What is hypoxia disease and what are the consequences. Hypoxia - oxygen starvation, symptoms and signs, types and degrees, causes and consequences, treatment and prevention

Oxygen starvation of the brain or hypoxia occurs due to a violation of the supply of oxygen to its tissues. The brain is the organ most in need of oxygen. A quarter of all inhaled air goes to serve the needs of the brain in it, and 4 minutes without it become critical for life. Oxygen enters the brain through a complex system of blood supply, then it is utilized by its cells. Any disturbances in this system lead to oxygen starvation.

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ICD-10 code

G93 Other disorders of brain

I67.3 Progressive vascular leukoencephalopathy

Epidemiology

Due to the variety of forms of pathological conditions inherent in oxygen starvation, it is difficult to determine its prevalence. Based on the reasons that give rise to it, the number of people who have experienced this state is very large. But the statistics of oxygen starvation in newborns are more definite and disappointing: fetal hypoxia is observed in 10 cases out of 100.

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Causes of oxygen starvation of the brain

There are various reasons for the occurrence of oxygen starvation of the brain. These include:

• decrease in oxygen in the environment (when climbing mountains, indoors, in spacesuits or submarines);
• disruption of the respiratory organs (asthma, pneumonia, chest trauma, tumors);
• failure in blood circulation in the brain (atherosclerosis of the arteries, thrombosis, embolism);
• violation of oxygen transport (lack of red blood cells or hemoglobin);
• blockade of enzyme systems involved in tissue respiration.

Pathogenesis

The pathogenesis of oxygen starvation consists in a change in the structure of the vascular walls, a violation of their permeability, which leads to cerebral edema. Depending on the causes that caused hypoxia, the pathogenesis develops according to a different algorithm. So, with exogenous factors, this process begins with arterial hypoxemia - a decrease in the oxygen content in the blood, which leads to hypocapnia - a lack of carbon dioxide, which disrupts the biochemical balance in it. The next chain of negative processes is alkalosis - a failure of the acid-base balance in the body. At the same time, blood flow in the brain and coronary arteries is disturbed, and blood pressure drops.

Endogenous causes due to pathological conditions of the body cause arterial hypoxemia along with hypercapnia (increased carbon dioxide content) and acidosis (increased organic acid oxidation products). Different types of hypoxia have their own scenarios of pathological changes.

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Symptoms of oxygen starvation of the brain

The first signs of oxygen deficiency are manifested in the excitation of the nervous system: breathing and heartbeat become more frequent, euphoria sets in, cold sweat appears on the face and limbs, motor restlessness. Then the state changes dramatically: lethargy, drowsiness, headache, darkening of the eyes, depression of consciousness appear. A person develops dizziness, constipation develops, muscle cramps and fainting, the onset of coma are possible. The most severe degree of a coma is a deep violation of the central nervous system: lack of brain activity, muscle hypotension, respiratory arrest with a beating heart.

Oxygen starvation of the brain in adults

Oxygen starvation of the brain in adults can develop as a result of a stroke, when the blood supply to the brain is disturbed, hypovolemic shock - a significant decrease in the volume of circulating blood that occurs with a large loss of blood, uncompensated loss of plasma during burns, peritonitis, pancreatitis, accumulation of a large volume of blood during injuries, dehydration during diarrhea. This condition is characterized by a decrease in pressure, tachycardia, nausea and dizziness, loss of consciousness.

Oxygen starvation of the brain in children and newborns

Analyzing various factors in the occurrence of oxygen starvation and the fact that it can accompany many diseases, it becomes clear that children are also in the affected area. Anemia, burns from fire and chemicals, gas poisoning, heart failure, various injuries, laryngeal edema due to an allergic reaction, etc. can lead to a state of oxygen starvation of the brain in children. But most often such a diagnosis is made to children at birth.

Diagnosis of oxygen starvation of the brain

Diagnosis of oxygen starvation of the brain is carried out on the basis of complaints from patients, if possible, data from the words of relatives, laboratory and instrumental studies are carried out.

The patient's condition is assessed on the basis of indicators of a general blood test. Analyzed indicators such as erythrocytes, ESR, hematocrit, leukocytes, platelets, reticulocytes. An analysis of the composition of the blood will also determine the acid-base balance of the body, the gas composition of the venous and arterial blood, and therefore indicate the diseased organ.

The most accessible methods of instrumental diagnostics include pulse oximetry - a special device worn on a finger measures the level of oxygen saturation in the blood (the optimal content is 95-98%). Other means are electroencephalogram, computed and magnetic resonance imaging of the brain, electrocardiogram, rheovasography, which determines the volume of blood flow and its intensity in arterial vessels.

Differential Diagnosis

Treatment of oxygen starvation of the brain

Treatment of oxygen starvation of the brain consists in etiotropic therapy (treatment of the cause). Thus, exogenous hypoxia requires the use of oxygen masks and pillows. For the treatment of respiratory hypoxia, drugs that dilate the bronchi, analgesics, antihypoxanes that improve oxygen utilization are used. In case of hemic (reduced oxygen in the blood), a blood transfusion is performed, antidote drugs are prescribed for histoxic or tissue, circulatory (heart attacks, strokes) - cardiotropic. If such therapy is not possible, actions are aimed at eliminating symptoms: they regulate vascular tone, normalize blood circulation, prescribe drugs for dizziness, headache, blood-thinning, restorative, nootropic drugs and lowering bad cholesterol.

Medications

Metered aerosols are used as bronchodilators: truvent, atrovent, berodual, salbutamol.

Truvent is an aerosol can, when using it is necessary to remove the protective cap, shake it several times, lower the spray head down, take it with your lips and press on the bottom, inhaling deeply and holding the breath for a few moments. One push equals a serving. The effect comes in 15-30 minutes. Every 4-6 hours, the procedure is repeated, making 1-2 clicks, this is how long the effect of the drug lasts. Do not prescribe during pregnancy, angle-closure glaucoma, allergies. The use of the drug can reduce visual acuity, increase intraocular pressure.

Analgesics include a large list of drugs from the well-known analgin to completely unfamiliar names, each of which has its own pharmacological effect. The doctor will determine what is necessary in a particular situation. Here is a list of some of them: acamol, anopyrin, bupranal, pentalgin, cefecon, etc.

Bupranal is a solution in ampoules for intramuscular and intravenous injections, in syringe tubes for intramuscular injection. The maximum daily dose is 2.4 mg. The frequency of administration is every 6-8 hours. Possible side effects in the form of nausea, weakness, lethargy, dry mouth. Contraindicated in children under 16 years of age, during pregnancy and lactation, increased intracranial pressure, alcoholism.

The list of antidote drugs includes atropine, diazepam (mushroom poisoning), eufillin, glucose (carbon monoxide), magnesium sulfate, almagel (organic acids), unithiol, cuprenil (heavy metal salts), naloxone, flumazenil (drug poisoning), etc. .

Naloxone - available in ampoules, there is a special form for newborns. The recommended dose is 0.4-0.8 mg, it may be necessary to increase it to 15 mg. With increased sensitivity to the drug, an allergy occurs; in drug addicts, taking the drug causes a specific attack.

For strokes, cerebrolysin, actovegin, encephabol, papaverine, no-shpa are used.

Actovegin - exists in various forms: dragees, solutions for injections and infusions, gels, ointments, creams. Doses and method of application are prescribed by the doctor depending on the severity of the disease. Burn wounds, bedsores are treated externally. The use of the drug can cause hives, fever, sweating. It has contraindications for pregnant women, during breastfeeding, with allergies.

vitamins

A number of vitamins in tissue oxygen starvation are antidotes of toxic substances. So, vitamin K1 blocks the action of warfarin - an antithrombotic agent, vitamin B6 - poisoning with anti-tuberculosis drugs, vitamin C is used for damage by carbon monoxide, anilines used in dyes, medicines, chemicals. To maintain the body, it is also necessary to saturate it with vitamins.

Physiotherapy treatment

With general or local hypoxia of various nature, a physiotherapeutic treatment method such as oxygen therapy is used. The most common indications for its use are respiratory failure, circulatory disorders, cardiovascular diseases. There are various ways of oxygen saturation: cocktails, inhalations, baths, skin, subcutaneous, intraband methods, etc. Oxygenobarotherapy - breathing compressed oxygen in a pressure chamber relieves hypoxia. Depending on the diagnosis that led to hypoxia, UHF, magnetotherapy, laser therapy, massage, acupuncture, etc. are used.

Alternative treatment

One of the recipes for alternative treatment is breathing exercises according to the following method. Inhale slowly and deeply, hold for a few seconds and exhale slowly. Do several times in a row, increasing the duration of the procedure. Count to 4 on the inhale, to 7 on the breath hold, and to 8 on the exhale.

Garlic tincture will help strengthen blood vessels, reduce their spasms: fill a third of the jar with chopped garlic, filling it with water to the brim. After 2 weeks of infusion, start taking 5 drops per spoon of water before meals.

A prepared mixture of buckwheat, honey and walnuts, taken in equal proportions, is able to raise hemoglobin: grind cereals and nuts to a state of flour, add honey, mix. Take on an empty stomach in a tablespoon half an hour before meals. Fresh beet juice is also effective, which must be allowed to stand for some time before taking it so that volatile substances come out.

Ginger can help with asthma attacks. Combining its juice with honey and pomegranate juice, drink a spoonful 3 times a day.

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Herbal treatment

It is effective in oxygen starvation to take decoctions, infusions, herbal teas with antispasmodic action: chamomile, valerian, St. John's wort, motherwort, hawthorn. For problems with the respiratory system, take decoctions of medicinal preparations from coltsfoot, pine buds, plantain, licorice root, elder flowers. Hemoglobin levels can be raised with herbs such as nettle, yarrow, dandelion, wormwood.

Homeopathy

In combination with the main treatment, homeopathic remedies are increasingly present. Here are some of the remedies that can be prescribed for oxygen starvation and are aimed at the causes of its occurrence.

• Accardium - granules, which include metallic gold, mountain arnica, coculus-like anamyrta. It is aimed at the treatment of angina pectoris, cardiovascular failures caused by heavy physical exertion. Twice a day, 10 granules for half an hour before meals or one hour after, keep under the tongue until completely resorbed. The average course of treatment lasts 3 weeks. The drug has no contraindications and side effects. For use during pregnancy and children, a doctor's consultation is necessary.
• Atma® - drops, a complex drug for the treatment of bronchial asthma. The dose for children under one year is 1 drop per teaspoon of water or milk. Under the age of 12, 2 to 7 drops per tablespoon. After 12 years - 10 drops in pure form or in water. Continue treatment up to 3 months. Side effects were not observed.
• Vertigoheel - oral drops, used for dizziness, atherosclerosis of cerebral vessels, strokes. Drops are dissolved in water, when swallowed, they are retained for some time in the mouth. Recommended from the age of the child. Up to 3 years - 3 drops, at the age of 3-6 years - 5, the rest - 10 drops 3-4 times a day for a month. Hypersensitivity reactions are possible. Contraindicated in children under one year old, during pregnancy and lactation - with the permission of a doctor.
• Hawthorn compositum - homeopathic cardiological remedy, liquid. Adults are prescribed 15-20 drops three times a day, children - 5-7 drops. The drug has contraindications in case of allergy to components.
• Aesculus-compositum - drops, are used for post-embolic circulatory disorders, post-infarction and post-stroke conditions. Single dose - 10 drops in water, holding in the mouth. Frequency - 3 times a day. The duration of treatment is up to 6 weeks. Side effects are unknown. Contraindicated in pregnant women and hypersensitive to the components of the drug.

Surgery

Surgical treatment on the heart or blood vessels may be needed in the circulatory form of oxygen starvation, the development of which occurs rapidly and is associated with violations of their functions.

Prevention

Prevention of oxygen starvation primarily consists in organizing a daily healthy well-established life, which provides for normal nutrition, moderate physical activity, proper sleep, lack of stressful situations, quitting smoking and alcohol, finding enough time in the fresh air. It is necessary to monitor blood pressure, timely take preventive courses of existing diseases.

HYPOXIA (hypoxia; Greek, hypo- + lat. oxy oxygen; syn.: oxygen deprivation, oxygen starvation) - the state arising at insufficient supply of fabrics of an organism with oxygen or disturbance of its utilization in the course of biol, oxidation.

Hypoxia is observed very often and serves as a pathogenetic basis for various pathological processes; it is based on insufficient energy supply of vital processes. Hypoxia is one of the central problems of pathology.

Under normal conditions, the efficiency of biol, oxidation, which is the main source of energy-rich phosphorus compounds necessary for the function and renewal of structures, corresponds to the functional activity of organs and tissues (see Biological Oxidation). If this correspondence is violated, a state of energy deficiency occurs, leading to a variety of functional and morphol disorders, up to tissue death.

Depending on etiol, the factor, the rate of increase and the duration of the hypoxic state, the degree of G., the reactivity of the organism, etc. G.'s manifestations can vary significantly. The changes that occur in the body are a combination of the immediate consequences of the impact of the hypoxic factor, secondary disorders, as well as developing compensatory and adaptive reactions. These phenomena are closely related to each other and are not always amenable to a clear distinction.

Story

Domestic scientists have played an important role in studying the problem of hypoxia. The basis for the development of the problem of hypoxia was laid by I. M. Sechenov with fundamental work on the physiology of respiration and the gas exchange function of blood under conditions of normal, low, and high atmospheric pressure. V. V. Pashutin was the first to create a general doctrine of oxygen starvation as one of the main problems of general pathology and to a large extent determined the further development of this problem in Russia. In Lectures on General Pathology, Pashutin (1881) gave a classification of hypoxic conditions close to modern. P. M. Albitsky (1853-1922) established the importance of the time factor in the development of hyperthyroidism, studied the compensatory reactions of the body in the event of a lack of oxygen, and described the hypothermia that occurs with primary disorders of tissue metabolism. The problem of hypoxia was developed by E. A. Kartashevsky, N. V. Veselkin, H. N. Sirotinin, and I. R. Petrov, who paid special attention to the role of the nervous system in the development of hypoxic conditions.

Abroad Bert (P. Bert) studied the effect of fluctuations in barometric pressure on living organisms; studies of high-altitude and some other forms of G. belong to Zuntz and Levy (N. Zuntz, A. Loewy, 1906), Van Leer (E. Van Liere, 1942); mechanisms of disturbances of system of external respiration and their role in G.'s development were described by J. Haldane, Priestley (J. Priestley). The importance of blood for oxygen transport in the body was studied by J. Barcroft (1925). The role of tissue respiratory enzymes in G.'s development was studied in detail by O. Warburg (1948).

Classification

The classification of Barcroft (1925), who distinguished three types of G. (anoxia), was widely used: 1) anoxic anoxia, with a cut, the partial pressure of oxygen in the inhaled air and the oxygen content in arterial blood are reduced; 2) anemic anoxia, the cut is based on a decrease in the oxygen capacity of the blood at a normal partial pressure of oxygen in the alveoli and its tension in the blood; 3) congestive anoxia, resulting from circulatory failure with a normal oxygen content in arterial blood. Peters and Van Slyke (J. P. Peters, D. D. Van Slyke, 1932) proposed to distinguish between the fourth type - histotoxic anoxia, which occurs with some poisonings as a result of the inability of tissues to properly use oxygen. The term "anoxia", used by these authors and meaning the complete absence of oxygen or the complete cessation of oxidative processes, is unsuccessful and is gradually falling into disuse, since the complete absence of oxygen, as well as the cessation of oxidation, almost never occurs in the body during life.

At a conference on the problem of G. in Kyiv (1949), the following classification was recommended. 1. Hypoxic G.: a) from a decrease in the partial pressure of oxygen in the inhaled air; b) as a result of difficulty in the penetration of oxygen into the blood through the respiratory tract; c) due to respiratory disorders. 2. Hemic G.: a) anemic type; b) as a result of hemoglobin inactivation. 3. Circulatory G.: a) stagnant form; b) ischemic form. 4. Tissue G.

In the USSR, the classification proposed by I. R. Petrov (1949) is also widespread; It is based on the causes and mechanisms of G.

1. Hypoxia due to a decrease in the partial pressure of oxygen in the inhaled air (exogenous hypoxia).

2. G. at patol, the processes breaking supply of fabrics with oxygen at its normal content in the environment or utilization of oxygen from blood at its normal saturation with oxygen; this includes the following types: 1) respiratory (pulmonary); 2) cardiovascular (circulatory); 3) blood (hemic); 4) tissue (histotoxic) and 5) mixed.

In addition, I. R. Petrov considered it expedient to distinguish between the general and local hypoxic state.

According to modern concepts, G. (usually short-term) can also occur without the presence in the body of any patol, processes that disrupt oxygen transport or its utilization in tissues. This is observed in those cases when the functional reserves of oxygen transport and utilization systems, even with their maximum mobilization, are unable to satisfy the body's need for energy, which has sharply increased due to the extreme intensity of its functional activity. G. can also occur in conditions of normal or increased, in comparison with the norm, consumption of oxygen by tissues as a result of a decrease in the energy efficiency of biol, oxidation and a decrease in the synthesis of high-energy compounds, primarily ATP, per unit of absorbed oxygen.

In addition to the classification of hypoxia, based on the causes and mechanisms of its occurrence, it is customary to distinguish between acute and hron. G.; sometimes allocate subacute and fulminant forms. Exact criteria for G.'s differentiation on rate of development and duration of a current do not exist yet; however in a wedge, practice it is accepted to refer to the lightning-fast form of G., which developed within several tens of seconds, to acute within several minutes or tens of minutes, subacute - within several hours or tens of hours; to hron, to forms carry G. proceeding weeks, months and years.

Etiology and pathogenesis

Hypoxia due to a decrease in the partial pressure of oxygen in the inhaled air (exogenous type) occurs hl. arr. when climbing to a height (see Altitude sickness, Mountain sickness). With a very rapid decrease in barometric pressure (eg, in violation of the tightness of high-altitude aircraft), a symptom complex occurs that differs in pathogenesis and manifestations from altitude sickness and is called decompression sickness (see). The exogenous type of gas also occurs when the total barometric pressure is normal, but the partial pressure of oxygen in the inhaled air is lowered, for example, when working in mines, wells, in case of malfunctions in the oxygen supply system of the cabin of an aircraft, in submarines, deep-seated vehicles, diving and protective suits, etc., as well as during operations in case of malfunction of anesthesia and respiratory equipment.

With exogenous G., hypoxemia develops, i.e., the oxygen tension in the arterial blood, the saturation of hemoglobin with oxygen and its total content in the blood decrease. The immediate pathogenetic factor that causes the disorders observed in the body during exogenous G. is the reduced oxygen tension and the shift in the oxygen pressure gradient between the capillary blood and the tissue environment, which is unfavorable for gas exchange, associated with it. Hypocapnia can also have a negative effect on the body (see), which often develops with exogenous G. due to compensatory hyperventilation of the lungs (see Pulmonary ventilation). Severe hypocapnia leads to a deterioration in the blood supply to the brain and heart, alkalosis, an imbalance of electrolytes in the internal environment of the body and an increase in oxygen consumption by tissues. In such cases, adding small amounts of carbon dioxide to the inhaled air, eliminating hypocapnia, can significantly alleviate the condition.

If, along with a lack of oxygen in the air, there is a significant concentration of carbon dioxide, which occurs in Ch. arr. in various production conditions, G. can be combined with hypercapnia (see). Moderate Hypercapnia does not adversely affect the course of exogenous G. and can even have a beneficial effect, which is associated with ch. arr. with increased blood supply to the brain and myocardium. Significant hypercapnia is accompanied by acidosis, ionic imbalance, decreased arterial oxygen saturation, and other adverse effects.

Hypoxia in pathological processes that disrupt the supply or utilization of oxygen by tissues.

1. Respiratory (pulmonary) type G. occurs as a result of insufficiency of gas exchange in the lungs due to alveolar hypoventilation, violations of ventilation-perfusion relations, excessive shunting of venous blood, or when oxygen diffusion is difficult. Alveolar hypoventilation may be due to a violation of the airway (inflammatory process, foreign bodies, spasm), a decrease in the respiratory surface of the lungs (pulmonary edema, pneumonia), an obstacle to straightening the lungs (pneumothorax, exudate in the pleural cavity). It can also be caused by a decrease in the mobility of the osteochondral apparatus of the chest, paralysis or spastic condition of the respiratory muscles (myasthenia gravis, curare poisoning, tetanus), as well as a disorder of the central regulation of respiration due to a reflex or direct effect on the respiratory center of pathogenic factors.

Hypoventilation can occur with severe irritation of the respiratory tract receptors, severe pain in respiratory movements, hemorrhages, tumors, trauma in the medulla oblongata, an overdose of narcotic and sleeping pills. In all these cases, the minute volume of ventilation does not correspond to the needs of the body, the partial pressure of oxygen in the alveolar air and the oxygen tension in the blood flowing through the lungs decrease, as a result of which hemoglobin saturation and oxygen content in arterial blood may decrease significantly. The removal of carbon dioxide from the body is also usually disturbed, and Hypercapnia joins G.. With acutely developing alveolar hypoventilation (eg, when the airways are blocked by a foreign body, paralysis of the respiratory muscles, bilateral pneumothorax), asphyxia occurs (see).

Violations of ventilation-perfusion relations in the form of uneven ventilation and perfusion can be caused by local impairment of airway patency, extensibility and elasticity of the alveoli, uneven inhalation and exhalation, or local disorders of pulmonary blood flow (with spasm of bronchioles, pulmonary emphysema, pneumosclerosis, local depletion of the vascular bed of the lungs) . In such cases, pulmonary perfusion or pulmonary ventilation becomes insufficiently effective in terms of gas exchange and the blood flowing from the lungs is not sufficiently enriched with oxygen even with normal total minute volume of respiration and pulmonary blood flow.

With a large number of arterio-venous anastomoses, venous (by gas composition) blood passes into the arterial system of the systemic circulation, bypassing the alveoli, through intrapulmonary arterio-venous anastomoses (shunts): from the bronchial veins to the pulmonary vein, from the pulmonary artery to the pulmonary vein, etc. During intracardiac shunting (see congenital heart defects), venous blood is discharged from the right heart to the left. In terms of their consequences for gas exchange, such disturbances are similar to true insufficiency of external respiration, although, strictly speaking, they refer to circulatory disorders.

The respiratory type G. connected with difficulty of diffusion of oxygen is observed at the diseases which are followed by so-called. alveolo-capillary blockade, when the membranes separating the gaseous environment of the alveoli and blood are sealed (lung sarcoidosis, asbestosis, emphysema), as well as with interstitial pulmonary edema.

2. Cardiovascular (circulatory) type G. occurs when circulatory disorders leading to insufficient blood supply to organs and tissues. A decrease in the amount of blood flowing through tissues per unit of time may be due to hypovolemia, i.e., a general decrease in the mass of blood in the body (with massive blood loss, dehydration of the body during burns, cholera, etc.), a drop in cardiovascular activity. Often there are various combinations of these factors. Disorders of cardiac activity can be caused by damage to the heart muscle (eg, heart attack, cardiosclerosis), overload of the heart, electrolyte imbalance and extracardiac regulation of cardiac activity, as well as mechanical factors that impede the work of the heart (tamponade, obliteration of the pericardial cavity, etc.) cases, the most important indicator and pathogenetic basis of circulatory G. of cardiac origin is a decrease in cardiac output.

Circulatory G. of vascular origin develops with an excessive increase in the capacity of the vascular bed due to reflex and centrogenic disorders of vasomotor regulation (eg, massive irritation of the peritoneum, depression of the vasomotor center) or vascular paresis as a result of toxic effects (eg, in severe infectious diseases), allergic reactions , disturbances of electrolytic balance, at insufficiency of catecholamines, glucocorticoids and other patol, states at which the tone of vascular walls is broken. G. can arise in connection with widespread changes in the walls of the vessels of the microcirculation system (see), an increase in blood viscosity and other factors that prevent the normal movement of blood through the capillary network. Circulatory G. can be local in nature with insufficient arterial blood flow to an organ or tissue site (see Ischemia) or difficulty in the outflow of venous blood (see Hyperemia).

Quite often at the heart of circulatory G. complex combinations of various factors changing at development patol, process, for example, acute cardiovascular insufficiency at a collapse of various origin, shock, Addison's disease, etc. lie.

Hemodynamic indicators in different cases of circulatory G. can vary widely. The blood gas composition in typical cases is characterized by normal tension and oxygen content in arterial blood, a decrease in these indicators in venous blood, and a high arterio-venous oxygen difference.

3. Bloody (hemic) type G. occurs as a result of a decrease in the oxygen capacity of the blood in anemia, hydremia, and a violation of the ability of hemoglobin to bind, transport and give oxygen to tissues. The expressed G.'s symptoms at anemias (see) develop only at considerable absolute decrease in erythrocyte mass or sharply lowered content of hemoglobin in erythrocytes. This type of anemia occurs when bone marrow hematopoiesis is depleted on the basis of hron, bleeding (with tuberculosis, peptic ulcer, etc.), hemolysis (with poisoning with hemolytic poisons, severe burns, malaria, etc.), with inhibition of erythropoiesis by toxic factors (for example, lead , ionizing radiation), with bone marrow aplasia, as well as with a deficiency of the components necessary for normal erythropoiesis and hemoglobin synthesis (lack of iron, vitamins, etc.).

The oxygen capacity of the blood decreases with hydremia (see), with hydremic plethora (see). Violations of the transport properties of blood in relation to oxygen may be due to qualitative changes in hemoglobin. Most often, this form of hemic G. is observed in carbon monoxide poisoning (the formation of carboxyhemoglobin), methemoglobin-forming agents (see Methemoglobinemia), as well as in some genetically determined hemoglobin anomalies.

Hemic G. is characterized by a combination of normal oxygen tension in the arterial blood with its reduced content, in severe cases - up to 4-5 vol. %. With the formation of carboxyhemoglobin and methemoglobin, the saturation of the remaining hemoglobin and the dissociation of oxyhemoglobin in the tissues can be difficult, as a result of which the oxygen tension in the tissues and in the venous blood is significantly reduced while reducing the arterio-venous difference in oxygen content.

4. Tissue type G.(not quite accurately - histotoxic G.) occurs due to a violation of the ability of tissues to absorb oxygen from the blood or due to a decrease in the efficiency of biol, oxidation due to a sharp decrease in the conjugation of oxidation and phosphorylation. Utilization of oxygen by tissues can be hampered as a result of inhibition of biol, oxidation by various inhibitors, disruption of enzyme synthesis, or damage to the membrane structures of the cell.

A typical example of tissue G. caused by specific inhibitors of respiratory enzymes is cyanide poisoning. Once in the body, CN- ions very actively combine with ferric iron, blocking the final enzyme of the respiratory chain - cytochrome oxidase - and suppressing oxygen consumption by cells. Specific inhibition of respiratory enzymes is also caused by sulfide ions, antimycin A, etc. The activity of respiratory enzymes can be blocked by the type of competitive inhibition by structural analogs of natural oxidation substrates (see Antimetabolites). G. occurs when exposed to substances that block the functional groups of a protein or coenzyme, heavy metals, arsenites, monoiodacetic acid, etc. Tissue G. due to the suppression of various biol links, oxidation occurs with an overdose of barbiturates, some antibiotics, with an excess of hydrogen ions, exposure to toxic substances (eg, lewisite), toxic substances biol, origin, etc.

The cause of tissue G. may be a violation of the synthesis of respiratory enzymes with a deficiency of certain vitamins (thiamine, riboflavin, pantothenic acid, etc.). Violation of oxidative processes occurs as a result of damage to the membranes of mitochondria and other cellular elements, which is observed with radiation injury, overheating, intoxication, severe infections, uremia, cachexia, etc. Often, tissue G. occurs as a secondary patol, a process with G. exogenous, respiratory, circulatory or hemic type.

With tissue G., associated with a violation of the ability of tissues to absorb oxygen, tension, saturation and oxygen content in the arterial blood can remain normal up to a certain point, and in the venous blood they significantly exceed normal values. A decrease in the arterio-venous difference in oxygen content is a characteristic sign of tissue G, which occurs when tissue respiration is disturbed.

A peculiar variant of G. of the tissue type occurs with a pronounced dissociation of the processes of oxidation and phosphorylation in the respiratory chain. At the same time, oxygen consumption by tissues may increase, however, a significant increase in the proportion of energy dissipated in the form of heat leads to an energy “depreciation” of tissue respiration. There is a relative insufficiency of biol, oxidation, with a cut, despite the high intensity of the functioning of the respiratory chain, the resynthesis of high-energy compounds does not cover the needs of tissues, and the latter are essentially in a hypoxic state.

Agents that uncouple the processes of oxidation and phosphorylation include a number of substances of exogenous and endogenous origin: dinitrophenol, dicoumarin, gramicidin, pentachlorophenol, some microbial toxins, etc., as well as thyroid hormones - thyroxine and triiodothyronine. One of the most active uncoupling substances is 2-4-dinidgrophenol (DNF), under the influence of certain concentrations, oxygen consumption by tissues increases and, along with this, metabolic shifts characteristic of hypoxic conditions occur. Thyroid hormones - thyroxine and triiodothyronine in a healthy body, along with other functions, play the role of fiziol, a regulator of the degree of conjugation of oxidation and phosphorylation, thus influencing heat generation. An excess of thyroid hormones leads to an inadequate increase in heat production, an increased consumption of oxygen by tissues, and, along with this, to a deficiency of macroergs. Some of the main wedge, symptoms of thyrotoxicosis (see) are based on G., resulting from the relative insufficiency of biol, oxidation.

The mechanisms of action of various uncoupling agents on tissue respiration are not the same and in some cases have not yet been sufficiently studied.

The processes of free-radical (non-enzymatic) oxidation, which take place with the participation of molecular oxygen and tissue catalysts, play an important role in the development of some forms of tissue hygrogenesis. These processes are activated when exposed to ionizing radiation, increased oxygen pressure, deficiency of certain vitamins (eg, tocopherol), which are natural antioxidants, i.e., inhibitors of free radical processes in biol, structures, and also with insufficient oxygen supply to cells. Activation of free radical processes leads to destabilization of membrane structures (in particular, lipid components), changes in their permeability and specific function. In mitochondria, this is accompanied by uncoupling of oxidation and phosphorylation, i.e., leads to the development of the form of tissue hypoxia described above. Thus, strengthening of free radical oxidation can act as an underlying cause of tissue G. or be a secondary factor that occurs in other types of G. and leads to the development of its mixed forms.

5. Mixed type G. it is observed most often and represents a combination of two or more main types of G. In some cases, the hypoxic factor itself affects several links fiziol, oxygen transport and utilization systems. For example, carbon monoxide, actively entering into contact with the ferrous iron of hemoglobin, in high concentrations also has a direct toxic effect on cells, inhibiting the cytochrome enzyme system; nitrites along with the formation of methemoglobin can act as uncoupling agents; barbiturates suppress oxidative processes in tissues and at the same time inhibit the respiratory center, causing hypoventilation. In such cases, hypoxic conditions of a mixed type occur. Similar states arise at simultaneous impact on an organism of several factors, different on the mechanism of action, causing G.

More complex patol, the condition occurs, for example, after massive blood loss, when, along with hemodynamic disturbances, Hydremia develops as a result of increased fluid inflow from the tissues and increased water reabsorption in the renal tubules. This leads to a decrease in the oxygen capacity of the blood, and at a certain stage of the posthemorrhagic state, hemic G. can join the circulatory G., i.e., the body’s reactions to posthemorrhagic hypovolemia), which are adaptive in terms of hemodynamics, cause the transition of circulatory G. into mixed.

A mixed form of G. is often observed, the cut mechanism is that the initially arising hypoxic state of any type, having reached a certain degree, inevitably causes dysfunction of various organs and systems involved in ensuring the delivery of oxygen and its utilization in the body. Thus, in severe G. caused by insufficiency of external respiration, the function of the vasomotor centers and the conduction system of the heart suffers, the contractility of the myocardium decreases, the permeability of the vascular walls, the synthesis of respiratory enzymes is disturbed, the membrane structures of cells are disorganized, etc. This leads to disruption of blood supply and absorption oxygen tissues, as a result of which the circulatory and tissue ones join the primary respiratory type of G.. Almost any severe hypoxic condition is of a mixed nature (for example, with traumatic and other types of shock, coma of various origins, etc.).

Adaptive and compensatory reactions. Under the influence of factors that cause G., the first changes in the body are associated with the inclusion of reactions aimed at maintaining homeostasis (see). If adaptive reactions are insufficient, functional disorders begin in the body; at the expressed degree of G. structural changes occur.

Adaptive and compensatory reactions are carried out in a coordinated manner at all levels of integration of the organism and can only conditionally be considered separately. Distinguish between reactions aimed at adapting to relatively short-term acute G., and reactions that provide stable adaptation to less pronounced, but long-term existing or recurring G. Reactions to short-term G. are carried out through the physiol, mechanisms available in the body and usually occur immediately or shortly after start of action of the hypoxic factor. For adaptation to long-term G. in the body there are no well-formed mechanisms, but there are only genetically determined prerequisites that ensure the gradual formation of mechanisms for adaptation to constant or repetitive G. An important place among the adaptive mechanisms belongs to the oxygen transport systems: respiratory, cardiovascular and blood, as well as tissue oxygen utilization systems.

Reactions of the respiratory system to G. are expressed in an increase in alveolar ventilation due to the deepening of breathing, the increase in respiratory excursions, and the mobilization of reserve alveoli. These reactions arise reflex owing to irritation of hl. arr. chemoreceptors of the aortic-carotid zone and the brain stem by a changed gas composition of the blood or substances that cause tissue G. An increase in ventilation is accompanied by an increase in pulmonary circulation. At recurring or hron. G. in the course of adaptation of an organism correlation between pulmonary ventilation and perfusion can become more perfect. Compensatory hyperventilation can cause hypocapnia), edges, in turn, are compensated by the exchange of ions between plasma and erythrocytes, increased excretion of bicarbonates and basic phosphates in the urine, etc. Long-term G. in some cases (for example, during life in the mountains) is accompanied by an increase in diffusion surface of the lung alveoli due to hypertrophy of the lung tissue.

Compensatory reactions of the circulatory system are expressed by an increase in heart rate, an increase in the mass of circulating blood due to the emptying of blood depots, an increase in venous inflow, stroke and minute volume of the heart, blood flow velocity and redistributive reactions that provide preferential blood supply to the brain, heart and other vital organs through expansion in them arterioles and capillaries. These reactions are due to reflex influences from the baroreceptors of the vascular bed and general neurohumoral shifts characteristic of G.

Regional vascular reactions are also largely determined by the vasodilating effect of ATP breakdown products (ADP, AMP, adenine, adenosine, and inorganic phosphorus), which accumulate in hypoxic tissues. With adaptation to longer G., the formation of new capillaries can occur, which, along with a stable improvement in the blood supply to the organ, leads to a decrease in the diffusion distance between the capillary wall and the mitochondria of the cells. In connection with the hyperfunction of the heart and changes in neuro-endocrine regulation, myocardial hypertrophy may occur, which is of a compensatory-adaptive nature.

The reactions of the blood system are manifested by an increase in the oxygen capacity of the blood due to increased leaching of erythrocytes from the bone marrow and activation of erythropoiesis due to increased formation of erythropoietic factors (see Erythropoietins). Of great importance are the properties of hemoglobin (see), which allow to bind an almost normal amount of oxygen even with a significant decrease in the partial pressure of oxygen in the alveolar air and in the blood of the pulmonary vessels. So, at pO 2 equal to 100 mm Hg. Art., oxyhemoglobin is 95-97%, at pO2 80 mm Hg. st.- ok. 90%, and at pO 2 50 mm Hg. Art. - almost 80%. Along with this, oxyhemoglobin is able to give the tissues a large amount of oxygen even with a moderate decrease in pO 2 in the tissue fluid. Enhanced dissociation of oxyhemoglobin in tissues experiencing hypoxia is facilitated by acidosis developing in them, since with an increase in the concentration of hydrogen ions, oxyhemoglobin more easily splits off oxygen. The development of acidosis is associated with a change in metabolic processes that cause the accumulation of milk, pyruvic and other organic acids (see below). When adapting to hron. G. there is a persistent increase in the content of erythrocytes and hemoglobin in the blood.

In muscular organs, an increase in the content of myoglobin (see), which has the ability to bind oxygen even at low blood pressure, has an adaptive value; the resulting oxymyoglobin serves as a reserve of oxygen, which it gives up with a sharp decrease in pO2, helping to maintain oxidative processes.

Tissue adaptive mechanisms are implemented at the level of oxygen utilization systems, macroerg synthesis and their consumption. Such mechanisms are the restriction of the functional activity of organs and tissues that are not directly involved in providing oxygen transport, an increase in the conjugation of oxidation and phosphorylation, and an increase in anaerobic ATP synthesis due to the activation of glycolysis. Tissue resistance to G. also increases as a result of excitation of the hypothalamic-pituitary system and increased production of glucocorticoids, which stabilize lysosome membranes. At the same time, glucocorticoids activate some enzymes of the respiratory chain and contribute to a number of other metabolic effects of an adaptive nature.

An increase in the number of mitochondria per unit cell mass and, accordingly, an increase in the capacity of the oxygen utilization system are of great importance for stable adaptation to G.. This process is based on the activation of the genetic apparatus of cells responsible for the synthesis of mitochondrial proteins. It is believed that a certain degree of deficiency of macroergs and a corresponding increase in the phosphorylation potential serve as an incentive signal for such activation.

However, compensatory and adaptive mechanisms have a certain limit of functional reserves, in connection with which the state of adaptation to G. with excessive intensity or long duration of exposure to factors that cause G. can be replaced by a stage of exhaustion and decompensation, leading to pronounced functional and structural disorders up to irreversible . These disorders in different organs and tissues are not the same. For example, a bone, a cartilage, a sinew are insensitive to G. and can keep normal structure and viability within many hours at complete cessation of supply with oxygen. The nervous system is most sensitive to G.; its various departments differ in unequal sensitivity. So, with a complete cessation of oxygen supply, signs of disturbance in the cerebral cortex are detected after 2.5-3 minutes, in the medulla oblongata - after 10-15 minutes, in the ganglia of the sympathetic nervous system and intestinal plexus neurons - after more than 1 hour. At the same time, parts of the brain that are in an excited state suffer more than those that are inhibited.

In the process of G.'s development, changes in the electrical activity of the brain occur. After a certain latent period, in most cases, an activation reaction occurs, which is expressed in desynchronization of the electrical activity of the cerebral cortex and increased high-frequency oscillations. The activation reaction is followed by a stage of mixed electrical activity consisting of delta and beta waves while maintaining frequent oscillations. In the future, delta waves begin to dominate. Sometimes the transition to the delta rhythm occurs suddenly. With further deepening of G., the electrocorticogram (ECoG) breaks up into separate groups of irregularly shaped oscillations, including polymorphic delta waves in combination with low oscillations of a higher frequency. Gradually, the amplitude of all types of waves falls and complete electrical silence sets in, which corresponds to deep structural disturbances. Sometimes it is preceded by low-amplitude frequent fluctuations that appear on the ECoG after the disappearance of slow activity. These ECoG changes can develop very quickly. So, after the cessation of breathing, the bioelectrical activity drops to zero after 4-5 minutes, and even faster after the circulatory arrest.

The sequence and expressiveness of functional disturbances at G. depends on etiol, a factor, rate of development of G., etc. blood is better than other organs and tissues (the so-called centralization of blood circulation), and therefore, despite the high sensitivity of the brain to G., it may suffer to a lesser extent than peripheral organs, for example, the kidneys, liver, where irreversible changes can develop, leading to death after the release of the body from the hypoxic state.

The change in metabolism first of all occurs in the field of carbohydrate and energy metabolism, closely related to biol. oxidation. In all cases of G., the primary shift is macroerg deficiency, which is expressed in a decrease in the content of ATP in cells with a simultaneous increase in the concentration of its decay products - ADP, AMP and inorganic phosphate. A characteristic indicator of G. is an increase in the so-called. phosphorylation potential, which is a ratio. In some tissues (especially in the brain), an even earlier sign of G. is a decrease in the content of creatine phosphate. So, after a complete cessation of blood supply, the brain tissue loses approx. 70% creatine phosphate, and after 40-45 sec. it disappears completely; somewhat slower, but in a very short time, the content of ATP falls. These shifts are due to the lag in the formation of ATP from its consumption in the processes of vital activity and occur the more easily, the higher the functional activity of the tissue. The consequence of these shifts is an increase in glycolysis due to the loss of the inhibitory effect of ATP on the key enzymes of glycolysis, as well as as a result of the activation of the latter by ATP decay products (other ways of activating glycolysis in G. are also possible). Increased glycolysis leads to a drop in glycogen content and an increase in the concentration of pyruvate and lactate. A significant increase in the content of lactic acid is also facilitated by its slow inclusion in further transformations in the respiratory chain and the difficulty in the processes of glycogen resynthesis that occur under normal conditions with the consumption of ATP. An excess of lactic, pyruvic and some other organic acids contributes to the development of metabolic acidosis (see).

The insufficiency of oxidative processes entails a number of other metabolic shifts that increase with the deepening of G. The intensity of the metabolism of phosphoproteins and phospholipids slows down, the content of essential amino acids in the serum decreases, the content of ammonia in tissues increases and the content of glutamine decreases, a negative nitrogen balance occurs.

As a result of lipid metabolism disorders, hyperketonemia develops, acetone, acetoacetic and beta-hydroxybutyric acids are excreted in the urine.

The exchange of electrolytes is broken, and first of all processes of active movement and distribution of ions on biol, membranes; increases, in particular, the amount of extracellular potassium. The processes of synthesis and enzymatic destruction of the main mediators of nervous excitation, their interaction with receptors, and a number of other important metabolic processes that occur with the consumption of energy of macroergic bonds are disrupted.

There are also secondary metabolic disorders associated with acidosis, electrolyte, hormonal, and other shifts characteristic of G. With further deepening of G., glycolysis is also inhibited, and the processes of destruction and decay are intensified.

pathological anatomy

Macroscopic G.'s signs are not numerous and nonspecific. In some forms of hypoxia, congestion in the skin and mucous membranes, venous plethora and edema of internal organs, especially the brain, lungs, abdominal organs, petechial hemorrhages in serous and mucous membranes can be observed.

The most universal sign of the hypoxic state of cells and tissues and an important pathogenetic element of G. is an increase in the passive permeability of biol, membranes (basement membranes of blood vessels, cell membranes, mitochondrial membranes, etc.). Disorganization of membranes leads to the release of enzymes from subcellular structures and cells into tissue fluid and blood, which plays a significant role in the mechanisms of secondary hypoxic tissue alteration.

An early sign of G. is a violation of the microvasculature - stasis, plasma soaking and necrobiotic changes in the vascular walls with a violation of their permeability, the release of plasma into the pericapillary space.

Microscopic changes in parenchymal organs in acute G. are expressed in granular, vacuolar, or fatty degeneration of parenchymal cells, and the disappearance of glycogen from cells. At sharply expressed G. there can be sites of a necrosis. Edema, mucoid or fibrinoid swelling develop in the intercellular space up to fibrinoid necrosis.

In a severe form of acute G., various degrees of damage to neurocytes are detected early, up to irreversible ones.

Vacuolization, chromatolysis, hyperchromatosis, crystalline inclusions, pycnosis, acute swelling, ischemic and homogenizing state of neurons, shadow cells are found in brain cells. During chromatolysis, a sharp decrease in the number of ribosomes and elements of the granular and agranular reticulum is observed, and the number of vacuoles increases (Fig. 1). With a sharp increase in osmiophilia, the nuclei and cytoplasm of mitochondria change dramatically, numerous vacuoles and dark osmiophilic bodies appear, and the cisterns of the granular reticulum are expanded (Fig. 2).

Changes in the ultrastructure make it possible to distinguish the following types of damage to neurocytes: 1) cells with a light cytoplasm, a decrease in the number of organelles, a damaged nucleus, and focal destruction of the cytoplasm; 2) cells with increased osmiophilia of the nucleus and cytoplasm, which is accompanied by changes in almost all components of the neuron; 3) cells with an increase in the number of lysosomes.

Vacuoles of various sizes appear in the dendrites, less often fine-granular osmiophilic material. An early symptom of axonal injury is mitochondrial swelling and destruction of neurofibrils. Some synapses change noticeably: the presynaptic process swells, increases in size, the number of synaptic vesicles decreases, sometimes they stick together and are located at a certain distance from the synaptic membranes. In the cytoplasm of presynaptic processes, osmiophilic filaments appear, which do not reach a significant length and do not acquire the shape of a ring, mitochondria change markedly, vacuoles, dark osmiophilic bodies appear.

The severity of changes in cells depends on the severity of G. In cases of severe G., a deepening of the pathology of the cell may occur after the elimination of the cause that caused G.; in cells that do not show signs of serious damage within a few hours, after 1-3 days. and later structural changes of varying severity can be detected. In the future, such cells undergo decay and phagocytosis, which leads to the formation of softening foci; however, a gradual restoration of the normal structure of cells is also possible.

Glial cells also show dystrophic changes. In astrocytes, a large number of dark osmiophilic glycogen granules appear. Oligodendroglia tends to proliferate, the number of satellite cells increases; they show swollen mitochondria without cristae, large lysosomes and accumulations of lipids, and an excess of elements of the granular reticulum.

In the endothelial cells of the capillaries, the thickness of the basement membrane changes, a large number of phagosomes, lysosomes, and vacuoles appear; this is associated with pericapillary edema. Changes in capillaries and an increase in the number and volume of astrocyte processes indicate cerebral edema.

At hron. G. morfol, changes in nerve cells are usually less pronounced; glial cells c. n. With. at hron. G. are activated and intensively proliferate. Violations in the peripheral nervous system are thickening, tortuosity and decay of the axial cylinders, swelling and decay of the myelin sheaths, spherical swellings of the nerve endings.

For chron. G. is characterized by a slowdown in regenerative processes in case of tissue damage: inhibition of the inflammatory reaction, slowing down the formation of granulations and epithelialization. Inhibition of proliferation can be associated not only with insufficient energy supply of anabolic processes, but also with excessive intake of glucocorticoids into the blood, which leads to a lengthening of all phases of the cell cycle; in this case, the transition of cells from the postmitotic phase to the phase of DNA synthesis is especially clearly blocked. Chron. G. leads to a decrease in lipolytic activity, in connection with which the development of atherosclerosis is accelerated.

Clinical signs

Respiratory disorders in typical cases of acute increasing G. are characterized by several stages: after activation, which is expressed in deepening of breathing and (or) increased respiratory movements, a dyspnoetic stage occurs, manifested by various rhythm disturbances, uneven amplitudes of respiratory movements. This is followed by a terminal pause in the form of a temporary cessation of breathing and terminal (agonal) breathing, represented by rare, short powerful respiratory excursions, gradually weakening until complete cessation of breathing. The transition to agonal breathing can also occur without a terminal pause through the stage of the so-called. apneustic breathing, characterized by long inspiratory delays, or through the stage of alternating agonal respiratory excursions with the usual and gradual reduction of the latter (see Agony). Sometimes some of these steps may be missing. The dynamics of respiration with increasing G. is determined by the afferent entering the respiratory center from various receptor formations excited by the shifts occurring during hypoxia in the internal environment of the body, and by a change in the functional state of the respiratory center (see).

Violations of cardiac activity and blood circulation can be expressed in tachycardia, which increases in parallel with the weakening of the mechanical activity of the heart and a decrease in stroke volume (the so-called thready pulse). In other cases, a sharp tachycardia is suddenly replaced by bradycardia, accompanied by a blanching of the face, cold extremities, cold sweat and fainting. Often there are various violations of the conduction system of the heart and rhythm disorders up to atrial fibrillation and ventricular fibrillation (see Cardiac arrhythmias).

At first, blood pressure tends to increase (if G. is not caused by circulatory failure), and then, as the hypoxic state develops, it decreases more or less rapidly, due to inhibition of the vasomotor center, impaired properties of the vascular walls, and a decrease in cardiac output and cardiac output. In connection with hypoxic alteration of the smallest vessels, a change in blood flow through the tissues, a disorder of the microcirculation system occurs, accompanied by difficulty in the diffusion of oxygen from capillary blood into cells.

The functions of the digestive organs are disturbed: the secretion of the digestive glands, the motor function of the digestive tract.

The function of the kidneys undergoes complex and ambiguous changes that are associated with disorders of general and local hemodynamics, hormonal effects on the kidneys, shifts in the acid-base and electrolyte balance, etc. With significant hypoxic alteration of the kidneys, insufficiency of their function develops up to the complete cessation of urine formation and uremia.

With the so-called lightning-fast G., advancing, for example, when inhaling nitrogen, methane, helium without oxygen, prussic to-you high concentration, fibrillation and cardiac arrest are observed, most of the wedge, there are no changes, because very quickly there is a complete cessation of vital bodily functions.

Hron, G.'s forms arising at long insufficiency of blood circulation, breath, at diseases of blood and other conditions which are followed by persistent disturbances of oxidizing processes in fabrics are clinically characterized by increased fatigue, an asthma and heartbeat at small physical. load, decreased immune reactivity, reproductive capacity and other disorders associated with gradually developing dystrophic changes in various organs and tissues. In bark of big hemispheres both at acute, and at hron. G. the functional and structural changes which are the main in a wedge, G.'s picture and in the prognostic relation develop.

Cerebral hypoxia is observed in cerebrovascular accidents, shock conditions, acute cardiovascular insufficiency, transverse heart block, carbon monoxide poisoning and asphyxia of various origins. G. of the brain can occur as a complication during operations on the heart and great vessels, as well as in the early postoperative period. At the same time various nevrol, syndromes and mental shifts develop, and all-cerebral symptoms, diffusive frustration of functions of c prevail. n. With.

Initially, active internal inhibition is disrupted; excitation, euphoria develops, a critical assessment of one's state decreases, motor anxiety appears. Following a period of excitement, and often without it, symptoms of depression of the cerebral cortex appear: lethargy, drowsiness, tinnitus, headache, dizziness, urge to vomit, sweating, general lethargy, deafness, and more pronounced disorders of consciousness. I can "appear clonic and tonic convulsions, involuntary urination and defecation.

With severe G., a soporous state develops: patients are stunned, inhibited, sometimes they perform elementary tasks, but after repeated repetition, they quickly stop vigorous activity. The duration of the soporous state ranges from 1.5-2 hours. up to 6-7 days, sometimes up to 3-4 weeks. Periodically, consciousness clears up, but the patients remain stunned. Pupil inequality (see. Anisocoria), uneven palpebral fissures, nystagmus (see), asymmetry of the nasolabial folds, muscle dystonia, increased tendon reflexes, abdominal reflexes are depressed or absent; patol, pyramidal symptoms of Babinsky, etc. appear.

With a longer and deeper oxygen starvation, mental disorders can occur in the form of Korsakov's syndrome (see), which is sometimes combined with euphoria, apathetic-abulic and astheno-depressive syndromes (see Apathetic syndrome, Asthenic syndrome, Depressive syndromes), sensory synthesis disorders (the head, limbs or the whole body seem to be numb, alien, the dimensions of body parts and surrounding objects are changed, etc.). A psychotic state with paranoid-hypochondriacal experiences is often combined with verbal hallucinations on a dreary-anxious affective background. In the evening and at night, episodes may occur in the form of delirious, delirious-oneiric and delirious-amental states (see Amental syndrome, Delirious syndrome).

With a further increase in G., a deepening of the coma occurs. The rhythm of breathing is disturbed, sometimes patol develops, Cheyne-Stokes, Kussmaul, etc. breathing develops. Hemodynamic parameters are unstable. Corneal reflexes are reduced, divergent strabismus, anisocoria, floating movements of the eyeballs can be detected. The tone of the muscles of the extremities is weakened, tendon reflexes are often depressed, rarely elevated, sometimes a bilateral Babinsky reflex is detected.

Clinically, four degrees of acute cerebral hypoxia can be distinguished.

I degree G. manifested by lethargy, stupor, anxiety or psychomotor agitation, euphoria, increased blood pressure, tachycardia, muscle dystonia, foot clonus (see Clonus). Tendon reflexes are increased with the expansion of reflexogenic zones, abdominal reflexes are depressed; there is patol, Babinsky's reflex, etc. Slight anisocoria, uneven palpebral fissures, nystagmus, weakness of convergence, asymmetry of the nasolabial folds, deviation (deviation) of the tongue. These disorders persist in the patient from several hours to several days.

II degree It is characterized by a soporous state for from several hours to 4-5 days, less often several weeks. The patient has anisocoria, uneven palpebral fissures, paresis of the facial nerve in the central type, reflexes from the mucous membranes (corneal, pharyngeal) are reduced. Tendon reflexes are increased or decreased; there are reflexes of oral automatism, bilateral pyramidal symptoms. Clonic convulsions may occur intermittently, usually starting in the face, then moving to the limbs and trunk; disorientation, weakening of memory, impaired mnestic functions, psychomotor agitation, delirious-amental states.

III degree manifested by deep stupor, mild, and sometimes severe coma. Quite often there are clonic convulsions; myoclonus of the muscles of the face and extremities, tonic convulsions with flexion of the upper and extension of the lower extremities, hyperkinesis such as chorea (see) and automated gestures, oculomotor disorders. There are reflexes of oral automatism, bilateral patol, reflexes, tendon reflexes are often reduced, grasping and sucking reflexes appear, muscle tone is reduced. When G. II - III degree, hyperhidrosis, hypersalivation, lacrimation occur; persistent hyperthermic syndrome can be observed (see).

With IV degree G. develops a deep coma: inhibition of the functions of the cerebral cortex, subcortical and stem formations. The skin is cold to the touch, the patient's face is amimic, the eyeballs are motionless, the pupils are wide, there is no reaction to light; the mouth is half-open, the parted eyelids rise in time with the breath, which is intermittent, arrhythmic (see Biot's breathing, Cheyne-Stokes' breathing). Cardiac activity and vascular tone fall, sharp cyanosis.

Then a terminal, or beyond, coma develops; the functions of the cerebral cortex, subcortical and stem formations of the brain fade away.

Sometimes vegetative functions are suppressed, trophism is disturbed, water-salt metabolism changes, tissue acidosis develops. Life is supported by artificial respiration and by means of tonic cardiovascular activity.

When a patient is taken out of a coma, the functions of the subcortical centers are first restored, then the cerebellar cortex, higher cortical functions, mental activity; there are transient movement disorders - involuntary erratic movements of the limbs or ataxia; overshooting and intentional tremor during the finger-nose test. Usually, on the second day after coming out of a coma and normalization of breathing, stupor and severe asthenia are observed; within a few days, the study causes reflexes of oral automatism, bilateral pyramidal and protective reflexes, sometimes visual and auditory agnosia, apraxia are noted.

Mental disorders (night episodes of abortive delirium, perception disorders) persist for 3-5 days. Patients are in a pronounced asthenic state for a month.

At hron. G. marked increased fatigue, irritability, lack of restraint, exhaustion, decreased intellectual and mnestic functions, disorders of the emotional-volitional sphere: narrowing of the range of interests, emotional instability. In advanced cases, intellectual insufficiency, weakening of memory and a decrease in active attention are determined; depressed mood, tearfulness, apathy, indifference, rarely complacency, euphoria. Patients complain of headache, dizziness, nausea, sleep disorders. They are often sleepy during the day and suffer from insomnia at night, fall asleep with difficulty, sleep is shallow, intermittent, often with nightmares. After sleep, patients feel tired.

Vegetative disorders are noted: pulsation, noise and ringing in the head, darkening in the eyes, a feeling of heat and flushes to the head, palpitations, pain in the heart, shortness of breath. Sometimes there are seizures with loss of consciousness and convulsions (epileptiform seizures). In hard cases hron. G. there may be symptoms of a diffuse disorder of the functions of c. n. N of page, corresponding to that at acute G.

Rice. 3. Electroencephalograms of patients with cerebral hypoxia (multichannel recording). The occipitocentral leads are presented: d - on the right, s - on the left. I. Normal type of electroencephalogram (for comparison). An alpha rhythm is recorded, well modulated, with a frequency of 10-11 oscillations per second, with an amplitude of 50-100 microvolts. II. Electroencephalogram of a patient with cerebral hypoxia of the 1st degree. Flashes of bilaterally synchronous oscillations of theta waves are recorded, which indicates changes in the functional state of the deep structures of the brain and a violation of the cortical-stem relationships. III. Electroencephalogram of a patient with cerebral hypoxia II degree. Against the background of dominance in all areas of multiple (slow) theta waves of an irregular beta rhythm, predominantly of low frequency, flashes of bilaterally synchronous groups of oscillations of theta waves with pointed peaks are recorded. This indicates a change in the functional state of meso-diencephalic formations and a state of "convulsive readiness" of the brain. IV. Electroencephalogram of a patient with cerebral hypoxia III degree. Significant diffuse changes in the form of the absence of an alpha rhythm, dominance in all areas of irregular slow activity - high-amplitude theta and delta and waves, individual sharp waves. This indicates signs of a diffuse disturbance of cortical neurodynamics, a broad diffuse reaction of the cerebral cortex to the pathological process. V. Electroencephalogram of a patient with IV degree cerebral hypoxia (in coma). Significant diffuse changes in the form of dominance in all areas of slow activity, mainly in the delta rhythm ///. VI. Electroencephalogram of the same patient in a state of transcendental coma. Diffuse decrease in the bioelectric activity of the brain, gradual "flattening" of the curves and their approach to the isoline, up to complete "bioelectric silence".

An electroencephalographic study of the brain (see Electroencephalography) with G. I degree on the EEG (Fig. 3, II) shows a decrease in the amplitude of biopotentials, the appearance of a mixed rhythm with a predominance of theta waves with a frequency of 5 oscillations per 1 second, an amplitude of 50-60 microvolts ; increased reactivity of the brain to external stimuli. At G. of the II degree on EEG (fig. 3, III) diffuse slow waves, flashes of a theta - and delta waves in all assignments are registered. The alpha rhythm is reduced to amplitude, not regular enough. Sometimes the condition of the so-called. convulsive readiness of the brain in the form of sharp waves, multiple spike potentials of paroxysmal discharges of high-amplitude waves. The reactivity of the brain to external stimuli is increased. On the EEG of patients with G. III degree (Fig. 3, IV), a mixed rhythm is recorded with a predominance of slow waves, sometimes paroxysmal flashes of slow waves, in some patients there is a low amplitude level of the curve, a monotonous curve consisting of high-amplitude (up to 300 μV) regular slow waves theta and delta. Brain reactivity is reduced or absent; in process of G.'s strengthening on EEG slow waves begin to prevail, the EEG curve is gradually flattened.

In patients with IV degree G. on the EEG (Fig. 3, V), a very slow, irregular, irregularly shaped rhythm is recorded (0.5-1.5 fluctuations per 1 sec.). The reactivity of the brain is absent. In patients in a state of transcendental coma, the reactivity of the brain is absent and the so-called. bioelectrical silence of the brain (Fig. 3, VI).

With a decrease in comatose phenomena and when the patient is removed from a coma, sometimes a monomorphic electroencephalographic curve is noted on the EEG, consisting of high-amplitude theta and delta waves, which reveals gross patol, changes - diffuse damage to the structures of brain neurons.

Rheoencephalographic study (see. Rheoencephalography ) at G. I and II degrees, an increase in the amplitude of REG waves, sometimes an increase in the tone of the cerebral vessels, is revealed. At G. III and IV degrees decrease and the progressing decrease in amplitude of REG waves is registered. A decrease in the amplitude of REG waves in patients with grade III and IV grades and a progressive course reflects a deterioration in the blood supply to the brain due to a violation of general hemodynamics and the development of cerebral edema.

Diagnostics

Diagnosis is based on symptoms that characterize the activation of compensatory mechanisms (shortness of breath, tachycardia), signs of brain damage and the dynamics of neurological disorders, hemodynamic data (BP, ECG, cardiac output, etc.), gas exchange, acid-base balance, hematological (hemoglobin, erythrocytes, hematocrit) and biochemical (milk and pyruvic to-you in the blood, sugar, blood urea, etc.) analyzes. Of particular importance is taking into account the dynamics of the wedge, symptoms and their comparison with the dynamics of electroencephalographic data, as well as indicators of the gas composition of the blood and acid-base balance.

To clarify the causes of the occurrence and development of G., the diagnosis of such diseases and conditions as cerebral embolism, cerebral hemorrhage (see Stroke), intoxication of the body with acute renal failure (see) and liver failure (see Hepatargy) is of great importance. , as well as hyperglycemia (see) and hypoglycemia (see).

Treatment and prevention

Due to the fact that in clinical practice mixed forms of G. are usually found, it may be necessary to use the complex to lay down. - prof. measures, the nature of which depends on the cause of G. in each case.

In all cases, gastroduodenitis caused by a lack of oxygen in the inhaled air, the transition to breathing with normal air or oxygen leads to rapid and, if gastronomy has not gone far, to the complete elimination of all functional disorders; in some cases, it is advisable to add 3-7% carbon dioxide to stimulate the respiratory center, expand the vessels of the brain and heart, and prevent hypocapnia. At inhalation of pure oxygen after rather long exogenous G. non-threatening short-term dizzinesses, clouding of consciousness can take place.

With respiratory G., along with oxygen therapy and stimulation of the respiratory center, measures are taken to eliminate obstacles in the airways (changing the position of the patient, holding the tongue, if necessary, intubation and tracheotomy), and surgical treatment of pneumothorax is performed.

Patients with severe respiratory failure or in cases of absence of spontaneous breathing are given auxiliary (artificial deepening of spontaneous breathing) or artificial respiration, artificial ventilation of the lungs (see). Oxygen therapy should be long-term, continuous, with a content of 40-50% oxygen in the inhaled mixture, sometimes short-term use of 100% oxygen is necessary. At circulatory G. appoint warm and hypertensive means, blood transfusion, electropulse therapy (see) and other measures normalizing blood circulation; in some cases oxygen therapy is shown (see). In case of cardiac arrest, indirect heart massage, electrical defibrillation, according to indications - endocardial electrical stimulation of the heart, adrenaline, atropine are injected and other resuscitation measures are carried out (see).

At hemic type G. carry out transfusion of blood or erythrocyte mass, stimulate hematopoiesis. In cases of poisoning with methemoglobin formers - massive bloodletting and exchange hemotransfusion; in case of carbon monoxide poisoning, along with the inhalation of oxygen or carbogen, exchange hemotransfusion is prescribed (see Blood transfusion).

For treatment, in some cases, hyperbaric oxygenation is used (see) - a method consisting in the use of oxygen under high pressure, which leads to an increase in its diffusion into hypoxic tissue areas.

For G.'s therapy and prevention, drugs are also used that have an antihypoxic effect that is not associated with an effect on oxygen delivery systems in tissues; some of them increase resistance to G. by reducing the overall level of vital activity, mainly the functional activity of the nervous system, and reducing energy consumption. To pharmakol, means of this type include narcotic and neuroleptic drugs, drugs that lower body temperature, etc.; some of them are used in surgical interventions together with general or local (craniocerebral) hypothermia to temporarily increase the body's resistance to G. In some cases, glucocorticoids have a beneficial effect.

If the acid-base balance and electrolyte balance are disturbed, appropriate drug correction and symptomatic therapy are carried out (see Alkalosis, Acidosis).

To intensify carbohydrate metabolism, in some cases, 5% glucose solution (or glucose with insulin) is administered intravenously. Improving the energy balance and reducing the need for oxygen in ischemic strokes, according to some authors (B. S. Vilensky et al., 1976), can be achieved by the introduction of drugs that increase the resistance of brain tissue to G.: sodium oxybutyrate affects the cortical structures, droperidol and diazepam (seduxen) - mainly on the subcortical-stem sections. Activation of energy metabolism is carried out by the introduction of ATP and cocarboxylase, an amino acid link - by intravenous administration of gammalon and cerebrolysin; use drugs that improve the absorption of oxygen by brain cells (desclidium, etc.).

Among the chemotherapeutic agents that are promising in terms of use to reduce the manifestations of acute G., there are benzoquinones - compounds with pronounced redox properties. Protective properties have preparations such as gutimin and its derivatives.

For the prevention and treatment of cerebral edema apply appropriate to lay down. measures (see Edema and swelling of the brain).

With psychomotor agitation, solutions of neuroleptics, tranquilizers, sodium hydroxybutyrate are administered in dosages corresponding to the condition and age of the patient. In some cases, if the excitement is not stopped, then barbituric anesthesia is performed. With convulsions, intravenous seduxen or barbituric anesthesia is prescribed. In the absence of effect and recurring seizures, artificial ventilation of the lungs is done with the introduction of muscle relaxants and anticonvulsants, inhalation oxygen-oxygen anesthesia, etc.

For the treatment of G.'s consequences, dibazol, galanthamine, glutamic acid, sodium oxybutyrate, gamma-aminobutyric acid preparations, cerebrolysin, ATP, cocarboxylase, pyridoxine, methandrostenolone (nerobol), tranquilizers, restorative agents, as well as massage and treatment are used in appropriate combinations. . physical education.

In experimental and partly in a wedge. conditions investigated a number of substances - the so-called. antihypoxants, the antihypoxic effect of which is associated with their direct influence on the processes of biological oxidation. These substances can be divided into four groups.

The first group includes substances that are artificial electron carriers, capable of unloading the respiratory chain and NAD-dependent cytoplasmic dehydrogenases from excess electrons. The possible inclusion of these substances as electron acceptors in the chain of respiratory enzymes during G. is determined by their redox potential and chemical features. structures. Among the substances of this group, the drug cytochrome C, hydroquinone and its derivatives, methylphenazine, phenazine metasulfate and some others were studied.

The action of the second group of antihypoxants is based on the ability to inhibit energetically low-value free (non-phosphorylating) oxidation in microsomes and the external respiratory chain of mitochondria, which saves oxygen for oxidation associated with phosphorylation. A number of thioamidines of the gutimine group have a similar property.

The third group of antihypoxic agents (eg, fructose-1, 6-diphosphate) are phosphorylated carbohydrates that allow the formation of ATP anaerobically and allow certain intermediate reactions in the respiratory chain to be carried out without the participation of ATP. The possibility of directly using ATP preparations introduced from the outside into the blood as an energy source for cells is doubtful: in realistically acceptable doses, these preparations can cover only a very small part of the body's energy needs. In addition, exogenous ATP can decompose already in the blood or undergo cleavage by nucleoside phosphatases of the endothelium of blood capillaries and other biol, membranes, without bringing energy-rich bonds to the cells of vital organs, but the possibility of a positive effect of exogenous ATP on the hypoxic state cannot be completely ruled out.

The fourth group includes substances (eg, pangamic acid), which remove the products of anaerobic metabolism and thereby facilitate oxygen-independent pathways for the formation of energy-rich compounds.

Improving energy supply can also be achieved through a combination of vitamins (C, B 1 , B 2 , B 6 , B 12 , PP, folic, pantothenic acid, etc.), glucose, substances that increase the conjugation of oxidation and phosphorylation.

Of great importance in the prevention of hypoxia are special exercises that increase the ability to adapt to hypoxia (see below).

Forecast

The prognosis depends primarily on the degree and duration of G., as well as on the severity of damage to the nervous system. Moderate structural changes in brain cells are usually more or less reversible, with pronounced changes, foci of softening of the brain can form.

In patients who have undergone acute G. I degree, asthenic phenomena usually persist for no more than 1-2 weeks. After removal from G. of the II degree at some patients the general spasms can arise within several days; during the same period, transient hyperkinesis, agnosia, cortical blindness, hallucinations, attacks of excitement and aggressiveness, dementia can be observed. Severe asthenia and some mental disorders can sometimes persist for a year.

In patients who have undergone G. III degree, intellectual-mnestic disorders, disorders of cortical functions, convulsive seizures, movement and sensitivity disorders, symptoms of damage to the brain stem and spinal disorders can be detected in long-term periods; psychopathization of the personality persists for a long time.

The prognosis worsens with increasing phenomena of edema and damage to the brain stem (paralytic mydriasis, floating movements of the eyeballs, inhibition of the pupillary reaction to light, corneal reflexes), prolonged and deep coma, intractable epileptic syndrome, with prolonged inhibition of the bioelectrical activity of the brain.

Hypoxia in conditions of aviation and space flight

Modern pressurized aircraft cabins and oxygen-respiratory equipment have reduced the danger of gas to pilots and passengers, but the possibility of an emergency cannot be completely ruled out in flight (cabin depressurization, malfunctions in oxygen-respiratory equipment and installations that regenerate air in the cabins of spacecraft).

In the pressurized cabins of various types of high-altitude aircraft, for technical reasons, a slightly lower air pressure than atmospheric pressure is maintained, so the crew and passengers in flight may experience a slight degree of H., as, for example, when climbing to a height of 2000 m. Although individual high-altitude kits equipment create an excess pressure of oxygen in the lungs at high altitudes, nevertheless, during their operation, moderate hypotension may occur.

For the flight personnel, the limits for reducing the partial pressure of oxygen in the inhaled air and, consequently, the limits for the permissible in-flight G. were determined. These limits were based on observations of the stay of healthy people for several hours at altitudes up to 4000 m, in a pressure chamber or in flight; at the same time, pulmonary ventilation and minute volume of blood increase, blood supply to the brain, lungs and heart increases. These adaptive responses keep pilots working at a level close to normal.

It has been established that pilots in the daytime can fly without the use of oxygen for breathing at altitudes up to 4000 m. may adversely affect the control of the aircraft, especially during landing. In this regard, pilots in flight are advised not to exceed an altitude of 2000 m at night or to start breathing oxygen from a height of 2000 m. From a height of 4000 m, breathing oxygen or an oxygen-enriched gas mixture is mandatory, symptoms of altitude sickness appear (see). When evaluating the symptoms that have arisen, it is necessary to take into account that in some cases their cause may be hypocapnia (see), with a cut, the acid-base balance is disturbed and gaseous alkalosis develops.

The great danger of acute G. in flight is connected with the fact that the development of disturbances in the activity of the nervous system, leading to a loss of working capacity, proceeds at first subjectively imperceptibly; in some cases, euphoria arises and the actions of the pilot and astronaut become inadequate. This necessitated the development of special electrical equipment designed to warn the flight crew and persons tested in the pressure chamber about the development of G. The work of these automatic hypoxic state alarms is based either on determining the partial pressure of oxygen in the inhaled air, or on the analysis of physiol, indicators in individuals subjected to the influence of G. By the nature of changes in the bioelectrical activity of the brain, the decrease in saturation of arterial blood with oxygen, the nature of changes in heart rate and other parameters, the device determines and signals the presence and degree of G.

Under the conditions of space flights, the development of aerodynamics is possible in the event of a failure of the atmosphere regeneration system in the spacecraft cabin, the spacesuit oxygen supply system during spacewalks, and also in the event of a sudden depressurization of the spacecraft cabin during flight. The superacute course of G., caused by process of a deoxygenation, will lead in such cases to acute development of heavy patol, the state, a cut is complicated by rough process of gas formation - an exit of the nitrogen dissolved in fabrics and blood (decompression frustration in narrow sense of the word).

The question of the permissible limit of the decrease in the partial pressure of oxygen in the air of the cabin of a spacecraft and the permissible degree of oxygenation in cosmonauts is decided with great care. There is an opinion that in long-term space flights, given the adverse effect of weightlessness, one should not allow G. exceeding that which occurs when ascending to a height of 2000 m. Therefore, if there is a normal earthly atmosphere in the cabin (pressure -760 mm Hg. Art. and 21% oxygen in the inhaled gas mixture, as it is created in the cabins of Soviet spacecraft), a temporary decrease in the oxygen content is allowed up to 16%. For the purpose of training to create an adaptation to G., the possibility and expediency of using the so-called spacecraft in the cockpits are being studied. dynamic atmosphere with a periodic decrease in the partial pressure of oxygen within physiologically acceptable limits, combined at certain moments with a slight increase (up to 1.5 - 2%) of the partial pressure of carbon dioxide.

Adaptation to hypoxia

Adaptation to hypoxia is a gradually developing process of increasing the body's resistance to G., as a result of which the body acquires the ability to carry out active behavioral reactions with such a lack of oxygen, which was previously incompatible with normal life activity. Researches allow to allocate in adaptation to G. four adaptive mechanisms coordinated among themselves.

1. Mechanisms, the mobilization of which can ensure a sufficient supply of oxygen to the body, despite its deficiency in the environment: hyperventilation of the lungs, hyperfunction of the heart, which ensures the movement of an increased amount of blood from the lungs to the tissues, polycythemia, an increase in the oxygen capacity of the blood. 2. Mechanisms that ensure, despite hypoxemia), a sufficient supply of oxygen to the brain, heart and other vital organs, namely: the expansion of arteries and capillaries (brain, heart, etc.), a decrease in the distance for oxygen diffusion between the capillary wall and mitochondria of cells due to the formation of new capillaries, changes in the properties of cell membranes and an increase in the ability of cells to utilize oxygen by increasing the concentration of myoglobin. 3. An increase in the ability of cells and tissues to utilize oxygen from the blood and form ATP, despite hypoxemia. This possibility can be realized by increasing the affinity of cytochrome oxidase (the end enzyme of the respiratory chain) for oxygen, i.e., by changing the quality of mitochondria, or by increasing the number of mitochondria per unit cell mass, or by increasing the degree of conjugation of oxidation with phosphorylation. 4. Increase in anaerobic resynthesis of ATP due to activation of glycolysis (see) that is estimated by many researchers as the essential mechanism of adaptation.

The ratio of these components of adaptation in the whole organism is such that at an early stage of G. (in the emergency stage of the adaptation process) hyperventilation occurs (see Pulmonary ventilation). The minute volume of the heart increases, blood pressure rises slightly, i.e., a syndrome of mobilization of transport systems occurs, combined with more or less pronounced phenomena of functional insufficiency - adynamia, impaired conditioned reflex activity, a decrease in all types of behavioral activity, weight loss. In the future, with the implementation of other adaptive shifts, and in particular those that occur at the cellular level, the energetically wasteful hyperfunction of transport systems becomes, as it were, redundant and a stage of relatively stable adaptation is established with slight hyperventilation and hyperfunction of the heart, but with high behavioral or labor activity of the body. . The stage of economical and rather effective adaptation can be replaced by the stage of depletion of adaptive capabilities, which is manifested by the syndrome of hron, altitude sickness.

It is established that at the heart of increase in power of transport systems and systems of utilization of oxygen at adaptation to G. activation of synthesis of nucleinic to - t and proteins lies. It is this activation that provides an increase in the number of capillaries and mitochondria in the brain and heart, an increase in the mass of the lungs and their respiratory surface, the development of polycythemia, and other adaptive phenomena. Introduction to animals of factors that inhibit RNA synthesis eliminates this activation and makes it impossible to develop the adaptation process, and the introduction of Co-factors of synthesis and precursors of nucleic acids accelerates the development of adaptation. Activation of the synthesis of nucleic acids and proteins ensures the formation of all structural changes that form the basis of this process.

An increase in the capacity of the systems of oxygen transport and ATP resynthesis, which develops during adaptation to H., increases the ability of people and animals to adapt to other environmental factors. Adaptation to G. increases force and speed of cordial reductions, the maximum work, to-ruyu the heart can carry out; increases the power of the sympathetic-adrenal system and prevents the depletion of catecholamine reserves in the heart muscle, usually observed with excessive physical. loads.

Preliminary adaptation to G. potentiates the development of subsequent adaptation to physical. loads. In animals adapted to H., an increase in the degree of preservation of temporal connections and an acceleration in the transformation of short-term, easily erased by extreme stimuli memory into long-term, stable memory have been established. This change of functions of a brain is result of activation of synthesis nucleinic to - t and proteins in neurons and glial cells of a cerebral cortex of the adapted animals. With preliminary adaptation to G., the body's resistance to various damages to the circulatory system, the blood system, and the brain increases. Adaptation to H. has been successfully used to prevent heart failure in experimental malformations, ischemic and sympathomimetic myocardial necrosis, DOC-salt hypertension, the consequences of blood loss, as well as to prevent behavioral disorders in animals in a conflict situation, epileptiform convulsions, and the effect of hallucinogens.

The possibility of using adaptation to G. to increase a person's resistance to this factor and increase the overall resistance of the organism in special conditions of activity, in particular in space flights, as well as for the prevention and treatment of human diseases, is the subject of clinical fiziol, research.

Blumenfeld L. A. Hemoglobin and reversible accession of oxygen, M., 1957, bibliogr.; Bogolepov N. K. Coma, M., 1962, bibliogr.; Bogolepov N.N., et al. Electron microscopic study of the human brain ultrastructure in stroke, Zhurn, neuropath, and psychiat., vol. 74, no. 9, p. 1349, 1974, bibliogr.; Van Leer, E. and Stickney K-Hypoxia, trans. from English, M., 1967; Vilensky B.S. Anticoagulants in the treatment and prevention of cerebral ischemia, L., 1976; Vladimirov Yu. A. and Archakov A. I. Lipid peroxidation in biological membranes, M., 1972; Voitkevich V, I. ​​Chronic hypoxia, L., 1973, bibliogr.; Gaevskaya M. S. Biochemistry of a brain at dying and revival of an organism, M., 1963, bibliogr.; Gurvich A. M. Electrical activity of the dying and reviving brain, L., 1966, bibliogr.; Kanshina N. F., To the pathological anatomy of acute and prolonged hypoxia, Arkh. patol., t. 35, Ns 7, p. 82, 1973, bibliogr.; K o-tovsky E. F. and Shimkevich L. L. Functional morphology at extreme influences, M., 1971, bibliogr.; Meyerson F. 3. The general mechanism of adaptation and prevention, M., 1973, bibliogr.; he, Mechanisms of adaptation to high-altitude hypoxia, in the book: Probl., hypoxia and hyperoxia, ed. G. A. Stepansky, p. 7, M., 1974, bibliography; Multi-volume guide to pathological physiology, ed. H. N. Sirotinina, v. 2, p. 203, M., 1966, bibliogr.; Negovsky V. A. Pathophysiology and therapy of an agony and clinical death, M., 1954, bibliogr.; Fundamentals of space biology and medicine, ed. O. G. Gazenko and M. Calvin, vol. 1-3, M., 1975, bibliogr.; Pashutin V. V. Lectures of general pathology, part 2, Kazan, 1881; Petrov I. R. Oxygen starvation of the brain. L., 1949, bibliogr.; he, the Role of the central nervous system, adenohypophysis and adrenal cortex in oxygen deficiency, L., 1967, bibliogr.; Sechenov I. M. Selected works, M., 1935; Sirotinin N. N. Basic provisions for the prevention and treatment of hypoxic conditions, in the book: Fiziol, and patol. respiration, hypoxia and oxygen therapy, ed. A. F. Makarchenko and others, p. 82, Kyiv, 1958; Charny A. M. Pathophysiology of anoxic states, M., 1947, bibliogr.; Barcroft J. The respiratory function of the blood, v, 1, Cambridge# 1925; Bert P. La pression baromStrique, P., 1878,

H. I. Losev; Ts. H. Bogolepov, G. S. Burd (neur.), V. B. Malkin (cosm.), F. 3. Meyerson (adaptation).

Hypoxia is a state of oxygen starvation that can be experienced both by the body as a whole and by its individual organs or organ systems.

A variety of factors can provoke hypoxia, including:

• Reduced oxygen content in the inhaled air (for example, during a stay in high mountainous areas);
• Partial or complete violation of air exchange in the lungs due to drowning, suffocation, edema of the lungs or bronchial mucosa, bronchospasm, etc.;
• A decrease in the oxygen capacity of the blood or, in other words, a decrease in the amount of hemoglobin capable of attaching oxygen, because it is he who performs the function of its main transporter (blood hypoxia can occur against the background of carbon monoxide poisoning, anemia or erythrocytolysis);
• Pathological conditions resulting from cardiovascular insufficiency and in which the movement of oxygenated blood to various tissues and organs is difficult or completely impossible (for example, with heart defects, diabetic vascular disease, etc.);
• Violations of the processes of oxygen uptake by body tissues (signs of hypoxia may develop due to blocking the activity of enzymes that take part in tissue respiration, toxic substances or salts of heavy metals);
• An increase in the functional load on a tissue or organ (symptoms of hypoxia can be provoked by hard physical work or increased sports loads, when the need for oxygen exceeds its actual intake into the body).

In some cases, oxygen starvation is the result of a combination of the factors listed above.

Hypoxia can also be observed in children during their prenatal development. If such a condition is noted for a long period, it can cause serious disturbances in the metabolism of the fetus. In especially severe cases, the consequences of hypoxia can be ischemia, necrosis of the child's tissues, and even his death.

The main causes of intrauterine fetal hypoxia are:

• Diseases transferred by the mother, including diseases of the heart, blood vessels, lungs, as well as diseases accompanied by a decrease in the concentration of hemoglobin in the blood;
• Congenital malformations of the fetus;
• Violations of the function of the umbilical cord and placenta, including deterioration of placental gas exchange due to premature detachment of the placenta, and interruption of the umbilical circulation due to the formation of knots, compression or entanglement of the fetus;
• Anemia, characterized by a reduced content of hemoglobin in the blood;
• Prolonged mechanical squeezing of the fetus.

Symptoms of hypoxia

Signs of hypoxia are quite diverse and are determined by the degree of severity of the condition, the duration of exposure to the body of an unfavorable factor, as well as the reactivity of the body itself.

In addition, the symptoms of hypoxia are determined by the form in which it occurs. In general, depending on the rate of development of the pathological process, there are:

• lightning fast;
• acute;
• Subacute;
• chronic hypoxia.

Fulminant, acute and subacute forms, in contrast to chronic hypoxia, are characterized by a more pronounced clinical picture. Symptoms of oxygen starvation develop in a fairly fast time frame, not giving the body the opportunity to adapt to them. Therefore, the consequences of acute hypoxia are often more serious for a person than the consequences of chronic oxygen starvation, which is gradually accustomed to. In some cases, they are irreversible.

Chronic hypoxia develops slowly. Thus, patients who are diagnosed with severe forms of respiratory failure on the background of chronic lung diseases can live for years without any dramatic symptoms. However, it should be noted that, like the acute form of oxygen starvation, the chronic one also leads to irreversible consequences. They just develop over a longer period of time.

The most common signs of hypoxia in acute form are:

• The appearance of shortness of breath;
• Increasing the frequency of breathing and its depth;
• Dysfunction of individual organs and systems.

The chronic form is most often characterized by an increase in the activity of erythropoiesis (the process of formation of erythrocytes in the bone marrow) against the background of the development of a pathological condition in which the concentration of erythrocytes per unit volume of blood significantly exceeds those considered physiologically normal. In addition, in the body there is a violation of the function of various organs and their systems.

Treatment of hypoxia

The treatment of hypoxia involves the appointment of a set of measures aimed at eliminating its cause, combating the lack of oxygen, as well as making adjustments to the body's homeostasis system.

In some cases, to eliminate the effects of hypoxia, it is enough to ventilate the room or walk in the fresh air. If the condition is provoked by more serious causes and is associated with diseases of the blood system, lungs, cardiovascular system, or poisoning with toxic substances, the following can be recommended for the treatment of hypoxia:

• Therapy using oxygen equipment (masks, pillows, balloons, etc.);
• Appointment of antihypoxants, bronchodilators, respiratory analeptics, etc.;
• The use of oxygen concentrators;
• Artificial ventilation of the lungs;
• Blood transfusion and stimulation of hematopoiesis;
• Surgical operations correcting the function of the heart and blood vessels;
• Prescribing drugs with a cardiotropic effect;
• The use of antidotes in combination with artificial ventilation of the lungs and the appointment of drugs whose action is aimed at improving the utilization of oxygen by tissues (in case of poisoning).

Causes of hypoxia:

1. various diseases of the body;
2. circulatory disorders;
3. paralysis of the respiratory muscles;
4. shock conditions;
5. heart and vascular insufficiency, heart block;
6. asphyxia;
7. alcohol;
8. carbon monoxide poisoning;
9. postoperative complications;
10. prolonged stay of a person in a gassed or stuffy room, at great depths or heights.

Regarding the rate of development, hypoxia happens:

Oxygen starvation is the cause of severe pathologies of the brain, heart, liver, kidneys. Severe hypoxia can lead to coma or death. Therefore, it is so important to take care of your health and in order to prevent or treat brain hypoxia, do not postpone a visit to the doctor.

Oxygen is a vital element for our body. It is involved in complex biochemical processes at the cellular level. Briefly, this process can be described as the synthesis of energy. And we need energy for everything: for the functioning of organs and systems (for example, the work of the heart, contraction of the intestinal walls), for our mental and physical activity.

With oxygen starvation, our body receives less energy - this is chronic tissue hypoxia. The function of the affected organ is impaired. And in especially severe cases, tissues do not receive energy at all - in case of poisoning, asphyxia.

It is not for nothing that experts call the brain a “critical organ” during hypoxia. After the cessation of blood supply, the dynamics of brain dysfunction is as follows:

Only 4 seconds in acute oxygen deficiency is able to withstand the brain tissue without disrupting activity.

With prompt qualified assistance, the state of coma can be reversible.

Signs of oxygen starvation depend on the type and causes of hypoxia. At an early stage, signs of hypoxia are subtle, but can have irreversible consequences.

Classification of types of oxygen starvation regarding the causes:

1. Exogenous hypoxia. It occurs as a reaction to low oxygen content, at low pressure, in stuffy rooms, when climbing to a height.
2. Hemic hypoxia- this is a lack of oxygen in the blood, for example, with anemia.
3. Respiratory hypoxia. Occurs when the body's ability to receive oxygen is impaired due to the pathology of the respiratory system.
4. Circulatory hypoxia associated with CVD pathology.
5. tissue hypoxia. It develops if oxygen is not absorbed by the tissues of the body.
6. Overload hypoxia. It can occur as a result of intense physical activity, when the body's need for oxygen increases.
7. Mixed hypoxia- prolonged oxygen starvation of a severe form with a combination of several reasons.

General signs of oxygen starvation.

With timely provided, adequate medical care, all body functions are restored.

They are quite varied and typical:

1. A sharp headache resulting from a pressure drop or lack of oxygen in the room.
2. A state of distraction and disorientation after a sudden deterioration in memory. Often the patient cannot understand where he is. Unable to remember where he went. This state does not last long. When it passes, the person calms down, attributing these symptoms to overwork or starvation.
3. A sharp transition from a state of excitement, euphoria, an increase in adrenaline to a state of lethargy and lethargy. There is a rapid heartbeat, dizziness, cold sweat, convulsions.
4. Involuntary and uncontrolled actions of the limbs, impaired skin sensitivity, lethargy, sensation of pain in the arms and legs.
5. Frequent mood swings, falling into extremes, the desire to laugh and cry for no particular reason.
6. Sleep disturbance, insomnia, awakenings in the middle of the night.
7. Aggression, irritability, weakness against the background of general fatigue of the body. A person cannot concentrate on a particular job.
8. Speech and vision impairment.
9. Decrease in mental abilities, difficulties with assimilation of new information.

By ignoring the symptoms of oxygen starvation of the brain, you are putting your health at serious risk. Timely access to specialists, early diagnosis and proper treatment will help prevent serious complications.

Hypoxia research methods:

Brain hypoxia is a serious pathological condition of the body, so treatment should be carried out at the first symptoms. Timely treatment will prevent negative consequences and avoid complications.

The treatment of oxygen starvation depends on the causes of the disease, by eliminating which positive dynamics can be achieved.

If signs of hypoxia appear before the doctor arrives, it is important to provide the patient with fresh air and, if necessary:

• unfasten clothes;
• to remove water from the lungs;
• ventilate a smoky or stuffy room;
• remove the patient to fresh air;
• do artificial respiration.

Doctors provide therapy, saturation of the body with oxygen, blood transfusion, resuscitation.

Treatment methods depend on the causes and types of hypoxia. In some cases, it is enough to ventilate the room and walk in the fresh air.

Depending on the severity of the patient's condition, treatment can take place in a hospital or at home. To normalize the patient's condition, medications and vitamins are prescribed.

Serious treatment will be required if the causes of oxygen starvation are problems of the heart, kidneys, blood, lungs. Therefore, the establishment of the work of the cardiovascular system, respiration, correction of the acid-base state of the blood, water-salt balance is of great importance.

1. In the case of exogenous hypoxia, oxygen equipment will be needed.
2. With respiratory hypoxia, one cannot do without bronchodilators, respiratory analeptics, antihypoxants.
3. In some cases, artificial lung ventilation, oxygen concentrators are used.
4. Treatment of hemic hypoxia requires blood transfusion.
5. In the treatment of circulatory hypoxia, corrective operations on the heart and blood vessels are used.

Prolonged oxygen starvation can cause cerebral edema, requiring the appointment of decongestants. With untimely resuscitation, fulminant and acute hypoxia often lead to death. Therefore, preventive measures, early diagnosis and timely complex treatment of hypoxia are so important.

To prevent hypoxia, it is necessary to eliminate all the causes that lead to a lack of oxygen.

1. Frequent walks in the fresh air - better outside the city or in the park.
2. If you have to stay indoors for a long time - frequent ventilation at any time of the year.
3. Periodic preventive examinations by specialists - for the early detection of diseases and their timely treatment.
4. Sufficient physical activity.
5. Prevention of beriberi: the use of fresh fruits and vegetables all year round. If necessary - taking vitamin and mineral complexes in courses.
6. Exclusion of smoking, drinking alcohol.

It all depends on the course of the process. If this is chronic oxygen starvation, then usually the cause is heart or blood disease. Accordingly, the cardiologist or therapist is engaged in the correction. And if the brain suffers, a neurologist is connected to the treatment.

Acute or fulminant hypoxia, as well as severe chronic hypoxia, require urgent resuscitation measures. Therefore, in these cases, you need to immediately call an ambulance.

• Pulse oximetry. The method is accessible and simple - just put a pulse oximeter on your finger. Blood oxygen saturation is determined within a few seconds. The norm is at least 95%.

• Determination of acid-base balance (ASCHR) and blood gas composition.

• Capnography, CO-metry– study of gases of exhaled air.

• Laboratory and instrumental methods studies can establish the fact of hypoxia, but to establish its causes, an additional examination, individual for each patient, will be needed.

Treatment of oxygen starvation of the brain consists in etiotropic therapy (treatment of the cause). Thus, exogenous hypoxia requires the use of oxygen masks and pillows. For the treatment of respiratory hypoxia, drugs that dilate the bronchi, analgesics, antihypoxanes that improve oxygen utilization are used. In case of hemic (reduced oxygen in the blood), a blood transfusion is performed, antidote drugs are prescribed for histoxic or tissue, circulatory (heart attacks, strokes) - cardiotropic. If such therapy is not possible, actions are aimed at eliminating symptoms: they regulate vascular tone, normalize blood circulation, prescribe drugs for dizziness, headache, blood-thinning, restorative, nootropic drugs and lowering bad cholesterol.

Metered aerosols are used as bronchodilators: truvent, atrovent, berodual, salbutamol.

Truvent is an aerosol can, when using it is necessary to remove the protective cap, shake it several times, lower the spray head down, take it with your lips and press on the bottom, inhaling deeply and holding the breath for a few moments. One push equals a serving. The effect comes in 15-30 minutes. Every 4-6 hours, the procedure is repeated, making 1-2 clicks, this is how long the effect of the drug lasts. Do not prescribe during pregnancy, angle-closure glaucoma, allergies. The use of the drug can reduce visual acuity, increase intraocular pressure.

Analgesics include a large list of drugs from the well-known analgin to completely unfamiliar names, each of which has its own pharmacological effect. The doctor will determine what is necessary in a particular situation. Here is a list of some of them: acamol, anopyrin, bupranal, pentalgin, cefecon, etc.

Bupranal is a solution in ampoules for intramuscular and intravenous injections, in syringe tubes for intramuscular injection. The maximum daily dose is 2.4 mg. The frequency of administration is every 6-8 hours. Possible side effects in the form of nausea, weakness, lethargy, dry mouth. Contraindicated in children under 16 years of age, during pregnancy and lactation, increased intracranial pressure, alcoholism.

The list of antidote drugs includes atropine, diazepam (mushroom poisoning), eufillin, glucose (carbon monoxide), magnesium sulfate, almagel (organic acids), unithiol, cuprenil (heavy metal salts), naloxone, flumazenil (drug poisoning), etc. .

Naloxone - available in ampoules, there is a special form for newborns. The recommended dose is 0.4-0.8 mg, it may be necessary to increase it to 15 mg. With increased sensitivity to the drug, an allergy occurs; in drug addicts, taking the drug causes a specific attack.

For strokes, cerebrolysin, actovegin, encephabol, papaverine, no-shpa are used.

Actovegin - exists in various forms: dragees, solutions for injections and infusions, gels, ointments, creams. Doses and method of application are prescribed by the doctor depending on the severity of the disease. Burn wounds, bedsores are treated externally. The use of the drug can cause hives, fever, sweating. It has contraindications for pregnant women, during breastfeeding, with allergies.

A number of vitamins in tissue oxygen starvation are antidotes of toxic substances. So, vitamin K1 blocks the action of warfarin - an antithrombotic agent, vitamin B6 - poisoning with anti-tuberculosis drugs, vitamin C is used for damage by carbon monoxide, anilines used in dyes, medicines, chemicals. To maintain the body, it is also necessary to saturate it with vitamins.

With general or local hypoxia of various nature, such a method of physiotherapeutic treatment as oxygen therapy is used. The most common indications for its use are respiratory failure, circulatory disorders, cardiovascular diseases. There are various ways of oxygen saturation: cocktails, inhalations, baths, skin, subcutaneous, intraband methods, etc. Oxygenobarotherapy - breathing compressed oxygen in a pressure chamber relieves hypoxia. Depending on the diagnosis that led to hypoxia, UHF, magnetotherapy, laser therapy, massage, acupuncture, etc. are used.

One of the recipes for alternative treatment is breathing exercises according to the following method. Inhale slowly and deeply, hold for a few seconds and exhale slowly. Do several times in a row, increasing the duration of the procedure. Count to 4 on the inhale, to 7 on the breath hold, and to 8 on the exhale.

Garlic tincture will help strengthen blood vessels, reduce their spasms: fill a third of the jar with chopped garlic, filling it with water to the brim. After 2 weeks of infusion, start taking 5 drops per spoon of water before meals.

A prepared mixture of buckwheat, honey and walnuts, taken in equal proportions, is able to raise hemoglobin: grind cereals and nuts to a state of flour, add honey, mix. Take on an empty stomach in a tablespoon half an hour before meals. Fresh beet juice is also effective, which must be allowed to stand for some time before taking it so that volatile substances come out.

Ginger can help with asthma attacks. Combining its juice with honey and pomegranate juice, drink a spoonful 3 times a day.

It is effective in oxygen starvation to take decoctions, infusions, herbal teas with antispasmodic action: chamomile, valerian, St. John's wort, motherwort, hawthorn. For problems with the respiratory system, take decoctions of medicinal preparations from coltsfoot, pine buds, plantain, licorice root, elder flowers. Hemoglobin levels can be raised with herbs such as nettle, yarrow, dandelion, wormwood.

In combination with the main treatment, homeopathic remedies are increasingly present. Here are some of the remedies that can be prescribed for oxygen starvation and are aimed at the causes of its occurrence.

• Accardium - granules, which include metallic gold, mountain arnica, coculus-like anamyrta. It is aimed at the treatment of angina pectoris, cardiovascular failures caused by heavy physical exertion. Twice a day, 10 granules for half an hour before meals or one hour after, keep under the tongue until completely resorbed. The average course of treatment lasts 3 weeks. The drug has no contraindications and side effects. For use during pregnancy and children, a doctor's consultation is necessary.
• Atma® - drops, a complex drug for the treatment of bronchial asthma. The dose for children under one year is 1 drop per teaspoon of water or milk. Under the age of 12, 2 to 7 drops per tablespoon. After 12 years - 10 drops in pure form or in water. Continue treatment up to 3 months. Side effects were not observed.
• Vertigoheel - oral drops, used for dizziness, atherosclerosis of cerebral vessels, strokes. Drops are dissolved in water, when swallowed, they are retained for some time in the mouth. Recommended from the age of the child. Up to 3 years - 3 drops, at the age of 3-6 years - 5, the rest - 10 drops 3-4 times a day for a month. Hypersensitivity reactions are possible. Contraindicated in children under one year old, during pregnancy and lactation - with the permission of a doctor.
• Hawthorn compositum - homeopathic cardiological remedy, liquid. Adults are prescribed 15-20 drops three times a day, children - 5-7 drops. The drug has contraindications in case of allergy to components.
• Aesculus-compositum - drops, are used for post-embolic circulatory disorders, post-infarction and post-stroke conditions. Single dose - 10 drops in water, holding in the mouth. Frequency - 3 times a day. The duration of treatment is up to 6 weeks. Side effects are unknown. Contraindicated in pregnant women and hypersensitive to the components of the drug.

Surgical treatment on the heart or blood vessels may be needed in the circulatory form of oxygen starvation, the development of which occurs rapidly and is associated with violations of their functions.

Oxygen starvation, or hypoxia, is a state of the body in which the normal supply of oxygen to the brain is disrupted. Hypoxia affects its outer part. But, as a rule, this term is also used to denote the absence of oxygen in the entire brain. Based on the latest statistical studies, the highest prevalence of this disease was found among residents of megacities and employees of enterprises that work in rooms where there is no normal air ventilation.

1. Inhalation of carbon monoxide.
2. Carbon monoxide poisoning.
3. Great height.
4. Suffocation.

Predisposing factors that provoke oxygen starvation of the brain include:

1. Inhalation of carbon monoxide.
2. Diseases that interfere with the normal functioning of the respiratory muscles.
3. Carbon monoxide poisoning.
4. Great height.
5. Suffocation.

There are several types of this disease:

1. Hypoxic. This variety is quite often diagnosed in people who climb to great heights. As a rule, this manifests itself in the following way: the higher the altitude, the greater the lack of oxygen.
2. Hemic. It is characterized by a decrease in the oxygen capacity of the blood.
3. Respiratory. A characteristic feature of such an ailment is the presence of pathological processes, which negatively affects the entire respiratory system.
4. Circulatory. Manifested in case of lack of blood circulation.
5. Tissue. The cause of its occurrence is considered to be a decrease in the activity of respiratory enzymes.
6. Mixed. As the name implies, it is manifested by a combination of different types of this disease.
7. Myocardial. It is manifested by a lack of oxygen in the heart muscle. The danger of this type of hypoxia lies in the high probability of developing a serious complication in the future - ischemia.

According to the period of flow, they distinguish:

1. Lightning, which develops in a split second and lasts a maximum of 3-5 minutes.
2. Sharp. It manifests itself, as a rule, after a heart attack or with a large loss of blood, which are predisposing factors for reducing the ability of blood to supply oxygen to tissues.
3. Chronic. Most often diagnosed with heart disease, cardiosclerosis or heart failure.

It is known that for normal functioning the brain needs about 3.3 million oxygen per 100 g of live weight. And if even the slightest deficiency occurs in the brain, to normalize the situation, cerebral blood flow increases almost instantly, which can exceed the norm by a maximum of two times. When this is not enough, hypoxia begins.

The initial stage of this disease is characterized by increased excitability. Most often, there is a state close to euphoria, an inability to exercise full control over one's actions, problems with performing simple mental tasks, and changes in gait.

Important! Changes in the upper skin of a person and the appearance of cold sweat can also serve as evidence of the onset of hypoxia.

If oxygen starvation continues for a significant period of time, then its characteristic features are severe vomiting and dizziness. In addition, the clarity of vision is significantly impaired, and periodic darkening in the eyes is observed. There are frequent cases of loss of consciousness.

For advanced cases, the appearance of cerebral edema is characteristic. In the future, serious deviations in the work of the brain can occur with a further loss of conditioned, and then unconditioned reflexes.

Attention! Medical practice includes several dozen cases when, as a result of prolonged hypoxia, the patient fell into a deep coma.

It should be remembered that oxygen starvation of the brain can be triggered by other factors. For example, constant stress, lack of sleep, excessive smoking or alcohol abuse.

But, as practice shows, the symptoms of this disease rarely occur alone, but to a greater extent complement each other.

The diagnosis of this disease, in addition to a general examination by the attending physician, also consists in conducting specific laboratory and instrumental tests.

Use of a pulse oximeter. Today, this method is not only the most accessible to determine whether oxygen starvation of the brain is present or absent, but it is also easy to use. To do this, just put a special device on the patient's finger - a pulse oximeter - and in just a couple of minutes it will become known how oxygenated the blood is. At the moment, the optimal level should not exceed 95%.

Determination of blood composition in veins and arteries. When this study is used, it becomes possible to establish the level of the main indicators of homeostasis, from which they emit: oxygen, partial pressure of carbon dioxide, the state of the bicarbonate and carbonate buffer.

The study of gases contained in the exhaled air (CO-metry and capnography are used).

It is no secret that people turn to medical institutions only when it becomes unbearable to endure. But if such an approach is still justified with a mild cold, then with manifestations of hypoxia, it can have very serious consequences. These include:

• bronchial asthma;
• serious metabolic disorders;
• stroke;
• deep coma.

The treatment of this disease is to use an integrated approach, which consists in the regular implementation of the prescribed procedures. The first step is to indicate to your doctor the reason that led to this condition. It could be chronic fatigue, stress, or a poorly ventilated room.

1. Herbal preparations, the action of which is aimed at accelerating the circulation of blood circulation in the patient's body and stabilizing his general well-being.
2. Hyperbaric oxygenation. The essence of this therapeutic method lies in the fact that the patient is placed in a special chamber, where the impact on the body of oxygen under high pressure is used.
3. Vitamins that restore brain tissue.

If weak oxygen starvation is diagnosed, the treatment in this case is to ventilate the room or take long walks in the fresh air. Hypoxia, which occurred as a result of heart disease or after poisoning, is treated much more difficult.

Treatment of respiratory hypoxia consists in prescribing drugs that dilate the bronchi, respiratory analeptics or antihypoxanes. In special cases, oxygen concentrators or artificial lung ventilation are used.

It should be remembered that with a timely visit to the doctor and in the presence of fairly mild symptoms, the prognosis for a speedy recovery is very favorable. But in more advanced cases, it is not always possible to eliminate the negative consequences that a lack of oxygen causes.

This disease is especially dangerous during pregnancy. And sadly, but every year the number of women who are faced with this phenomenon is only increasing. But it should be borne in mind that hypoxia during pregnancy most often means no longer a full-fledged disease, but the course of processes due to which various pathological abnormalities occur in the body of a baby in the mother's womb. This happens due to the fact that blood with oxygen does not flow in the proper amount to the internal organs of the fetus. But it is worth remembering that mother and child are one, therefore, if the child suffers, then, accordingly, the mother also suffers.

Hypoxia during pregnancy is a very alarming sign, especially if it has been diagnosed more than once over several trimesters. Therefore, so that this disease does not develop into a chronic form, it is recommended not to hope that this is an accident, and not to attribute everything to an “interesting” situation and possible deviations from the norm that usually occur in this case, but to consult a doctor as soon as possible at the place of observation.

Oxygen starvation of the fetus can manifest itself in both acute and chronic forms. And, as practice shows, different predisposing factors are necessary for each of the cases. So, chronic hypoxia develops gradually and for a fairly long period of time. It occurs most often due to placental insufficiency, when, due to the presence of bad habits, serious chronic diseases (asthma), the placenta does not perform its functions in full.

Most often, chronic hypoxia manifests itself in the second trimester of pregnancy.

Acute oxygen starvation of the fetus, unlike chronic, occurs unexpectedly and, as a rule, occurs during the 2nd stage of labor. The main reasons leading to this condition are called placental abruption and the appearance of nodules on the umbilical cord.

Of the symptoms indicating the imminent onset of hypoxia, we can distinguish:

1. Rapid heart rate early and slower later.
2. Fetal immobility.
3. Weak tremors of the child in the later stages.
4. Changes in the skin of a newborn baby from natural to green or blue.

As a rule, at regular gynecological examinations, each expectant mother is recommended to remember not only the day when the baby moves for the first time, but also carefully observe them (movements) in the future. This is necessary first of all in order to fix, and in the future to prevent the development of serious pathologies.

Attention! The presence of up to 10 series of active stirring of the child is considered the norm.

Also, at each scheduled gynecological examination, the expectant mother listens to the abdominal wall through a special tube - an obstetrician's stethoscope. The purpose of this test is to determine the baby's heart rate. Indicators of 110-160 beats per minute are considered normal. If other indicators are present, then this is considered an indication for additional examinations using a dopplerometer or cardiotocograph.

In addition, oxygen starvation can also be determined by visual examination, since with this disease the volume of the abdomen decreases very much, and the baby himself, although he is in the last stages, looks unnaturally thin during an ultrasound examination.

Manifestations of this disease in newborns are often the cause of irreversible disturbances in the activity of vital organs (lungs, kidneys, heart and central nervous system). Therefore, when identifying the initial stage of hypoxia in a baby, it is necessary to warm him up as soon as possible and give him artificial respiration. In more serious cases, it is necessary to free the airways from the mucus accumulated there. For this, special solutions are introduced there. It is also recommended to perform an external heart massage.

As a rule, the transferred oxygen starvation in newborns in the future requires constant monitoring by a pediatrician at the place of residence.

In most cases, women who have even the slightest hint of intrauterine hypoxia are gradually transferred to inpatient treatment. There they are prescribed injections of drugs containing vitamins and substances that help thin the blood. But, as a rule, such events do not always achieve their goal, since oxygen starvation in a child will pass only when the factors that contributed to its occurrence are completely eliminated.

Therefore, preventive measures include:

1. Daily two-hour walk in the fresh air. If for some reason this becomes impossible, then it is recommended to ventilate the room or install an air conditioner with an air ionization function. But remember that constant sitting in a closed room, even with daily ventilation, is strongly discouraged.
2. Rejection of bad habits. Since this is not only a predisposing factor for the development of this disease, but also causes serious harm to the unborn baby.
3. Eat foods that are high in iron. As a rule, these are pomegranate, beef liver, beans, herbs, onions. In addition, oxygenated drinks, oxygen cocktails, have proven themselves well.
4. Avoid colds and infectious diseases.
5. If possible, avoid places with large crowds of people.
6. Stick to a specific daily routine. Remember that for the full recovery of the body, you need up to 8 hours of uninterrupted sleep.
7. Minimize the manifestation of stressful situations.

Important! Acute oxygen starvation in an unborn baby requires a caesarean section.

With insufficient oxygen supply to the brain, hypoxia develops. Tissue starvation occurs due to a lack of oxygen in the blood, a violation of its utilization by peripheral tissues, or after the cessation of blood flow to the brain. The disease leads to irreversible changes in brain cells, disruption of the central nervous system and other serious consequences.

At the initial stages, dysfunction of the microcirculation of the brain, a change in the state of the walls of blood vessels, neurocytes, and degeneration of parts of the brain tissue are observed. In the future, there is a softening of the cells or their gradual recovery with timely treatment.

The main causes of acute cerebral hypoxia:

• acute heart failure;
• asphyxia;
• transverse heart block;
• traumatic brain injury;
• atherosclerosis;
• undergone heart surgery;
• carbon monoxide poisoning;
• thromboembolism of cerebral vessels;
• ischemic disease;
• stroke;
• diseases of the respiratory system;
• anemia.

Chronic hypoxia develops when working in adverse conditions, living in mountainous areas where the air is rarefied. The gradual deposition of atherosclerotic plaques on the walls of blood vessels leads to a decrease in the lumen of the arteries, slowing down blood flow. If there is a complete blockage of the vessel, the brain tissue dies, a heart attack develops, which can cause severe complications, death.

Signs of oxygen starvation vary depending on the form of pathology. In acute hypoxia, patients experience motor and psycho-emotional arousal, increased heart rate and respiration, pale skin, increased sweating, "flies" before the eyes. Gradually, the state changes, the patient calms down, becomes lethargic, sleepy, his eyes darken, tinnitus appears.

At the next stage, the person loses consciousness, clonic convulsions, chaotic muscle contractions may occur. Motor disorders are accompanied by spastic paralysis, an increase, and then the extinction of muscle reflexes. The attack develops very quickly, within 1-2 minutes a coma may occur, so the patient needs urgent medical attention.

Hypoxia of the brain of a chronic form proceeds slowly. It is characterized by constant fatigue, dizziness, apathy, depression. Hearing and vision often deteriorate, performance decreases.

Depression is characteristic of brain hypoxia

Neurological signs of hypoxia in adults:

• With diffuse organic damage to the brain, posthypoxic encephalopathy develops, accompanied by visual, speech disorders, impaired coordination of movements, tremor of the limbs, twitching of the eyeballs, muscle hypotension.
• With a partial impairment of consciousness, the symptoms of hypoxia are manifested by lethargy, stupor, and stunning. A person is in a depressed state, from which he can be brought out with persistent treatment. Patients retain protective reflexes.
• Asthenic condition: increased fatigue, exhaustion, deterioration of intellectual abilities, motor restlessness, low efficiency.

Hypoxia of the brain is fulminant, acute and chronic. In the acute stage, signs of oxygen deficiency develop rapidly, and the chronic disease proceeds, gradually progressing, with less pronounced signs of malaise.

Acute hypoxia is accompanied by cerebral edema, degenerative changes in neurons. Even after normalization of oxygen delivery to brain cells, degenerative processes persist and progress, leading to the formation of softened foci. Chronic hypoxia of brain tissues does not cause pronounced changes in nerve cells, therefore, when the causes of pathology are eliminated, patients fully recover.

Depending on the causes that caused oxygen starvation, brain hypoxia is classified:

• The exogenous form of the disease develops with a lack of oxygen in the air.
• Respiratory hypoxia of brain tissue occurs when the upper respiratory tract is disrupted (asthma, pneumonia, tumors), overdose of narcotic drugs, mechanical injuries of the chest.
• Hemic hypoxia of the brain is diagnosed when there is a violation of the transport of oxygen by blood cells. Pathology develops with a lack of hemoglobin, red blood cells.
• Circulatory develops in violation of the blood circulation of the brain due to heart failure, thromboembolism, atherosclerosis.
• Tissue hypoxia is caused by a violation of the process of oxygen utilization by cells. Blockade of enzyme systems, poisoning with poisons, medicines can lead to this.

When the supply of O₂ is stopped, the brain tissues can live for 4 seconds, after 8-10 seconds the person loses consciousness, after another half a minute the activity of the cerebral cortex disappears and the patient falls into a coma. If blood circulation is not restored within 4-5 minutes, the tissues die.

Symptoms of acute oxygen starvation of the brain, that is, coma:

• Subcortical coma causes inhibition of the cerebral cortex and subcortical formations. The patient is disoriented in space and time, reacts badly to speech, external stimuli, does not control urination and defecation, he has increased muscle tone, depressed reflexes, and increased heart rate. Breathing is independent, the reaction of pupils to light is preserved.
• Hyperactive coma causes dysfunction of the anterior parts of the brain, symptoms are manifested by convulsions, lack of speech, reflexes, hyperthermia, jumps in blood pressure, respiratory depression, weak pupillary response to light.
• With a "flaccid coma" the medulla oblongata is affected. Reactions to external stimuli completely disappear, reflexes are absent, muscle tone is reduced, shallow breathing, blood pressure indicators decrease, pupils are dilated and do not respond to light, convulsions periodically occur.
• Terminal coma is a complete cessation of the brain. A person cannot breathe on his own, blood pressure and body temperature drop sharply, there are no reflexes, muscle atony is observed. The patient is on artificial life support.

Prolonged oxygen starvation of the brain, stage 4 coma has a high risk of death, death occurs in more than 90% of cases.

With low oxygen pressure in the air, hypoxic hypoxia develops. The cause of the pathology is:

• breathing in confined spaces: tanks, submarines, bunkers;
• during rapid ascent on aircraft;
• during a long climb or stay in the mountains.

The lack of oxygen in the air leads to a decrease in its concentration in the alveoli of the lungs, blood and peripheral tissues. As a result, the level of hemoglobin decreases, chemoreceptors are irritated, the excitability of the respiratory center increases, hyperventilation, alkalosis develop.

The water-salt balance is disturbed, vascular tone decreases, blood circulation in the heart, brain and other vital organs worsens.

Symptoms of hypoxic hypoxia:

• A surge of energy, acceleration of movements and speech.
• Tachycardia and dyspnea on exertion.
• Violation of coordination of movements.
• Rapid breathing, shortness of breath at rest.
• Decreased performance.
• Deterioration of short-term memory.
• Lethargy, drowsiness;
• Paresis, paresthesia.

At the last stage, brain hypoxia is characterized by loss of consciousness, the appearance of convulsions, muscle rigidity, involuntary urination, defecation, and coma occurs. When rising to a height of 9-11 km above sea level, cardiac activity is sharply disturbed, oppressed, and then breathing completely disappears, coma and clinical death occur.

One of the signs of hypoxia may be fainting.

Therapy Methods

If a patient is diagnosed with acute cerebral hypoxia, it is important for the attending physician to ensure the maintenance of the cardiovascular and respiratory systems, normalize metabolic processes, and prevent acidosis, which worsens the state of brain tissues.

How to treat hypoxia in violation of cerebral circulation? Patients are prescribed vasodilators, anticoagulants, blood thinners. Medications are selected taking into account the causes of the development of pathology.

For the treatment of hypoxia, methods are also used:

• craniocerebral hypothermia;
• hyperbaric oxygenation;
• extracorporeal circulation.

This is how hyperbaric oxygen therapy works

Neuroprotectors, nootropics and antihypoxants protect nerve cells and promote their recovery. Decongestants are used for cerebral edema. Therapy of the consequences of hypoxia is carried out with narcotic drugs, neuroleptics.

If cerebral hypoxia has led to a coma, the patient is connected to a ventilator, intravenously administered drugs that increase blood pressure, normalize heart rate and circulating blood volume. Symptomatic treatment is also applied, the causes of oxygen deficiency are eliminated.

Acute or chronic hypoxia of the brain occurs when there is a violation of the oxygen supply of the brain structures. The disease can lead to irreversible changes in the cells of the organ, nerve trunks, severe disability and death of the patient. With timely assistance, it is possible to minimize the pathological process and restore the functioning of the brain.

Oxygen starvation, or hypoxia, is a pathological process associated with insufficient oxygen supply to cells due to its lack in the surrounding atmosphere, disorders of the blood or the cells themselves. Hypoxia can manifest itself in both acute and chronic forms, but always requires immediate recognition and therapy due to possible irreversible consequences for the body.

Hypoxia is not a separate disease or syndrome. This is a general pathological process that underlies a variety of diseases and is caused by an extraordinary variety of reasons, ranging from the composition of the surrounding air to the pathology of certain types of cells in the human body.

Although oxygen starvation has certain symptoms, it is a non-specific process that can play a key role in the pathogenesis of many diseases. Hypoxia occurs in adults, newborn babies, fetuses growing in utero and has rather stereotypical structural manifestations that differ only in severity.

In the initial phase of oxygen deficiency, compensatory-adaptive mechanisms are activated, implemented mainly by the cardiovascular system, respiratory organs, and intracellular biochemical reactions. As long as these mechanisms work, the body does not feel a lack of oxygenation. As they are depleted, a phase of decompensation begins with a developed picture of tissue hypoxia and its complications.

Clinically compensated acute oxygen starvation is achieved by an increase in heart rate and respiration, an increase in pressure and cardiac output, the release of reserve erythrocytes from depot organs, if necessary, the body "centralizes" blood circulation, directing blood to the most vulnerable and hypoxia-sensitive tissues - the brain and myocardium. The remaining organs for some time are able to tolerate the lack of oxygen relatively painlessly.

If the gas balance of the blood is restored before the defense mechanisms are exhausted, the victim of hypoxia can count on a full recovery. Otherwise, irreversible intracellular structural changes will begin, and the consequences will most likely not be avoided.

At chronic oxygen deficiency the defense mechanism is somewhat different: the number of constantly circulating red blood cells increases, the proportion of hemoglobin and enzymes in them increases, the alveolar and vascular networks of the lungs expand, breathing becomes deeper, the myocardium thickens, maintaining sufficient cardiac output. Tissues "acquire" a more extensive microcirculatory network, and cells - additional mitochondria. With the decompensation of these mechanisms, active production of collagen by connective tissue cells begins, culminating in diffuse sclerosis and dystrophy of the organ cells.

In prognostic terms, acute hypoxia seems to be more dangerous. due to the fact that the reserves of compensation are temporary, and the body does not have time to adjust to a new breathing regime, so untimely treatment threatens with serious consequences and even death. Chronic oxygen starvation, on the contrary, causes persistent adaptive reactions, so this condition can last for years, the organs will perform their function even with moderate sclerosis and dystrophy.

Varieties of oxygen starvation

The classification of hypoxic conditions has been revised many times, but its general principle has been preserved. It is based on identifying the cause of the pathology and determining the level of damage to the respiratory chain. Depending on the etiopathogenetic mechanism, there are:

• Exogenous oxygen starvation - associated with external conditions;
• Endogenous form - in diseases of internal organs, endocrine system, blood, etc.

Endogenous hypoxia happens:

• Respiratory;
• Circulatory - with damage to the myocardium and blood vessels, dehydration, blood loss, thrombosis and thrombophlebitis;
• Hemic - due to the pathology of erythrocytes, hemoglobin, enzyme systems of red blood cells, with erythropenia, lack of hemoglobin (anemic), poisoning with poisons that block hemoglobin, the use of certain drugs (aspirin, citramon, novocaine, vikasol, etc.);
• Tissue - due to the inability of cells to absorb blood oxygen due to disorders in various parts of the respiratory chain under conditions of normal oxygenation;
• Substrate - occurs due to a lack of substances that serve as a substrate for oxidation during tissue respiration (hunger, diabetes);
• Overload - a variant of physiological oxygen starvation due to excessive physical activity, when oxygen reserves and the capabilities of the respiratory system become insufficient;
• Mixed.

According to the rate of development of pathology, a fulminant form (up to 3 minutes), acute (up to 2 hours), subacute (up to 5 hours) and chronic, which can last for years, are distinguished. In addition, hypoxia can be general and local.

Why is oxygen becoming scarce?

The development of oxygen starvation is based on exogenous and endogenous causes. External ones are caused by a lack of oxygen in the air, which can be clean, but mountainous, urban, but dirty.

Exogenous hypoxia appears when:

1. Low oxygen content in the inhaled air - mountainous terrain, frequent flights (for pilots);
2. Being in a closed space with a large number of people, in a mine, wells, on a submarine, etc., when there is no communication with open air;
3. Inadequate room ventilation;
4. Work under water, in a gas mask;
5. Dirty atmosphere, gas pollution in large industrial cities;
6. Breakage of equipment for anesthesia and artificial pulmonary ventilation.

Endogenous hypoxia associated with internal adverse conditions that predispose to a lack of oxygen in the blood:

As you can see, the causes of endogenous oxygen starvation are extremely diverse. It is difficult to name an organ, the defeat of which in one way or another would not affect the respiration of cells. Especially severe changes occur in the pathology of erythrocytes and hemoglobin, blood loss, lesions of the respiratory center, acute occlusion of the arteries of the lungs.

In addition to hypoxia in adults, it is also possible lack of oxygen in the fetus during fetal development or a newborn baby. The reasons for it are:

• Diseases of the kidneys, heart, liver, respiratory organs in the expectant mother;
• Severe anemia in pregnancy;
• Late with pathology of hemocoagulation and microcirculation;
• Alcoholism, drug addiction of the expectant mother;
• Intrauterine infection;
• Anomalies of the placenta and umbilical vessels;
• congenital deformities;
• Anomalies of labor activity, trauma in childbirth, placental abruption, entanglement of the umbilical cord.

Structural changes and symptoms with lack of oxygen

With a lack of oxygen in the tissues, characteristic ischemic-hypoxic changes develop. Brain damage is caused by disorders with erythrocyte aggregation, impregnation of blood vessel walls with plasma and their necrotic changes. As a result, vascular permeability increases, the liquid part of the blood enters the perivascular space, giving rise to edema.

A severe lack of oxygen in the blood contributes to irreversible changes in neurons, their vacuolization, chromosome breakdown and necrosis. The more severe hypoxia, the more pronounced dystrophy and necrosis, moreover, cell pathology can increase even after the cause of oxygen deficiency has been eliminated.

So, in severe hypoxia, several days after the restoration of oxygenation in neurons that did not have structural changes before, irreversible degenerative processes begin. Then these cells are absorbed by phagocytes, and softening areas appear in the parenchyma of the organ - voids in place of destroyed cells. In the future, this threatens chronic and.

Chronic hypoxia is accompanied by a lower intensity of necrotic reactions, but it provokes the multiplication of glial elements that play a supporting and trophic role. Such gliosis underlies.

brain changes in chronic dyscirculatory encephalopathy

Depending on the depth of oxygen deficiency in tissues, it is customary to isolate several degrees of severity of pathology:

1. Light - signs of hypoxia become noticeable only during physical exertion;
2. Moderate - symptoms occur even at rest;
3. Severe - severe hypoxia with dysfunction of internal organs, cerebral symptoms; precedes coma;
4. Critical - coma, shock, agony and death of the victim.

The lack of oxygen in the body is manifested mainly by neurological disorders, the severity of which depends on the depth of hypoxia. As metabolic disorders worsen, the kidneys, liver, and myocardium are involved in the pathogenetic chain, the parenchyma of which is also extremely sensitive to a lack of oxygenation. In the terminal phase of hypoxia, multiple organ failure occurs, severe hemostasis disorders with bleeding, necrotic changes in the internal organs.

Clinical signs of oxygen starvation are characteristic of all types of pathology, while lightning-fast hypoxia may not have time to manifest itself with any symptoms due to the sudden (in a matter of minutes) death of the victim.

Acute oxygen starvation develops over 2-3 hours, during which the organs have time to feel the lack of oxygen. First, the body will try to correct it by accelerating the pulse, increasing pressure, however, compensatory mechanisms are quickly depleted due to the severe general condition and the nature of the underlying disease, hence the symptoms of acute hypoxia:

• bradycardia;
• Decreased blood pressure;
• Irregular, shallow, rare breathing or its pathological types.

If oxygen deficiency is not eliminated at this moment, then irreversible ischemic-dystrophic changes in vital organs will develop, the victim will plunge into a coma, agony and death will occur from multiple organ failure, cardiac arrest.

Subacute and chronic varieties lack of oxygen in the body in an adult or a child is manifested by hypoxic syndrome, which, of course, affects the most vulnerable organ to a lack of oxygen - the brain. Against the background of oxygen deficiency in the nervous tissue, ischemia and death of neurons begin, circulatory disorders occur with microthrombosis and hemorrhage, and edema progresses.

Symptoms of oxygen starvation of the brain are:

1. Euphoria, agitation, unmotivated anxiety, restlessness;
2. Motor excitation;
3. Reduced criticism of one's condition, inadequate assessment of what is happening;
4. Signs of oppression of cortical structures - cranialgia, noises in the ears or head, dizziness, lethargy;
5. Violations of consciousness up to coma;
6. Spontaneous urination and defecation;
7. Nausea, vomiting;
8. Loss of coordination, inability to walk and make purposeful movements;
9. Convulsive muscle contractions with irritation from outside - begin with the facial muscles, then the muscles of the limbs and abdomen are involved; the most severe form is opisthotonus, when all the muscles of the body contract, including the diaphragm (as in tetanus).

Neurological symptoms, as hypoxic-ischemic disorders deepen in the tissues, are joined by cardialgia, the pulse becomes more frequent over 70 heart beats per minute, hypotension increases, breathing becomes irregular, shortness of breath increases, and body temperature decreases.

Against the background of metabolic disorders and disorders of peripheral blood flow (cyanosis) of the skin develops, however, in case of intoxication with cyanides, carbon monoxide, nitro compounds, the skin of the victim may, on the contrary, turn pink.

Chronic oxygen starvation with constant cerebral hypoxia is accompanied by mental disorders in the form of hallucinations, delirious state, agitation, disorientation, memory loss and dementia. In severe hypotension, perfusion of already suffering tissues decreases, coma develops with inhibition of vital nerve centers and death.

A milder course of chronic hypoxia observed in residents of megacities, office workers and other closed poorly ventilated premises is accompanied by drowsiness, weakness, fatigue, headaches, mood swings, a tendency to depressive disorders, a decrease in the ability to concentrate at work, dizziness. Such hypoxia brings rather subjective discomfort, makes it difficult to perform professional duties, but does not threaten life. Nevertheless, it is necessary to deal with it in order to maintain an active life and adequate working capacity.

Oxygen starvation in the fetus and newborn

Oxygen starvation has a very unfavorable effect on the fetus developing during pregnancy, whose cells constantly multiply, forming tissues, and therefore are very sensitive to hypoxia. Today, pathology is diagnosed in every tenth newborn baby.

Fetal hypoxia can occur in both acute and chronic forms. In the early stages of gestation, chronic oxygen starvation provokes a slowdown in the formation of the embryo, congenital malformations, and in the later stages - disorders of the central nervous system, growth retardation, and a decrease in adaptive reserves.

Acute oxygen starvation during childbirth is usually associated with complications of childbirth itself - rapid or too prolonged labor, clamping of the umbilical cord, weakness of labor forces, placental abruption, etc. In this case, dysfunction of the internal organs of the fetus is pronounced, tachycardia of up to 160 or more strokes is observed heart rate per minute or bradycardia less than 120 beats. Heart sounds are muffled, movements are weak. The most severe variant of intrauterine hypoxia is asphyxia.

Chronic hypoxia develops slowly, with a moderately pronounced lack of oxygen, while malnutrition is diagnosed - a slowdown in weight gain by the fetus, more rare movements, bradycardia.

A developing baby can subsequently lead to a convulsive syndrome or cerebral palsy. Perhaps the formation of congenital anomalies of the heart, pneumopathy due to impaired maturation of the lung tissue.

Asphyxia during childbirth is extremely dangerous due to the death of a newborn, severe brain damage with necrosis and hemorrhage, respiratory disorders, and multiple organ failure. This condition requires resuscitation.

Oxygen starvation of the fetus is manifested:

• Tachycardia at the beginning of hypoxia and slowing of the pulse with its aggravation;
• Deafness of heart sounds;
• An increase in motor activity at the beginning of the development of pathology and in mild degrees, and a decrease with a deep lack of oxygen;
• The appearance of meconium in the amniotic fluid;
• An increase in hypoxia with periods of tachycardia and hypertension, followed by bradycardia and hypotension;
• The appearance of edema in the tissues;
• Hemorrhages due to a violation of blood viscosity, a tendency to intravascular aggregation of red blood cells;
• Disorders of electrolyte metabolism, acidosis.

serious consequences oxygen starvation during pregnancy can be birth trauma to the fetus, intrauterine death, severe asphyxia in the womb or during childbirth. Children born or born under conditions of oxygen starvation are hypotrophic, poorly adapted to life outside the fruiting place, suffer from neurological and mental disorders in the form of delayed speech and mental development, convulsive syndrome, and cerebral palsy.

In a newborn child with hypoxia, a sharp bradycardia, the absence of crying and the first breath, a sharp cyanosis of the skin, the absence of spontaneous respiration and a sharp metabolic imbalance are possible, requiring emergency care.

Treatment of oxygen starvation

Treatment of oxygen starvation should be comprehensive and timely, aimed at eliminating the cause of hypoxia and restoring adequate perfusion and tissue oxygenation. In acute forms and asphyxia, emergency therapy and resuscitation are necessary.

Regardless of the type of oxygen starvation, hyperbaric oxygenation is used as one of the main methods of pathogenetic therapy, in which oxygen is supplied to the lungs under high pressure. Due to the high pressure, oxygen can immediately dissolve in the blood, bypassing the connection with the erythrocyte, so its delivery to the tissues will be fast and not dependent on the morphological and functional features of red blood cells.

Hyperbaric oxygenation allows you to saturate the cells with oxygen, promotes the expansion of the arteries of the brain and heart, the work of which is enhanced and improved. In addition to oxygenation, cardiotonic agents, drugs to eliminate hypotension are prescribed. If necessary, transfusion of blood components is performed.

Hemic hypoxia is treated:

1. Hyperbaric oxygen therapy;
2. Hemotransfusions (blood transfusion);
3. The introduction of drugs-carriers of active oxygen - perftoran, for example;
4. Methods of extracorporeal detoxification - hemosorption, plasmapheresis to remove toxins from the blood;
5. The use of drugs that normalize the respiratory chain - ascorbic acid, methylene blue;
6. The introduction of glucose to meet the energy needs of cells;
7. Glucocorticosteroids.

Oxygen starvation during pregnancy requires hospitalization in the clinic and correction of both obstetric and extragenital pathology of the woman with the restoration of adequate blood circulation in the placenta. Rest and bed rest, oxygen therapy are prescribed, antispasmodics are introduced to reduce uterine tone (papaverine, eufillin, magnesia), drugs that improve blood rheology (chimes, pentoxifylline).

In chronic fetal hypoxia, vitamins E, C, group B, administration of glucose, antihypoxic agents, antioxidants and neuroprotectors are indicated. As the condition improves, the pregnant woman masters breathing exercises, water aerobics, undergoes physiotherapy (ultraviolet irradiation).

If severe fetal hypoxia cannot be eliminated, then in the period from the 29th week of gestation, it is necessary to urgently deliver the woman by caesarean section. Natural childbirth in chronic oxygen deficiency is carried out with monitoring of fetal cardiac activity. If a child is born in conditions of acute hypoxia or asphyxia, he is given resuscitation assistance.

In the future, babies who have undergone hypoxia are observed by a neurologist, the participation of a psychologist and a speech therapist may be required. With severe consequences of hypoxic brain damage, children need long-term drug therapy.

Dangerous complications of oxygen starvation are:

• Persistent neurological deficit;
• parkinsonism;
• dementia;
• Coma development.

Often, after hypoxia, not cured in a timely manner, psychological problems and fatigue remain.

Prevention oxygen starvation is to prevent conditions accompanied by a lack of oxygen: an active lifestyle, walking in the fresh air, physical activity, good nutrition and timely treatment of somatic pathology. "Office" work requires ventilation of the premises, and the types of professions that are more dangerous in terms of hypoxia (miners, divers, etc.) require strict observance of precautionary measures.