic acidosis, the anion gap delta is calculated to detect concomitant metabolic alkalosis and, using Winter's formula, it is determined whether respiratory compensation is adequate or reflects a second acid-base imbalance.

When using a segment of the small or large intestine, hyperchloremic metabolic acidosis may develop. When part of the stomach is used, hypochloremic metabolic acidosis may develop.

The diagnosis is made on the basis of arterial blood gas parameters, while the pH will be low (<7,35). Избыток оснований может быть меньше чем 3 ммоль/л. Кроме этого, важными являются данные анализа венозной крови, показывающие уровень электролитов, бикарбоната (низкий, <20 ммоль/л), хлоридов, показателей функций почек, концентрации глюкозы в крови, а также результаты общего анализа крови. Анализ мочи необходим для определения ее кислотности/защелачивания, а также наличия кетоновых тел. Следует рассчитать анионную разницу по формуле: (Na + + К +) - (С1 + + HCO 3 -), которая должна быть в норме (<20) при адекватном отведении мочи.

Treatment of metabolic acidosis

• Eliminate the cause.
• In rare cases, the introduction of NaHCO 3 is indicated.

The use of NaHCO 3 - in the treatment of acidemia is indicated only in some circumstances, and in others it can be dangerous. When metabolic acidosis is due to loss of HCO 3 - or accumulation of inorganic acids, administration of HCO 3 - is generally safe and adequate. However, when the acidosis is due to the accumulation of organic acids, there is no clear evidence that would indicate a decrease in mortality with the introduction of HCO 3 - associated with many risks. In the treatment of the underlying disease, lactate and keto acids are converted back into HCO 3 - . Therefore, the introduction of exogenous HCO 3 - may cause "overlap", ie. development of metabolic alkalosis. In many conditions, the introduction of HCO 3 - can also cause an overload of Na and volume, hypokalemia and (due to inhibition of the activity of the respiratory center) hypercapnia. In addition, since HCO 3 - does not diffuse through cell membranes, its administration does not lead to the correction of intracellular acidosis and, moreover, it can paradoxically worsen the condition, since part of the administered HCO 3 - is converted into carbon dioxide, which penetrates into cells and is hydrolyzed with the formation of H + and HCO 3 - .

Despite these and other risks, most experts still recommend IV HCO 3 - in severe metabolic acidosis in order to achieve a pH of 7.20.

Such treatment requires two preliminary calculations. The first is to determine the amount to which the level of HCO 3 - should be increased; the calculation is carried out according to the Cassirer-Bleich equation, taking the value of H + at pH 7.2 equal to 63 nmol / l: 63 \u003d 24xPCO 2 /HCO 3 - or the desired level of HCO 3 - \u003d 0.38xPCO 2 The amount of NaHCO 3 - that needs to be entered to reach this level is calculated as follows:

The amount of NaHCO 3 - (make) \u003d (desired - measured) x 0.4 x body weight (kg).

This amount of NaHCO 3 is administered over several hours. Serum pH and NaHCO 3 - should be determined every 30 minutes - 1 hour, allowing time to equilibrate with extravascular HCO 3 - .

Instead of NaHCO 3 - you can use:

• tromethamine - an amino alcohol that neutralizes acids formed during both metabolic (H +) and respiratory acidosis;
• carbicarb - an equimolar mixture of NaHCO 3 - and carbonate (the latter binds CO 2 to form HCO 3 -);
• dichloroacetate, which enhances lactate oxidation.

The benefits of all these compounds have not been proven, and they have their own negative effects.

It is necessary to frequently determine the level of K + in serum in order to timely diagnose its decrease, which usually occurs with metabolic acidosis, and, if necessary, administer KCl orally or parenterally.

Provided that the patient can be treated on an outpatient basis, acidosis is corrected with sodium bicarbonate tablets.

At a pH value of less than 7.1, an intravenous infusion of a hypertonic sodium bicarbonate solution [two 50 ml ampoules of 8.4% NaHCO 3 (50 mEq)] is indicated with strict control of the arterial blood gas composition. This therapy should be carried out under the supervision of a nephrologist and resuscitator. In case of hypokalemia, potassium citrate should be added.

lactic acidosis

Lactic acidosis develops with hyperproduction of lactate, a decrease in its metabolism, or both.

Lactate is a normal by-product of glucose and amino acid metabolism. The most severe form of lactic acidosis, type A, develops with hyperproduction of lactate, which is necessary for the formation of ATP in ischemic tissues (02 deficiency). In typical cases, excess lactate is formed by insufficient tissue perfusion due to hypovolemic, cardiac or septic shock and is further increased by slowing lactate metabolism in a poorly supplied liver. Lactic acidosis is also observed in primary hypoxia due to pulmonary pathology and in various types of hemoglobinopathies.

Type B lactic acidosis develops under conditions of normal overall tissue perfusion and is a less dangerous condition. The reason for the increase in lactate production may be local relative hypoxia of the muscles during their increased work (for example, during physical exertion, convulsions, trembling in the cold), malignant tumors and the intake of certain medicinal or poisonous substances. Such substances include reverse transcriptase inhibitors and biguanides - phenformin and metformin. Although phenformin has been discontinued in most countries, it is still used in China.

An unusual form of lactic acidosis is D-lactate acidosis, caused by the absorption of D lactic acid (a carbohydrate metabolism product of bacteria) in the colon in patients with jejunoileal anastomosis or after bowel resection. This substance is stored in the blood because human lactate dehydrogenase only breaks down lactate.

Diagnosis and treatment of lactic acidosis types A and B are similar to those for other types of metabolic acidosis. In D-lactate acidosis, the anion gap is less than expected for the present reduction in HCO 3 - ; the appearance of an osmolar gap in the urine (the difference between the calculated and measured urine osmolarity) is possible. Treatment consists of fluid resuscitation, carbohydrate restriction, and (sometimes) antibiotics (eg, metronidazole).

Acidosis is a condition characterized by an increase in acidity and a decrease in blood pH less than 7.35 (normal blood pH is 7.35-7.38).

In other words, this is a violation of the acid-base balance of the body, in which the organic acids contained in the tissues and in the blood are either not removed quickly enough or are produced in excess.

Causes

It should be understood that acidosis is always the result of another disease. This means that it should not be considered as an independent disease, but as a symptom.

Acidosis can appear in the following situations:

Fever.
When the body temperature reaches 38.5, metabolic processes in the body begin to proceed differently. So, due to high temperature, the metabolism of proteins, fats and carbohydrates is accelerated, in the process of transformation of which acids are produced. After formation, acids are released into the bloodstream, which causes the phenomenon of acidosis.

Pregnancy.
During the intrauterine development of the fetus, the same metabolic processes occur in its organs and tissues as in the mother's body. This means that during the growth of the fetus, there are more organic acids in the blood of a pregnant woman, which causes a state of acidosis.

Starvation.
In order to maintain the normal functions of organs and systems, during fasting, the body begins to process the previously accumulated reserves of nutrients. Since the organic acids produced during their metabolism are able to combine and be excreted from the body with substances supplied with food, their concentration in the blood increases sharply during fasting.

Diabetes .
Since diabetes mellitus disrupts the metabolism of carbohydrates, in some severe cases there is an accumulation of acids in the tissues and in the blood, which can lead to acetonuria (the presence of acetone in the urine), keto-acidotic coma. Also, acidosis can occur during hypoglycemic coma due to an overdose of insulin.

Respiratory failure.
The appearance of acidosis in patients with respiratory failure is associated with an increase in the partial pressure of CO 2 in the blood, due to a decrease in lung ventilation. Also, long-term exposure to high concentrations of CO 2 leads to acidosis.

Heart failure with symptoms of circulatory failure in the small circle (chronic left ventricular failure). Heart failure of this type leads to an increase in blood pressure in the vessels of the lungs, which causes edema, a decrease in gas exchange and the development of acidosis.

Kinds

Compensated acidosis (pH 7.35)

Subcompensated acidosis (pH level 7.25-7.34)

Decompensated (pH less than 7.25)

Acidosis symptoms

The main symptoms of acidosis:

• Weakness, drowsiness. These symptoms are explained by the inhibitory effect of excess organic acids on the structures of the central nervous system.
• Nausea. As well as weakness, it is caused by inhibition of the structures of the central nervous system.
• Feeling of suffocation, smell of acetone from the mouth. This is due to the fact that excess organic acids are able to be excreted from the body through the lungs, in the form associated with gas molecules.

Diagnostics

The only way to laboratory diagnose the state of acidosis is to measure the pH of the blood (blood pH).

Normally, the value of this indicator is 7.35-7.38. It is important to understand that at a pH level of 7.35 (although the figure is at the lower limit of the norm), so-called compensation processes can already occur in the body, in which the excretory systems operate in an increased load mode.

This means that if the cause of acidosis is not eliminated, in the near future the compensatory mechanisms will weaken, and the stage of subcompensation will begin (pH 7.25-7.35), at which a general deterioration in the condition will occur.

Finally, pH values ​​less than 7.25 indicate the onset of a decompensation stage, in which the body can no longer cope with the excretion of excess organic acids and coma may occur.

In addition to measuring the pH level, the state of acidosis is indirectly indicated by:

• Increasing the partial pressure of CO 2
• Decrease in standard bicarbonate (SB)
• Reduced base excess (BE)

Treatment of acidosis

Since acidosis is never an independent disease, its etiological treatment is to eliminate the underlying disease.

There is also symptomatic therapy aimed at alleviating the patient's condition. It includes the appointment of drinking plenty of water and ingestion of soda (from 5 to 40 g per day, depending on the current pH value).

It is important to understand that such symptomatic treatment in some cases can cause an exacerbation of the underlying disease (for example, heart failure), so that only the doctor treating the underlying disease can prescribe adequate treatment.

Complications and prognosis

Acidosis is a manifestation of metabolic disorders in the body, often associated with serious diseases.

Therefore, if the cause of its appearance is not eliminated, the amount of organic acids in the blood will constantly increase, depleting compensatory mechanisms, which can ultimately lead to a coma.

A shift in the acid-base balance with an increase in acidity and a decrease in the pH of the body's media characterizes its pathological conditions, united by a common definition - acidosis.

The etiology of this condition is based on the accumulation and complexity of removing organic acid oxidation products from the body.

Causes

The presence of a large accumulation of acidic products in acidosis can be caused by various reasons.

Factors affecting the development of acidosis can be both external and internal. External causes of acidosis include inhalation of air or vapors with a high content of carbon dioxide.

Internal causes include functional disorders of the body systems that affect metabolic processes and the excretion of products of organic acids.

The reasons for the development of acidosis can be certain processes in the body: diabetes mellitus, circulatory disorders, tumor processes, pregnancy, hypoglycemia, hypoxic conditions of various origins, disorders in the activity of the kidneys, intoxication, starvation, side effects of medications, etc. In some cases, obvious reasons, leading to the appearance of acidosis are not determined.

Regardless of the cause that caused it, acidosis adversely affects the entire body of the patient. The worst prognosis for severe acidosis is shock or death.

The consequences of acidosis can be dehydration of the body, blood clotting, thrombosis, unstable blood pressure, myocardial infarction, liver, spleen, etc., functional disorders in the blood circulation of the brain and the flow of metabolic processes in it, i.e. the state of acidosis entails a violation of the activity of all vital organs.

Types of acidosis

The type of mechanism for the appearance of acidosis determines three types of acidosis: respiratory, non-respiratory and mixed type of acidosis.

Non-respiratory acidosis is classified in turn into several subspecies:

• A condition characterized by impaired renal function, accompanied by a lack of excretion of acids from the body, is called excretory acidosis.
• The most severe and complex condition, expressed by a significant accumulation of endogenous acids, refers to metabolic acidosis.
• The intake of a significant amount of a substance, which is then processed into acids, is referred to as an exogenous form of acidosis.

There is a classification of types of acidosis according to the level of pH. In this case, compensated, subcompensated and decompensated acidosis are determined.

Compensated acidosis is characterized by an insignificant change in the pH and the ratio of the sodium salt of carbonic acid to the components of the carbonate buffer. With compensated acidosis, with the help of hyperventilation of the lungs, a significant part of carbon dioxide and hydrogen ions are removed from the body, which cause a shift in the acid-base balance to the acid side.

As a response, with compensated acidosis, the kidneys also begin to intensively excrete hydrogen ions in the urine, and the process of reabsorption of sodium bicarbonate in the tubules increases.

The absence or lack of compensatory actions in the body provokes the development of decompensated acidosis.

The ratio of carbonic acid and sodium bicarbonate in decompensated acidosis changes significantly, and the pH decreases.

Metabolic, the most common acidosis, is subdivided into hyperchloremic acidosis, lactic acidosis and diabetic.

In hyperchloremic acidosis, the acid-base balance is disturbed due to the high content of chlorine in the blood plasma. This disruption results in a deficiency or total loss of sodium bicarbonate. The causes of hyperchloremic acidosis can be diseases of the kidneys, intestines, the introduction of ammonium chloride or hydrochloric acid into the body.

Lactic acidosis develops as a result of an excess of lactic acid in the body. Violations of the production of enzymes, unstable supply of muscles and tissues with blood or oxygen are the main causes of lactic acidosis. Often this type of acidosis develops against the background. The cause of lactic acidosis can be malnutrition, the presence of an excess of meat, flour products in it, and the lack of fresh vegetables and fruits in the diet.

Diabetic acidosis appears as a complication of diabetes mellitus and indicates the presence of hyperglycemia and ketonemia. An increased content of lactic or p-hydrobutyric acid is found in the patient's blood. In diabetic acidosis, there is an acute shortage of carbohydrates in the cells of the body. This is the most severe manifestation of acidosis. The reason for it may be the untimely taking of the necessary drugs or infection of the body with diabetes. The consequence of diabetic acidosis may be coma or death of the patient.

Symptoms and diagnosis of acidosis

Mild forms of acidosis do not give any characteristic clinic. Differentiating acidosis from other diseases is quite difficult, because. symptoms of acidosis do not indicate the development of disorders of the acid-base balance in the body. The presence of general malaise, mild nausea, vomiting, shortness of breath and palpitations, high blood pressure, disturbances in the functioning of the central nervous system should be alarming and serve as a reason for contacting a medical institution.

Diagnosis of acidosis is carried out on the basis of an analysis of the results of the arterial blood pH, for analysis, blood is taken at the wrist from the radial artery. To determine the causes of acidosis in the blood, the amount of carbon dioxide and bicarbonate is checked. In the study of anamnesis, for the diagnosis of acidosis , the previous condition and illnesses of the patient are taken into account.

Diagnosis of acidosis is also carried out on the basis of the pH level in the urine, serum electrolytes and blood gases are examined. Other tests are done to determine the cause of the acidosis.

Acidosis correction

Considering that acidosis is not an independent disease, but occurs as a result of other disorders, the correction of acidosis is primarily aimed at treating the underlying disease or regulating dysfunctions in the body.

To correct acidosis of metabolic origin, intravenous fluid is prescribed, and treatment of the underlying pathology.

Sodium bicarbonate in combination with glucose or sodium chloride is used in severe cases of acidosis.

Symptomatic treatment is used for mild acidosis. Dialysis is used in cases of acute poisoning of the body.

Prevention of acidosis

For the prevention of acidosis, it is necessary to carefully approach the issue of a balanced diet and the timely treatment of existing diseases. White bread, eggs, cheeses, meats, animal fats, eaten without restrictions, do more harm than good. Therefore, to prevent acidosis, it is necessary to use these products in moderation. Do not abuse coffee and alcohol. It is advisable to consume as many vegetables and fruits in raw form as possible.

Indispensable conditions for the prevention of acidosis are preventive visits to the doctor and careful treatment of already acquired diseases.

metabolic acidosis- a pathological condition characterized by a high level of acidity of the circulating blood, caused by a decrease in the plasma concentration of bicarbonate or the accumulation of acids other than carbonic. Integral indicators of metabolic acidosis are a decrease in blood pH below 7.35 and a concentration of standard bicarbonates (SB) less than 21 mmol/l. Metabolic acidosis is the most common and most severe form of acid-base disorder (ABS).

Etiology of metabolic acidosis

1. Accumulation of acidic products in metabolic disorders:
   a) ketoacidosis (diabetes mellitus, hypoxia, prolonged fasting, liver pathology, alcohol intoxication, prolonged fever);
   b) lactic acidosis (heart failure, shock conditions, hypoxia, severe infections, liver pathology);
   c) accumulation of acids during the activation of catabolism (massive injuries, burns, extensive inflammatory processes).
2. Accumulation in the body of acidic products in violation of their excretion (acute and chronic renal failure, shock).
3. Significant loss of bicarbonate with intestinal juice (with diarrhea).
4. Increased intake of acidic foods with food, poisoning with acids and certain drugs (salicylates, ethanol, methanol, etc.).

Most often, metabolic acidosis is observed in decompensated diabetes mellitus, liver failure, prolonged starvation, acute hypoxia of any origin, including after cardiac arrest.

Compensation for metabolic acidosis

The key role in the compensation of metabolic acidosis belongs to pulmonary hyperventilation and hydrocarbon buffer. Excess hydrogen ions are neutralized when interacting with the main component of the hydrocarbonate buffer (NaHCO 3) with the formation of carbonic acid, which quickly dissociates into CO 2 and H 2 O. As a result of hyperventilation of the lungs, excess CO 2 is quickly excreted from the body. In this case, the metabolic acidosis is said to be compensated by respiratory alkalosis.

The protein buffer also plays a certain role in the binding of hydrogen ions. The kidneys and liver can also participate in compensation mechanisms, only if the pathology of these organs did not cause the development of acidosis. Part of the protons goes into the bone tissue in exchange for sodium and calcium ions.

With metabolic acidosis, intense and rather dynamic shifts occur in the ionic composition of plasma and cells. However, it should be borne in mind that the exchange of potassium, sodium, calcium, magnesium, chlorine and other ions mainly depends on the nature of the underlying disease, the state of water-salt metabolism, the functional state of the kidneys, liver and other organs. Therefore, the correction of the concentration of ions in the blood should be strictly individual.

Clinic of metabolic acidosis

According to the degree of compensation, compensated and decompensated acidosis are distinguished. Compensated acidosis is characterized by a change in the absolute amounts of the components of the carbonate buffer, while the ratio of the sodium salt of carbonic acid to carbonic acid remains within the normal range (20:1) and the blood pH does not change significantly. With decompensated acidosis, not only the absolute amount of sodium bicarbonate and carbonic acid changes, but also their ratio, resulting in a decrease in blood pH.

The main indicators of the severity of metabolic acidosis
(average summary data)

Clinically mild acidosis may be asymptomatic. With a decrease in pH to 7.2 (decompensation), respiration increases markedly. With a further decrease in pH, the activity of the respiratory center is suppressed, the myocardium is inhibited, and the sensitivity of receptors to catecholamines decreases. The performance of the heart decreases, the minute volume of the heart (MOV) falls, hypoxic encephalopathy occurs, up to the development of a coma.

Principles of correction of metabolic acidosis

Treatment of metabolic acidosis is aimed at correcting the underlying cause. In renal failure, and in some cases, in case of poisoning with ethylene glycol, salicylates or methanol, hemodialysis is prescribed. In general, the principles of correction of metabolic acidosis are as follows:

1. Elimination of the etiological factor (pathology of the respiratory and cardiovascular systems, abdominal organs, etc.).
2. Normalization of hemodynamics - elimination of hypovolemia, restoration of microcirculation, improvement of the rheological properties of blood.
3. Improving pulmonary ventilation (up to the transition to mechanical ventilation).
4. Correction of electrolyte metabolism.
5. Improvement of renal blood flow.
6. Elimination of hypoproteinemia.
7. Improvement of tissue oxidative processes by introducing glucose, insulin, thiamine, pyridoxine, riboxin, ascorbic, pantothenic and pangamic acids.
8. Strengthening the hydrocarbon buffer system.

Sources:
1. Anzimirov V.L., Bazhenova A.P., Bukharin V.A. and etc.; Ed. Yu.M. Pantsyreva / Clinical Surgery: Reference Guide // Medicine, 1988.
2. Sumin S.A. / Emergency conditions // Pharmaceutical world, 2000.

Metabolic acidosis is one of the most frequent and dangerous forms of ASC disorders. Such acidosis can be observed in heart failure, many types of hypoxia, impaired liver and kidney function in the neutralization and excretion of acidic substances, depletion of buffer systems (for example, as a result of blood loss or hypoproteinemia).

causes of metabolic acidosis

Metabolic disorders leading to the accumulation of excess non-volatile acids and other substances with acidic properties.

† Lactic acidosis and increased levels of pyruvic acid in tissues ((for example, with various types of hypoxia: respiratory, cardiovascular, hemic, tissue; prolonged intense physical work, during which the formation of UA increases, and its oxidation is reduced due to oxygen deficiency; lesions liver).

† Accumulation of other organic and inorganic acids formed during the development of pathological processes that affect large arrays of tissues and organs. The development of this variant of metabolic acidosis is observed with extensive burns of the skin and mucous membranes; various types of inflammation (for example, with erysipelas, peritonitis, purulent pleurisy); massive injuries (for example, with prolonged crush syndrome, multiple body injuries).

† Ketoacidosis (due to acetone, acetoacetic and -hydroxybutyric acids), as a rule, is observed in patients with diabetes; with prolonged fasting, especially with a deficiency of carbohydrates; with prolonged febrile conditions; alcohol intoxication; extensive burns and inflammation.

Lack of buffer systems and physiological mechanisms to neutralize and remove excess non-volatile acids from the body.

TYPICAL CHANGES IN AFR

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

Typical directions of changes in indicators of acid-base balance (capillary blood) in all non-gas acidosis:

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

Compensation mechanisms for metabolic acidosis

Compensation mechanisms for metabolic acidosis according to the speed of their activation and duration of functioning are divided into urgent and long-term (Fig. 13–5).

Rice. 13–5. Compensation mechanisms for metabolic acidosis.

Urgent Mechanisms for Reversal of Metabolic Acidosis

Urgent mechanisms for eliminating metabolic acidosis are to activate:

Bicarbonate buffer system of intercellular fluid and blood plasma. This system is able to eliminate even significant acidosis (due to its large buffer capacity).

Bicarbonate buffer of erythrocytes and other cells. This occurs with a significant acid load on the body.

Protein buffer system of cells of various tissues. It is observed in conditions of significant accumulation of non-volatile acids in the body.

Bicarbonate and hydrophosphate buffers of bone tissue.

Respiratory center, which provides an increase in the volume of alveolar ventilation, rapid removal of CO 2 from the body and often normalization of pH. It is significant that the "buffer capacity" of the external respiration system under conditions of metabolic acidosis is approximately two 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 metabolic acidosis compensation

Long-term mechanisms of metabolic acidosis compensation are implemented mainly by the kidneys and to a much lesser extent with the participation of bone tissue buffers, liver and stomach.

renal mechanisms. With the development of metabolic acidosis, the following are activated:

† ammoniogenesis (main mechanism),

† acidogenesis,

† secretion of monosubstituted phosphates (NaH 2 PO 4),

† Na + ,K + ‑exchange mechanism.

Collectively, renal mechanisms provide an increase in H + secretion in the distal renal tubule and bicarbonate reabsorption in the proximal nephron.

The participation of bone tissue buffers (bicarbonate and phosphate) in chronic acidosis also remains.

Hepatic compensation mechanisms consist in the intensification of ammonia formation and gluconeogenesis, detoxification of substances with the participation of glucuronic and sulfuric acids and their subsequent removal from the body.

The chronic course of metabolic acidosis is also characterized by an increase in the formation of hydrochloric acid by the parietal cells of the stomach.

Due to the activation of these mechanisms, metabolic acidosis can be compensated: the pH does not fall below 7.35. However, in case of insufficiency of buffer systems and physiological mechanisms to eliminate the shift in the acid-base balance, the pH of the blood drops beyond the normal range. In these cases, significant disorders of the body's vital functions are possible, including the development of coma.