With a decrease in barometric pressure, 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 virtually unchanged. So atmospheric air under normal conditions (at sea level) it contains 21% oxygen, 78% nitrogen, 0.03% carbon dioxide and almost % is inert gases: helium, xenon, argon, etc.

Partial pressure(lat. partialis - partial, from lat. pars - part) - the pressure of a single 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 a gas in atmospheric air is determined by the formula:

Ph is the barometric pressure at the actual altitude.

A decisive role in maintaining human life is played by gas exchange between the body and external environment. Gas exchange is carried out due to respiration and blood circulation: oxygen continuously enters the body, and carbon dioxide and other metabolic products are released from the body. In order for this process not to be disturbed, it is necessary to support partial pressure of oxygen in the inhaled air at a level close to the earth.

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

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

where αO 2 \u003d 21% is the gas content in atmospheric air in%;

P h \u003d 0 - barometric pressure at sea level

As the height increases total pressure gases decreases, however, the partial pressure of such constituent parts, as carbon dioxide and water vapor in the alveolar air, remains virtually unchanged.

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

· for water vapor РН 2 О=47mm Hg;

· for carbon dioxide РСО 2 =40 mm Hg.

This significantly changes the rate of oxygen pressure drop in the alveolar air.

Atmospheric pressure and air temperature at heights

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 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 some disease states, changes in the composition occur, which can lead to hypoxia.

The main air parameters that determine the physiological state of a person are:

absolute pressure;

percentage of oxygen;

temperature;

relative humidity;

harmful impurities.

Of all the listed air parameters, the absolute pressure and the percentage of oxygen are of decisive importance for a person. Absolute pressure determines the partial pressure of oxygen.

The partial pressure of any gas in a gas mixture is the fraction of the total pressure of the gas mixture attributable to that gas in proportion to its percentage.

So for partial pressure oxygen we have

where
− percentage of oxygen in the air (
);

R H − air pressure at altitude H;

− partial pressure of water vapor in the lungs (backpressure for breathing
).

The partial pressure of oxygen is of particular importance for the physiological state of a person, since it determines the process of gas exchange in the body.

Oxygen, like any gas, tends to move from a space in which its partial pressure is greater to a space with a lower pressure. Consequently, the process of saturation of the body with oxygen occurs only when the partial pressure of oxygen in the lungs (in the alveolar air) is greater than the partial pressure of oxygen in the blood flowing to the alveoli, and this latter will be greater than the partial pressure of oxygen in the tissues of the body.

To remove carbon dioxide from the body, it is necessary to have the ratio of its partial pressures opposite to that described, i.e. highest value partial pressure of carbon dioxide should be in the tissues, less - in the venous blood and even less - in the alveolar air.

At sea level at R H= 760 mmHg Art. the partial pressure of oxygen is ≈150 mm Hg. Art. With such
normal saturation of human blood with oxygen in the process of breathing is ensured. With increasing flight altitude
decreases due to the decrease P H(Fig. 1).

Special physiological studies have established that the minimum partial pressure of oxygen in the inhaled air
This number is called the physiological limit of a person's stay in an open cabin in terms of size
.

The partial pressure of oxygen is 98 mm Hg. Art. corresponds height H= 3 km. At
< 98 mmHg Art. visual impairment, hearing impairment, slow reaction and loss of consciousness by a person are possible.

To prevent these phenomena on the aircraft, oxygen supply systems (OSS) are used, providing
> 98 mmHg Art. in the inhaled air in all flight modes and in emergency situations.

Practically in aviation, the height H = 4 km as a limit for flights without oxygen devices, i.e. aircraft with a service ceiling of less than 4 km may not have an SPC.

1. Partial pressure of oxygen and carbon dioxide in the human body in terrestrial conditions

When changing the values ​​​​specified in the table
and
disrupted normal gas exchange in the lungs and throughout the human body.

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

Rudyard Kipling

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

During the voyage there was a storm and the captain ordered all passengers to get off the deck. The common cabin for third-class passengers was 18 feet long, 11 wide, and 7 high. Passengers crowded in this cramped space; they would only be very cramped if the hatches were left open; but the captain ordered to close them, and for some unknown reason ordered to tighten the entrance to the cabin tightly 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 followed, with the groans of the dying and curses of stronger ones: it stopped only after one of the passengers managed to forcefully escape onto the deck and call on the lieutenant, before whom a terrible sight opened up: seventy-two of the passengers had already died, and many were dying ; their limbs were writhing convulsively, and blood oozed from their eyes, nostrils, and ears. After 152 years, history repeated itself, and on June 19, 2000, in another English port - Dover, the customs service found in the back of a Dutch truck in a tightly closed container designed to transport tomatoes, 58 corpses and two living illegal emigrants from the country.

Of course, the cases cited are egregious, out of the ordinary. However, the same reason causes the paleness of people leaving a church full of people; fatigue after a few hours in the theatre, in a concert hall, in a lecture hall, in any badly ventilated room. At the same time, clean air leads to the disappearance of all unfavorable manifestations.

The ancients did not imagine this reason; and the scientists of the sixteenth and seventeenth centuries were not well versed in it. The impetus for its decoding was the work of Prestle, who discovered that the oxygen contained in the atmospheric air tends to turn 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 by a number of experiments that when the atmosphere remains unchanged, death inevitably occurs. Bisha concluded from many striking experiments that there is a close connection between respiration, 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. Legallois extended these observations to the spinal cord as well. 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 tissues and cells of the body or violations of its use during biological oxidation.

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

For reasons of hypoxia, it can be exogenous, caused by external factors (this is 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 reduced partial pressure of oxygen in the inhaled air (for example, when staying in closed rooms 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 with malfunctions of anesthesia and respiratory equipment), and hypobaric, due to 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 subdivided into

Respiratory (a variant of hypoxic hypoxia): difficulty in the supply of oxygen to the body, violation of the alveolar venous hylation;

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 during 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 connection of oxygen with hemoglobin, forming a stable compound - carboxyhemoglobin (with a CO content in the air of the order of 0.005, up to 30% of hemoglobin turns into HbCO, and at 0.1% CO, about 70% HbCO, which is deadly for the body); when hemoglobin is exposed to strong oxidizing agents (nitrates, nitrites, nitrogen oxides, aniline derivatives, benzene, some infectious toxins, medicinal substances: phenacytine, amidopyrine, sulfonamides - methemoglobin-forming agents that convert heme divalent iron into trivalent form) methemoglobin is formed; c- replacement of normal hemo globin for pathological forms - hemoglobinopathies; d - blood dilution - hemodilution;

Circulatory: a - congestive type - a decrease in cardiac output, b - ischemic type - a violation of 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 - heavy metal salts, alkylating agents; d - competitive inhibition - inhibition of succinate dehydrogenase malonic and other dicarboxylic acids), beriberi (group "B"), disintegration of biological membranes, hormonal disorders;

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

Mixed type of hypoxia.

According to the prevalence of hypoxia, a) local (often with local hemodynamic disturbances) and b) general are distinguished.

According to the speed of development: a) fulminant (develops to a severe and even fatal degree within a few seconds, b) acute (within 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 (fatal).

In the pathogenesis of hypoxia, several fundamental mechanisms can be distinguished: the development of an energy deficit, a violation of the renewal of protein structures, a violation of the structure of cell and organoid membranes, activation of proteolysis, and the development of acidosis.

Metabolic disorders develop first of all 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 (Of-

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

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

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

Blocking energy-dependent mechanisms for maintaining ionic balance and impaired cell membrane permeability 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. Unabsorbed by mitochondria and located in the cytoplasm, Ca~ +, in turn, is 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 shifts in cells and tissues result in impaired functions of organs and body systems.

Nervous system. First of all, complex analytic-synthetic processes suffer. Often initially there is a kind of euphoria, a loss of the ability to adequately assess the situation. With an increase in hypoxia, gross violations of the GNI develop, up to the loss of the ability to simply count, stupefaction, and complete loss of consciousness. Already in the early stages, coordination disorders are observed at first complex (cannot thread a needle), and then the simplest movements, and then adynamia is noted.

The cardiovascular system. With increasing hypoxia, tachycardia, weakening of the contractility of the heart, arrhythmia up to atrial and ventricular fibrillation are detected. Blood pressure after the initial rise progressively falls until the development of collapse. Disorders of microcirculation are also expressed.

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

a stepping short-term stop, terminal (agonal) breathing appears in the form of rare deep convulsive "sighs", gradually weakening until complete cessation. Ultimately, death occurs from paralysis of the respiratory center.

The mechanisms of adaptation of the body to hypoxia can be divided, firstly, into the mechanisms of passive, and secondly, active adaptation. According to 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 a decrease in the body's need for oxygen.

Active adaptation includes reactions of four orders:

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

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

Reactions of the III order - 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).

Reactions of the IV order - an increase in 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 more perfect correlation of ventilation and blood flow, compensatory myocardial hypertrophy, an increase in hemoglobin in the blood, activation of erythropoiesis, and an increase in the number of mitochondria per cell mass unit.

MOUNTAIN SICKNESS is a variant of exogenous hypobaric hypoxic hypoxia. It has long been known that climbing to great heights causes a morbid condition, the typical symptoms of which are nausea, vomiting, gastrointestinal disturbances, and physical and mental depression. Individual resistance to oxygen starvation has a wide range of fluctuations, which was noted by many researchers in the study of mountain 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 pointed out that climbing to 3050 m can cause some people to experience symptoms of altitude sickness, while others can reach an altitude of 4270 m without any manifestations of altitude sickness. However, very few people can climb 5790 m without showing noticeable symptoms of altitude sickness.

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

Systematic experiments on deciphering the pathogenesis of mountain (altitude) illness were carried out by Paul Baer, ​​who came to the conclusion that a decrease in the pressure of the atmosphere surrounding the animal acts only in so far as it reduces the tension of oxygen in this atmosphere, i.e. the observed changes in the animal's organism during the rarefaction of the atmosphere turn out to be in all respects completely identical with those observed during a decrease in the amount of oxygen in the inhaled air. There is a parallelism between the one and the other state, not only qualitative, but also quantitative, if only the comparison is based not on the percentage of oxygen in the inhaled mixture, but only on the tension of this gas in it. So, a decrease in the amount of oxygen in the air, when its voltage is from 160 mm Hg. Art. drops to 80 mm Hg. Art., can be quite comparable with the rarefaction of air by half, 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 air out of it. With a decrease in air pressure by 1/3 (when the pressure drops to 500 mm Hg or when the oxygen tension drops 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., at an oxygen tension of about 80 mm Hg), the animals showed only a somewhat apathetic state and a desire to remain immobile; finally, with a further decrease in pressure, all the phenomena associated with a lack of oxygen developed. The onset of death was usually observed with a decrease in oxygen tension to 20-30 mm Hg. Art.

In another version of the experiments, Paul Bert placed the animal already 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. So, the first signs of the influence of rarefaction in the form of a slight increase in breathing appear at a pressure of 80 mm Hg. Art. - in case of air 380 mm Hg. Art. Thus, in order to obtain the same phenomena in rarefied oxygen as in air, the degree of oxygen rarefaction must be 5 times greater than the degree of atmospheric rarefaction.

air. Taking into account that atmospheric air contains 1/5 of oxygen 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 affected by motor 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 at the usual atmospheric pressure, the pig's run was quite unhindered, and she did not seem to experience any particular fatigue. If the pressure was brought to half atmospheric or slightly lower, then the pig, not prompted to move, remained motionless, without showing any signs of suffering, while the animal inside the "squirrel" wheel showed obvious difficulties in running, constantly stumbled and , finally, in exhaustion, fell on his back and remained without any active movements, allowing himself 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 an animal in a state of complete rest, turns out to be fatal for an animal forced to produce increased muscular movements.

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

Prevention - oxygen prophylaxis, acidic foods and stimulants.

The increased supply of oxygen to the body is called HYPEROXIA. 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 is largely natural conditions does not occur 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 pulse rate), a decrease in the amount of hemoglobin and erythrocytes (example: decompression anemia). A person can breathe a mixture of gases with a high oxygen content for a sufficiently long period. The first flights of American astronauts were carried out on vehicles in the cabins of which an atmosphere with an excess of oxygen was created.

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

Life is impossible without oxygen, but oxygen itself is capable of exerting 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. There is the formation of free oxygen radicals that disrupt the formation of DNA and thereby pervert protein synthesis. The consequence of systemic enzyme deficiency is a drop in the content of γ-aminobutyrate in the brain, the main inhibitory mediator of gray matter, which causes convulsive syndrome of cortical origin.

The toxic effect of oxygen can manifest itself during prolonged breathing with 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 mainly 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 reflex spasm of the microvessels of the lungs and impaired microcirculation and as a result of 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 lung atelectasis is observed in pilots who begin to breathe oxygen long before climbing, which requires additional gas supply.

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 the tissues.

Breathing with 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 an excess of oxygen, including in the first couple of the same mechanisms as during hypoxia, but with the opposite direction (decrease in respiration and its depth, decrease in pulse, decrease in the mass of circulating blood, the number of erythrocytes), but with the development of hyperoxic hypoxia, adaptation proceeds as and 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 individual muscle twitches.