Acid-base state. Carboxyhemoglobin

Hemoglobin (Hb)

— blood pigment, whose role is to transport oxygen to organs and tissues. Outside of red blood cells (in blood plasma), hemoglobin is practically undetectable.

Chemically hemoglobin belongs to the group of chromoproteins. Its prosthetic group, including iron, is called heme, and its protein component is called globin. The hemoglobin molecule contains 4 hemes and one globin. Heme is a metalloporphyrin, a complex of iron and protoporphyrin. Protoporphyrin is based on four pyrrole rings connected via methyl bridges (CH) to form a porphyrin ring. Heme is identical for all varieties of human hemoglobin.

In red blood cells of circulating blood hemoglobin is in a state of continuous reversible reaction, either adding an oxygen molecule (in the pulmonary capillaries) or giving it away (in the tissue capillaries).

When the blood is completely saturated with oxygen, 1 g of hemoglobin binds 1.34-1.36 ml of oxygen. At a high oxygen content in the environment (in the lungs), reduced hemoglobin easily and quickly turns into oxyhemoglobin, while at low concentrations of oxygen in the environment (in tissues in which oxygen is utilized), oxyhemoglobin easily splits off oxygen from itself. In case of worsening conditions of blood arterialization due to impaired diffusion of oxygen through the alveolar membrane or an increase in the speed of blood flow in the pulmonary circulation, as well as increased tissue oxygen consumption, the content of oxyhemoglobin in the blood decreases, and the amount of restored hemoglobin increases accordingly. Normally, the content of oxyhemoglobin in arterial blood is 95-96% of the total amount of hemoglobin. In venous blood this value decreases to 60%.

Carboxyhemoglobin (HbCO)

- oxycarbon hemoglobin - dissociates several hundred times slower than oxyhemoglobin, therefore even a small concentration (0.07%) of carbon monoxide (CO) in the air, binding about 50% of the hemoglobin present in the body and depriving it of the ability to carry oxygen, is fatal.

Education carboxyhemoglobin begins from the periphery of erythrocytes in contact with CO in the pulmonary capillaries. During subsequent blood circulation, redistribution of CO between red blood cells does not occur. As the concentration of CO in the air increases, the formation of carboxyhemoglobin spreads from the periphery of red blood cells to their center. Each gram of globin is capable of binding 1.33-1.34 ml of O2 or CO. This quantity is called the Huefner constant. However, the affinity for CO is 200-290 times greater than for O2-

The equilibrium constant for this reaction is:

In this regard, even with a low CO content in the inhaled air in the body, a competitive relationship is created between these gases to capture hemoglobin with a significant advantage for CO.

Determination of carboxyhemoglobin content

(according to L.E. Gorn). The method is based on photometric determination of the difference in light absorption of solutions of oxy- and carboxyhemoglobin after their denaturation with alkali.

Equipment and reagents. Universal photometer FM or horizontal photometer; 0.04% ammonia solution; 0.2 n. a solution of sodium or potassium oxide hydrates (caustic potassium or soda).

Methodology. 4.9 and 5.9 ml of 0.04% ammonia solution are poured into 2 test tubes, after which 0.1 ml of blood is added to each. In the first test tube, designed to determine the light absorption of the original denatured blood containing the desired amount of carboxyhemoglobin (HbO2 + HbCO), quickly add 5 ml of 0.2 N. alkali solution, quickly mix by tipping twice and photometer the sample 1 minute after adding the alkali (50-70 s, no more!) with light filter No. 5 (M-55 or M-52, effective wavelength of transmitted light 550 or 520 nm). The contents of the second test tube, in which the total amount of hemoglobin is determined, is directly photometered using filter No. 5 (M-50, 496 nm). Photometry is carried out according to generally accepted rules in 10 mm cuvettes using distilled water. When using filter No. 5 (M-55), the carboxyhemoglobin content is calculated using the formula:

where E is extinction.

If filter No. 5 is brand M-52 and not M-55, then the coefficient 132 is replaced by 123.

Norm and evaluation of carboxyhemoglobin test results

In the blood of persons who do not come into contact with carbon monoxide under production conditions, carboxyhemoglobin is usually present in some quantity, which is due to the almost constant pollution of the atmosphere with products of incomplete combustion of all types of fuel. According to various authors, urban residents who are not exposed to carbon monoxide have up to 15% carboxyhemoglobin in their blood. Its average concentration varies, according to various sources, from 2-4 to 6-8%. Smoking leads to an increase in this value by 2-3%. The source of carboxyhemoglobin formation is not only exogenous carbon monoxide, but also, to some extent, carbon monoxide formed in the body as a result of incomplete oxidation of certain metabolic products, in particular hemoglobin. Since when a victim is transferred to a clean atmosphere, especially when oxygen is inhaled, the dissociation of carboxyhemoglobin occurs relatively quickly (in the first hour the carboxyhemoglobin content is halved), the results laboratory research blood taken for analysis some time after first aid may give a false impression of the initial maximum concentration carboxyhemoglobin and thereby distort the idea of ​​the severity of the clinical picture of intoxication. This justifies the need to minimize the intervals between removing the victim from the poisoned atmosphere and taking blood for analysis. With chronic carbon monoxide intoxication, the dissociation of carboxyhemoglobin in the blood slows down significantly.

Determination of carboxyhemoglobin in the blood is a valuable indicator that clarifies the diagnosis and determines rational therapy. Thus, in cases where, after a certain time, a balance between the formation and removal of carbon monoxide occurs in the victim’s blood, oxygen therapy may lose its significance.

Qualitative reaction to the presence of carboxyhemoglobin in the blood:

1. Blood in the amount of 0.01 ml is taken from a finger with a needle prick and diluted with distilled water 100 times (up to 1 ml). A test tube with diluted blood is placed in front of the spectroscope and two absorption bands are observed in natural or artificial light in the yellow-green (A = 579-564 nm) and green (k = 548 - 530 nm) parts of the spectrum, coinciding with the spectrum of oxyhemoglobin (A = 598-577 and 556-536 nm).

To differentiate, a qualitative reaction is performed: a substance is added to the test tube that quickly reacts with oxygen and converts oxyhemoglobin in the blood into reduced hemoglobin (1 - 2 drops of ammonium sulfide NH4S or 4-5 mg of sodium dithionite Na2S204). The test tube is shaken and placed again in front of the spectroscope.

In the absence of carboxyhemoglobin, only one broad absorption band is visible, corresponding to reduced hemoglobin and located in the yellow-green part of the spectrum (A = 596-543 nm). In the presence of carboxyhemoglobin, no changes in the spectrum occur, and upon repeated spectroscopy, two absorption bands continue to be determined - in the yellow-green and green parts of the spectrum. The sensitivity of the spectroscopic test corresponds to 15 - 20% carboxyhemoglobin in relation to whole blood. More accurate results are obtained using gasometric and especially spectroscopic methods.

2. The spectroscopic method for determining carboxyhemoglobin is based on the ability of carboxyhemoglobin and reduced hemoglobin to varying degrees absorb light rays at a wavelength of 534-563 nm. The difference between the light absorption of carboxyhemoglobin and the light absorption of reduced hemoglobin, which is obtained by adding sodium dithionite, is calculated.

0.1 ml of blood is taken from a finger for analysis. The blood is aspirated with a micropipette previously rinsed with sodium citrate solution; Place in a 10 ml measuring tube and adjust the volume to the 0.005 N mark. sodium hydroxide solution. A reducing agent - 8 mg of sodium dithionite - is added to 5 ml of a transparent solution and the optical density of the solution is measured spectrometrically at waves of 534 and 536 nm. The content of СОНb in the blood is calculated using the formula:

where E1 is the optical density at a wavelength of 534 nm; E2 - the same at a wavelength of 536 nm.

There is no consensus on physiologically acceptable levels of carboxyhemoglobin in the blood. Thus, in urban residents, the level of carboxyhemoglobin in the blood can reach 4 - 7%.

It should be noted that in patients with chronic carbon monoxide intoxication, the level of carboxyhemoglobin in the blood usually corresponds to normal values. Determination of carboxyhemoglobin in them can occur in cases of dysfunction of the lungs and heart with abnormalities in the metabolism of carbonic acid, as well as in cases of sigmoidemia, diabetes, silicosis and heart diseases.

3. In cases where there is no spectroscope at hand, an indicative, technically simple method for determining carboxyhemoglobin using copper sulfate can be used. A drop of blood from a victim suspected of carbon monoxide poisoning is applied to a piece of white paper (glass, earthenware, porcelain). A drop of blood from a healthy person is placed nearby. Add a drop of 2% copper sulfate solution to each drop of blood and mix with a wooden stick (matches). After 30 s - 1 min, a grayish-brown or chocolate-colored paste-like mass forms in the blood containing carboxyhemoglobin. After some time it becomes reddish-brown in color. When the content of SONY in the blood is very high (close to 100%), the ointment-like mass has a crimson-red color, which darkens when standing, acquiring a brown tone. Carbon monoxide poisoning occurs with an increase in the content of hemoglobin and red blood cells in the peripheral blood.

Determination of methemoglobin. When intoxicated with aniline, nitro- and dinitrobenzene, berthollet salt and other compounds capable of oxidizing the iron of hemoglobin, methemoglobin is formed with the transition of iron from divalent to trivalent.

There is an opinion that there is always a certain (physiologically acceptable) amount of methemoglobin in the blood of a healthy person and animals. In the body of warm-blooded animals, processes of formation and reduction of methemoglobin to hemoglobin oxide constantly occur. IN normal conditions these processes are well balanced. The level of methemoglobin in a healthy person does not exceed 1% in relation to the total hemoglobin in the blood:

1. A qualitative reaction to methemoglobin is carried out using spectral analysis. Methemoglobin gives a characteristic spectrum with a wide absorption band in the red part of the spectrum (k = 630 nm) and two bands in the orange and yellow parts of the spectrum.

2. Quantitative determination of methemoglobin is of great importance for assessing the severity of intoxication. It is produced on a spectrophotometer. In this case, methemoglobin, after its preliminary determination by the absorption band of light at a wavelength of 633 nm, is converted into cyanmethemoglobin, which does not give an absorption band at all in this part of the spectrum. The method is based on photometry of methemoglobin and cyanmethemoglobin in the red part of the spectrum at a wavelength of 630 nm, in which they have different absorption spectra. The change in light absorption intensity after adding potassium cyanide (to convert MtHb to cyanmethemoglobin) is directly proportional to the concentration of MtHb.

Two blood samples are taken for testing. Hemoglobin from one sample is converted to methemoglobin by adding a drop of a saturated solution of KjFe (CN)6. In another sample, hemoglobin is oxidized due to oxygen dissolved in the medium. Next, the degree of absorption of light with a wavelength of 619 nm is determined in both samples, followed by calculation of the difference in light absorption between methemoglobin and oxyhemoglobin. If there are known general values ​​of the difference for normal blood, its decrease is regarded as a loss of part of the hemoglobin due to its transition to methemoglobin.

3. Quantitative determination of methemoglobin can also be carried out using a hand-held spectroscope. Blood diluted 5 times with distilled water (0.2 ml blood and 0.8 ml water) is placed in a cylinder and viewed through a hand-held spectroscope. If there is an absorption band in the red part of the spectrum, the solution is diluted with water until the band becomes slightly visible. The total volume of blood salt K3Fe(CN)6 is noted, which causes the remaining oxyhemoglobin to be converted to methemoglobin. The absorption band reappears in the red part of the spectrum. The solution is again, as the first time, diluted with water and the total volume value is obtained again (Vi). The calculation is carried out according to the formula:

where V is the first volume in milliliters; Vx is the second volume in milliliters.

One of the promising methods of laboratory diagnostics is gas-liquid chromatography. It differs from others primarily in its high specificity and sensitivity, as well as the speed of analysis (5-15 minutes), small amount of test material, comparative ease of research and its sufficient objectivity. Using this method, it is possible to quantitatively and qualitatively determine such toxic substances as dichloroethane, carbon tetrachloride, chloroform, acetone, ethyl and methyl alcohols, and organophosphorus pesticides.

Emergency care for occupational intoxication, Artamonova V.G., 1981.

Carbon monoxide CO belongs to the group of blood poisons that form pathological pigments.

Carbon monoxide is a colorless gas, the most toxic component of the products of incomplete combustion of carbon-containing substances, CO is part of many gas mixtures (lighting, water, blast furnace, generator, coke oven gas, etc.).

If sanitary and hygienic requirements are not met and technological conditions are violated, high concentrations of CO can be observed in blast furnace and open-hearth production, in foundries, gas-generating shops, when testing engines, in car garages, in the cabins of diesel locomotives and airplanes, in chemical industry enterprises during the synthesis of a number of substances. CO can be found in elevated concentrations during blasting operations in mines, and can be released as part of the volatile products of partial destruction of polymers during the production of various materials from them at high temperatures.

Carbon monoxide enters the body through the respiratory tract and is released primarily through exhaled air.

Pathogenesis. Penetrating into the blood, CO is absorbed by red blood cells, interacts with the iron of hemoglobin, forming a stable compound carboxyhemoglobin. It is known that every gram of hemoglobin is capable of binding CO. However, the “affinity” of hemoglobin for CO is 200-290 times greater than for O2. The formation of carboxyhemoglobin leads to inhibition of hemoglobin oxygenation, disruption of its transport function and the development of hemic hypoxia. In the presence of carboxyhemoglobin. The dissociation of oxyhemoglobin slows down, and therefore oxygen deficiency develops. In addition, CO acts on tissue biochemical systems containing iron - myoglobin, cytochrome, cytochrome oxidase, cytochrome C, peroxidase, catalase. In the pathogenetic mechanisms of chronic carbon monoxide intoxication, an important role is played by the increase in non-hemoglobin iron in plasma, which has a higher affinity for carbon monoxide than hemoglobin iron and, by binding CO, is a protective buffer that prevents the formation of HbCO. At the same time, there are disturbances in porphyrin metabolism, indicating a possible direct effect of CO on enzyme systems involved in the biosynthesis of porphyrins.

Symptoms of carboxyhemoglobinemia. The clinical picture of acute CO intoxication is characterized by polymorphism. There are three degrees of intoxication: mild, moderate and severe. Mild CO intoxication is manifested by subjective sensations: headache in the temples and forehead (“pulsation in the temples”), heaviness in the head, dizziness, weakness, tinnitus, nausea, sometimes vomiting, drowsiness. The HbCO content in the blood is 20-30%.

Moderate intoxication occurs with more or less prolonged loss of consciousness, motor restlessness, convulsions, shortness of breath, and palpitations. These phenomena may be preceded by severe headache, muscle weakness, dizziness, nausea, and vomiting. Visible mucous membranes acquire a crimson-red hue. The HbCO content in the blood reaches 35-40%.

At severe forms intoxication, prolonged loss of consciousness, clonic and tonic convulsions, coma are observed, involuntary urination or defecation, shortness of breath with respiratory distress, tachycardia. There may be a high body temperature (38-40°C). Increase in carboxyhemoglobin level up to 50%.

During acute intoxication and in its long-term period, damage to various organs and systems is possible. The nervous system suffers the most, its sensitivity to toxic effect CO is explained by its exceptional requirement for a regular supply of oxygen. In case of severe intoxication, after emerging from a coma, motor restlessness appears, followed by lethargy, lethargy, and drowsiness. Retrograde amnesia may develop mental disorders, which occur with various phobias, hallucinations, manic states, and hallucinatory delusions. Parkinsonism syndrome, as well as mental disorders in the form of the Korsakoff symptom complex, have been described.

On the first day of intoxication, pulmonary edema may develop, characteristic feature which is the scarcity of percussion and auscultation data compared to the severity of x-ray morphological changes (“silent” forms). To more late complications These include cases of pneumonia that occur on the 2-3rd day after poisoning.

Along with functional disorders in the form of tachycardia, extrasystole, changes in atrioventricular conduction, attacks are observed atrial fibrillation, signs of damage to the heart muscle and impaired coronary circulation up to focal myocardial infarction. These changes are transient and disappear after 2-3 weeks.

Blood changes are characterized by an increase in the number of red blood cells and hemoglobin content, which leads to an increase in blood viscosity and a slowdown in ESR. Changes in white blood are manifested by short-term neutrophilic leukocytosis with a band shift, appearing on the first day of intoxication with subsequent normalization. The central place is occupied by disturbances in the gas composition of the blood: a decrease in the oxygen content in arterial blood, a decrease in the carbon dioxide content, a decrease in the arteriovenous oxygen difference and the coefficient of oxygen utilization by tissues are characteristic. The severity of hypoxemia is directly dependent on the amount of carboxyhemoglobin formed and the severity of intoxication.

A prolonged unconscious state, accompanied by positional pressure of one’s own body on the skin and muscles, leads to disruption of microcirculation in certain areas, which can cause trophic disorders in the form of erythema, edema, blistering, trophic ulcers on the skin of the limbs, back, buttocks. These trophic disorders may be complicated by impaired renal function.

Chronic carbon monoxide toxicity may be due to a combination of repeated acute lungs poisoning with long-term effects of low concentrations of CO.

The early stage of chronic CO exposure is most characterized by functional disorders of the central nervous system, manifested autonomic dysfunction and angiodystonic syndrome with a tendency to vasospasms. In this case, cerebral vascular disorders dominate, combined with cardiac disorders, and often with arterial hypertension. Against the background of exposure to increased concentrations of CO, a pronounced asthenic state develops, diencephalic crises, and organic diffuse brain damage - toxic encephalopathy - are possible.

Long-term exposure to CO in concentrations slightly higher than the maximum permissible concentration can lead to moderate damage to the heart muscle in the form of its dystrophy, often with signs of coronary circulatory failure.

Changes in the blood are manifested by erythrocytosis or a tendency towards it, an increase in hemoglobin content.

The most characteristic and constant sign of chronic exposure to CO, even of low intensity, is an increase in non-hemoglobin iron in the plasma, which is an important compensatory factor that maintains homeostasis of the body at the initial stage of intoxication. At the same time, certain changes in porphyrin metabolism are observed: the content of coproporphyrin in erythrocytes is increased, and the excretion of levulinic acid and coproporphyrin in the urine is increased.

Diagnosis of carboxyhemoglobinemia. The diagnosis of acute carbon monoxide intoxication is made on the basis of characteristic clinical symptoms, as well as sanitary and hygienic characteristics of working conditions. Headache localized mainly in the temple area. Characteristic is the bright scarlet color of the mucous membranes and skin. Diagnostic value has a combination of changes in the nervous, cardiovascular and respiratory systems, as well as trophic changes in the skin. An absolute sign of acute CO exposure is the presence of carboxyhemoglobin in the blood, and blood samples should be taken directly at the scene of the incident. The absence of HbCO does not provide grounds to reject the diagnosis of intoxication, since under normal air conditions carboxyhemoglobin dissociates quickly.

The diagnosis of chronic carbon monoxide intoxication is difficult due to polymorphism clinical symptoms and its non-specific character. It can be diagnosed only on the basis of detailed familiarization with the working conditions of the sick person, long work experience and taking into account the totality of detected clinical syndromes. In this case, a strict differentiated approach is required in each specific case in order to exclude non-professional causes that cause similar violations in a particular system. If during acute intoxication a reliable sign is the formation of carboxyhemoglobin, then during chronic exposure the content of carboxyhemoglobin in the blood slightly exceeds the physiological norm (10% or more, with the norm being up to 5%), and in addition, there is no parallelism between the severity of intoxication and the level of HbCO in the blood. Have diagnostic value increased content iron in blood plasma and changes in porphyrin metabolism.

First aid and treatment of carboxyhemoglobinemia. In case of acute CO intoxication, first aid is provided outside the room where the victim was located. In mild cases, hot drinks (tea, coffee) are recommended, 1-2 ml of caffeine solution is injected under the skin, a heating pad is prescribed to the legs, and humidified oxygen is inhaled through nasal catheters. Positive effect has application ascorbic acid, vitamins B1, B2, B6, cytochrome C (injections 10-50 mg).

If the breathing rhythm is disturbed, 0.3-0.5 ml of 1% lobeline solution is administered intravenously. If breathing stops, use artificial respiration, which must be combined with oxygen supply - continuously for the first 2-4 hours, then for 30-40 minutes with 10-15 minute breaks. For hypocapnia, short-term inhalation of carbogen is indicated. In addition, they use intravenous administration mixtures of the following composition: 500 ml of 5% glucose solution, 20-30 ml of 5% ascorbic acid solution, 50 ml of 2% novocaine solution. When excited it is shown intramuscular injection 2 ml of a 2.5% solution of aminazine, 1 ml of a 1% solution of diphenhydramine, 2 ml of a 2.5% solution of pipolfen, 1 ml of a 2% solution of promedol. For convulsions, 3 ml of 10% barbamyl solution is prescribed intravenously. Cardiovascular drugs are prescribed depending on the state of the circulatory system ((hypotensive drugs, either caffeine, cordiamine, or corglycon, strophanthin).

In case of severe intoxication, in order to remove CO by accelerating its dissociation and combating brain hypoxia, it is indicated hyperbaric oxygen therapy(under pressure 2-3 atm).

In case of prolonged coma, in order to prevent and treat cerebral edema, head hypothermia (ice cooling), forced osmotic diuresis without water load, hydrocortisone, and repeated lumbar punctures with the removal of 10-15 ml of cerebrospinal fluid are used. Broad-spectrum antibiotics should be prescribed early to prevent infectious complications. The use of iron supplements is indicated, among which Ferkoven (5 ml intravenously) is the most effective.

In case of chronic intoxication, long-term combined use of vitamins A, B1, B2, B6, B12, C, PP, folic acid in combination with oxygen therapy or carbogen. The administration of glucose, calcium pantothenate, glutamic acid, ATP is indicated, and according to indications - cardiac and vasodilator drugs.

Work ability examination. After acute mild poisoning, the victim is able to work at his previous job. After moderate or severe intoxication, a transfer to another job with the issuance of an additional paid sick leave is indicated. In the presence of persistent long-term consequences, it is recommended to refer to the VTEK to establish disability due to an occupational disease or determine the percentage of loss of professional ability.

In the initial stages of chronic CO intoxication, after a temporary break from work on additional paid sick leave (1-2 months) and appropriate treatment, complete restoration of impaired functions occurs, so the worker can resume his previous work. At expressed forms Chronic intoxication requires transfer to work away from contact with toxic substances and rational employment. A referral to the VTEK is indicated to determine the disability group for an occupational disease and the degree of urate of professional work ability.

Prevention. It is necessary to seal equipment and pipelines where carbon monoxide may be released. Carry out systematic monitoring of the concentration of carbon monoxide in indoor air and quick removal released gas through the use of powerful ventilation devices, automatic alarm dangerous concentrations CO.

Study of acid-base state (ABC) or acid-base status (ABS) is important in the diagnosis and treatment of various emergency conditions, including surgical ones.

Acidity and alkalinity mean the concentration of free hydrogen ions (H +) in a solution, i.e. Blood pH. For the efficient functioning of vital processes, the concentration of free hydrogen ions (H +) must be within strict limits. In fact, the study of acid-base balance includes, along with measuring pH, the determination of physiologically important gases present in the blood (oxygen - O 2 and carbon dioxide - CO 2) and about 20 other parameters. All these indicators and their values ​​are closely interrelated with each other.

Patients in the intensive care unit and operating room may experience significant changes in these indicators over short periods of time. Research on acid-basic acid, unlike all other types laboratory tests, performed on arterial blood samples.

For normal functioning All cells of the body require oxygen (O 2). The decisive role in the transport of oxygen to tissues belongs to the hemoglobin contained in red blood cells. The term “hemoglobin” refers to several forms of hemoglobin that are present in human blood, both normally and in pathology. More than 98% of the oxygen absorbed by the lungs from the inhaled air is transferred to the body's cells in the blood in the form of oxyhemoglobin. Normally in the blood large quantities there are hemoglobin fractions that are not capable of carrying O2 - dishemoglobins (sulfhemoglobin, methemoglobin, carboxyhemoglobin).

Methemoglobin is constantly formed as a result of normal metabolism of body cells. Methemoglobin contains ferric iron and is not capable of transporting oxygen! When significant amounts of methemoglobin are formed, the transport function of the blood is sharply disrupted. The body has a mechanism for regulating the level of methemoglobin in the blood, which maintains the proportion of this fraction not higher than 1.0 - 1.5% of total hemoglobin.

Carboxyhemoglobin- a strong compound of hemoglobin (Hb) and carbon monoxide (CO). Carboxyhemoglobin is formed very quickly, since the ability of carbon monoxide to attach to hemoglobin is approximately 200 times higher than that of oxygen. Carboxyhemoglobin is not capable of carrying oxygen to the tissues of the body, therefore, in case of carbon monoxide poisoning, death can quickly occur in a person. Carboxyhemoglobin is formed in large quantities during poisoning carbon monoxide, and in small ones it is always present in the blood of all smokers and residents of large cities.

Indications:

ABL analysis is required

· To make a diagnosis Blood gas analysis is an integral part of diagnosing respiratory failure and primary hyperventilation. It also reveals metabolic acidosis and alkalosis.

· To assess the severity of the disease

· To monitor the effectiveness of treatment Such analysis is very important for selecting oxygen (O2) therapy for patients with chronic respiratory failure type 2 and for optimizing ventilator settings.

An increase in methemoglobin (FMetHb) in the blood develops when:

· poisoning with nitrites, nitrates, nitroso compounds, aniline, sulfonamides, acetanilide, chlorides, bromides, etc.

hereditary deficiency of NADH-methemoglobin reductase: low enzyme activity manifests itself in early childhood. Clinical implications As a rule, this disease does not have, manifesting itself as a minor cosmetic defect.

presence of abnormal variants of hemoglobin, designated hemoglobin M

An increase in carboxyhemoglobin (FCOHb) in the blood develops when:

· carbon monoxide poisoning. When FСOHb levels are above 30%, severe headaches are observed, general weakness, vomiting, shortness of breath, tachycardia, and at a level of 50% - convulsions, coma; above 70%, respiratory failure occurs and death is possible.

Methodology:

Determination of blood gases, acid-base status, oximetry parameters are carried out on the ABL 800 FLEX analyzer from RADIOMETR, Denmark, determination of up to 50 parameters.