Respiratory acidosis. Chronic respiratory acidosis

RESPIRATORY ACIDOSIS honey.
Respiratory acidosis characterized by a decrease in blood pH and an increase in blood pCO2 (more than 40 mmHg).

Etiology

Respiratory acidosis is associated with a decreased ability to excrete CO2 through the lungs. Causes: all disorders that depress lung function and CO2 clearance
Primary lung damage (alveolar-capillary dysfunction) can lead to CO2 retention (usually as a late manifestation).
Neuromuscular lesions. Any pathology of the respiratory muscles that leads to decreased ventilation (for example, pseudoparalytic myasthenia gravis) can cause CO2 retention
Pathology of the central nervous system. Any severe damage to the brainstem may be associated with decreased ventilation capacity and CO2 retention
Drug-induced hypoventilation. Any drug that causes significant depression of the central nervous system or muscle function can lead to the development of respiratory acidosis.
Clinic
Various symptoms generalized central nervous system depression
Cardiac disorders: decrease cardiac output, pulmonary hypertension- effects that can lead to a critical decrease in blood flow to vital organs.

Diagnosis

Acute CO2 retention leads to an increase in blood pCO2 with minimal changes in plasma bicarbonate levels. With an increase in pCO2 for every 10 mm Hg. Plasma bicarbonate levels increase by approximately 1 mEq/L, and blood pH decreases by approximately 0.08. In acute respiratory acidosis, serum electrolyte concentrations are close to normal.
Chronic respiratory acidosis. After 2-5 days, renal compensation occurs: plasma bicarbonate levels increase uniformly. Gas composition analysis arterial blood shows that with an increase in pCO2 for every 10 mm Hg. plasma bicarbonate content increases by 3-4 mEq/l, and blood pH decreases by 0.03.

Treatment

Treatment of the underlying disease
Breathing therapy. pCO2 exceeding 60 mm Hg may be an indication for mechanical ventilation in cases of severe depression of the central nervous system or respiratory muscles.
See also, (()) 2,4-Dienoyl-CoA reductase
c Enzyme deficiency

ICD

E87.2 Acidosis

Directory of diseases. 2012 .

See what "RESPIRATORY ACIDOSIS" is in other dictionaries:

respiratory acidosis- (a. respiratoria) see Gas acidosis... Large medical dictionary

respiratory acidosis of newborns- (a. respiratoria neonatorum) gas A., observed in newborns with respiratory distress syndrome ... Large medical dictionary

Acidosis- ICD 10 E87.287.2 ICD 9 276.2276.2 DiseasesDB ... Wikipedia

Acidosis- I Acidosis (acidosis; lat. acidus sour + ōsis) one of the forms of acid disorders alkaline balance body; characterized by an absolute or relative excess of acids, i.e. substances that donate hydrogen ions (protons) to bases... Medical encyclopedia - a decrease in acidity due to insufficient ventilation of the lungs (respiratory acidosis) or non-pulmonary etiology (metabolic acidosis).

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

Hypoventilation can occur due to:

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

Hypoventilation leads to the accumulation of CO 2 in the body (hypercapnia) and, accordingly, an increased amount of carbonic acid synthesized in the carbonic anhydrase reaction:

H 2 0 + CO 2 H 2 C0 3

Carbonic acid dissociates into a 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, emphysema of smokers, etc.), leading to moderate hypercapnia. Sometimes chronic alveolar hyperventilation and moderate hypercapnia are caused by extrapulmonary disorders, in particular significant body fat in area chest in extremely obese patients. Such localization of fatty deposits increases the load on the lungs when breathing. To restore normal ventilation in these patients, weight loss is very effective.

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
pH	7,0-7,35	pH	Moderately reduced (5.0-6.0)
Total CO 2 content	Increased	[NSO 3 - ]	Not defined
R C0 2	45-100 mm Hg. Art.	Titratable acidity	Slightly elevated
Standard bicarbonates	At first the norm, with partial compensation - 28-45 mmol/l	Potassium level	Demoted
Buffer bases	At first the norm, with a prolonged course - 46-70 mmol/l	Chloride level	Promoted
Potassium	Tendency towards hyperkalemia
Chloride content	Downgraded

Compensatory reactions of the body during respiratory acidosis

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

• actions 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 accounted for by bone tissue and more than 50% by the hemoglobin buffer system.

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

Effect of intracellular buffers in respiratory acidosis

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

The bicarbonate formed as a result of these reactions diffuses from red blood cells into the extracellular fluid in exchange for 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 in P C0 2.

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

Renal compensatory reactions in respiratory acidosis

The functional activity of the kidneys during hypercapnia contributes to pH stabilization along with the action of intracellular buffers. Renal compensatory reactions in respiratory acidosis are aimed at:

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

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

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

The amount of bicarbonate in the 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 quickly excreted.

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LITERATURE [show] .

1. Gorn M.M., Heitz W.I., Swearingen P.L. Water-electrolyte and acid-base balance. Per. from English - St. Petersburg; M.: Nevsky Dialect - Binom Publishing House, 1999. - 320 p.
2. Berezov T. T., Korovkin B. F. Biological chemistry. - M.: Medicine, 1998. - 704 p.
3. Dolgov V.V., Kiselevsky Yu.V., Avdeeva N.A., Holden E., Moran V. Laboratory diagnostics of acid-base status. - 1996. - 51 p.
4. SI units in medicine: Transl. from English / Rep. ed. Menshikov V.V. - M.: Medicine, 1979. - 85 p.
5. Zelenin K.N. Chemistry. - St. Petersburg: Special. literature, 1997.- pp. 152-179.
6. Fundamentals of human physiology: Textbook / Ed. B.I.Tkachenko - St. Petersburg, 1994.- T. 1.- P. 493-528.
7. Kidneys and homeostasis in normal and pathological conditions. / Ed. S. Clara - M.: Medicine, 1987, - 448 p.
8. Ruth G. Acid-base state and electrolyte balance. - M.: Medicine 1978. - 170 p.
9. Ryabov S.I., Natochin Yu.V. Functional nephrology. - St. Petersburg: Lan, 1997. - 304 p.
10. Hartig G. Modern infusion therapy. Parenteral nutrition.- M.: Medicine, 1982.- P. 38-140.
11. Shanin V.Yu. Typical pathological processes. - St. Petersburg: Special. literature, 1996 - 278 p.
12. Sheiman D. A. Pathophysiology of the kidney: Trans. from English - M.: Eastern Book Company, 1997. - 224 p.
13. Kaplan A. Clinical chemistry.- London, 1995.- 568 p.
14. Siggard-Andersen 0. The acid-base status of the blood. Copenhagen, 1974.- 287 p.
15. Siggard-Andersen O. Hidrogen ions and. blood gases - In: Chemical diagnosis of disease. Amsterdam, 1979.- 40 p.

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

Chronic respiratory acidosis develops long time, sufficient to activate the renal compensation mechanism. An increase in blood PCO 2 is accompanied by a moderate decrease in pH. At the same time, the excess of bases and HCO 2 increase (PaCO 2 > 44 mm Hg, BE > +2 mmol/l, pH< 7,35). Из организма выводятся H + и С1 - . С мочой выделяется NH 4 Cl, обладающий свойствами сильной кислоты. Компенсаторный характер мета­болического алкалоза очевиден. Несмотря на почечную компенсацию, ды­хательные нарушения могут прогрессировать. Хронический дыхательный ацидоз может перейти в острый, но непосредственной угрозы для жизни больного не представляет.

Treatment of the underlying disease is necessary.

ACUTE RESPIRATORY ALKALOSIS

Acute respiratory alkalosis is characterized by a primary acute loss of CO 2 due to excess (in relation to metabolic needs) alveolar ventilation. This occurs as a result of passive hyperventilation during mechanical ventilation or stimulation of the respiratory center and carotid bodies caused by hypoxemia or metabolic disorders. Acute respiratory alkalosis in traumatic brain injury may be caused by stimulation of chemoreceptors by lactic acid accumulating in the brain. Due to a decrease in PCO 2, the pH of the extracellular fluid increases, BE does not change (PCO 2< 36 мм рт.ст., BE ± 2 ммоль/л, рН >7.44). Plasma catecholamine concentrations fall. MOS decreases. Dilatation of blood vessels in the lungs and muscles and spasm of cerebral vessels occur. Cerebral blood flow And intracranial pressure are decreasing. Dysregulation of breathing and brain disorders are possible: paresthesia, muscle twitching, convulsions.

It is necessary to treat the underlying disease (trauma, cerebral edema) or condition (hypoxia) that caused respiratory alkalosis. Monitoring of CBS and blood gases. The mode of respiratory alkalosis during mechanical ventilation is indicated for neurotrauma (RSO 2 = 25 mm Hg). With moderate respiratory alkalosis under mechanical ventilation, no correction is required.

CHRONIC RESPIRATORY ALKALOSIS

Chronic respiratory alkalosis develops over a period of time sufficient for compensation by the kidneys. Urinary excretion of HCO 2 increases and the release of non-volatile acids decreases. Base deficiency increases in the blood plasma, pH is within normal limits or slightly increased (PCO 2< 35 мм рт.ст., BE < -2 ммоль/л, рН > 7,40-7,45).

Treatment. It is necessary to eliminate the main reason causing the stimulation of breathing.

Respiratory alkalosis, acute and chronic, as a rule, is a compensatory reaction caused by metabolic acidosis or some other reasons (hypoxemia, pain, shock, etc.).

METABOLIC ACIDOSIS

Metabolic acidosis is characterized by a deficiency of bases in the extracellular fluid. Accumulation of fixed acids or loss of bases leads to a decrease in buffer bases and pH. Acids penetrate into the cerebrospinal and extracellular fluid of the brain. Peripheral and central chemoreceptors stimulate breathing. However, compensation processes are gradually being exhausted.

Causes of metabolic acidosis:

increased plasma lactic acid levels (lactic acidosis);

Increased levels of acetoacetic and beta-hydroxybutyric acids (ketoacidosis);

Increase in content uric acid and SO 4 2- ( renal failure);

Accumulation inorganic acids HSO 4 - and H 2 PO 4 - (protein breakdown during shock and parenteral nutrition, liver failure);

Losses of bicarbonate (direct losses due to diarrhea, the presence of intestinal and biliary fistulas, diseases digestive tract; loss of bicarbonate, depending on the loss of Na + and K + ions - as a result of the loss of these ions HCO 3 - loses the properties of bicarbonate);

Infusions of acidic solutions and electrolyte solutions that change the ionic composition of the extracellular fluid (massive transfusions of “old blood” containing ammonium chloride, which has the properties of a strong acid; infusions of solutions with low pH; an increase in the concentration of H + ions leads to a decrease in bicarbonate).

With uncompensated metabolic acidosis BE< -2 ммоль/л, РСО 2 35-45 мм рт.ст., рН < 7,36, при полной или частичной дыхательной компенсации BE < -2 ммоль/л, РСО 2 < 36 мм рт.ст, рН < 7,36.

Due to the huge production of H +, the most important thing is to treat the underlying disease. Symptomatic treatment of acidosis without understanding its cause and the entire metabolic catastrophe can be ineffective and harmful. Let us remember that uncontrolled alkalization of the blood leads to a deterioration in the oxygen supply to tissues. For diabetic acidosis, insulin is predominantly prescribed. Even with circulatory arrest, the need for urgent administration of bicarbonate is questioned.

Effective and reliable methods of treating metabolic acidosis are infusion of balanced solutions, maintaining adequate hydration and circulation in patients with preserved renal function.

LACTATE ACIDOSIS

Lactic acid is the end product of anaerobic glycolysis in the body. Normally, its serum concentration is 2 mmol/L or less. Most lactic acid is metabolized by the liver through the process of gluconeogenesis. As an energy source, lactic acid is absorbed by the heart muscle. An increase in the amount of lactic acid in the blood serum is observed with metabolic disorders associated with increased anaerobic glycolysis. An increase in the level of lactic acid in the blood serum is always an indicator of significant metabolic disorders.

Causes of lactic acidosis:

decreased tissue oxygenation - tissue hypoxia. Highest value cause circulatory disorders (cardiogenic, septic, hypovolemic shock). The possibility of lactic acidosis during arterial hypoxemia, especially short-term and shallow, is doubtful. There is also no direct evidence of increased blood lactic acid levels in anemia unless there are clinical symptoms of shock. However, the presence of all forms of hypoxemia theoretically contributes to the development of lactic acidosis. The latter is assumed in all cases of clinically severe disease, in patients with unstable hemodynamics, inotropic support, compartment syndrome, etc. It is necessary to determine the CBS indicators using the Astrup method, the anion difference and the level of lactate in the blood;

liver dysfunction lead to a decrease in its ability to convert lactic acid into glucose and glycogen. A normally functioning liver processes significant amounts of lactate, but in shock this ability is impaired;

deficiency of thiamine (vitamin B 1) may lead to the development of lactic acidosis in the absence of cardiovascular failure. Thiamine deficiency is observed in critical conditions, often in patients who abuse alcohol with Wernicke’s symptom complex. Thiamine deficiency contributes to an increase in lactic acid levels due to inhibition of pyruvate oxidation in mitochondria. The level of lactate in the blood serum increases during excessive drinking, and after 1-3 days, lactic acidosis turns into ketoacidosis;

increase in the level of dextrorotatory isomer of lactic acid - D-lactic acidosis. This isomer is formed as a result of the action of microorganisms that break down glucose in the intestines. D-lactic acidosis is more common in patients after abdominal operations: extensive resections small intestine, interintestinal anastomoses, etc., as well as in obese individuals. Standard laboratory techniques allow the determination of only the levorotatory isomer of lactic acid. The presence of D-lactic acidosis should be assumed in patients with uncompensated metabolic acidosis and a high anion gap. Functional disorders gastrointestinal tract, diarrhea, organ surgery abdominal cavity, possibly dysbiosis, may indicate this disorder. Apparently, this disease is more common, but is often not diagnosed [Marino P., 1998];

other possible reasons lactic acidosis in the departments intensive care - lactic acidosis associated with drug therapy. Lactic acidosis can be caused by long infusions adrenaline solution. Adrenaline accelerates the breakdown of glycogen in skeletal muscles and increases lactate production. An increase in lactic acidosis is promoted by peripheral vasoconstriction, leading to anaerobic metabolism.

Lactic acidosis may develop with the use of sodium nitroprusside. The metabolism of the latter is associated with the formation of cyanides, which can disrupt the processes of oxidative phosphorylation and cause lactic acidosis. Cyanide formation can occur without an increase in lactate levels. The possibility of an increase in lactic acid levels with prolonged passive hyperventilation and the administration of alkaline solutions (initiated lactic acidosis) cannot be ruled out.

Diagnostics. The following signs indicate the possibility of lactic acidosis:

The presence of metabolic acidosis associated with an increased anion gap;

Marked base deficiency;

The anion difference is more than 30 mmol/l, while there are no other causes that can cause acidosis (ketoacidosis, renal failure, administration of toxic substances);

The level of lactic acid in venous blood exceeds 2 mmol/l. This indicator reflects the intensity of lactate formation in tissues.

Treatment is etiological, i.e. aimed at eliminating the cause of lactic acidosis. In case of shock or circulatory failure, measures should be taken to improve tissue perfusion, delivery and oxygen consumption by tissues. All patients with alcoholic encephalopathy require treatment with thiamine. The average dose of thiamine, in case of deficiency, is 100 mg/day.

Administration of sodium bicarbonate is indicated at pH less than 7.2, HCO 3 less than 15 mmol/l, in the absence of respiratory acidosis. The recommended concentration of HCO 3 in blood plasma is 15 mmol/l. This level of HCO 3 - will keep the pH above 7.2. Half of the HCO 3 deficiency is eliminated by the initial intravenous administration of bicarbonate followed by measuring its level in the blood. Further intravenous administration bicarbonate is produced slowly drip-by-drop with periodic monitoring of the pH level and HCO 3 -, PSO 3 - and all indicators of CBS.

The main causes of respiratory acidosis are:
chronic diseases lungs (fibrosis, emphysema, asthma, etc.);
depression of the respiratory center (for example, drug overdose);
weakening of neuromuscular functions (for example, with the introduction of blocking drugs);
inadequate operation of the ventilator, contributing to an increase in the concentration of CO2 in the inhaled gas mixture;
increased CO2 production (during fever, metabolization of solutions used as energy substrates in parenteral nutrition, etc.);
traumatic injury to the chest;
thromboembolism pulmonary artery;
pulmonary edema, diffusion disorders of the permeability of pulmonary membranes.

The body easily adapts to the state of chronic respiratory acidosis, compensating for the low pH by increasing the reabsorption of bicarbonate by the kidneys and returning it to the blood, and arterial hypoxemia by increasing the number of red blood cells.
Development of acute respiratory acidosis is a serious complication that can lead to a very unfavorable outcome. This is due to the fact that CO2 passes through the cerebrospinal barrier much faster than H ions, and the decrease in blood pH due to the accumulation of CO2 occurs faster than the decrease in bicarbonate ions. In conditions of acute respiratory acidosis, a decrease in pH cerebrospinal fluid occurs faster than a decrease in blood pH, which is accompanied by depression of the central nervous system. Acute respiratory acidosis has a more adverse effect on the body than metabolic acidosis.

Clinical complications caused by acute respiratory acidosis:
Carbon-Dioxide Narcosis syndrome;
EEG depression (up to deep coma);
heart rhythm disturbances (tachycardia, ventricular fibrillation);
unstable level blood pressure;
hyperkalemia.

I would like to pay special attention to the first of these complications, since in this situation the accumulation of CO2 is accompanied by a decrease in arterial blood pO2. IN in this case It must be remembered that normally the respiratory center is very sensitive to the amount of CO2, but when the concentration of pCO2 in arterial blood exceeds 65 mm Hg. Art., then the main stimulus of the respiratory center is a decrease in arterial blood p02 below 85 mm Hg. Art. In other words, under these conditions, arterial hypoxemia is a protective-compensatory reaction of the body aimed at stimulating the respiratory center when the latter reacts inadequately to an increased concentration of CO2. If in this situation, to correct hypoxemia, the patient is given oxygen, then the protective reaction is disrupted, and, consequently, the rate of CO2 excretion is disrupted.
In turn, the accumulation of carbon dioxide contributes to an even greater decrease in blood pH, which ultimately can lead to deep coma and even to the death of the patient. The possibility of this syndrome occurring must be remembered during anesthesia, as well as in the early postoperative period, when, against the background of high arterial blood pCO2 values, patients are given oxygen to correct hypoxemia. In the presence of carbon dioxide syndrome, the actions of clinicians should first of all be aimed at reducing CO2, which in the future will automatically lead to the normalization of arterial blood p02.

Treatment of acute respiratory acidosis:
1. Constant sanitation of the respiratory tract, since hypercapnia contributes to the accumulation of viscous bronchial secretions.
2. Introducing an additional amount of fluid, which, along with improving hemodynamics, helps soften bronchial secretions and improve their removal.
3. Administration of alkaline solutions: NaHC03 (at pH > 7.30) or TNAM-E if the patient is on mechanical ventilation, since the Tris buffer depresses the respiratory center and can contribute to an even greater increase in CO2.
4. Humidification of inhaled air to reduce the viscosity of bronchial secretions.
5. If, despite the therapy, a combination of pCO2 > 70 mm Hg is observed in the arterial blood. Art. and p02 > 55 mm Hg. Art., then it is recommended to transfer the patient to mechanical ventilation.

Must be remembered:
Give oxygen to the patient only when arterial blood pO2 is below 55 mmHg:
the oxygen concentration in the inhaled air should not exceed 40%.

Training video for acid base analysis in respiratory and metabolic acidosis

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Main indicators of severity various degrees respiratory acidosis:

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

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

Pathogenesis. With excessive accumulation of carbon dioxide in the body, the hemoglobin dissociation curve shifts to the right, resulting in an increase in the concentration of hydrogen cations and bicarbonate anions. 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 entry of bicarbonate into the plasma. This compensatory mechanism is activated 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 take their place. A decrease in K + in cardiomyocytes can create a condition for cardiac arrhythmias.

Correction of respiratory acidosis

The basis of treatment for respiratory acidosis is transfer of the patient to artificial ventilation lungs. In this case, it is necessary to provide for the need to gradually reduce pCO 2, because Metabolic alkalosis of the cerebrospinal fluid that occurs in the post-hypercapnic period leads to damage to the central nervous system with the development of seizures and other neurological symptoms.

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