What is the partial pressure of oxygen in arterial blood. Partial pressure of oxygen in arterial blood Determination of partial pressure of oxygen and carbon dioxide

The meaning of breathing

Breathing is a vital process of constant exchange of gases between the body and its surrounding environment. In the process of breathing, a person absorbs oxygen from the environment and releases carbon dioxide.

Almost all complex reactions of transformation of substances in the body require the participation of oxygen. Without oxygen, metabolism is impossible, and a constant supply of oxygen is necessary to preserve life. In cells and tissues, as a result of metabolism, carbon dioxide is formed, which must be removed from the body. The accumulation of significant amounts of carbon dioxide inside the body is dangerous. Carbon dioxide is carried by the blood to the respiratory organs and exhaled. Oxygen entering the respiratory organs during inhalation diffuses into the blood and is delivered to organs and tissues by the blood.

There are no reserves of oxygen in the human and animal bodies, and therefore its continuous supply into the body is a vital necessity. If a person, in necessary cases, can live without food for more than a month, without water for up to 10 days, then in the absence of oxygen, irreversible changes occur within 5-7 minutes.

Composition of inhaled, exhaled and alveolar air

By alternately inhaling and exhaling, a person ventilates the lungs, maintaining a relatively constant gas composition in the pulmonary vesicles (alveoli). A person breathes atmospheric air with a high content of oxygen (20.9%) and a low content of carbon dioxide (0.03%), and exhales air in which there is 16.3% oxygen and 4% carbon dioxide (Table 8).

The composition of alveolar air differs significantly from the composition of atmospheric, inhaled air. It contains less oxygen (14.2%) and a large amount of carbon dioxide (5.2%).

Nitrogen and inert gases that make up the air do not take part in respiration, and their content in inhaled, exhaled and alveolar air is almost the same.

Why does exhaled air contain more oxygen than alveolar air? This is explained by the fact that when you exhale, air that is in the respiratory organs, in the airways, is mixed with the alveolar air.

Partial pressure and tension of gases

In the lungs, oxygen from the alveolar air passes into the blood, and carbon dioxide from the blood enters the lungs. The transition of gases from air to liquid and from liquid to air occurs due to the difference in the partial pressure of these gases in air and liquid. Partial pressure is the part of the total pressure that accounts for the share of a given gas in a gas mixture. The higher the percentage of gas in the mixture, the correspondingly higher its partial pressure. Atmospheric air, as is known, is a mixture of gases. Atmospheric air pressure 760 mm Hg. Art. The partial pressure of oxygen in atmospheric air is 20.94% of 760 mm, i.e. 159 mm; nitrogen - 79.03% of 760 mm, i.e. about 600 mm; There is little carbon dioxide in the atmospheric air - 0.03%, therefore its partial pressure is 0.03% of 760 mm - 0.2 mm Hg. Art.

For gases dissolved in a liquid, the term “voltage” is used, corresponding to the term “partial pressure” used for free gases. Gas tension is expressed in the same units as pressure (mmHg). If the partial pressure of a gas in the environment is higher than the voltage of that gas in the liquid, then the gas dissolves in the liquid.

The partial pressure of oxygen in the alveolar air is 100-105 mm Hg. Art., and in the blood flowing to the lungs the oxygen tension is on average 60 mm Hg. Art., therefore, in the lungs, oxygen from the alveolar air passes into the blood.

The movement of gases occurs according to the laws of diffusion, according to which gas spreads from a medium with high partial pressure to a medium with lower pressure.

Gas exchange in the lungs

The transition of oxygen from the alveolar air into the blood in the lungs and the flow of carbon dioxide from the blood into the lungs obey the laws described above.

Thanks to the work of the great Russian physiologist Ivan Mikhailovich Sechenov, it became possible to study the gas composition of the blood and the conditions of gas exchange in the lungs and tissues.

Gas exchange in the lungs occurs between alveolar air and blood by diffusion. The alveoli of the lungs are intertwined with a dense network of capillaries. The walls of the alveoli and capillaries are very thin, which facilitates the penetration of gases from the lungs into the blood and vice versa. Gas exchange depends on the size of the surface through which gases diffuse and the difference in partial pressure (tension) of the diffusing gases. With a deep breath, the alveoli stretch, and their surface reaches 100-105 m2. The surface area of ​​the capillaries in the lungs is also large. There is, and a sufficient, difference between the partial pressure of gases in the alveolar air and the tension of these gases in the venous blood (Table 9).

From Table 9 it follows that the difference between the tension of gases in the venous blood and their partial pressure in the alveolar air is 110 - 40 = 70 mm Hg for oxygen. Art., and for carbon dioxide 47 - 40 = 7 mm Hg. Art.

Experimentally, it was possible to establish that with a difference in oxygen tension of 1 mm Hg. Art. in an adult at rest, 25-60 ml of oxygen can enter the blood in 1 minute. A person at rest needs approximately 25-30 ml of oxygen per minute. Therefore, an oxygen pressure difference of 70 mmHg. Art. is sufficient to provide the body with oxygen under different conditions of its activity: during physical work, sports exercises, etc.

The rate of diffusion of carbon dioxide from the blood is 25 times greater than that of oxygen, therefore, with a pressure difference of 7 mm Hg. Art., carbon dioxide has time to be released from the blood.

Carrying gases in the blood

Blood carries oxygen and carbon dioxide. In blood, as in any liquid, gases can be in two states: physically dissolved and chemically bound. Both oxygen and carbon dioxide dissolve in very small quantities in the blood plasma. Most oxygen and carbon dioxide are transported in chemically bound form.

The main carrier of oxygen is hemoglobin in the blood. 1 g of hemoglobin binds 1.34 ml of oxygen. Hemoglobin has the ability to combine with oxygen, forming oxyhemoglobin. The higher the partial pressure of oxygen, the more oxyhemoglobin is formed. In the alveolar air, the partial pressure of oxygen is 100-110 mm Hg. Art. Under such conditions, 97% of blood hemoglobin binds to oxygen. Blood brings oxygen to tissues in the form of oxyhemoglobin. Here the partial pressure of oxygen is low, and oxyhemoglobin - a fragile compound - releases oxygen, which is used by the tissues. The binding of oxygen by hemoglobin is also influenced by carbon dioxide tension. Carbon dioxide reduces the ability of hemoglobin to bind oxygen and promotes the dissociation of oxyhemoglobin. Increasing temperature also reduces the ability of hemoglobin to bind oxygen. It is known that the temperature in the tissues is higher than in the lungs. All these conditions help dissociate oxyhemoglobin, as a result of which the blood releases the oxygen released from the chemical compound into the tissue fluid.

The property of hemoglobin to bind oxygen is vital for the body. Sometimes people die from lack of oxygen in the body, surrounded by the cleanest air. This can happen to a person who finds himself in low pressure conditions (at high altitudes), where the thin atmosphere has a very low partial pressure of oxygen. On April 15, 1875, the Zenit balloon, with three balloonists on board, reached an altitude of 8000 m. When the balloon landed, only one person remained alive. The cause of death was a sharp decrease in the partial pressure of oxygen at high altitude. At high altitudes (7-8 km), arterial blood in its gas composition approaches venous blood; all tissues of the body begin to experience an acute lack of oxygen, which leads to serious consequences. Climbing to altitudes above 5000 m usually requires the use of special oxygen devices.

With special training, the body can adapt to the low oxygen content in the atmospheric air. A trained person’s breathing deepens, the number of red blood cells in the blood increases due to their increased formation in the hematopoietic organs and their supply from the blood depot. In addition, heart contractions increase, which leads to an increase in minute blood volume.

Pressure chambers are widely used for training.

Carbon dioxide is carried by the blood in the form of chemical compounds - sodium and potassium bicarbonates. The binding of carbon dioxide and its release into the blood depend on its tension in the tissues and blood.

In addition, blood hemoglobin is involved in the transfer of carbon dioxide. In tissue capillaries, hemoglobin enters into a chemical combination with carbon dioxide. In the lungs, this compound breaks down to release carbon dioxide. About 25-30% of the carbon dioxide released in the lungs is carried by hemoglobin.

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Hypoxia is most clearly detected during stay in a rarefied space, when the partial pressure of oxygen drops.

In an experiment, oxygen starvation can occur at relatively normal atmospheric pressure, but with a low oxygen content in the surrounding atmosphere, for example, when an animal is in a confined space with a low oxygen content. The phenomena of oxygen starvation can be observed when climbing mountains, rising in an airplane to a high altitude - mountain and altitude sickness(Fig. 116).

The first signs of acute mountain sickness can often be observed already at an altitude of 2500 - 3000 m. For most people, they appear when climbing to 4000 m and above. The partial pressure of oxygen in the air, equal (at atmospheric pressure 760 mm Hg) to 159 mm, drops at this altitude (430 mm atmospheric pressure) to 89 mm. At the same time, arterial blood oxygen saturation begins to decrease. Symptoms of hypoxia usually appear when arterial oxygen saturation is around 85%, and death can occur when arterial oxygen saturation falls below 50%.

Climbing a mountain is accompanied by characteristic phenomena also due to temperature conditions, wind and muscle activity performed during the ascent. The more the metabolism increases due to muscle tension or a decrease in air temperature, the sooner signs of illness appear.

Disorders that arise during ascent to altitude develop more strongly the faster the ascent occurs. Training is of great importance in this regard.

Oxygen starvation when ascending in an airplane to a high altitude has some peculiarities. Climbing the mountain is slow and requires intense muscle work. Airplanes can reach altitude within a very short time. A pilot's stay at an altitude of 5000 m in the absence of sufficient training is accompanied by sensations of headache, dizziness, heaviness in the chest, palpitations, expansion of gases in the intestines, as a result of which the diaphragm is pushed upward, and breathing becomes even more difficult. The use of oxygen devices eliminates many of these phenomena (Fig. 117).

The effect on the body of low oxygen content in the air is expressed in disorders of the nervous system, breathing and circulation.

Some excitement is followed by fatigue, apathy, drowsiness, heaviness in the head, mental disorders in the form of irritability followed by depression, some loss of orientation, motor function disorders, and disorders of higher nervous activity. At medium altitudes, a weakening of internal inhibition develops in the cerebral cortex, and at higher altitudes, diffuse inhibition develops. Disorders of autonomic functions also develop in the form of shortness of breath, increased heart activity, changes in blood circulation and digestive disorders.

With acute oxygen starvation, the breath. It becomes superficial and frequent, which is the result of stimulation of the respiratory center. Sometimes a peculiar, intermittent, so-called periodic breathing (Cheyne-Stokes type) occurs. In this case, pulmonary ventilation noticeably suffers. With the gradual onset of oxygen starvation, breathing becomes frequent and deep, air circulation in the alveoli improves noticeably, but the carbon dioxide content and its tension in the alveolar air drop, i.e., hypocapnia develops, complicating the course of hypoxia. Impaired breathing may cause loss of consciousness.

Acceleration and intensification of the activity of the heart arise due to an increase in the function of its accelerating and amplifying nerves, as well as a decrease in the function of the vagus nerves. Therefore, increased heart rate during oxygen starvation is one of the indicators of the reaction of the nervous system that regulates blood circulation.

At high altitudes, a number of other circulatory disorders also occur. Blood pressure initially increases, but then begins to decrease in accordance with the state of the vasomotor centers. With a sharp decrease in the oxygen content in the inhaled air (up to 7 - 6%), the activity of the heart noticeably weakens, blood pressure drops, and venous pressure rises, cyanosis and arrhythmia develop.

Sometimes it is also observed bleeding from the mucous membranes of the nose, mouth, conjunctiva, respiratory tract, and gastrointestinal tract. Great importance in the occurrence of such bleeding is attached to the expansion of superficial blood vessels and disruption of their permeability. These changes occur partly due to the action of toxic metabolic products on the capillaries.

Dysfunction of the nervous system from being in a rarefied space also manifests itself gastrointestinal disorders usually in the form of lack of appetite, inhibition of the digestive glands, diarrhea and vomiting.

During high altitude hypoxia, the metabolism. Oxygen consumption initially increases, and then, with severe oxygen starvation, it decreases, the specific dynamic effect of protein decreases, and the nitrogen balance becomes negative. Residual nitrogen in the blood increases, ketone bodies accumulate, especially acetone, which is excreted in the urine.

A decrease in the oxygen content in the air to a certain limit has little effect on the formation of oxyhemoglobin. However, later, when the oxygen content in the air decreases to 12%, the oxygen saturation of the blood becomes about 75%, and when the oxygen content in the air is 6 - 7%, it is 50 - 35% of normal. The oxygen tension in capillary blood is especially reduced, which significantly affects its diffusion into the tissue.

Increased pulmonary ventilation and an increase in the tidal volume of the lungs during hypoxia cause depletion of alveolar air and blood in carbon dioxide (hypocapnia) and the occurrence of relative alkalosis, as a result of which the excitability of the respiratory center can be temporarily inhibited and the activity of the heart is weakened. Therefore, inhalation of carbon dioxide at altitudes, causing an increase in the excitability of the respiratory center, helps to increase the oxygen content in the blood and thereby improves the condition of the body.

However, the continuing decrease in the partial pressure of oxygen during ascent to altitude contributes to the further development of hypoxemia and hypoxia. The phenomena of insufficiency of oxidative processes are increasing. Alkalosis is again replaced by acidosis, which is again somewhat weakened due to an increase in the respiratory rate, a decrease in oxidative processes and the partial pressure of carbon dioxide.

Noticeably changed when rising to altitude and heat exchange. Heat transfer at high altitude increases mainly due to the evaporation of water by the surface of the body and through the lungs. Heat production gradually lags behind heat loss, as a result of which body temperature, which initially increases slightly, then decreases.

The onset of signs of oxygen starvation largely depends on the characteristics of the body, the state of its nervous system, lungs, heart and blood vessels, which determine the body’s ability to tolerate a rarefied atmosphere.

The nature of the action of rarefied air also depends on the rate of development of oxygen starvation. In acute oxygen starvation, dysfunction of the nervous system comes to the fore, while in chronic oxygen starvation, due to the gradual development of compensatory processes, pathological phenomena from the nervous system are not detected for a long time.

A healthy person generally copes satisfactorily with lowering barometric pressure and partial pressure of oxygen to a certain limit, and the better the slower the ascent and the easier the body adapts. The limit for a person can be considered a decrease in atmospheric pressure to one third of normal, i.e., up to 250 mm Hg. Art., which corresponds to an altitude of 8000 - 8500 m and an oxygen content in the air of 4 - 5%.

It has been established that during stay at heights there occurs device body, or its acclimatization, providing compensation for breathing disorders. Residents of mountainous areas and trained climbers may not develop mountain sickness when climbing to an altitude of 4000 - 5000 m. Highly trained pilots can fly without an oxygen apparatus at an altitude of 6000 - 7000 m and even higher.

As barometric pressure decreases, the partial pressure of the main gases that make up the atmosphere also decreases. The quantitative composition of the air mixture in the troposphere remains practically unchanged. Thus, atmospheric air under normal conditions (at sea level) contains 21% oxygen, 78% nitrogen, 0.03% carbon dioxide and almost % is inert gases: helium, xenon, argon, etc.

Partial pressure(Latin partialis - partial, from Latin pars - part) - the pressure of an individual component of the gas mixture. The total pressure of a gas mixture is the sum of the partial pressures of its components.

The partial pressure of gas in atmospheric air is determined by the formula:

Рh – barometric pressure at actual altitude.

Gas exchange between the body and the external environment plays a decisive role in maintaining human life. Gas exchange is carried out through respiration and blood circulation: oxygen continuously enters the body, and carbon dioxide and other metabolic products are released from the body. To ensure that this process is not disrupted, it is necessary to maintain partial pressure of oxygen in the inhaled air at a level close to that on earth.

Partial pressure of oxygen (O 2) in the air is called the part of the total air pressure attributable to O 2.

So, at sea level (H=0m), in accordance with (1.1), the partial pressure of oxygen will be:

where αО 2 = 21% is the gas content in atmospheric air in %;

P h =0 – barometric pressure at sea level

As altitude increases, the total gas pressure drops, but the partial pressure of such components as carbon dioxide and water vapor in the alveolar air remains virtually unchanged.

And equally, at a human body temperature of 37 0 C approximately:

· for water vapor pH 2 O = 47 mm Hg;

· for carbon dioxide RSO 2 =40 mm Hg.

In this case, the rate of drop in oxygen pressure in the alveolar air changes significantly.

Atmospheric pressure and air temperature at altitudes

According to international standard

Table 1.4

Alveolar air- a mixture of gases (mainly oxygen, carbon dioxide, nitrogen and water vapor) contained in the pulmonary alveoli, directly involved in gas exchange with the blood. The supply of oxygen to the blood flowing through the pulmonary capillaries and the removal of carbon dioxide from it, as well as the regulation of respiration, depend on the composition maintained in healthy animals and humans within certain narrow limits due to ventilation of the lungs (in humans it normally contains 14-15% oxygen and 5-5.5% carbon dioxide). With a lack of oxygen in the inhaled air and certain painful conditions, changes in composition occur, which can lead to hypoxia.

From Liverpool Harbor, ships always set sail for distant shores on Thursdays.

Rudyard Kipling

On December 2, 1848, on Friday, and not at all on Thursday (according to R. Kipling), the Londoidery steamer set off from Liverpool to Sligo with two hundred passengers, most of them emigrants.

During the voyage, a storm occurred and the captain ordered all passengers to leave the deck. The general cabin for third-class passengers was 18 feet long, 11 wide, and 7 high. The passengers were crowded in this cramped space; it would only be very cramped for them if the hatches remained open; but the captain ordered them to be closed, and for some unknown reason ordered the entrance to the cabin to be tightly covered with oilcloth. The unfortunate passengers thus had to breathe the same, non-renewable air. It soon became unbearable. A terrible scene of violence and madness ensued, with the groans of the dying and the curses of the stronger: it stopped only after one of the passengers managed to force his way onto the deck and call for the lieutenant, before whom a terrible sight opened: seventy-two of the passengers had already died, and many were dying ; their limbs were convulsively writhed, and blood came out of their eyes, nostrils and ears. 152 years later, history repeated itself and on June 19, 2000, in another English port - Dover, the customs service found 58 corpses and two living illegal emigrants from the country in the back of a Dutch truck in a tightly closed container intended for transporting tomatoes.

Of course, the cases cited are blatant and out of the ordinary. However, the same reason determines the pallor of people leaving a church filled with people; fatigue after several hours spent in the theater, in a concert hall, in a lecture hall, in any poorly ventilated room. At the same time, clean air leads to the disappearance of all adverse manifestations.

The ancients did not imagine this reason; and the scientists of the sixteenth and seventeenth centuries were poorly versed in it. The impetus for its deciphering came from the works of Presley, who discovered that oxygen contained in atmospheric air has the property of converting venous blood into arterial blood. Lavoisier completed this discovery and founded the chemical theory of respiration. Goodwin (1788) applied new views to asphyxia (suffocation) and proved through a series of experiments that when the atmosphere remains unchanged, death inevitably occurs. Bisha concluded from many striking experiments that there is a close connection between breathing, blood circulation and nervous activity; he showed that the rush of venous blood to the brain stops its activity and then the activity of the heart. Legalois extended these observations to the spinal cord. Claude Bernard proved that venous blood is not poisonous, although it lacks the ability to support life.

HYPOXIA (hypoxia; Greek hypo - under, below, little + lat. oxygenium - oxygen) or “oxygen starvation”, “oxygen deficiency” is a typical pathological process that causes insufficient oxygen supply to the tissues and cells of the body or disturbances in its use during biological oxidation.

Along with hypoxia, “anoxia” is distinguished - i.e. complete absence of oxygen or complete cessation of oxidative processes (in reality, such a condition does not occur) and “hypoxemia” - low voltage and oxygen content in the blood.

For reasons of hypoxia, it can be exogenous, caused by external factors (primarily a lack of oxygen in the inhaled air - hypoxic hypoxia, and vice versa, an excess of oxygen in the inhaled air - hyperoxic hypoxia) and endogenous, due to the pathology of the body.

Exogenous hypoxic hypoxia, in turn, can be normobaric, i.e. developing at normal barometric pressure, but with a reduced partial pressure of oxygen in the inhaled air (for example, when being in confined spaces of small volume, as was the case in the case described above, working in mines, wells with faulty oxygen supply systems, in the cabins of aircraft, underwater boats, in medical practice for malfunctions of anesthesia-respiratory equipment), and hypobaric, caused by a general decrease in barometric pressure (when climbing mountains - “mountain sickness” or in unpressurized aircraft without individual oxygen systems - “altitude sickness”).

Endogenous hypoxia can be divided into

Respiratory (a variant of hypoxic hypoxia): difficulty in the supply of oxygen to the body, impaired alveolar vengillation;

Hemic as a result of the pathology of the oxygen carrier - hemoglobin, leading to a decrease in the oxygen capacity of the blood: a - hemoglobin deficiency due to blood loss, hemolysis of erythrocytes, impaired hematopoiesis, b - impaired binding of 0 2 to hemoglobin (carbon monoxide or carbon monoxide CO has an affinity for hemoglobin of 240 times more than oxygen, and when poisoned by this gas, it blocks the temporary combination of oxygen with hemoglobin, forming a stable compound - carboxyhemoglobin (with a CO content in the air of about 0.005, up to 30% of hemoglobin turns into HbCO, and at 0.1% CO, about 70% HbCO, which is fatal for the body); under the influence of strong oxidizing agents on hemoglobin (nitrates, nitrites, nitrogen oxides, aniline derivatives, benzene, some infectious toxins, medicinal substances: phenacytin, amidopyrine, sulfonamides - methemoglobin formers, converting divalent heme iron into ferric form) methemoglobin is formed; in - replacement of normal hemoglobin with pathological forms - hemoglobinopathies; d - blood dilution - hemodilution;

Circulatory: a - congestive type - decreased cardiac output, b - ischemic type - impaired microcirculation;

Tissue (histotoxic - as a result of impaired oxygen utilization by tissues): blockade of oxidative enzymes (a - specific binding of active centers - potassium cyanide; b - binding of functional groups of the protein part of the molecule - salts of heavy metals, alkylating agents; d - competitive inhibition - inhibition of malonic succinate dehydrogenase and other dicarboxylic acids), vitamin deficiencies (group “B”), disintegration of biological membranes, hormonal disorders;

Associated with a decrease in the permeability of hematoparenchymal barriers: limitation of 0 2 diffusion through the capillary membrane, limitation of 0 2 diffusion through the intercellular spaces, limitation of 0 2 diffusion through the cell membrane.

Mixed type of hypoxia.

Based on the prevalence of hypoxia, hypoxia is divided into a) local (often with local hemodynamic disturbances) and b) general.

According to the speed of development: a) fulminant (develops to a severe and even fatal degree within a few seconds, b) acute (within several minutes or tens of minutes, c) subacute (several hours or tens of hours), d) chronic (lasts for weeks, months, years).

By severity: a) mild, b) moderate, c) severe, d) critical (deadly).

In the pathogenesis of hypoxia, several fundamental mechanisms can be identified: the development of energy deficiency, disruption of the renewal of protein structures, disruption of the structure of cellular and organelle membranes, activation of proteolysis, and development of acidosis.

Metabolic disorders first develop in energy and carbohydrate metabolism, as a result of which the content of ΛΤΦ in cells decreases with a simultaneous increase in the products of its hydrolysis - ADP and AMP. In addition, NAD H 2 accumulates in the cytoplasm (From-

excess of “own” intramitochondrial NAD*H? , which is formed when the respiratory chain is turned off, inhibits the work of shuttle mechanisms and cytoplasmic NADH 2 loses the ability to transfer hydride ions to the mitochondrial respiratory chain). In the cytoplasm, NAD-H 2 can be oxidized, reducing pyruvate to lactate, and it is this process that is initiated when there is a lack of oxygen. Its consequence is excessive formation of lactic acid in the tissues. An increase in ADP content as a consequence of insufficient aerobic oxidation activates glycolysis, which also leads to an increase in the amount of lactic acid in tissues. The insufficiency of oxidative processes also leads to disruption of other types of metabolism: lipid, protein, electrolyte, and neurotransmitter metabolism.

At the same time, the development of acidosis entails hyperventilation of the lungs, the formation of hypocapnia and, as a consequence, gas alkalosis.

Based on electron microscopy data, the main role in the development of irreversible cell damage during hypoxia is attributed to changes in cellular and mitochondrial membranes, and it is probably the mitochondrial membranes that are affected first.

Blocking energy-dependent mechanisms for maintaining ion balance and disrupting the permeability of cell membranes under conditions of insufficient ATP synthesis changes the concentration of K\Na + and Ca 2+, while mitochondria lose the ability to accumulate Ca~ + ions and its concentration in the cytoplasm increases. Ca~ + not absorbed by mitochondria and located in the cytoplasm is, in turn, an activator of destructive processes in mitochondrial membranes, acting indirectly through stimulation of the enzyme phospholipase A 3, which catalyzes the hydrolysis of mitochondrial phospholipids.

Metabolic changes in cells and tissues result in dysfunction of organs and systems of the body.

Nervous system. First of all, complex analytical and synthetic processes suffer. Often, a kind of euphoria and loss of the ability to adequately assess the situation are initially observed. With increasing hypoxia, severe violations of the internal nervous system develop, up to the loss of the ability to simple count, confusion and complete loss of consciousness. Already in the early stages, coordination disorders are observed, first of complex ones (he cannot pull a thread into a needle), and then of simple movements, and then adynamia is noted.

The cardiovascular system. With increasing hypoxia, tachycardia, weakened contractility of the heart, arrhythmia up to atrial and ventricular fibrillation are detected. Blood pressure, after an initial rise, progressively falls until collapse develops. Microcirculation disorders are also evident.

Respiratory system. The stage of respiratory activation is replaced by dyspneic phenomena with various disturbances in the rhythm and amplitude of respiratory movements (Cheyne-Sgox, Kussmaul breathing). After often

After a short stop, terminal (agonal) breathing appears in the form of rare deep convulsive “sighs”, gradually weakening until it stops completely. Ultimately, death occurs from paralysis of the respiratory center.

The body’s adaptation mechanisms to hypoxia can be divided, firstly, into passive and, secondly, active adaptation mechanisms. Based on the duration of the effect, they can be divided into urgent (emergency) and long-term.

Passive adaptation usually means limiting the body’s mobility, which means reducing the body’s need for oxygen.

Active adaptation includes reactions of four orders:

First order reactions - reactions aimed at improving the delivery of oxygen to cells: an increase in alveolar ventilation due to increased frequency and deepening of respiratory movements - tachypnea (shortness of breath), as well as mobilization of reserve alveoli, tachycardia, an increase in pulmonary blood flow, a decrease in the radius of the tissue cylinder, an increase in circulating mass blood due to its release from the depot, centralization of blood circulation, activation of erythropoiesis, change in the rate of release of 0 2 by hemoglobin.

Second order reactions - reactions at the tissue, cellular and subcellular levels, aimed at increasing the ability of cells to utilize oxygen: activation of respiratory enzymes, activation of mitochondrial biogenesis (during hypoxia, the function of an individual mitochondria decreases by 20%, which is compensated by an increase in their number in the cell), decrease critical level p0 2 (i.e. the level below which the rate of respiration depends on the amount of oxygen in the cell).

III order reactions - a change in the type of metabolism in the cell: the share of glycolysis in the energy supply of the cell increases (glycolysis is 13-18 times inferior to respiration).

IV order reactions - increasing tissue resistance to hypoxia due to the power of energy systems, activation of glycolysis and a decrease in the critical level of p0 2.

Long-term adaptation is characterized by a persistent increase in the diffusion surface of the pulmonary alveoli, a better correlation between ventilation and blood flow, compensatory myocardial hypertrophy, an increase in hemoglobin content in the blood, activation of erythropoiesis, and an increase in the number of mitochondria per unit cell mass.

MOUNTAIN SICKNESS is a variant of exogenous hypobaric hypoxic hypoxia. It has long been known that ascent to high altitude causes a painful condition, the typical symptoms of which are nausea, vomiting, gastrointestinal disorders, physical and mental depression. Individual resistance to oxygen starvation has a wide range of fluctuations, which many researchers paid attention to when studying altitude sickness. Some people suffer from altitude sickness already at relatively low altitudes (2130-

2400 m above sea level), while others are relatively resistant to high altitudes. It has been stated that the 3050m elevation may cause symptoms of altitude sickness in some people, while others can reach 4270m without any symptoms of altitude sickness. However, very few people can reach an altitude of 5790 m without developing noticeable symptoms of altitude sickness.

A number of authors, along with mountain sickness, also identify altitude sickness, which occurs during rapid (in a few minutes) ascents to high altitudes, which often occurs without any unpleasant sensations - subjectively asymptomatic. And this is her cunning. It occurs when flying at high altitudes without the use of oxygen.

Systematic experiments to decipher the pathogenesis of mountain (high-altitude) illness were carried out by Paul Baer, ​​who came to the conclusion that a decrease in the pressure of the atmosphere surrounding an animal acts only insofar as it reduces the tension of oxygen in this atmosphere, i.e. the observed changes in the animal's body when the atmosphere becomes rarefied turn out to be in all respects completely identical to those observed when the amount of oxygen in the inhaled air decreases. There is a parallelism between one and the other state, not only qualitative, but also quantitative, if only the basis for comparison is not the percentage of oxygen in the inhaled mixture, but only the tension of this gas in it. Thus, a decrease in the amount of oxygen in the air when its tension is from 160 mm Hg. Art. drops to 80 mmHg. Art., can be quite comparable to the air being halved when the pressure drops from 760 mm Hg. Art. (normal atmospheric pressure) up to 380 mm Hg. Art.

Paul Bert placed an animal (mouse, rat) under a glass bell and pumped the air out of it. When the air pressure decreased by 1/3 (when the pressure dropped to 500 mm Hg or when the oxygen tension decreased to approximately 105 mm Hg), no abnormal phenomena were noted on the part of the animal; when the pressure was reduced by 1/2 (at a pressure of 380 mm Hg, i.e., with an oxygen tension of about 80 mm Hg), the animals showed only a somewhat apathetic state and a desire to maintain a motionless state; finally, with a further decrease in pressure, all the phenomena associated with a lack of oxygen developed. The onset of death was usually observed when the oxygen tension decreased to 20-30 mm Hg. Art.

In another version of the experiments, Paul Bert placed the animal in an atmosphere of pure oxygen and then discharged it. As one would expect a priori, the vacuum could be brought to much greater degrees than air. Thus, the first signs of the influence of vacuum in the form of a slight increase in breathing appear at a pressure of 80 mm Hg. Art. - in the case of air 380 mm Hg. Art. Thus, to obtain the same phenomena in rarefied oxygen as in air, the degree of rarefaction of oxygen must be 5 times greater than the degree of rarefaction of atmospheric

air. Taking into account that atmospheric air contains 1/5 of oxygen in its composition by volume, i.e. oxygen accounts for only a fifth of the total pressure, it is clearly seen that the observed phenomena depend only on the oxygen tension, and not on the pressure of the surrounding atmosphere.

The development of mountain sickness is also significantly influenced by physical activity, which was brilliantly proven by Regnard’oM (1884) using the following demonstrative experiment. Two guinea pigs were placed under a glass bell - one was given complete freedom of behavior, and the other was in a “squirrel” wheel driven by an electric motor, as a result of which the animal was forced to constantly run. As long as the air in the bell remained under normal atmospheric pressure, the pig ran quite unhindered, and she apparently did not experience any particular fatigue. If the pressure was brought to half atmospheric or slightly lower, then the pig, not encouraged to move, remained motionless, not showing any signs of suffering, while the animal inside the “squirrel” wheel showed obvious difficulties in running, constantly stumbled and finally, exhausted, she fell on her back and remained without any active movements, allowing herself to be carried away and thrown from place to place by the rotating walls of the cage. Thus, the same decrease in pressure, which is still very easily tolerated by animals in a state of complete rest, turns out to be fatal for an animal forced to produce increased muscle movements.

Treatment of mountain sickness: pathogenetic - descent from the mountain, giving oxygen or carbogen, giving acidic foods; symptomatic - effect on the symptoms of the disease.

Prevention - oxygen prophylaxis, acidic foods and stimulants.

The increased supply of oxygen to the body is called HYPEROXY. Unlike hypoxia, hyperoxia is always exogenous. It can be obtained: a) by increasing the oxygen content in the inhaled gas mixture, b) by increasing the pressure (barometric, atmospheric) of the gas mixture. Unlike hypoxia, hyperoxia does not occur to a large extent in natural conditions and the animal organism could not adapt to it in the process of evolution. However, adaptation to hyperoxia still exists and in most cases is manifested by a decrease in pulmonary ventilation, a decrease in blood circulation (decreased heart rate), a decrease in the amount of hemoglobin and red blood cells (example: decompression anemia). A person can breathe a mixture of gases with a high oxygen content for quite a long period. The first flights of American astronauts were carried out on devices in the cabins of which an atmosphere with excess oxygen was created.

When oxygen is inhaled under high pressure, HYPEROXIC HYPOXIA develops, which should be discussed specifically.

Without oxygen, life is impossible, but it itself can have a toxic effect comparable to strychnine.

During hyperoxic hypoxia, high oxygen tension in tissues leads to oxidative destruction (destruction) of mitochondrial structures, inactivation of many enzymes (enzymes), especially those containing sulfhydryl groups. The formation of free oxygen radicals takes place, disrupting the formation of DNA and thereby distorting protein synthesis. The consequence of systemic enzyme deficiency is a drop in the brain content of γ-aminobutyrate, the main inhibitory neurotransmitter of the gray matter, which causes convulsive syndrome of cortical origin.

The toxic effect of oxygen can occur with prolonged breathing of a mixture of gases with a partial pressure of oxygen of 200 mm Hg. Art. At partial pressures less than 736 mm Hg. Art. the histotoxic effect is expressed predominantly in the lungs and manifests itself either in the inflammatory process (high partial pressure of oxygen in the alveoli, arterial blood and tissues is a pathogenic irritant, leading to a reflex spasm of the microvessels of the lungs and impaired microcirculation and, as a result, cell damage, which predisposes to inflammation), or in diffuse microatelectasis of the lungs due to the destruction of the surfactant system by free radical oxidation. Severe pulmonary atelectasis is observed in pilots who begin to breathe oxygen long before reaching altitude, at which additional gas is required.

At 2500 mm Hg. Art. Not only arterial and venous blood is saturated with oxygen, due to which the latter is not able to remove CO 2 from tissues.

Breathing a gas mixture, the partial pressure of oxygen in which is higher than 4416 mm Hg. Art., leads to tonic-clonic convulsions and loss of consciousness within a few minutes.

The body adapts to excess oxygen, turning on in the first couple the same mechanisms as during hypoxia, but with the opposite direction (decreased breathing and its depth, decreased pulse, decreased mass of circulating blood, number of red blood cells), but with the development of hyperoxic hypoxia, adaptation proceeds as follows: and with other types of hypoxia.

ACUTE OXYGEN POISONING clinically occurs in three stages:

Stage I - increased breathing and heart rate, increased blood pressure, dilated pupils, increased activity with occasional muscle twitching.