Respiratory acidosis. Acute respiratory acidosis

Respiratory acidosis is a pathological condition due to an increase in the concentration of protons in the extracellular fluid and blood ([H +]), due to a delay in the body of carbon dioxide due to the predominance of the release of CO2 into the internal environment during its formation during metabolism over the release of carbon dioxide during external environment during external respiration.

Respiratory acidosis is indicated by the pH of arterial blood at a level lower than the lower limit of the normal range (7.38), with a carbon dioxide voltage in it greater than 43 mm Hg. Art.

The leading link in the pathogenesis of respiratory acidosis is to reduce the ability of the external respiration system to emit carbon dioxide into the external environment. It is caused by dysregulation in the external respiration system and damage by diseases and pathological processes of its effectors, which, through the action of certain mechanisms, reduce the purification of the alveolar gas mixture from carbon dioxide.

The most common causes of respiratory acidosis are:

1. Chronic lung diseases, which mainly characterize obstructive respiratory disorders. It should be noted that these diseases (bronchial asthma and chronic obstructive bronchitis) lead to respiratory acidosis only at an extreme degree of exacerbation of obstructive alveolar ventilation (external respiration) disorders, which, in particular, occurs in status asthmaticus. In this case, the direct cause of respiratory acidosis is a critical decrease in the number of those respirons in which ventilation is sufficient for the normal cleansing of the alveolar spaces from carbon dioxide. The reason for this is the pathological increase in the resistance of the respiratory tract of the respiratory system, parts and parts of the lungs.

2. A decrease in the strength of contractions of the respiratory muscles as a result of their pathological changes and impaired transmission of excitation in neuromuscular synapses (myasthenia gravis, the action of antidepolarizing muscle relaxants). Weakness of the respiratory muscles as a cause of respiratory acidosis occurs in diseases such as Guillain-Barré syndrome (acute idiopathic demyelinating polyneuropathy), as well as polymyositis and dermatomyositis. In botulism, the cause of respiratory acidosis is a drop in alveolar ventilation due to a botulinum exotoxin blockade of the release of acetylcholine from presynaptic nerve endings at the neuromuscular junction. The action of a similar pathogenetic mechanism leads to respiratory acidosis in patients with Eaton-Lambert syndrome.

3. Inhibition of the functional activity of the inspiratory neurons of the respiratory center as a result of the side effects of narcotic analgesics and other drugs that upset the central regulation of external respiration.

In chronic respiratory acidosis, the duration of which exceeds 48 hours, there is a complete mobilization of all possible compensation mechanisms, as a result of which the kidneys begin to extremely intensively form and retain the bicarbonate anion in the body. Therefore, in chronic respiratory acidosis, in response to an increase in PaCOr, the concentration of bicarbonate anion in the blood plasma increases to a greater extent, and a smaller decrease in pH occurs than in acute respiratory acidosis.

An increase in the tension of carbon dioxide in arterial blood to a level higher than 60 mm Hg. Art., (severe respiratory acidosis) is an absolute indication for mechanical ventilation. Do not wait for acid-base and blood gas data if symptoms suggest severe respiratory acidosis. The extreme severity of respiratory acidosis, in particular, is evidenced by its symptoms such as drowsiness and lethargy. They are associated with an increase in cerebrospinal fluid pressure due to an increase in cerebral blood flow in response to an increase in carbon dioxide tension in arterial blood. As the respiratory acidosis progresses, arterial hypotension is added to its symptoms as a result of acute circulatory failure (Scheme 17.1).

Respiratory alkalosis is a pathological condition due to excessive excretion of carbon dioxide during external respiration relative to the formation of carbon dioxide during metabolism. The development of respiratory acidosis is indicated by a decrease in the carbon dioxide tension in the arterial blood to a level lower than 37 mm Hg. Art., with an increase in pH to values ​​exceeding 7.42.

The leading link in the pathogenesis of respiratory alkalosis is the pathogenically excessive excretion of carbon dioxide by the external respiration system. Metabolic alkalosis is caused by changes in the regulation of external respiration and pathological changes in its effectors, which increase the purification of the alveolar gas mixture from carbon dioxide.

The most common cause of acute respiratory alkalosis is neuroses, in which the intracentric relationship and regulation of external respiration are upset in such a way that the external respiration system begins to excessively eliminate CO2. An abnormally increased release of carbon dioxide reduces its tension in arterial blood, which, in accordance with the Henderson-Hasselbach equation, reduces the concentration of protons in the extracellular fluid, that is, it causes respiratory alkalosis.

Hyperventilation syndrome is the result of an exacerbation of neurosis, in which excessive ventilation of the lungs causes respiratory alkalosis. At the same time, hyperventilation increases in parallel with an increase in anxiety. Anxiety (unmotivated anxiety) becomes extremely pronounced and can be transformed first into lethargy, and then (in a small part of patients) into a state of pre-coma. Preku is characterized by the extreme difficulty of contact with the patient, which is still possible, in contrast to coma. A drop in the pumping function of the heart as a cause of precoma in patients with respiratory alkalosis occurs when the pH of the arterial blood rises to a level of 7.7 and above. Respiratory alkalosis in hyperventilation syndrome leads to a decrease in the contractility of voluntary muscles, which can lead to acute muscle weakness (false paralysis). Other complaints of patients with hyperventilation syndrome include a feeling of difficulty breathing, dizziness without fainting, and numbness of the arms and legs. The electroencephalographic equivalent of the syndrome is bilateral synchronous theta waves, which are replaced by delta waves with periodic peak and slow discharges.

Salicylate poisoning leads to respiratory acidosis through a state of pathologically enhanced excitation of the inspiratory neurons of the respiratory center. In addition, a chronically increased level of excitation of inspiratory neurons can be a consequence of cerebral circulation disorders, brain tumors, infectious lesions of the central nervous system, and also occur as a result of craniocerebral wounds and trauma.

In syndromes (pathological conditions) of sepsis and a systemic inflammatory reaction, respiratory alkalosis is a consequence of persistent excitation of inspiratory neurons due to the supra-segmental effect of cytokines that cause these syndromes when circulating with blood at high concentrations (hypercytokinemia).

Arterial hypoxemia of any origin can be the cause of respiratory alkalosis, which develops due to hyperventilation in response to excitation of peripheral chemoreceptors due to a drop in oxygen tension in arterial blood. This is the mechanism of development of respiratory alkalosis in patients with embolism of the pulmonary artery and its branches, pneumonia, bronchial asthma and other pulmonary diseases. In addition, the cause of respiratory alkalosis in patients with lung diseases is the excitation of the corresponding receptors of the pathologically altered pulmonary parenchyma, bronchi and pleura, which is a stimulus for hyperventilation.

If in patients with respiratory alkalosis the arterial blood pH rises to a level higher than 7.6, then breathing with gas mixtures enriched with carbon dioxide may be advisable for correcting respiratory alkalosis.

Acidosis is one of the forms of acid-base imbalance, in which acidification of the internal environment occurs due to the accumulation of acidic products and hydrogen ions. Normally, these products are quickly removed due to the work of the buffer systems and excretory organs, but in a number of pathological conditions, pregnancy, etc. Acidic foods accumulate, pass into the urine and can lead to coma.

An excess of acids appears with their excessive production or lack of excretion, leading to a decrease in pH and the development of acidosis, which is not an independent disease, but only reflects the development of another pathology and is considered one of the possible complications.

The norm is 7.35-7.38. Deviations from this value are fraught with serious disturbances in homeostasis, the work of vital organs and can even threaten life, therefore the indicator is very carefully monitored in severe pathology of internal organs, in patients of intensive care units, cancer patients, in pregnant women predisposed to such disorders.

The excess of acidic products can be absolute or relative, compensated or uncompensated. Short-term fluctuations in pH are also normal, reflecting an intensive metabolism, exposure to stress factors, etc., however, the acid-base balance quickly returns to normal due to the well-coordinated work of the buffer systems, kidneys and lungs. Such acidosis does not have time to give symptoms and therefore fits into the framework of the physiological adaptive mechanism.

Acidification of the internal environment can occur chronically with errors in nutrition, to which many people, both young and mature, are prone. This type of acidosis can be lifelong, without causing pronounced symptoms or disruption of vital functions. In addition to nutrition, the acidity of the internal environment is influenced by the quality of drinking water, the level of physical activity, psycho-emotional state, hypoxia due to lack of fresh air.

Determination of blood pH level is not included in the list of necessarily determined parameters of vital activity. It is specified when symptoms of acid-base balance disorders appear, most often in patients in intensive care units and intensive care units. It is necessary to treat acidosis immediately, since a decrease in pH is fraught with severe disorders of brain activity, coma and death of the patient.

Causes and types of acidosis

It is important to remember that acidosis is just one of the symptoms, in which finding out the true cause of the disorder is a primary task for specialists.

Acidosis can be caused by:

• Diseases occurring with an increase in body temperature;
• Kidney pathology;
• Prolonged diarrhea;
• Fasting or unbalanced diet;
• The state of pregnancy;
• Violation of pulmonary ventilation in inflammatory processes, cardiac pathology;
• Endocrine metabolic disorders (diabetes mellitus, thyrotoxicosis).

An increase in body temperature that accompanies various pathologies of both infectious and non-infectious nature, accompanied by an intensification of metabolism and the production of special protective proteins - immunoglobulins. If the temperature exceeds 38.5 degrees, the metabolism changes towards catabolism, when the breakdown of proteins, fats and carbohydrates increases, resulting in acidification of the internal environment.

Pregnancy- a special state of the organism of the expectant mother, many of whose organs are forced to work in an enhanced mode. Providing the fetus with nutrients and oxygen requires an increase in the level of metabolism, while the decay products become more not only due to their own, maternal, but also due to those secreted by the fetus growing in the uterus.

Inadequate intake of nutrients is another important factor that provokes acidosis. During starvation, the body seeks to provide itself with energy from the already available reserves - fatty tissue, liver and muscle glycogen, etc. The breakdown of these substances entails a breakdown in acid-base balance with a shift in pH towards acidification due to an overabundance of acidic products by the body itself.

However, not only the lack of food, but also its improper composition also contributes to the growth of chronic acidosis. It is believed that animal fats, salt, carbohydrates, refined foods, with a simultaneous lack of fiber and trace elements, contribute to the development of acidosis.

A significant shift in acid-base balance can occur for respiratory disorders... With a decrease in the volume of pulmonary ventilation in the blood, an excess amount of carbon dioxide accumulates, which will inevitably lead to acidosis. This phenomenon can be observed with pulmonary edema, severe respiratory failure against the background of emphysema or asthma, pneumonia - respiratory acidosis.

Depending on the pathogenetic mechanism of the development of acidosis and the degree of organ dysfunction, there are several varieties acidosis. According to the pH value, it can be:

• Compensated - when the acidity does not go beyond the extreme lower limit of the norm, equal to 7.35, while the symptoms are usually absent;
• Subcompensated - the pH decreases even more, reaches 7.25, signs of dysmetabolic processes in the myocardium in the form of arrhythmias, as well as shortness of breath, vomiting and diarrhea are possible;
• Decompensated - the acidity indicator becomes below 7.24, violations from the outside, the heart, the digestive system, the brain, up to loss of consciousness are clearly expressed.

According to the causal factor, they are distinguished:

1. Gas acidosis- its reasons may consist in a violation of pulmonary gas exchange (pathology of the respiratory system) and then it will be called respiratory (respiratory), as well as in a change in the composition of the air with an excess of carbon dioxide, hypoventilation in case of chest injuries, etc.
2. Non-gas;
3. Metabolic acidosis- develops in violation of metabolic processes, the impossibility of binding or destruction of acidic components of the blood (diabetes mellitus, etc.);
4. Excretory (excretory)- if the kidneys are not able to remove acids dissolved in the blood (renal) from the body, or more than normal is lost from the intestines and stomach, the amount of alkalis is a gastrointestinal variety;
5. Exogenous- when a large amount of acids or substances that can be converted into acids in the process of biochemical reactions in the body are received from outside;
6. Mixed option acidification of the internal environment, in which there is a combination of several mechanisms for the development of pathology. For example, diseases of the heart and lungs, lungs and kidneys, diabetes and simultaneous damage to the kidneys, lungs, intestines, etc.

Metabolic acidosis

One of the most common forms is metabolic acidosis, in which the concentration of lactic, acetoacetic and β-hydroxybutyric acids in the blood increases. It proceeds more severely than other varieties, is accompanied in the blood and a decrease in hemoperfusion in the kidneys.

metabolic acidosis

Diabetes mellitus, thyrotoxicosis, starvation, alcohol abuse and other causes lead to non-respiratory acidosis, and depending on the type of acid that predominantly accumulates in the body, there is lactic acidosis (lactic acidosis) and ketoacidosis characteristic of diabetes mellitus.

With lactic acidosis in the blood increases, with ketoacidosis - metabolic products of acetoacetic acid. Both types can be severe in diabetes and lead to coma, requiring immediate qualified help. Rarely, lactic acidosis develops with excessive physical exertion, especially in people who do not play sports regularly. Lactic acid builds up in the muscles, causing soreness, and in the blood, acidifying it.

Manifestations of acidosis

Symptoms of acidosis depend on the degree of pH shift towards the acidic side. In the case of compensated forms of pathology, a mild course of symptoms does not arise or they are few in number and barely noticeable, however, with an increase in the amount of acidic foods, weakness, fatigue will appear, breathing will change, shock and coma are possible.

Symptoms of acidosis can be masked by manifestations of the underlying pathology or are very similar to it, which makes diagnosis difficult. Mild acidosis is often asymptomatic, severe - always gives a clinic of impaired breathing, it is possible to reduce the contractility of the heart muscle and the reaction of the peripheral vascular bed to adrenaline, which leads to cardiogenic shock and coma.

Metabolic acidosis accompanied by a very characteristic breathing disorder of the Kussmaul type, which is aimed at restoring acid-base balance by increasing the depth of respiratory movements, in which a larger volume of carbon dioxide is emitted into the surrounding air.

With respiratory (respiratory) acidosis due to a decrease in alveolar gas exchange, breathing will become shallow, perhaps even faster, but will not deepen, since the alveoli are not able to provide an increased level of ventilation and gas exchange.

respiratory acidosis

The most accurate information on the concentration of carbon dioxide in the patient's blood, which a doctor can obtain without involving additional examination methods, is given by an assessment of the type of breathing. After it became clear that the patient really has acidosis, specialists will have to find out its cause.

The least diagnostic difficulties arise with respiratory acidosis, the causes of which are usually quite easily recognized. Most often, obstructive emphysema, pneumonia, interstitial pulmonary edema act as a trigger. To clarify the causes of metabolic acidosis, a number of additional studies are being carried out.

Moderately expressed compensated acidosis proceeds without any symptoms, and the diagnosis consists in the study of the buffer systems of blood, urine, etc. As the severity of the pathology deepens, the type of respiration changes.

With the decompensation of acidosis, disorders occur in the brain, heart and blood vessels, the digestive tract, associated with ischemic-dystrophic processes against the background of hypoxia and the accumulation of excess acids. An increase in the concentration of hormones in the adrenal medulla (adrenaline, norepinephrine) contributes to tachycardia, hypertension.

The patient, with an increase in the formation of catecholamines, experiences palpitations, complains of an increase in pulse rate and fluctuations in blood pressure. As the acidosis worsens, arrhythmia may join, bronchospasm often develops, the secretion of the digestive glands increases, so vomiting and diarrhea may be among the symptoms.

The influence of acidification of the internal environment on the activity of the brain provokes drowsiness, fatigue, lethargy, apathy, headaches. In severe cases, impaired consciousness manifests itself in a coma (in diabetes mellitus, for example), when the patient does not respond to external stimuli, the pupils are dilated, breathing is rare and shallow, muscle tone and reflexes are reduced.

With respiratory acidosis, the patient's appearance changes: the skin changes color from cyanotic to pinkish, becomes covered with sticky sweat, puffiness of the face appears. In the early stages of respiratory acidosis, the patient may be agitated, euphoric, talkative, but as acidic products accumulate in the blood, behavior changes towards apathy, drowsiness. Decompensated respiratory acidosis occurs with stupor and coma.

An increase in the depth of acidosis in pathology of the respiratory organs is accompanied by hypoxia in the tissues, a decrease in their sensitivity to carbon dioxide, inhibition of the respiratory center in the medulla oblongata, while gas exchange in the lung parenchyma progressively decreases.

The metabolic one joins the respiratory mechanism of acid-base imbalance. The patient's tachycardia increases, the risk of cardiac arrhythmias increases, and if treatment is not started, a coma will develop with a high risk of death.

If acidosis is caused by uremia in the presence of chronic renal failure, then among the signs may be convulsions associated with a drop in concentration. With an increase in blood, a lack of breathing will become noisy, a characteristic ammonia smell will appear.

Diagnosis and treatment of acidosis

Diagnosis of acidosis is based on laboratory studies of the composition of blood and urine, determination of blood pH, assessment of the effectiveness of the buffer systems. There are no reliable symptoms that can reliably accurately judge the presence of acidosis.

In addition to lowering the pH of the blood to 7.35 and below, the following are also characteristic:

• An increase in carbon dioxide pressure (with respiratory acidosis);
• Decrease in indicators of standard bicarbonate and bases (with metabolic variant of violation of acid-base balance).

Correction of mild forms of acidosis is carried out by prescribing abundant drinking and alkaline liquids, products that contribute to the formation of acid metabolites are excluded from the diet. A comprehensive examination is mandatory to determine the cause of the pH shift.

Recently, the theory has become widespread, according to which a variety of pathological processes are associated with acidification of the internal environment. Alternative medicine advocates urge the use of regular baking soda as a universal cure for all diseases. However, you need to first figure out whether ordinary soda is so useful and really harmless for a sick person with anything?

In the case of malignant tumors, undoubtedly, soda treatment will not have the desired effect and even harm, with gastritis, it will aggravate existing secretory disorders and, possibly, provoke atrophic processes in the mucous membrane, and with alkalosis, it will contribute to the normalization of acid-base balance, but only if adequate dose, regimen of administration and constant laboratory monitoring of the pH level, bases and blood bicarbonate.

Pathogenetic treatment of acidosis consists in eliminating the main pathology that caused the pH shift to the acidic side - respiratory failure, pulmonary edema, diabetes mellitus, uremia, etc. For this purpose, bronchodilators are prescribed (beta-adrenomimetics - salbutamol, salmeterol, isoprenaline, theophylline) , mucolytics and expectorants (acetylcysteine, ambroxol), antihypertensive drugs (enalapril, captopril), the dose of insulin is adjusted for diabetes. In addition to medication support, airway sanitation and positional drainage of the bronchi are carried out to restore their patency.

Symptomatic therapy to normalize the acid-base balance consists in the use of soda and drinking plenty of fluids. In the case of decompensated acidosis and coma, sterile sodium bicarbonate solution is injected intravenously under constant control of the acid-base balance of the blood and under conditions of resuscitation.

Respiratory acidosis is a pathological condition of the body, which is caused by an imbalance of acid-base components in the blood and lymph of a person. It arises in connection with prolonged stay in the environment, where there is an increased concentration of carbon dioxide. In fact, this is carbon dioxide poisoning.

With respiratory acidosis, the acid-base balance shifts towards an increase in the acidity of all body fluids, and the alkaline environment is suppressed by the action of acids. In connection with this factor, the metabolic process is disrupted in all organs and systems, a malfunction develops in their work, which leads to a general deterioration in well-being. The most severe forms of respiratory acidosis provoke severe poisoning with organic acids, coma and the onset of death of the poisoned person.

Inhalation of carbon dioxide and vapors of other acids saturates the blood and gradually all tissues of the body with chemical compounds of the organic type, therefore, the negative reaction of the body occurs immediately and intensifies as the toxic effect increases. Each organ and system of the body reacts differently to a sharp change in the acid-base balance, due to its physiological structure and functional purpose.

In general, with respiratory acidosis, patients develop the following critical conditions of the body:

Classification

According to the type of development of the clinical picture, respiratory acidosis is classified based on functional disorders of the body's activity, as well as on the basis of how intensively accumulated acids are removed from it.

The following types of respiratory acidosis are distinguished:

• excretory (develops after impaired renal function, when the concentration of inhaled acids reaches a critical level);
• metabolic (occurs as a result of acid poisoning, when metabolic processes in the body are disrupted);
• exogenous (a complicated form of respiratory acidosis, caused not only by the intake of acids through the organs of the respiratory system, but also by their synthesis inside the body in the form of amino acids of protein origin);
• compensated (this is a mild degree of poisoning with acid vapors);
• subcompensated (the patient has a serious change in the acid-base balance with a threat to life);
• decompensated (the patient's health condition requires urgent resuscitation measures to prevent the onset of irreversible processes to change the tissues of internal organs).

The latter type of respiratory acidosis is characterized by complete denaturation of protein compounds in the body. This is already a pathological condition of the patient, which often ends in coma and death.

Respiratory acidosis symptoms

Signs of acid-base imbalance due to respiratory acidosis are very difficult to diagnose in differential diagnosis, so they can be easily confused with another pathology.

To make an accurate diagnosis, it is important for the doctor to know what conditions the patient was in before he began to experience the following symptoms:

The severity of a symptom directly depends on the severity of acid vapor poisoning and how much the acid-base balance in the patient's body is changed.

Treatment

Therapy of a pathological condition is reduced to simultaneously restoring the impaired functions of vital organs and stabilizing the acid-base balance in the body.

For this, in most cases, the patient is prescribed the following course of treatment, which must be carried out in a hospital setting:

1. Intravenous droppers are placed, which saturate the body with salts of alkaline components in order to equalize the imbalance and extinguish the excess concentration of acids in the blood.
2. Intramuscular and intravenous injections of drugs based on sodium bicarbonate are administered. Drinking medicines can also be used. Their purpose is to raise the acidity index to a pH of 7.2. It is this ratio that is optimal for such an unsatisfactory state of health of the patient.
3. Intravenous administration of a glucose solution together with the medication sodium chloride. This medicinal complex helps to restore disturbed blood volumes and prevent tissue destruction of vital organs.
4. Connecting the patient to a ventilator. This is an extreme method of therapy aimed at saving the patient's life. It is used in cases when the patient's condition is critical and organs begin to fail, acute oxygen starvation develops.

The timing of the patient's complete recovery depends on how strong the poisoning was with acid fumes, as well as on the promptness of the medical care provided. The average recovery period after suffering respiratory acidosis is 5-6 days.

Respiratory (respiratory) acidosis- This is an uncompensated or partially compensated decrease in pH as a result of hypoventilation.

Hypoventilation can occur due to:

1. Damage (disease) of the lungs or respiratory tract (pneumonia, pulmonary fibrosis, pulmonary edema, foreign bodies in the upper respiratory tract, etc.).
2. Injuries (diseases) of the respiratory muscles (potassium deficiency, pain in the postoperative period, etc.).
3. Oppression of the respiratory center (opiates, barbiturates, tabloid paralysis, etc.).
4. Incorrect ventilation mode.

Hypoventilation leads to the accumulation of CO2 in the body (hypercapnia) and, accordingly, an increased amount of synthesized carbonic acid in the carbonic anhydrase reaction:

H 2 0 + CO 2 H 2 C0 3

Carbonic acid dissociates into hydrogen ion and bicarbonate according to the reaction:

H 2 C0 3 H + + HCO 3 -

There are two forms of respiratory acidosis:

• acute respiratory acidosis;
• chronic respiratory acidosis.

Acute respiratory acidosis develops with severe hypercapnia.

Chronic respiratory acidosis develops in chronic obstructive pulmonary diseases (bronchitis, bronchial asthma, smokers' emphysema, etc.), leading to moderate hypercapnia. Sometimes chronic alveolar hyperventilation and mild hypercapnia cause extrapulmonary disturbances, in particular, significant fatty deposits in the chest area in overweight patients. Such localization of fatty deposits increases the load on the lungs when breathing. Weight loss is very effective in restoring normal ventilation in these patients.

Laboratory data for respiratory acidosis are presented in table. 20.5.

Table 20.5. Laboratory data for respiratory acidosis (according to Mengele, 1969)
Blood plasma		Urine
Index	Result	Index	Result
NS	7,0-7,35	NS	Moderately reduced (5.0-6.0)
Total CO 2	Increased	[NSO 3 -]	Not determined
P C0 2	45-100 mm Hg Art.	Titratable acidity	Slightly increased
Standard bicarbonates	First, the norm, with partial compensation - 28-45 mmol / l	Potassium level	Downgraded
Buffer bases	First, the norm, with a prolonged course - 46-70 mmol / l	Chloride level	Promoted
Potassium	Tendency towards hyperkalemia
Chloride content	Lowered

Compensatory reactions of the body in respiratory acidosis

The complex of compensatory changes in the body during respiratory acidosis is aimed at restoring the physiological optimum pH and consists of:

• the action of intracellular buffers;
• renal processes of excretion of excess hydrogen ions and an increase in the intensity of re-absorption and synthesis of bicarbonate.

The action of intracellular buffers occurs in both acute and chronic respiratory acidosis. 40% of the intracellular buffer capacity is in the bone tissue and more than 50% in the hemoglobin buffer system.

The secretion of hydrogen ions by the kidneys is a relatively slow process, in this regard, the effectiveness of renal compensation mechanisms in acute respiratory acidosis is minimal and significant in chronic respiratory acidosis.

Action of intracellular buffers in respiratory acidosis

The effectiveness of the bicarbonate buffer system (the leading extracellular buffer system), determined, among other things, by the normal respiratory function of the lungs, during hypoventilation is ineffective (bicarbonate is not able to bind CO 2). Neutralization of excess H + is carried out by the carbonate of the bone tissue, which causes the release of calcium from it into the extracellular fluid. Under chronic acid load, the contribution of bone buffers to the total buffering capacity exceeds 40%. The mechanism of action of the hemoglobin buffer system with an increase in PCO 2 is illustrated by the following sequence of reactions:

The bicarbonate formed as a result of these reactions diffuses from the erythrocytes into the extracellular fluid in exchange for a chlorine ion. As a result of the action of the hemoglobin buffer, the plasma bicarbonate concentration increases by 1 mmol / L for every 10 mm Hg. Art. increase Р С0 2.

An increase in the amount of plasma bicarbonate with a one-step fold increase in PCO 2 is not effective. So, according to calculations using the Henderson-Hasselbach equation, the bicarbonate buffer system stabilizes the pH at the point of 7.4 at a ratio of HCO 3 - / H 2 CO 3 = 20: 1. An increase in the amount of bicarbonate by 1 mmol / l, and PCO 2 by 10 mm Hg. Art. reduce the ratio HCO 3 - / H 2 CO 3 from 20: 1 to 16: 1. Calculations using the Henderson-Hasselbach equation show that such a ratio HCO 3 - / H 3 CO 3 will provide a pH of 7.3. The effect of bone buffers, in addition to the acid-neutralizing activity of the hemoglobin buffer system, contributes to a less significant decrease in pH.

Renal Compensatory Responses in Respiratory Acidosis

Functional renal activity in hypercapnia contributes to pH stabilization along with the action of intracellular buffers. Renal compensatory responses in respiratory acidosis are directed at:

• removal of excess amounts of hydrogen ions;
• maximum reabsorption of filtered and glomerular bicarbonate:
• creation of a reserve of bicarbonate through the synthesis of HCO 3 - in the reactions of acido- and ammoniogenesis.

A decrease in the arterial blood pH due to an increased PCO 2 leads to an increase in the CO 2 voltage in the tubular epithelium cells. As a result, the production of carbonic acid and the formation of HCO 3 - and H + during its dissociation increase. Hydrogen ions are secreted into the tubular fluid, and bicarbonate enters the blood plasma. The functional activity of the kidneys to stabilize pH is able to compensate for the deficiency of bicarbonate and remove the excess of hydrogen ions, but this requires a significant amount of time, measured in hours.

In acute respiratory acidosis, the renal mechanisms of pH stabilization are practically not involved. In chronic respiratory acidosis, the increase in HCO 3 - is 3.5 mmol / L of bicarbonate for every 10 mm Hg. Art., while in acute respiratory acidosis, the increase in HCO 3 - by 10 mm Hg. Art. P CO 2 is only 1 mmol / l. Renal processes of stabilization of CBS provide a moderate decrease in pH. According to calculations using the Henderson-Hasselbach equation, an increase in the concentration of bicarbonate by 3.5 mmol / l, and PCO 2 - by 10 mm Hg. Art. will lower the pH to 7.36. with chronic respiratory acidosis.

The amount of bicarbonate in blood plasma in untreated chronic respiratory acidosis corresponds to the renal threshold for bicarbonate reabsorption (26 mmol / L). In this regard, parenteral administration of sodium bicarbonate to correct acidosis will be practically ineffective, since the administered bicarbonate will be rapidly excreted.

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Source: Medical laboratory diagnostics, programs and algorithms. Ed. prof. Karpishchenko A.I., St. Petersburg, Intermedica, 2001

The main indicators of the severity of various degrees of respiratory acidosis:

Etiology... Respiratory acidosis is a consequence of decreased alveolar ventilation, which causes an increase in blood pCO 2. Respiratory acidosis causes:

• depression of the respiratory center: brain injury, infection, the effect of morphine, etc.;
• violation of neuromuscular conduction: myasthenia gravis, poliomyelitis;
• deformation of the chest: kyphoscoliosis;
• pulmonary diseases: chronic obstructive pulmonary disease, status asthmaticus, pulmonary edema, respiratory distress syndrome.

Pathogenesis... With an excessive accumulation of carbon dioxide in the body, the hemoglobin dissociation curve shifts to the right, as a result of which the concentration of hydrogen cations and bicarbonate anions increases. Hemoglobin and protein buffers partially block H +, which leads to a further shift of the dissociation curve to the right until a new equilibrium level is reached. Renal compensation increases the production of HCO 3 - and the release of bicarbonate into the plasma. Such a compensatory mechanism turns on in the presence of chronic respiratory failure and reaches a maximum on days 2-4, while subcompensation of respiratory acidosis occurs, in which potassium cations leave the cell, and hydrogen and sodium cations come in their place. A decrease in K + in cardiomyocytes can create a condition for disturbances in the rhythm of cardiac activity.

Correction of respiratory acidosis

The basis of the treatment of respiratory acidosis is the transfer of the patient to mechanical ventilation. In this case, it is necessary to provide for the need for a gradual decrease in pCO 2, since The metabolic alkalosis of the cerebrospinal fluid that occurs in the posthypercapnic period leads to damage to the central nervous system with the development of seizures and other neurological symptoms.

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