What is metabolic acidosis and what causes it. Acidosis: main causes, symptoms and treatment Decompensated metabolic acidosis

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Metabolic acidosis is characterized by the accumulation in the body as a result of a metabolic disorder of an excess amount of persistent (non-volatile) acids.

The main causes of the development of metabolic acidosis.

Increased acid formation:

• keto acids in diabetes mellitus, prolonged fasting and alcohol intoxication;
• lactic acid in shock and tissue hypoxia;
• sulfuric acid with increased catabolism (postoperative period, prolonged fasting);
• increased absorption of chlorides in patients with ureterointestinal anastomosis.

Violation of the excretion of acids (uremic acidosis):

• chronic glomerulonephritis;
• primary or secondary wrinkled kidney;
• shock kidney.

Excess loss of bicarbonate:

• fistulas of the duodenum or small intestine, gallbladder;
• diarrhea;
• ulcerative colitis.

Excessive administration of sodium chloride:

• iatrogenic disorder associated with excessive infusion of a number of solutions.

Diagnosis of metabolic acidosis is based on the study of indicators of the acid-base state. Only in advanced cases, especially in patients with ketoacidosis, a significant decrease in pH is manifested by shortness of breath (Kussmaul breathing), which is aimed at reducing the concentration of carbon dioxide, and the diagnosis of an acid-base disorder can be made "at a distance". When examining acid-base parameters, metabolic acidosis is indicated by a decrease in BE< -2,3 и НСОЗ < 22 ммоль/м. Ниже приведены примеры компенсированного и декомпенсированного метаболического ацидоза.

With compensated metabolic acidosis, no special therapeutic measures are required. With decompensation, in order to increase the pH of the plasma, it is necessary to administer alkaline solutions. Sodium bicarbonate is prescribed to increase the capacity of the plasma bicarbonate buffer. The required dose of a 1-molar solution (8.4%) is calculated by the formula:

BE x body weight x 0.3

It should be remembered that the introduction of sodium bicarbonate is accompanied by an increased formation of carbon dioxide, to remove which, if the patient is undergoing mechanical ventilation, it is necessary to correct its parameters. An excess of sodium bicarbonate can lead to the development of iatrogenic alkalosis.

Trometamol is also used to correct metabolic acidosis. The introduction of this drug binds hydrogen ions and removes them through the kidneys. Part of the drug penetrates through the cell membrane into cells, which allows for the treatment of intracellular acidosis. The appointment of this tool is possible only with normal kidney function. In addition to the administration of sodium bicarbonate and trometamol, the treatment of metabolic acidosis should include correction of the low CO syndrome, optimization of oxygen delivery to organs and tissues, correction of water and electrolyte balance disorders, carbohydrate metabolism, improvement of microcirculation, and adequate infusion therapy.

Saveliev V.S.

Surgical diseases

The body is a very complex system consisting of various parts: organs, tissues, cells. And if there is a failure at some level, then the functioning of the whole organism will certainly be disrupted.

For example, if the amount of acids (they are certainly present in tissues, blood) increases, then acidosis will occur. What are its symptoms? And how should effective treatment be carried out?

Acidosis is not a disease in itself, but a condition that occurs as a result of an imbalance in the acid-base balance of the body.

Every body contains acids, they are necessary for its functioning. And in the normal state, these same acids should be excreted, which provides a balance.

But if this does not happen for some reason, then they will accumulate in the blood, urine and even in some organs. Alarming symptoms will certainly tell about this. It is worth noting that the treatment should be timely, since strong oxidation is not normal, it can lead to sad consequences.

There are several varieties of this disease. For example, if we take the mechanism of state development as the basis for classification, then we can distinguish the following types:

• Respiratory acidosis occurs due to insufficient removal of carbon dioxide during breathing. It turns out that it accumulates in the blood and changes its composition.
• Non-respiratory acidosis occurs due to the accumulation of non-volatile acids in the blood, which for some reason are not excreted, but remain in the body.

There is also a mixed form, in which both carbon dioxide and non-volatile acids accumulate.

Non-respiratory acidosis can also be classified:

• Metabolic. This is the most common and at the same time complex form, in which endogenous acids begin to accumulate in the tissues of the body, disrupting their functioning. The symptoms are the most pronounced, immediate treatment is required.
• Excretory. It occurs in case of violation of the excretory function of the body, for example, in renal failure.
• Exogenous. Its main reason is the intake of an excess amount of such substances into the body, which in the process of processing turn into acids and begin to accumulate, not having time to be excreted.

Depending on the concentration of acids (it is determined by the pH level), there are:

• If the pH level is close to the lower limits of the norm, compensated acidosis is diagnosed. In this state, a person may not be aware of such changes for a long time, but they will gradually (sometimes over several years) disrupt the functioning of the body.
• With a slight excess of normal values, we are talking about a subcompensated form.
• With a significant excess of the norm, they speak of a decompensated form. Usually the symptoms are obvious, the consequences can be sad, so immediate and competent treatment is required.

Causes

Such a state cannot develop unreasonably. There are many negative factors that can provoke acid-base imbalance:

Manifestations

Symptoms of a disease such as acidosis, with a mild form of the disease or at its initial stage, may not appear in any way and do not bother. And sometimes they are expressed only in signs of the underlying disease, which led to the accumulation of acids and the development of this condition.

But it is important to recognize the manifestations in time in order to start treatment and avoid serious consequences, one of which is coma, and subsequently death.

Here are the symptoms to watch out for:

Diagnostics

You can identify acidosis with the help of blood and urine tests, since their composition will certainly change.

How to treat?

With a disease such as acidosis, immediate treatment is required, since in severe cases a fatal outcome is likely. So if there are alarming symptoms, consult a doctor immediately.

Here are the main steps:

1. Elimination of the cause of the development of the condition, that is, the treatment of the underlying disease or the elimination of pathologies. For example, diabetes mellitus requires the introduction of insulin. If the ventilation of the lungs is impaired, then it will be carried out artificially. You will also need to drain the lungs, remove sputum (suction) and take expectorants.
2. You have to follow a certain diet. The patient should consume more berries, vegetables, fruits, cereals, plant products. And strong tea and coffee, alcohol, fried, flour, smoked, pickled, sweet and salty should be abandoned.
3. The blood must be cleansed of toxins and acids. Plasmapheresis may be required.
4. In some cases, dialysis is effective.
5. In severe forms, fluid is administered intravenously, as well as sodium bicarbonate. If the patient can drink on his own, he should do so. It is effective to take soda dissolved in water.
6. If necessary, symptomatic treatment is carried out.

Acidosis is curable if measures are timely. Health to you!

The main cause of this variant of acidosis is a violation of tissue metabolism with the formation of an excess amount of non-volatile endogenous acids (lactic acidosis, ketoacidosis). When oxygen delivery is disturbed, cell metabolism is rebuilt to the path of anaerobic glycolysis with intracellular accumulation of hydrogen ions due to the formation of organic and inorganic acids. Metabolic acidosis is often associated with a primary metabolic disorder, such as diabetes, fasting, fever, hypoxia due to circulatory disorders.

lactic acidosis develops with excessive formation of lactic acid or a decrease in its excretion from the blood. The most common cause of it is a violation of the processes of anaerobic oxidation during tissue hypoxia in patients in the postoperative period, pancreatitis, leukemia, anemia. Acidosis activates cellular cathepsins, protein breakdown increases, and the content of free amino acids in the blood increases. Lactic acidosis in peripheral blood flow disorders may be a complication of ketoacidosis.

Lactate is formed during the anaerobic metabolism of glucose. Under the right conditions, virtually all tissues can produce lactic acid. Most often, lactic acidosis is transient with shock, postoperative trauma, with intense physical activity, during which there is an imbalance between the delivery of oxygen and the need for it in contracting muscles. The liver and, to a lesser extent, the kidneys utilize lactate, using it in energy metabolism or converting it back into glucose. In most clinical cases, lactic acidosis is associated with inadequate tissue oxygen supply, as in shock or cardiac arrest. Under such conditions, lactic acid production is increased and its clearance is reduced due to poor liver perfusion. In patients with decompensated lactic acidosis in shock with severe tissue hypoxia, a high percentage of deaths is noted.

Lactic acidosis may be associated with disorders in which there is no tissue hypoxia. Such variants of acidosis are described in patients with leukemia, lymphomas, lymphogranulomatosis and other malignant neoplasms, uncorrected diabetes, and severe liver failure. The mechanisms causing acidosis in these conditions are not well understood. In neoplasms, tissue metabolism may locally increase with lactate production, or blood flow to non-carcinomatous cells may be obstructed. In most cases, there is an extensive tumor lesion of the liver. It is possible that it is a violation of liver function that causes the accumulation of lactate in the blood. Lactic acidosis also often develops in unrecognized ischemia or infarction of the intestine, as well as in patients with heart failure receiving vasoconstrictors.

Various drugs that inhibit mitochondrial function can also cause life-threatening lactic acidosis. Drugs that can have this effect include biguanides used to treat diabetes mellitus and antiviral nucleoside analogues used to treat acquired immunodeficiency syndrome (AIDS).

Lactic acidosis can be observed when there is a violation of the delivery and utilization of oxygen by tissues (shock, heart failure, severe anemia, defects in mitochondrial enzymes or their inhibition by carbon monoxide and cyanides), as well as excessive formation or insufficient utilization of L-lactate (glycogenoses, epileptic seizures, diabetes mellitus). , alcohol intoxication.Ethanol causes a slight increase in lactic acid, but with alcohol intoxication, clinically significant lactic acidosis does not develop, unless there are other complications, such as liver failure., liver failure, malignant neoplasms).

Lactic acidosis may be due to the accumulation in the blood of D-lactate (a product of the metabolism of intestinal bacteria) in blind loop syndrome and intestinal obstruction. In these cases, unabsorbed carbohydrates enter the colon, where they are converted to D-lactic acid by an overgrowth of Gram-positive anaerobes. These patients experience intermittent episodes of metabolic acidosis, which are triggered by carbohydrate-rich foods. Manifestations include confusion, cerebral ataxia, slurred speech, and memory lapses. They may show symptoms of intoxication. Treatment includes the use of antimicrobials to reduce the number of D-lactate-producing microorganisms in the gut, along with a carbohydrate-restricted diet.

Lactic acidosis can also be associated with hereditary metabolic disorders: glucose-6-phosphatase deficiency or other congenital diseases with a defect in gluconeogenesis or pyruvate oxidation. Lactic acidosis can develop with a weakening of oxidative metabolism in mitochondria. Lactic acidosis has been described in genetic mitochondrial disorders in which lactic acid builds up. One such disease, referred to as MELAS, includes mitochondrial encephalopathy (ME), lactic acidosis (LA), and stroke-like episodes (S). Children with this pathology do not complain during the first years of life, but then motor and cognitive development disorders begin to appear. Mitochondrial defects also lead to growth retardation, seizures, and recurrent strokes. During therapy, a decrease in the level of lactic acid in plasma in children with severe lactic acidosis can lead to a pronounced clinical improvement.

With normal liver function, self-compensation of lactic acidosis occurs, since 50% of it is utilized in the liver.

The clinical picture of severe lactic acidosis is characterized by depression of consciousness (from stunning to stupor), tachycardia, hypotension, frequent deep "acidotic" breathing, impaired peripheral circulation, and, often, oligo-or anuria. With acidosis, resistance to the vasoconstrictive action of catecholamines develops, which leads to the development of stasis and impaired microcirculation, aggravating hypoxia. A decrease in pH below 7.2 can lead to a decrease in cardiac output.

Under the influence of hypoxia and acidosis, the level of kinins in plasma and extracellular fluid increases, which causes vasodilation and a sharp increase in the permeability of the vascular wall. Increased catabolism in acidosis leads to overhydration by increasing the production of endogenous water. Due to the fact that the mucous membranes of the gastrointestinal tract and respiratory tract are involved in the excretion of protons, it is possible to develop acidotic laryngotracheobronchitis, bronchiolitis and alveolitis, gastroesophagitis with prolonged cough, vomiting, sometimes with an admixture of blood.

Fig.10. Scheme of lactic acidosis.

Ketoacidosis develops with incomplete oxidation of free fatty acids, which are formed in excess with increased lipolysis and a decrease in the formation of triglycerides in the liver due to the low activity of the acylcarnitine transferase enzyme. Keto acids (acetoacetic and β-hydroxybutyric), formed in the liver from fatty acids, are a source of energy in many body tissues. Hyperproduction of ketoacids occurs when there is an insufficient supply of carbohydrates or the inability to use available carbohydrates in energy metabolism. Under these conditions, fatty acids are mobilized from adipose tissue and enter the liver, where they are converted into ketones. Ketoacidosis develops when the production of ketones exceeds the ability of tissues to use them.

The most common cause of ketoacidosis is decompensated diabetes mellitus.

Diabetic ketoacidosis (DKA) ranks first among the acute complications of endocrine diseases. Mortality in DKA reaches 6-10%. In diabetic ketoacidosis, keto acids accumulate in the blood: acetoacetate and β-hydroxybutyrate. DKA results from an absolute or relative deficiency of insulin, which can develop over hours or days.

In patients receiving insulin injections, the causes of DKA may include:

- the appointment of inadequate (too low) doses of insulin;

- Violation of the regimen of insulin therapy;

- a sharp increase in the need for insulin: infectious diseases (sepsis, especially urosepsis, pneumonia, other respiratory and urinary tract infections, meningitis, sinusitis, cholecystitis, pancreatitis, etc.), concomitant endocrine disorders (thyrotoxicosis, Itsenko-Cushing's syndrome, acromegaly , pheochromocytoma), myocardial infarction, stroke, trauma, surgical interventions, drug therapy (glucocorticoids, estrogens, including oral contraceptives), pregnancy, stress (in all these cases, an increase in insulin demand is due to an increase in the concentration of contrainsular hormones - adrenaline, cortisol, glucagon and growth hormone, as well as tissue resistance to insulin).

Due to the increasing deficiency of insulin in the body, there is a depletion of liver glycogen, an increase in gluconeogenesis, and a decrease in glucose utilization by tissues. The increase in insulin deficiency is largely facilitated by the simultaneous decrease in the number of receptors and their sensitivity to insulin in peripheral tissues. This leads to significant hyperglycemia and glycosuria. The development of hyperglycemia is due not only to insulin deficiency in the body, but also to excessive secretion of glucagon, which stimulates gluconeogenesis and glycogenolysis. Due to hyperglycemia, the osmotic pressure in the extracellular fluid increases and the process of cellular dehydration develops. A decrease in the content of glycogen in the liver causes an increase in the mobilization of fat from the depot, followed by its entry into the liver. This eventually leads to fatty liver, and subsequently to ketosis, which exacerbates insulin deficiency. The consequence of hyperketonemia and ketonuria is a violation of water-salt metabolism - a decrease in the content of sodium, phosphorus, calcium, potassium, magnesium and chlorides in the blood. The level of potassium in the blood is initially elevated and then lowered, which is associated with increased excretion of it in the urine. Sometimes early hypokalemia is possible , which is caused by massive destruction of cells, their loss of potassium and its intensive excretion with urine. This, in turn, leads to dehydration and a shift of acid-base balance towards acidosis.

Fig.11. Mechanisms of development of ketoacidosis.

The role of contrainsular hormones:

- adrenaline, cortisol and growth hormone suppress insulin-mediated utilization of glucose by muscle tissue;

- adrenaline, glucagon and cortisol increase glycogenolysis and gluconeogenesis;

- adrenaline and growth hormone enhance lipolysis and suppress residual secretion of insulin.

Clinical picture DKA

The most common symptoms are polydipsia, polyuria, weakness; the severity of these symptoms depends on the degree and duration of hyperglycemia. Patients may complain of lack of appetite, nausea, vomiting, abdominal pain associated with ketonemia, which can mimic various surgical diseases. Hypokalemia and hypocaligistia can cause atony of the smooth muscles of the gastrointestinal tract, and, as a result, intestinal obstruction and acute dilatation of the stomach, which leads to severe vomiting.

Hyperventilation is also characteristic due to an increase in the depth of breathing; when the pH drops below 7.2, Kussmaul breathing usually occurs, accompanied by the smell of acetone. Tachycardia often occurs. In the absence of severe dehydration, hypotension is absent. Hypothermia is usually observed. There may be hyporeflexia caused by hypokalemia. In severe diabetic ketoacidosis, arterial hypotension, stupor, coma are observed.

Another cause of ketoacidosis is stage 2 fasting. From the 2nd - 3rd day of complete fasting, due to the mobilization of large amounts of fat from the depot and the formation of ketone bodies, transient ketosis occurs, which does not require treatment, since under conditions of hypoglycemia and hypoinsulinemia, cells begin to use ketones as the main energy substrate. There may be signs of acidosis - headache, dizziness, nausea, weakness, insomnia. In therapeutic starvation in this case, enterally alkaline solutions are prescribed.

Alcoholic ketoacidosis occurs in patients with chronic alcoholism after a sharp cessation of ethanol. It is usually caused by vomiting, malnutrition due to anorexia, hypovolemia (a decrease in the volume of extracellular fluid). In acute alcohol intoxication and chronic alcoholism, the processes of β-oxidation of fatty acids can also be activated. Due to an increase in the ratio of NADP / NAD, ketone bodies accumulate in the blood, mainly β-hydroxybutyrate (for the same reason, a slight lactic acidosis is possible), which then turns into acetoacetic acid.

Violations of the acid-base balance in metabolic acidosis are caused by the movement of ions from the cell to the interstitial sector and vice versa. More than 90% of the movements relate to potassium, sodium, chlorine, hydrogen, bicarbonate ions.

In response to an increase in the concentration of protons in the blood plasma and, accordingly, a decrease in the pH value, an excess of protons is bound by bicarbonate and protein buffer systems. Hydrogen ions move inside the cell, where the protein (including hemoglobin) buffer is a proton acceptor. The potassium released by the buffer is released into the plasma (a phenomenon of biological cell injury), transient hyperkalemia occurs with concomitant progressive hypocaligistia. Potassium is intensively excreted in the urine, daily hyperkaliuria can exceed the norm by 4-5 times. Due to this, within 4-5 days, under the conditions of the presence of acidosis, the potassium content in the plasma is normalized, then hypokalemia develops.

For every 3 potassium ions leaving the cell, 2 sodium ions and one hydrogen ion move into it (transmineralization of the cell). This leads to aggravation of cellular acidosis and restructuring of enzyme systems. Hypernatremia causes cellular overhydration.

Compensation mechanisms in metabolic acidosis, they are aimed at reducing the concentration of hydrogen ions and are carried out by extra- and intracellular buffer systems, lungs and kidneys. In plasma, the content of bicarbonate decreases due to the depletion of the bicarbonate buffer.

An increase in proton concentration causes stimulation of the respiratory center, hyperventilation and tachypnea develop, pCO 2 of the extracellular fluid decreases until it becomes sufficient to equalize H 2 CO 3 / HCO 3 - (with a decrease in HCO 3 - by 2 mEq / l pCO 2 is compensatory decreases by 1.3 mm Hg). When the pH drops below 7.2, Kussmaul respiration may develop. However, respiratory compensation cannot fully normalize the proton concentration, since it is the high level of [H + ] that stimulates the respiratory center. In addition, the increased work of the respiratory muscles contributes to the additional formation of carbon dioxide. In case of failure of the respiratory mechanisms (respiratory diseases, violations of the central regulation of respiration, etc.), rapid compensation is impossible, severe mixed acidosis develops with a sharp decrease in pH and an almost unchanged content of bicarbonate.

The renal mechanism of metabolic acidosis compensation is activated later, after 16-18 hours from the onset of exposure to the damaging factor. The mechanism is aimed at enhancing proton excretion and plays an important role only in patients with unchanged renal function. In the kidneys, the processes of acido- and ammoniogenesis are enhanced, as well as replenishing the deficiency of plasma bicarbonate due to its formation and reabsorption. Enhanced reabsorption of bicarbonate ions leads to active excretion of chlorine (HCO 3 ˉ Cl - ions are reciprocal), hypochloremia develops.

In the liver, the processes of deamination of amino acids are activated, lactate and pyruvate are involved in the metabolism, thereby reducing the level of acid-reactive products.

Laboratory indicators of metabolic acidosis

Decreased plasma pH

Reducing the values ​​of pCO 2 , AB, SB, BB

BE shift in the negative direction

A sharp drop in urine pH (below 4.0)

Hyperkalemia (in the initial stage), followed by subsequent hypokalemia

Hypochloremia

Hypernatremia

Therapy metabolic acidosis includes, first of all, the elimination of the causes leading to respiratory hypoxia (the fight against hypoventilation, oxygen therapy, assisted breathing, if necessary, intubation and transfer of the patient to mechanical ventilation).

The next important point is the fight against circulatory disorders (elimination of hypovolemia, anemia, improvement of the rheological properties of blood, microcirculation, treatment of heart failure).

Intravenous administration of alkaline solutions: sodium bicarbonate, sodium lactate, lactasol, trisamine, acesol. Sodium bicarbonate is used in severe acidosis (pH below 7.2) to improve myocardial contractility and increase lactate utilization. However, since sodium bicarbonate activates phosphofructokinase, its use may paradoxically exacerbate acidosis by increasing lactate production.

The amount of sodium bicarbonate is calculated using the buffer base deficiency formula (DBD).

DBO = 0.3 BE body weight (mmol)

The question of the use of alkaline solutions in moderate acidosis has not yet been resolved. The introduction of sodium bicarbonate can lead to arterial hypertension and pulmonary edema due to increased venous tone and oliguria. If it is possible to eliminate the cause of acidosis, then the introduction of bicarbonate can lead to the development of alkalosis.

The question of the advisability of using bicarbonate to eliminate acidosis in DKA has not yet been resolved, since its use causes undesirable effects:

– In DKA, due to the loss of phosphorus, the level of 2,3-diphosphoglycerate in erythrocytes decreases, and as a result, the oxyhemoglobin dissociation curve shifts to the left (oxygen binds more strongly to hemoglobin). Acidosis shifts the dissociation curve to the right (Bohr effect), so that oxygen supply to tissues is not disturbed. Bicarbonate again shifts the dissociation curve to the left, and tissues receive less oxygen.

– With proper treatment (infusion therapy plus insulin), ketone bodies are converted to bicarbonate and administration of additional bicarbonate can cause alkalosis.

– Commercially available bicarbonate solutions are hyperosmolar and can increase already high plasma osmolality.

– Treatment with bicarbonate can cause neurological complications ranging from confusion to coma. HCO 3 - anions, combining with H + ions, form carbonic acid. When it dissociates, CO 2 and water are formed. CO 2 easily penetrates the blood-brain barrier and causes acidification of the cerebrospinal fluid (bicarbonate itself practically does not penetrate into it). Therefore, the normalization of plasma pH may be accompanied by paradoxical acidosis in the CNS, which leads to neurological disorders.

The use of bicarbonate is justified in the following cases:

- if DKA is complicated by severe lactic acidosis;

- if there is severe acidosis (pH less than 6.9), especially complicated by shock, which is not amenable to infusion therapy aimed at increasing cardiac output (0.9% NaCl solution, plasma, albumin).

With an increase in pH to 7.1-7.15, bicarbonate is canceled.

Trisamine is used for excess sodium in the blood and unchanged kidney function. The effect of trisamine is based on the free penetration of the drug into the cell and the correction of intracellular acidosis. It has side effects: promotes the migration of potassium from the cell, can cause hypoglycemia and hypocalcemia.

The calculation is made according to the formula:

Number of solution = body weight (kg) BE

Lactate is less commonly used. Its use will be effective if the patient has preserved oxidative processes in the cell. If there is hypoxia, then lactic acid will accumulate in the blood.

One of the important problems in the treatment of metabolic acidosis is the correction of electrolyte disturbances, in particular, the exchange of potassium and chlorine. As acidosis resolves with fluid resuscitation and insulin administration in DKA, potassium is re-introduced into cells and serum levels decrease, which can cause hypokalemia. Hypokalemia causes severe complications (eg, life-threatening ventricular arrhythmias). If there is no urinary retention, potassium replacement is started simultaneously with fluid therapy. If the level of potassium is initially elevated, it is prescribed only after its concentration in the serum is normal. Potassium doses are adjusted based on ECG data and clinical and laboratory findings of hypokalemia.

A 22-year-old man, who has been suffering from insulin-dependent diabetes mellitus for 15 years, had nausea and vomiting for three days. He complained of marked thirst and frequent urination. The patient had Kussmaul breathing.

pO 2 94 mm Hg

pCO 2 25 mm Hg

SB 6.8 mmol/l

BB 25.0 mmol/l

The level of glucose in the blood is 23.0 mmol/L.

Clinical and laboratory findings are typical of decompensated diabetic ketoacidosis. A low concentration of bicarbonate, a pronounced shift of buffer bases in the negative direction, hyperventilation with a sharp decrease in pCO 2 indicate the presence of metabolic acidosis with partial respiratory compensation.

For the normal functioning of the body, it is necessary to maintain all its functions in a state of balance. This applies not only to the level of hormones, the activity of the sympathetic and parasympathetic nervous systems, but also the acid-base composition of the blood. Normally, the amount of substances with low and high acidity (abbreviated as pH) are in a certain balance. Due to this, the blood has a slightly alkaline environment. With an increase in the concentration of alkalis, a person develops "alkalosis", with an increase in acids - "acidosis".

Metabolic acidosis develops in various diseases that are not associated with damage to the respiratory system. It cannot arise on its own and is always a complication of some other disease. You can get all the necessary information about the causes, symptoms and methods of treating this condition from this article.

Why is acidosis dangerous?

This is a serious complication that can occur due to severe infections, against the background of diabetes, in violation of the functions of the liver, kidneys, and in a number of other pathologies. "Acidification" of blood causes a number of additional disorders in the functioning of organs and tissues, among which the most dangerous are:

• Damage to cells throughout the body. A large amount of free acids corrodes the outer membrane of cells, which leads to a violation of their functions. Since toxins are carried to all organs and tissues, pathological changes can be very diverse;
• Respiratory disorders. Oxygen in the body is an alkali, in its chemical role. Therefore, patients are characterized by deep frequent breathing - this is how the body tries to reduce acidity. Unfortunately, this process leads to a narrowing of the cerebral vessels and an increase in blood pressure. As a result, the human condition only worsens and increases the risk of hemorrhages in various organs;
• An increase in blood pressure. The mechanism of occurrence is associated with the presence of respiratory disorders;
• Damage to the digestive organs. In most patients, acute metabolic acidosis causes abdominal pain, stool disorders, and other dyspeptic phenomena. With this violation, aggressive substances such as acetone and hydroxybutyric acid are often formed, which corrode the mucous membrane of the stomach, esophagus and intestines. In some cases, patients even bleed from these organs;
• Oppression of consciousness. Toxins produced by the body negatively affect the nerves and medulla. With a mild course, the patient may experience irritability, weakness, drowsiness, and with a severe one, coma;
• Violation of the heart. Damage to cells and nervous tissue, imbalance of trace elements and a number of other factors inevitably affect the myocardium. In the first stages, this influence can be manifested by frequent and strong heartbeat, rhythm disturbances. In severe pathology, heart contractions weaken and become more rare. The final stage is cardiac arrest.

All of these violations can not only worsen well-being, but also pose a threat to life. That is why the first signs of the disease must be detected and treated as early as possible.

Types of metabolic acidosis

Diagnosing a specific form of pathology is very important - this allows not only to find out the cause of its development, but also to determine the optimal medical tactics. At the moment, doctors use 2 main classifications that help make a diagnosis.

The first reflects the connection with diabetes. It is necessary to find out if the patient has this disease before starting treatment, since metabolic acidosis in diabetes mellitus has its own characteristics. His therapy necessarily includes the correction of glucose (sugar) levels. Without this nuance, any other medical procedures will be ineffective.

The criterion for the second classification is the type of poisoning of the organism. Various acids can rise in human blood, the most dangerous of which are lactic acid and ketone bodies (acetone, butyric acids). Depending on the "acidifying" substance, there are:

1. Ketoacidosis. In the patient's blood, the presence of hydroxybutyric acids and acetone is noted. It often develops against the background of diabetes, but can also occur with other diseases;
2. lactic acidosis. Accompanied by an increase in the concentration of lactic acid. It can occur with a large number of diseases, including due to disruption of the liver or kidneys, the development of a severe infection, in case of poisoning, etc .;
3. Combined form. It often occurs in people with high sugar levels and in the presence of provoking factors. The latter may include severe stress, physical overload, infectious diseases, and a number of other conditions.

The reasons for the appearance of various forms are somewhat different from each other. They need to be known in order to quickly assume the type of disease and correctly treat metabolic acidosis.

Causes

As mentioned above, this pathology does not occur by itself. This is always a consequence of another disease, which leads to metabolic disorders and the accumulation of toxins. Mechanisms and causes of metabolic acidosis differ in different forms. All the necessary information on this issue is presented in the table below.

View	Causes	The mechanism of development of pathology
diabetic ketoacidosis	This form occurs in patients with diabetes, the course of which has become more severe. The following factors can lead to this: Lack of adequate treatment; Accession of a purulent infection; Severe injury or emergency surgery; Stress; Starvation; Pregnancy; Vascular accidents - strokes or heart attacks; A sharp increase in sugar levels: after eating sweet foods (chocolate or pastries), drinking alcohol, unreasonably reducing the dose of insulin or pharmacological preparations.	The main manifestation of diabetes is a violation of the body's control over glucose levels. Due to damage to certain receptors or a lack of insulin, the body cannot detect the level of sugar, and then constantly increases its amount. The release of glucose into the blood occurs during the breakdown of fats and proteins. By-products of this chemical reaction are toxic acids - acetone and hydroxybutyric acid. Their accumulation leads to a change in the acidity of the blood.
Non-diabetic ketoacidosis	This condition can occur when there is insufficient intake of carbohydrates in the body or when their absorption is impaired. Non-diabetic ketoacidosis develops when: Prolonged fasting; Cyclic Vomiting Syndrome is a hereditary disease that manifests itself with alternating periods of vomiting and complete well-being, without any apparent cause; Profuse and prolonged vomiting due to infections, poisoning, etc.	The lack of carbohydrates in the blood and tissues leads to a lack of energy in all organs. If there are no carbohydrates, the body takes energy from the breakdown of proteins and fats. This leads to the release of toxic substances and the development of ketoacidosis.
lactic acidosis	Some hereditary diseases (von Gierke's disease, MELAS syndrome); Severe infection that occurs with fever over 38 ° C and intoxication (manifested by weakness, fatigue, headache and other symptoms); Poisoning by some pharmacological preparations: diphenhydramine, sweeteners, sodium nitroprusside, iron preparations, etc.; Oncological diseases (cancer, sarcoma); Poisoning by alcohol and surrogates; Lack of liver function in the presence of cirrhosis, hepatitis, sclerosing cholangitis, Wilson-Konovalov disease, Budd-Chiari syndrome; Chronic kidney disease of a severe stage with glomerulonephritis, tubulointerstitial nephritis, in the outcome of hypertension and a number of other diseases.	A certain amount of lactic acid is constantly produced in a healthy body. A significant increase in its amount can occur if its excretion is impaired (for example, if the kidneys are damaged), metabolic disorders, or insufficient oxygen delivery to the tissues. The latter situation may arise due to damage to oxygen carrier cells (erythrocytes) or some hereditary metabolic disorders.

Some doctors additionally highlight the hyperchloremic form, which occurs in conjunction with lactic acidosis. However, according to information from modern scientific publications, chlorine metabolism disorders are a less significant condition. They practically do not affect the tactics of treatment, so now they are not distinguished into a separate species.

Symptoms

This condition does not have any characteristic features. The change in acidity is accompanied by a large number of different symptoms, which can be quite difficult to relate to each other. That is why it is quite difficult to identify the disease at home.

Common manifestations that can be observed in any form of the disease include:

• Constant nausea with vomiting, after which there is no improvement in well-being;
• A sharp weakness that forces the patient to stay in bed;
• The appearance of shortness of breath at rest. A person cannot "breathe", because of which his breathing becomes frequent and deep;
• Paleness of the skin and visible mucous membranes (eyes, mouth and nasal cavity);
• The appearance of cold sweat on the skin;
• Slowing the heartbeat and lowering blood pressure;
• Perhaps the development of convulsions, severe dizziness and loss of consciousness (up to coma).

As we have already said, the change in acidity does not happen by itself. This condition is always preceded by some other disease. Simplistically, we can say that a sharp deterioration in well-being against the background of the disease is often the first symptom. In this case, it is necessary to call an ambulance team, which will assess the situation and, if necessary, hospitalize the patient. In the hospital, the doctors will establish the final diagnosis, conduct the necessary studies and therapeutic measures.

Diagnostics

Conventionally, all studies are carried out with three goals: to assess the level of blood acidity, to determine the type of pathology and to find out the causes of the pathology. For the first purpose, it is enough to conduct one study - to determine the acid-base state. Significantly more diagnostic measures may be required to find out the cause of the pH change.

Acid-base blood test

The simplest and most reliable way to confirm the presence of metabolic acidosis is to conduct this test. This does not require any special preparation from the patient. As needed, blood is taken from the patient from a vein, which is sent to the laboratory. As a rule, the finished result can be obtained within a few hours.

To decipher the results, it is necessary to know the normal values ​​\u200b\u200bof the indicators and their deviations during the disease. This information is presented in the table below:

Index	Norm	Changes in metabolic acidosis	Important to pay attention
pH (acidity)	7,35-7,45	There is a decrease in pH	At a pH of 7.35-7.38 and the presence of symptoms, a diagnosis of compensated metabolic acidosis is made. pH less than 7.35 indicates the development of decompensated acidosis.
PaO 2 - reflects the amount of oxygen contained in the blood.	80-100 mmHg	There are no changes or an increase in PaO 2 is observed.	If, against the background of reduced acidity, there is an increase in the concentration of carbon dioxide and a decrease in oxygen, we are talking about respiratory, and not metabolic acidosis.
PaCO 2 - shows the amount of carbon dioxide in the blood.	35-45 mmHg	There are no changes or a decrease in PaCO 2 is observed.

This analysis is sufficient to confirm the presence of pathology. However, to elucidate its form and cause of development, a number of additional studies are needed.

Determination of the type of pathology

To this end, doctors prescribe to the patient a general urinalysis and a biochemical blood test, which necessarily includes the determination of glucose and lactic acid levels. These two studies allow you to quickly determine the specific type of acid-base disorder.

Determination of the cause

In order to find out the cause, doctors may order a large number of different studies, depending on their assumptions. However, there are tests that are mandatory for all patients with this disease. They allow you to assess the condition of the main organs and systems at the lowest cost. This "diagnostic minimum" includes:

Study	Norms	Possible changes
Clinical blood test	ESR - up to 15 mm/hour The level of leukocytes is 4-9*10 9 /liter. Including: Neutrophils 2.5-5.6 * 10 9 / liter (46-72%) Lymphocytes 1.2-3.1 * 10 9 / liter (17-36%) Monocytes 0.08-0.6*10 9 /liter (3-11%).	A significant increase in the level of ESR and leukocytes can be observed against the background of an infectious process. The predominant increase in neutrophils indicates the bacterial nature of the infection; An increase in the concentration of lymphocytes often indicates a viral disease; An increase in the content of monocytes is often a sign of infectious mononucleosis.
General urine analysis	Density 1015-1026; Blood cells (leukocytes, erythrocytes) 2-3 in the field of view; Protein - less than 0.03 g / l; Cylinders - absent; Glucose is absent.	A decrease in the density of urine and the appearance of pathological impurities in it (cells, cylinders, etc.) may indicate kidney failure - one of the common causes of lactic acidosis.
Biochemistry of blood	Total protein 65-87 g/l; ALT 7-45 IU; AST 8-40 IU; Total bilirubin 4.9-17.1 µmol/l; Creatinine 60-110 µmol/l.	An increase in the level of bilirubin and liver enzymes (ALT, AST) often indicates acute liver damage. An excess of creatinine is usually a sign of severe kidney disease or the development of chronic kidney disease (CKD for short). A decrease in total protein with a slight increase in other indicators may be a sign of chronic liver pathology, such as cirrhosis or chronic hepatitis. A multiple increase in total protein is an indirect sign of multiple myeloma.

In addition to these laboratory diagnostic methods, doctors may recommend ultrasound, magnetic resonance or computed tomography, scintigraphy of individual organs, and a number of other procedures. The decision on the required amount of research is determined individually, depending on the alleged cause of the decrease in acidity.

Principles of treatment

Correction of metabolic acidosis is a rather difficult task even for an experienced doctor. Each patient with a suspected disease is offered to be hospitalized, as they need constant monitoring, regular intravenous infusions of solutions and periodic various studies.

All goals of treatment can be divided into two groups - the restoration of normal blood acidity and the elimination of the cause of the pathology.

pH recovery

First of all, doctors try to find out what disease led to the development of pathology. If it is diabetes, glucose-lowering therapy with insulin and pharmacological preparations begins immediately. With the development of a severe infection, complex treatment is carried out using antibacterial / antiviral drugs. If the decrease in pH has caused severe damage to the organ, the attending physician tries to restore its function or replace them with drugs and instrumental techniques (for example, hemodialysis).

Simultaneously with the above activities, infusion therapy is mandatory - drip intravenous infusion of solutions. The choice of solution is carried out depending on the type:

Form of pathology	Features of infusion therapy	Optimal Solutions
diabetic ketoacidosis	In patients with this condition, it is necessary to replenish the loss of fluid and beneficial trace elements. In this case, solutions containing glucose are contraindicated for use.	Preparations containing electrolytes: potassium, sodium, calcium, magnesium, etc. Sterofundin; Ringer's solution; Trisol; It is also possible to use normal saline (0.9%) and disol.
lactic acidosis	The main goal of therapy is to eliminate the lack of fluid, reduce the concentration of lactic acid and restore the deficiency of alkalis.
Non-diabetic ketoacidosis	This form shows solutions with anti-ketone action. In addition, they must make up for the deficiency of glucose (if any) and fluid.	The optimal drug for therapy (in the absence of contraindications) is a 20-40% glucose solution. Additionally, it is possible to use Rheosorbilact and Xylate preparations, which effectively eliminate acetone and butyric acids from the blood.

Infusion therapy in children is carried out according to the same principles as in adults. The main thing is to correctly determine the cause and variant of the disease. The only difference is in the volume of intravenous fluids - the child needs a much smaller amount of fluids. Doctors calculate the required amount by body weight.

Features of therapy of individual forms

Since different pathological mechanisms operate in each of the forms, some aspects of their treatment differ from each other. In this section, we present the most important principles that should be followed when prescribing therapy:

1. In lactic acidosis, in addition to infusion therapy, B vitamins (thiamine, pyridoxine, cyanocobalamin) must be prescribed every 12 hours. These substances improve metabolism and contribute to the normalization of acidity. To combat the lack of air, patients are given a constant inhalation of oxygen through a mask or nasal cannulas. In severe acidosis, when the level of lactic acid rises 4-5 times, doctors can "purify" the blood - hemodialysis;
2. In ketoacidosis without diabetes, as an addition to standard therapy, it is recommended to prescribe drugs that restore the digestive system (Domperidone, Metoclopramide). This will reduce the loss of fluid with vomiting and improve the digestion of food. Nutrition must be carried out through the mouth (using a gastric tube or frequent fractional feedings). It should be high in calories, high in carbohydrates and low in fat. Also, patients are shown vitamin therapy;
3. In diabetic ketoacidosis, the main method of treatment is the introduction of insulin. Sugar reduction and adequate intravenous fluids are the most effective treatments. After carrying out these activities, in most cases, the pH is restored to normal values ​​and the patient's well-being improves.

Treatment of a child is carried out according to the same principles as the therapy of an adult patient. However, it should be remembered that children are more difficult to tolerate any diseases, and especially those accompanied by a change in acidity. Therefore, timely hospitalization and properly provided medical care are especially important for them.

FAQ

It depends on the cause of the disease. If the patient has diabetes, he is prescribed a table without easily digestible carbohydrates and with a predominant amount of protein food. In contrast, when glucose levels are low (due to non-diabetic ketoacidosis), carbohydrates should become the main component of food to compensate for the lack of energy.

Question:
How long will the treatment of this disease take?

Depends on the severity of the disease and the condition of the patient. The minimum duration of therapy, in most cases, is 2 weeks.

Question:
What are the most common causes of acidosis in newborns?

In the vast majority of cases, this condition develops with various intrauterine pathologies that lead to oxygen starvation of the child and disrupt the supply of nutrients through the placenta. The cause may be premature detachment of the placenta, post-term pregnancy, premature birth, pathologies of the umbilical cord, etc. In this case, both ketoacidosis and lactate accumulation can occur. Treatment of such children is carried out according to the same principles that were described above.

Question:
Is it possible to develop complications after an illness?

Decreased blood pH itself can cause severe damage to the brain, heart, or kidneys. It should also be remembered that the disease that caused it can lead to damage to other organs.

Question:
Are there any distinguishing symptoms of ketoacidosis and lactic acidosis?

Of the characteristic signs, two should be noted: the appearance of the smell of acetone and the rate of development of coma. The appearance of a specific odor from the patient's skin is characteristic only for ketoacidosis, while a patient with impaired lactic acid metabolism smells normal. According to the time of development of coma, one can also assume a variant of the disease - with lactic acidosis, most often, impaired consciousness occurs quickly (within a few hours). While in a patient with a high content of ketone bodies in the blood, consciousness can persist for 12-20 hours.

The acid-base balance is regulated by the body systems, which allows the latter to function normally. When acidosis occurs, we are talking about the development of an acid disorder in the direction of increase, which is the main symptom. Reasons lead to treatment. Metabolic acidosis is considered separately.

If the amount of acid in the body increases, then acidosis develops. The reason is its insufficient excretion from the body and oxidation. This is also facilitated by intestinal disorders, starvation and a feverish state, which leads to the formation of acetoacetic acid, acetone in the urine, and a coma in severe cases.

The site site identifies several types of acidosis:

• compensated type.
• subcompensated type.
• uncompensated type.
• Gas in case of violation of ventilation of the lungs and inhalation of a large amount of CO2.
• Non-gas - is divided into:

1. Metabolic - the accumulation in the tissues of acidic products that are destroyed in the body.
2. Excretory - the absence of excretion of non-volatile acids by the kidneys and an increase in the gastrointestinal tract loss of bases.
3. Exogenous - the intake of a large number of elements involved in the formation of acids.
4. Mixed.

metabolic acidosis

The most common type of acidosis is metabolic. In this form, a lot of acid is produced, which is excreted in very small quantities.

Metabolic acidosis is divided into types:

• Diabetic ketoacidosis, in which there is an excess of ketone bodies in the body.
• Hyperchloraemic acidosis is formed when bicarbonate is lost, for example, after diarrhea.
• Lactic acidosis - the accumulation of lactic acid due to alcohol abuse, strenuous physical activity, malignant tumors, hypoglycemia, the use of certain medications, anemia, convulsions, etc.

Metabolic acidosis manifests itself in the following symptoms:

1. A stunned, soporous or inhibited state.
2. Rapid breathing.
3. Shock and, as a result, death.

This type of disease is diagnosed by a blood test for acid-base balance. Treatment is aimed at eliminating the underlying cause. Sodium bicarbonate or sodium bicarbonate solution is administered intravenously. To avoid the fatal outcome that metabolic acidosis leads to, it should be treated.

lactic acidosis

Lactic acidosis is another common disease in which there is a significant accumulation of lactic acid. Type A is marked by obvious tissue anoxia. Type B practically does not manifest itself.

Type A is more common. Type B manifests itself very quickly, the reasons for which scientists have not yet reliably identified.

Type A lactic acidosis develops due to:

1. Diabetes.
2. epilepsy.
3. Convulsive conditions.
4. Hodgkin's disease.
5. Diseases of the liver and kidneys.
6. Neoplasia.
7. Myelomas.
8. infections.
9. Leukemia.
10. Bacteremia.
11. Generalized lymphoma.

Type B lactic acidosis develops due to exposure to pesticides, toxins, and drugs.

Causes of acidosis

Maintaining a normal acid-base balance is as important a factor as the absence of any infectious diseases. The main causes of acidosis are lifestyle, sedentary day regimen and malnutrition. It also affects the environment in which a person lives.

Nutrition plays a very important role. It seems that only acidic foods contribute to the development of acidosis. In fact, the acid in the body is the result of the breakdown and oxidation of food elements. It is important that the kidneys and lungs work well at the same time. The kidneys help in the elimination of non-volatile elements, and the lungs - volatile ones.

In addition, the metabolism should not be disturbed in the body, and there should also be no chronic diseases that provoke a latent course of acidosis. These include tumors, allergic reactions, neurosis, rheumatism, tissue inflammation, etc.

Acidosis symptoms

Acidosis is often manifested by the symptoms that express the main disease. In a mild form, it may not appear at all. Sometimes it causes nausea, vomiting and fatigue. The severe form is manifested in violations of the frequency and depth of breathing, heart contractions and stupor. Also, the severe form is marked by metabolic disorders in the brain. This leads to constant drowsiness and coma.

The acute form of acidosis is recognized by the appearance of diarrhea and insufficient blood supply to the tissues. Reduced blood flow provokes dehydration, shock, acute blood loss and heart disease.

In children, acidosis may occur due to congenital disease. This affects its development, leads to convulsions and inhibition of character.

The initial stage can be recognized by:

• Weaknesses.
• Headache.
• Drowsiness.
• Lethargy.
• Depression of the nervous system.

The aggravation of acidosis is accompanied by the appearance of:

Increased breathing and heart rate.

Digestive problems: diarrhea, vomiting, nausea, leading to dehydration.

In diabetes, there is a smell of fruits in the mouth, among other signs.

acidosis and alkalosis

are deviations in violation of metabolic processes in the body. Acidosis is an increase in the level of acids. Alkalosis is a deviation towards alkalis.

With a compensated form of diseases, a change in sodium bicarbonate and carbonic acid occurs. In the decompensated form, there is a violation of the amount of acids and alkalis in the direction of an excess of one of the substances.

Quite often, acidosis occurs against the background of non-respiratory causes. This is the accumulation of lactic acid, acetoacetic or hydroxybutyric acid. The accumulation of lactic acid is often noted due to disorders in the functioning of the heart or lungs (oxygen starvation). Also, the disease develops against the background of diarrhea. In this case, the body turns on compensatory functions when there is a balance between acids and alkalis.

Alkalosis and acidosis affect the functioning of the body. Breathing changes, vascular tone decreases, cardiac output and blood pressure decrease. Violated water and electrolyte balance. The bones lose their hardness, gradually there are changes in the work of the heart.

Treatment of acidosis

Since acidosis practically does not manifest itself, the treatment is aimed at eliminating the causes of its occurrence. However, the phenomenon itself is not ignored. Acidosis is treated with protein foods with a mild form of its manifestation. Of the drugs, sodium bicarbonate is prescribed orally for a mild form or intravenously for a severe one. Calcium carbonate is prescribed if it is necessary to limit the amount of sodium and with hypocalcemia.

Metabolic acidosis is treated:

1. sodium bicarbonate.
2. Nicotinic acid.
3. Cocarboxylase.
4. Riboflavin mononucleotide.
5. Glutamic acid.
6. dichloroacetate.

In case of pathologies in the gastrointestinal tract, Rehydration salt, Dimephosphone is taken orally.

The main emphasis is on proper nutrition. During treatment, coffee and alcoholic beverages should be avoided. Fruits, vegetable fats, berries, fresh vegetables are taken along with white bread, pasta, animal fats. It is actively recommended to take a decoction of rice to remove toxins, toxins and other harmful elements.

Forecast

Acidosis affects the functionality of the whole organism. If the acid-base balance is disturbed, then other systems are also disturbed. The heart, lungs and kidneys are mainly affected. However, acidosis often indicates the development of other diseases that affect metabolic disorders. The prognosis depends entirely on therapeutic measures to eliminate the cause and the acidosis itself.

Life expectancy depends on how quickly a person treats acidosis. In some cases, we are talking about a fatal outcome if the patient does not take any measures.