Caisson disease is one of those that are among the so-called “occupational” diseases. The correct name according to medical reference books is decompression sickness, or DCS. In common parlance, it is often called “divers’ disease,” and scuba diving enthusiasts themselves succinctly call this disease “caisson.” What is this unusual disease, characteristic of those who often descend to the depths of the sea or underground?

History and description of the disease

DCS is a disease caused by a sharp decrease in the pressure of gases inhaled by a person - nitrogen, oxygen, hydrogen. At the same time, dissolved in human blood, these gases begin to be released in the form of bubbles, which block normal blood supply and destroy the walls of blood vessels and cells. In a severe stage, this disease can lead to paralysis or even death. This condition often develops in those who work in conditions of high atmospheric pressure during the transition from it to normal pressure without taking proper precautions. This transition is called decompression, which gives the disease its name.

Similar decompression is experienced by workers constructing bridges, ports, foundations for equipment, digging underwater tunnels, as well as miners developing new deposits and divers, both professionals and amateurs of underwater sports. All this work is carried out under compressed air in special caisson chambers or in special wetsuits with an air supply system. The pressure in them specifically increases with immersion in order to balance the growing pressure of the water column or water-saturated soil above the chamber. Staying in caissons, like scuba diving, consists of three stages:

Compression (period of increased pressure);
Working in a caisson (being under consistently high pressure);
Decompression (a period of pressure reduction during ascent).

It is when the first and third stages are carried out incorrectly that decompression sickness occurs.

A potential risk group is recreational divers. Moreover, news reports often talk about how military doctors have to “pump out” reckless divers.

For the first time, humanity encountered this disease after the invention of the air pump and caisson chamber in 1841. Then workers began to use similar cameras when constructing tunnels under rivers and securing bridge supports in wet soil. They began to complain of joint pain, numbness of the limbs and paralysis after the chamber was returned to normal pressure of 1 atmosphere. These symptoms are currently called DCS type 1.

Typology of decompression sickness

Doctors currently divide decompression sickness into two types, depending on which organs are involved in the symptoms and the complexity of the disease.

Type I decompression sickness is characterized by a moderate danger to life. With this type of progression, the disease involves the joints, lymphatic system, muscles and skin. Symptoms of type 1 decompression sickness are as follows: increasing pain in the joints (elbow and shoulder joints are particularly affected), back and muscles. Painful sensations become stronger when moving, they acquire a boring character. Other symptoms are skin itching, rash, also with this type of disease the skin becomes covered with spots, the lymph nodes become enlarged.
Type II decompression sickness is much more dangerous for the human body. It affects the spinal cord, brain, respiratory and circulatory systems. This type is manifested by paresis, difficulty urinating, intestinal dysfunction, and tinnitus. In particularly difficult cases, loss of vision and hearing, paralysis, and convulsions leading to coma may occur. Less common is suffocation (shortness of breath, chest pain, cough), but this is a very alarming symptom. When a person spends a long time in rooms with high pressure, such an insidious symptom as dysbaric osteonecrosis is possible - a manifestation of aseptic necrosis of bones.

Decompression sickness occurs within an hour of decompression in 50% of patients. Especially often these are the most severe symptoms. In 90% of cases, signs of decompression sickness are detected 6 hours after decompression, and in rare cases (this applies primarily to those who rise to altitude after leaving the caisson) they can appear even after a day or more.

The mechanism of occurrence of the “divers problem”

To understand the causes of this disease, one should turn to Henry’s physical law, which states that the solubility of a gas in a liquid is directly proportional to the pressure on this gas and liquid, that is, the higher the pressure, the better the gas mixture that a person breathes dissolves in the blood. And the opposite effect - the faster the pressure decreases, the faster the gas is released from the blood in the form of bubbles. This applies not only to blood, but also to any fluid in the human body, so decompression sickness also affects the lymphatic system, joints, bone and spinal cord.

Gas bubbles formed as a result of a sharp decrease in pressure tend to group and block blood vessels, destroy tissue cells, blood vessels, or compress them. As a result, blood clots form in the circulatory system, rupturing the vessel and leading to its necrosis. And bubbles in the bloodstream can reach the most distant organs of the human body and further cause destruction.

The main causes of decompression sickness during scuba diving are as follows:

A sharp non-stop rise to the surface;
Immersion in cold water;
Stress or fatigue;
Obesity;
Age of the diving person;
Flight after a deep sea dive;

When diving in a caisson, the usual causes of decompression sickness are:

Long-term work under high pressure conditions;
Diving in a caisson to a depth of over 40 meters, when the pressure rises over 4 atmospheres.

Diagnosis and treatment of decompression sickness

To make a correct diagnosis, the doctor must provide a complete clinical picture of the symptoms that arose after decompression. Also, when diagnosing, a specialist can rely on data from studies such as magnetic resonance imaging of the brain and spinal cord to confirm the diagnosis based on characteristic changes in these organs. However, you should not rely solely on these methods - the clinical picture they produce may coincide with the course of arterial gas embolism. If one of the symptoms is dysbaric osteoncrosis, then only a combination of radiography can reveal it.

Caisson disease is successfully cured in 80% of cases. To do this, it is necessary to take into account the time factor - the faster the symptoms are identified and treatment is provided, the faster the body will recover and gas bubbles will be eliminated.

The main treatment method for DCS is recompression. This involves using special equipment that pumps large amounts of oxygen into the patient's blood to flush out excess nitrogen under high pressure. This method is used directly at the victim’s location; subsequently, it is important to transport him to the nearest medical facility. In the future, therapy is added to eliminate other symptoms of the disease - relieving joint pain, restorative and anti-inflammatory therapy.

A decompression chamber used to treat decompression sickness.

To prevent the occurrence of DCS, you should correctly calculate the decompression mode, set the correct intervals between decompression stops during the ascent to the surface, so that the body has time to adapt to changing pressure. Most often, these calculations are carried out by computer programs designed for these purposes, but in 50% of cases they do not take into account the individual characteristics of each diver or caisson chamber worker, as well as the fact that many of them are negligent in following recommendations for correct recovery from the high area. pressure on the surface.

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(decompression sickness)

What is decompression sickness?

Decompression sickness is a condition that develops as a result of a transition from an environment with increased atmospheric pressure to an environment with normal pressure. It should be emphasized that the pathological changes that characterize decompression sickness do not develop while under high pressure, but with too rapid a transition to normal atmospheric pressure, i.e., during decompression.

Caisson disease can occur in divers who have to work under high pressure under water, as well as in construction workers engaged in work carried out in the so-called caisson method under water or in the ground in water-saturated soils.

Who is at risk for decompression sickness?

The clinical picture observed in caisson workers, divers, and recently also in people using scuba gear for scuba diving, when the transition from high atmospheric pressure to normal is not slow enough, is also described in the literature under the name “divers paralysis”, “compression sickness” , “high pressure sickness”, “decompression sickness”, etc.

A similar clinical picture is also observed in so-called decompression illnesses of pilots (“decompression sickness”, “aviators’ disease”). This condition develops in them as a result of a violation of the airtightness of the aircraft cabin at high altitudes or when flying in a regular cabin at an altitude of over 8000 m.

Both decompression sickness of divers, as well as caisson workers, and decompression sickness of pilots, according to modern concepts, are varieties of “decompression sickness”, but with decompression sickness, disturbances in the body are associated with the transition from increased atmospheric pressure to normal, and with decompression sickness of pilots - aircraft to the sharply reduced pressure of high altitudes.

During caisson work, carried out, for example, when laying foundations for hydraulic structures or bridge supports, a person works in a closed room filled with compressed air. Compressed air squeezes water out of the ground and the workspace becomes accessible to people. The air pressure in the caisson corresponds to the pressure under which the water is located at a given level.

As you know, for every 10 m of depth the pressure increases by 1 atm. Consequently, at a depth of 30 m, the pressure is 3 atm higher than normal, i.e. equal to 4 atm.

The highest pressure allowed when working in a caisson should not exceed 4 atm according to existing regulations. -atmospheres of excess pressure. At a pressure of 7 atm. and above, a person begins to be exposed to the toxic and then narcotic effects of nitrogen. Therefore, when descending under water to a depth of 70 m or more, the diver is supplied for breathing not with ordinary compressed air, but with a helium-oxygen mixture. However, replacing air nitrogen with another indifferent gas (helium) does not eliminate the possibility of decompression sickness if decompression rules are violated.

The main part of the caisson is an iron or reinforced concrete working chamber. From the ceiling of this chamber extends upward a pipe or shaft with a ladder for lifting and lowering people, as well as mechanisms, for lifting soil, etc. The shaft ends in a cylindrical extension, the so-called central chamber, to which two sluices are adjacent on the sides, communicating with the outside atmosphere with heavy, pneumatically closed doors. Through special pipes, the compressor station supplies compressed air into the working chamber at a pressure equal to the water pressure at the bottom of the caisson.

Workers are lowered into the working chamber through a hermetically sealed airlock, which is connected to the outside air and separated from the central chamber by a door that opens only inward.

After the worker has entered the airlock, compressed air begins to be pumped into it. When the pressure in the airlock reaches the same pressure as in the central chamber, the inner door automatically opens and descent into the working chamber becomes possible.

Egressing is carried out in the reverse order, i.e., after the worker leaves the central chamber into the airlock, the pressure gradually decreases to atmospheric pressure.

Working in a caisson involves not only exposure to increased atmospheric pressure, but often also the significant physical stress of excavating and transporting soil. In addition, work in a caisson usually takes place under unfavorable meteorological conditions (high humidity, high or low air temperature). While working in a caisson, workers may be exposed to a number of toxic substances (carbon dioxide, hydrogen sulfide), as well as oil vapors and aerosols from compressors.

The work of a diver is essentially no different from work in a caisson, since both divers and caisson workers work under conditions of high pressure. However, divers usually work at greater depths and their work is more strenuous, although the duration of their stay under water is much shorter.

How does decompression sickness occur?

When a person transitions from normal atmospheric pressure to increased pressure, a number of changes are observed, especially in persons with little experience of caisson work and in the case of unfavorable sluicing progress, which actually have nothing to do with decompression sickness. These changes are explained by an imbalance between the internal air pressure in the body and external pressure. There is a feeling of stuffiness in the ears, caused by the pressing of the eardrum by the outside air. The depression of the eardrum due to obstruction of the Eustachian tubes can be so significant that tears with hemorrhages and even perforation form on it.

Due to an imbalance between the air in the frontal sinuses and the outside atmosphere, especially with a runny nose, pain in the frontal sinuses may occur.

The influence of increased pressure also explains other changes that are noted in individuals during their stay in the caisson: due to the depression of the abdomen due to compression of intestinal gases and lowering of the diaphragm, the vital capacity and ventilation of the lungs increase, the respiratory and pulse rates decrease, as well as the minute volume of the heart, working capacity muscle increases slightly. When under high blood pressure, the senses of smell, touch and taste are dulled.

Dryness of the mucous membranes is noted, hearing decreases, intestinal motility increases, and metabolism slows down. However, if the pressure is increased gradually and there are no pathological changes in the body, workers usually tolerate staying in the caisson without any particular discomfort, especially with some training.

Increased air pressure causes significant changes in the human circulatory system. The reason for these changes is the high partial pressure of oxygen and the narcotic effect of nitrogen.

Under pressure up to 7 atm. There is a slowdown in the heart rate and a decrease in the speed of peripheral blood flow, which deepens with increasing time spent under high pressure. These hemodynamic changes are determined mainly by the height of the partial pressure of oxygen.

At air pressure above 7 atm. The narcotic effect of nitrogen plays a major role in changing hemodynamics in humans, which is characterized by an acceleration of peripheral blood flow, an increase in the stroke and cardiac output and the amount of blood circulating in the body.

With increasing time under pressure, the primary narcotic reaction will decrease, and the state of the cardiovascular system will change in accordance with changes in the partial pressure of oxygen.

As mentioned above, changes characteristic of decompression sickness develop with improper decompression, that is, with an insufficiently slow transition from increased atmospheric pressure to normal.

When atmospheric pressure increases, the gases that make up the inhaled air dissolve in the blood and tissues of the body in much larger quantities than usual. It is known that the physical solubility of gases in the blood and tissues of the body is proportional to their partial pressure and solubility coefficient. A person in a caisson is oversaturated with gases, mainly nitrogen. The higher the pressure and the time spent under pressure, the greater the saturation of the blood and tissues with gases entering with the inhaled air, primarily nitrogen.

At normal atmospheric pressure and normal body temperature, 100 ml of blood contains 1.2 ml of nitrogen. With increasing air pressure, the content of dissolved nitrogen in the blood increases as follows: at a pressure of 2 atm. -2.2 ml per 100 ml, at 3 atm. -3 ml, at 4 atm. -3.9 ml, etc.

Thus, with a significant increase in atmospheric pressure, the amount of nitrogen dissolved in the blood increases several times. The gas dissolved in the blood passes into the tissues of the body. The largest amount of nitrogen is absorbed by adipose and nervous tissues, which contain large amounts of fats and lipoids. Adipose tissue dissolves approximately 5 times more nitrogen than blood. When a person moves from an environment with high atmospheric pressure to an environment with normal pressure, the reverse process occurs; excess gases dissolved in the body are removed from the tissues into the blood, and from the blood through the lungs to the outside.

During decompression, the body releases excess nitrogen relatively slowly. This is explained by the fact that the amount that can be excreted by the lungs does not exceed approximately 150 ml per minute. However, when a person is under high blood pressure, the amount of excess nitrogen in the body can exceed several liters.

Therefore, it takes a certain amount of time for the excess nitrogen to be released through the lungs. With slow, gentle decompression, excess nitrogen is gradually released from the body, diffusing from the blood through the lungs to the outside without forming bubbles.

During a rapid transition of a person from high pressure to normal, gases dissolved in the body in large quantities do not have time to diffuse from the blood into the lungs and come out of solution in gaseous form, as a result of which free gas bubbles, consisting mainly of nitrogen, form in the blood and tissues. In addition to nitrogen, they contain oxygen and carbon dioxide. Gas bubbles can clog (embolism) or rupture blood vessels, which causes the clinical phenomena described below that are characteristic of decompression sickness.

Thus, the essence of decompression sickness is the blockage of the blood vessels of various organs by bubbles of free gas, consisting mainly of nitrogen. Gas embolism leads to disruption of blood circulation, and, consequently, tissue nutrition, hence pain and dysfunction of certain organs and systems.

The occurrence of decompression sickness is possible, as a rule, only during decompression from a pressure of at least 1.25 atm. or 2.25 atm., which corresponds to a depth of 12-13 m. This is explained by the fact that gas bubbles are formed if the amount of dissolved nitrogen in the body after decompression exceeds 2 times the saturation of the body with nitrogen at ambient air pressure. During rapid decompression from high pressure, which exceeds normal pressure by at least 1.25 atm, just such conditions are created. At pressures up to 1.8 atm. Most often mild forms of the disease are observed and only in some cases serious lesions occur. With increasing additional pressure, the frequency of caisson diseases and especially severe forms increases.

Clinical picture of decompression sickness

The clinical picture of decompression sickness depends on the size, quantity and location of the gas bubbles formed. Therefore, it can be very diverse in its nature, course and severity. It should be emphasized that adipose and nervous tissues, which, as mentioned above, have the greatest ability to absorb nitrogen, are relatively poorly supplied with vessels and, therefore, they have the worst conditions for the return release of nitrogen into the blood.

Causes of decompression sickness

A number of factors can contribute to the development of decompression sickness. Hypothermia of the body due to unfavorable meteorological conditions in the caisson (low temperature, high air humidity) leads to a slowdown in blood flow and vascular spasms, which makes it difficult to denature the body from nitrogen. Overwork also weakens the body in the fight against disease. Drinking alcohol and smoking adversely affect the cardiovascular system, the condition of which is important in the development of the disease. Violation of the diet, for example, eating food that causes fermentation in the intestines before descending into the caisson, can also contribute to the development of the disease.

For the occurrence of decompression sickness, the age, individual characteristics and health status of the worker are of a certain importance. A number of authors believe that in older people the incidence of decompression diseases increases. Obese people with significant deposits of fat, which absorbs nitrogen well, have a greater chance of developing decompression sickness. This is confirmed by animal experiments.

If the circulatory apparatus, which plays a major role in the body’s fight against decompression sickness, is insufficient, the release of nitrogen from the body will undoubtedly slow down.

Changes in the gastrointestinal tract, in particular constipation, can obviously also contribute to the development of decompression sickness. There is good reason to think that changes in the lungs, such as diffuse fibrosis, may make it difficult to remove nitrogen from the blood. Therefore, in addition to the main cause of decompression sickness, a number of other factors may play an important role in the development of the disease.

Symptoms of decompression sickness

There is no generally accepted classification of decompression sickness. However, most authors divide acute cases of decompression sickness into mild and severe.

There is also a chronic form of decompression sickness. The vast majority of observed cases of disease are mild forms of the disease. Severe and even fatal cases of decompression sickness are also well known.

Decompression sickness usually occurs in the form of acute phenomena that develop after improper decompression, but residual or secondary phenomena can be observed that limit the patient’s ability to work for a long time.

Although decompression sickness can cause damage to any organs and systems, the most frequently observed are pathological changes in the skin, blood vessels and muscles, as well as disorders in the nervous system, circulatory system and respiration.

Acute phenomena caused by improper decompression usually develop some time after it, that is, after a latent period. However, divers working under high pressure may experience symptoms of decompression sickness during decompression. The latent period after decompression in the vast majority of cases lasts no more than an hour, in 20% of cases - several hours, and in rare cases - up to 24 hours.

In almost all cases of decompression sickness, there is itching of the skin of the extremities, and sometimes of the entire surface of the skin. Itching of the skin often precedes the appearance of other signs of decompression disease.

Changes in the skin appear as a result of the formation of gas bubbles in the skin and subcutaneous tissue. The bubbles, squeezing and stretching the tissue, irritate the corresponding receptors and cause itching, burning, a crawling sensation, etc. Sometimes the skin takes on a marbled appearance due to the rupture of the superficial vessels of the skin.

In mild forms of decompression sickness, itchy skin and joint pain are the main symptoms of the disease and are often not accompanied by other pathological changes. A rash (small hemorrhages) may appear.

One of the most common manifestations of decompression sickness is osteoarthralgia and myalgia (workers often call this condition “breakdown”). Patients complain of pain in the bones or joints, most often in the knees, shoulders and hips. The pain can vary in intensity and is often intermittent. The pain usually gets worse with movement.

There is pain when pressing, crunching and crepitus, and sometimes swelling of the periarticular tissues (rarely effusion).

Osteoarthralgia is often accompanied by an increase in body temperature and changes in the peripheral blood (shift to the left, eosinophilia, monocytosis).

An X-ray examination of the joints during an attack of decompression sickness reveals accumulations of gas in the form of bubbles in the soft tissues, in the cavities of the joints and around them. A mild form of decompression sickness lasts 7-10 days and usually goes away without a trace.

In an acute attack of decompression sickness, as a result of blockage of blood vessels, an asymptomatic bone infarction and local aseptic necrosis can also develop, which is detected only after a long time, already during the development of a complication - deforming osteoarthritis. Bone infarcts most often occur in the cancellous portions of the femur.

Pain in the limbs during decompression sickness can also be associated with changes in the peripheral nervous system, often accompanied by myalgia. Neuralgia is much less common than osteoarthralgia. The development of neuralgia during decompression sickness is obviously caused by oxygen starvation of nerve fibers or is of embolic origin (embolism of vessels supplying the nerve, extravascular accumulation of gas in the perineurium or endoneurium).

Local cooling, trauma and some other factors can contribute to the development of the disease. Sometimes neuralgia accompanies osteoarthralgia. Most often, neuralgia develops on the upper extremities. Trigeminal neuralgia is also observed.

Neuralgia usually progresses favorably and ends after a few days.

As a result of gas embolism of the labyrinthine vessels, Meniere's syndrome can develop. In this case, headache, dizziness, nausea, vomiting, loss of balance, general weakness and malaise are observed.

Dizziness, which is the leading symptom of this form of decompression sickness, is often combined with tinnitus, and in some cases with hearing loss. The patient is pale, the skin is covered with cold sweat; Nystagmus and bradycardia are noted.

An attack of dizziness may be accompanied by loss of consciousness. Usually the disease ends well, although relapses are noted.

Cases of diseases that involve damage to the central nervous system seem to be much more serious.

When the spinal cord is damaged, most often its lumbar and sacral parts, which are comparatively less well supplied with blood vessels, paresis, monoplegia, and paraplegia develop (most often of the lower extremities). Disorders of the bladder and rectum are less common. Due to damage to the central nervous system, trophic skin disorders may be observed.

Cases of impotence have been described. When the brain is damaged, depending on the location, hemiparesis, hemiplegia, aphasia, mental disorders, and rarely, irritation of the meninges develop.

Changes in the central nervous system may be associated with the formation of bubbles in the white matter of the brain, which is poorly supplied with blood vessels. The most serious phenomena develop with prolonged ischemia or rupture of blood vessels in the brain tissue.

Disorders of the central nervous system can be combined with visual impairment and vestibular disorders. Changes in the central nervous system are often accompanied by residual effects that can limit the patient’s ability to work for a long time.

Caisson disease sometimes manifests itself in changes in the lungs, which is expressed in asthmatic attacks, pulmonary infarction, most often in the right lower lobe. Cases of pulmonary edema and spontaneous pneumothorax have been described.

Changes in the cardiovascular system during decompression sickness often result in coronary disorders. In these cases, pain appears in the chest, general weakness, dizziness, muffled heart sounds, and arrhythmia are noted. Sometimes, after exiting the caisson, a collaptoid state is observed.

Along with the above acute disorders caused by improper decompression, disorders of other organs and systems may also be observed.

These include changes in the gastrointestinal tract (flatulence, pain, nausea, vomiting, sometimes with blood, loose stools, in rare cases, a picture of an acute abdomen), eyes (quickly passing blindness, optic neuritis and cataracts).

It must be emphasized that the acute clinical forms of decompression sickness listed above are often combined with each other and can have varying severity. Sometimes extremely severe and even fatal cases of the disease are observed, caused by severe changes in the most important organs and systems (brain, heart and lungs). Lethal cases of the disease are usually caused by massive embolism of the vessels of the lungs, heart, brain and are associated with severe disturbances of pulmonary circulation, acute heart failure, and respiratory paralysis.

In addition to acute forms, there are also chronic forms of decompression sickness. They can obviously have two origins. One group includes the so-called secondary chronic cases associated with air embolism and developing after acute decompression sickness. These are most often changes in the nervous system that developed as a result of prolonged circulatory disorders after a gas embolism. Among these changes, aeropathic myelosis and chronic Meniere's syndrome are most often detected.

However, along with these changes, which are the consequences of long-term circulatory disorders in parts of the nervous system that are especially sensitive to oxygen starvation, with decompression sickness, chronic changes that are not associated with air embolism may occur.

Chronic forms of the disease can be caused by the deposition of small, non-embolic gas bubbles on the vessel wall, which contribute to the development of the thrombotic process. This form of decompression sickness is called primary chronic and develops slowly, having a long latent period.

Most often, thrombotic processes develop in the bones in the form of deforming osteoarthritis. In our opinion, the existence of chronic forms of decompression sickness in the form of deforming osteoarthritis is supported.

At the same time, it is possible that deforming osteoarthritis, often detected in people working under high pressure, has two origins:

1) as a consequence of an acute form of decompression disease;

2) as a manifestation of chronic decompression sickness. In people working at high atmospheric pressure, radiological signs of osteoarticular changes include narrowing of the joint spaces, calcification of articular cartilage in the area of the epiphyseal angles and soft tissues at the site of attachment of the joint capsules, alternation of areas of osteoporosis and osteosclerosis, calcification of the endosteum and restructuring of the bone structure .

The possibility of developing another form of primary chronic decompression disease - cardiac myodegeneration - is possible due to the slow development of the thrombotic process in the small vessels of the heart. However, it should be noted that the question of the mechanism of development of changes in the heart in workers under conditions of high blood pressure is very complex and cannot be considered sufficiently resolved. Available observations show that those who work in a caisson for a long time actually show relatively often changes in the heart muscle (dullness of tones, expansion of the boundaries, arrhythmias). These changes are reflected on the electrocardiogram. However, they can not only be caused by thrombotic phenomena due to the formation of small gas bubbles in the corresponding vessels, but are also directly related to prolonged work under high atmospheric pressure and other conditions in which the caisson workers work (considerable physical stress, exposure to adverse meteorological factors, toxic substances etc.). The same reasons can cause some other diseases observed in people employed in work carried out using the caisson method. Such diseases include earlier development of atherosclerotic changes, decreased weight and hemoglobin percentage, as well as frequent catarrhal diseases of the middle ear.

Treatment and prevention of decompression sickness

The main method of treating a patient with acute symptoms of decompression sickness is to return the patient to the pressure conditions under which he was at work.

Recompression is carried out in a special room - the so-called treatment gateway. The presence of a treatment airlock is mandatory when working above 1.5 additional atmospheres. The treatment airlock is a closed chamber - actually a hospital ward, where you can quickly increase the pressure and provide the patient with the necessary medical care.

The essence of the therapeutic effect of recompression is that, under the influence of increased pressure created in the therapeutic airlock, gas bubbles previously formed during rapid decompression in the blood and tissues quickly decrease and the gases dissolve again. In the vast majority of cases, with recompression, especially if it is combined with other treatment methods, it is enough to increase the pressure to the values at which the patient worked. In some cases, with massive embolism, recompression requires applying pressure higher than the initial one.

Recompression should be done as quickly as possible and continue until the painful symptoms disappear - at least 30 minutes, after which the patient is slowly decompressed.

In a treatment airlock, decompression is much slower than under normal conditions. Decompression in the treatment airlock should be carried out at a rate of at least 10 minutes for every 0.1 atm, and in mild cases - at a pressure below 1.5 atm. at least 5 minutes.

When the pressure in the treatment airlock drops below 2 atm, it is recommended to inhale oxygen to accelerate nitrogen denaturation.

Along with recompression, which is a specific treatment method for decompression sickness, symptomatic therapy is important, which is used depending on the form and severity of the disease. In this regard, you must first of all keep in mind the means that normalize and stimulate the activity of the cardiovascular system (cardiazol, cordiamine, camphor, caffeine, adrenaline, strychnine, ephedrine, etc.).

If the pain is severe, you may need to use painkillers (substances from the morphine group are not recommended!). For osteoarthralgia, local heat and rubbing may provide some benefit.

In case of coronary events, it is necessary to prescribe vasodilators (amyl nitrite, nitroglycerin), in case of collapse - infusion of glucose, saline solutions, blood plasma, etc. It is recommended to give warm coffee, strong tea, and warm the patient.

If there are no contraindications, rubbing the body and light exercise, which promotes the release of nitrogen from tissues, may also be beneficial.

After leaving the treatment lock, physiotherapeutic procedures are carried out - warm baths, solux, etc.

Therapeutic recompression should be performed in all cases of decompression sickness, regardless of its severity.

The result of therapeutic recompression largely depends on how quickly the patient was placed in the therapeutic airlock, i.e., again in conditions of high pressure.

In most cases, with timely and quickly performed recompression, as well as appropriate symptomatic treatment, the clinical phenomena of decompression sickness quickly disappear without any significant consequences.

Only in a small percentage of cases does recompression fail to produce positive results. This happens when it was carried out incorrectly or irreversible changes quickly developed.

If painful phenomena resume after exiting the treatment gateway, recompression should be repeated.

After staying in the treatment lock, the patient should be under observation for several hours, depending on the form of manifestation of decompression sickness and the severity of the disease.

Prevention of caisson disease consists, first of all, in the correct organization of work in the caisson. Particular emphasis should be placed on the need for strict adherence to working hours under high pressure, compression rules and decompression regimes.

The work procedures of divers are regulated by special safety rules.

In diving practice, a stepwise decompression method is adopted, in which the diver ascends with stops at certain depths (using diving platforms).

By using a moving Davis decompression chamber, the diver's time in the water during decompression can be significantly reduced.

Divers are also decompressed on the surface. In these cases, after the first stop, the diver is raised to the surface and quickly placed in a recompression chamber (after removing the helmet, belt and galoshes), in which the pressure is immediately raised to the pressure at the first stop. Decompression is carried out according to the appropriate tables.

Hygienic working conditions play a significant role in the prevention of decompression sickness. It is necessary to systematically monitor the degree of cleanliness and temperature of the air supplied to the caisson, as well as prevent body cooling and change wet clothing in a timely manner. Those working in the caisson should be provided with a warm shower after work, as well as hot food.

An analysis was carried out of the circumstances surrounding the development of many cases of decompression sickness. In addition to rapid decompression, the development of the disease was facilitated by a sharp increase in the amount of carbon dioxide in the chamber, heavy physical activity immediately before decompression, as well as sharp chills resulting from the difference between the worker’s high body temperature and the low temperature of the chamber. Along with the preventive measures listed above, it is also recommended to introduce a 10-minute rest before decompression.

Inhalation of oxygen during decompression is recommended to prevent decompression sickness. When oxygen is inhaled, a lower partial pressure of nitrogen is created in the alveoli, which contributes to a more intense release of it from the body. To avoid the toxic effect of oxygen, it should be inhaled at a pressure below 2 atm.

For those working in caissons, the duration of stay under pressure, including locking and venting, is set in accordance with the excess pressure.

The higher the additional pressure, the shorter the duration of work in the caisson. So, according to existing rules, the duration of the working day under pressure conditions above 3.5 atm. set to 2 hours 40 minutes.

The working day of caisson workers is usually divided into 2 half shifts. In cases of single shift work, the time spent under pressure is significantly reduced.

When the pressure in the caisson is over 1.2 atm. all persons who have not previously worked under high pressure conditions or have had a break from working in a caisson for more than a month must work for a reduced time during the first 4 days.

In accordance with the current regulations, all applicants for caisson work are subject to a preliminary medical examination.

Only healthy males are allowed to perform physical work in caissons: at a pressure of up to 1.9 atm. - at the age of 18 to 50 years, at a pressure above 1.9 atm. - from 18 to 45 years.

Women are allowed to work in the caisson only as engineering, technical, medical and instructor personnel. For these personnel, the above upper age limits are increased by 10 years.

The following changes in the body are contraindications to entering caisson work:

I. Diseases of internal organs

1. Severe general physical underdevelopment.

2. Pulmonary tuberculosis in the subcompensation stage.

3. Tuberculous and non-tuberculous diseases of the respiratory tract, lungs and pleura, if they are accompanied by a tendency to hemoptysis or impaired respiratory function.

4. Organic diseases of the heart muscle, regardless of the degree of compensation.

5. Hypertension (blood pressure is 20-30 mmHg higher than that corresponding to a given age).

6. Hypotension (maximum blood pressure below 95 mmHg).

7. Endarteritis.

8. Chronic diseases of the abdominal organs with persistent, pronounced changes in their functions (peptic ulcer, ulcerative colitis, kidney and bladder diseases, etc.) or a tendency to bleeding.

9. Blood diseases. Hemorrhagic diathesis. Severe anemia (hemoglobin content below 50%).

10. Endocrine-vegetative diseases. Graves' disease, diabetes mellitus and diabetes insipidus, severe pituitary disorders, etc.

11. Morbid obesity.

12. Chronic inflammatory diseases of the lymph nodes.

13. Chronic diseases of bones and joints, clinically expressed.

II. Nervous system diseases

1. Organic diseases of the central nervous system or their residual effects, expressed in paralysis, paresis, hyperkinesia, and coordination disorders.

2. All mental illnesses.

3. Chronic recurrent neuritis (polyneuritis) and severe radiculitis.

4. Clinically pronounced myositis and neuromyositis.

5. Convulsive seizures of any origin.

6. Pronounced phenomena of the so-called traumatic neurosis.

III. Diseases of the upper respiratory tract and ears

1. Lesions of the upper respiratory tract - neoplasms or other diseases, as well as their consequences that impede respiratory function (nasal polyps, adenoids, infectious granulomas, atrophy of the nasal passages, hypertrophy of the inferior turbinates, especially their posterior ends, paralysis of the laryngeal muscles, etc. .).

2. Severe atrophic catarrh of the nasal mucosa with the development of crusts.

3. Severe diseases of the paranasal sinuses.

4. Atrophic scars of the eardrum.

5. Chronic purulent mesotympanitis, often aggravated by minor perforation of the eardrum (a pinhead or less).

6. Chronic purulent epitympanitis with caries of the walls of the tympanic cavity or cholesteatomy.

7. Persistent hearing loss in one or both ears (perception of whispered speech at a distance of 1 m or less) due to a disease of the sound-conducting and sound-receiving apparatus.

8. Hyperfunction or dysfunction of the vestibular apparatus.

9. Poor patency of the Eustachian tube.

IV. Surgical diseases

1. All types of hernia.

2. Severe and widespread nodular dilatation of the veins of the lower extremities with a tendency to ulceration.

3. Severe hemorrhoids with bleeding.

In addition, for women, contraindications to working in a caisson are:

1. Diseases of the female genital organs with a tendency to bleeding.

2. Pregnancy of any stage and the postpartum period (2 months).

3. Menstrual period.

All those involved in caisson work undergo a weekly medical examination, which is carried out by a therapist and an otolaryngologist.

Catarrhal symptoms from the upper respiratory tract are grounds for temporary removal from work.

After mild cases of illness (osteoarthralgia, neuralgia, skin changes), patients can be returned to work after the elimination of painful phenomena, subject to medical supervision. Severe cases of the disease require longer removal from work. In the presence of persistent effects after illnesses, the patient must be referred to VTEK to determine the group of professional disability.

Decompression sickness is well known to representatives of those professions whose work involves immersion in water, to great depths in the bowels of the earth, or with flight into space. The difference in air pressure between the two environments in which a person works can cause paralysis or death.

Caisson disease - what is it?

Decompression sickness, otherwise called decompression sickness or divers' sickness, occurs in people after they rise to the surface of the earth or water from the depths. Caisson disease occurs when atmospheric pressure changes. Decompression can be experienced by representatives of those professions that are involved in the construction of surface bridges, ports, miners, scuba divers, deep sea explorers, and astronauts. Decompression sickness is dangerous for the crew of the bathyscaphe only in emergency cases when a quick ascent is required.

Work underwater or deep underground is carried out in professional wetsuits or caisson chambers with an air supply system. These devices and suits have a built-in pressure control mechanism. When diving, the pressure in the caissons increases so that a person can breathe safely. The return to the surface of the earth must be gradual so that the body has time to rebuild itself. Rapid ascent is fraught with decompression sickness and death.

Mechanism of decompression sickness

Caisson disease is a blockage of blood vessels by a gaseous thrombus, which is based on nitrogen bubbles. Decompression sickness occurs as a result of changes in the concentration of gases in body fluids. To understand the mechanism of the disease, it is necessary to recall Henry's law, which states that increased pressure leads to better dissolution of gases in liquids. Descending to depth, the diver breathes compressed air. At the same time, nitrogen, which under normal conditions does not enter the human bloodstream, penetrates into the blood vessels under conditions of high pressure.

When the external pressure begins to decrease during ascent, gases leave the liquid. If a diver rises to the surface of the water slowly, the nitrogen has time to leave the blood in the form of small bubbles. When the gas rises quickly upward, it tends to leave the liquid as quickly as possible, but without having time to reach the lungs, it clogs the vessels with microthrombi. Bubbles attached to the vessels can break off along with pieces of the vessels, leading to hemorrhages. If nitrogen bubbles do not enter the vessels, but into the tissues, tendons or joints, then an extravascular form of decompression sickness occurs.

Caisson disease - causes

Among the main reasons why decompression sickness occurs are the following:

improper diving;
fast ascent;
failure to comply with diving rules;
incorrect use of underwater equipment.

Factors that provoke this disease include:

age - the older a person is, the more difficult it is for him to bear pressure-related loads;
vascular diseases;
dehydration – water helps to quickly remove unnecessary gases from the body;
increased physical activity before diving;
excess weight - fats increase the retention of gas bubbles;
alcohol in the blood.

Caisson disease - symptoms

Decompression sickness, the symptoms of which depend on the location of the gas bubbles, can manifest itself almost immediately after ascent. Sometimes decompression sickness occurs when ascending to the surface not immediately, but after a day. The main symptoms of decompression sickness include the following:

In type 1 disease, which affects the tendons, joints, skin and lymphatic system, symptoms will include joint and muscle pain, skin spots and.
In type 2 disease, which affects the brain, circulatory and respiratory systems, the main symptoms will be: tinnitus, headache, problems with the intestines and urination. In severe cases, the following symptoms will appear: paralysis, convulsions, suffocation, loss of hearing and vision.

Caisson disease - treatment

Before treating decompression sickness, it is necessary to carry out a clarifying diagnosis to distinguish decompression sickness from gas embolism. If the diagnosis is confirmed, therapeutic measures should be started immediately. The only true method of treatment is therapy in a special pressure chamber using a face mask. In the pressure chamber, a recompression mode is created using pressure, and the patient breathes pure oxygen all the time (except for short intervals). The effectiveness and duration of treatment depend on the severity of the damage to the body.

Caisson disease - consequences

Even timely and correctly provided assistance is not a guarantee that a person will not have the consequences of this disease. Caisson disease is dangerous for organ systems:

respiratory;
visual;
cardiac;
digestive;
motor.

Caisson disease occurs during a rapid transition from high pressure to normal pressure. It occurs among those working in caissons during the construction of bridges, dams, docks, tunnels, etc. Under the influence of increased pressure in the caisson, nitrogen from the inhaled air is excessively absorbed by tissues and blood. During a rapid transition to an atmosphere with normal pressure (decompression), the nitrogen released from the tissues does not have time to be released through the lungs and accumulates in the tissues, blood and lymphatic vessels in the form of bubbles that clog the lumen of the vessels (decompression sickness). This causes circulatory and tissue nutrition disorders. Death can occur immediately, several hours or several (1-20) days after leaving the coffered chamber. It occurs in emergency situations due to a forced violation of safety rules, when a person moves too quickly from conditions of high atmospheric pressure to normal. The main danger is decompression, i.e. the period when workers leave the caisson, during which damage to the eardrum, which is very sensitive to pressure disturbances from the outside, from the ear canal, and from the inside, from the middle ear, is possible.

Forms:

Mild form of decompression sickness

Moderate decompression sickness

Severe form of decompression sickness

The main danger is decompression, i.e. the period when workers exit the caisson, during which damage to the eardrum, which is very sensitive to pressure disturbances from the outside, from the ear canal, and from the inside, from the middle ear, is possible.

Pathogenesis

The disease develops as a result of the transition of blood gases and body tissues from a dissolved state to a free one.

The resulting gas bubbles disrupt normal blood circulation, irritate nerve endings, and deform and damage body tissues.

During decompression, the body undergoes a process of removing dissolved nitrogen from the tissues. Depending on its speed, excess nitrogen in the tissues enters the blood in a dissolved state or in the form of bubbles. They are the cause of gas embolism and the development of decompression sickness.

Symptoms

The symptoms of decompression sickness are characterized by polymorphism.

The disease does not develop immediately: its first symptoms appear 10–15 minutes or later after decompression, i.e. during the formation of more or less large gas bubbles.

Workers complain of ear pain, “dilation of the abdomen,” a feeling of malaise, cold, and pain in the joints. Subsequently, certain clinical symptoms develop, the manifestation and severity of which is determined by the size, quantity and localization of gas bubbles in the body.

Mild form of decompression sickness

Manifests itself in the form of extremely severe pain in the area of a joint or several joints suddenly. The mechanism of pain is caused by a malnutrition of the embolized tissue area (periosteum, bone, joint, fascia, muscle, nerve). Most often, persistent pain occurs in one or more joints of the extremities, especially in the knees and shoulders, as well as in the wrists, elbows and ankles.

The mild form includes all skin cases (“caisson scabies”). Itching is usually felt on the trunk or proximal extremities. The nature of the itching resembles the itching of the skin caused by an insect bite.

An objective examination reveals pain in the nerve trunks, muscles and joints upon palpation. Swelling of the periarticular tissue and joint effusion are often observed. Certain areas of the skin have a “marbled” pattern due to embolism of cutaneous vessels. The accumulation of gas in the subcutaneous tissue gives rise to the development of subcutaneous emphysema.

Therapeutic recompression relieves pain and leads to rapid recovery.

Moderate decompression sickness

First of all, Meniere's syndrome is formed as a result of the formation of gas bubbles in the labyrinth of the inner ear. Severe weakness, heaviness and pain appear in the head. These symptoms intensify and are combined with severe dizziness, vomiting, noise and ringing in the ears, and hearing loss. Severe pallor, sweating, and weakness appear. Dizziness bothers me even when lying down.

Gastrointestinal lesions are characterized by the accumulation of gas in the intestines and mesenteric vessels and are accompanied by the appearance of very severe abdominal pain and frequent bowel movements. The abdomen is tense, palpation is painful. Visual acuity decreases, which is accompanied by dilation of the pupils and suppression of their reaction to light. The fundus picture varies from normal to varying degrees of hyperemia of the optic discs.

The prognosis is usually favorable provided timely and correct therapeutic recompression is performed.

Severe form of decompression sickness

Develops during the transition from the highest pressures (3-4 Atm). Characterized by the formation of emboli in the vessels of the central nervous system, heart and lungs. Patients note severe general weakness and weakness in the legs, a sharp cough, severe pain in the chest, especially when inhaling, and shortness of breath. Subsequently, clinical signs of pulmonary edema appear.

With multiple aeroembolism, a significant number of gas bubbles of various sizes accumulate in the cavities of the right heart and the vessels of the lungs, causing disruption of cardiovascular activity. In such cases, pallor, severe weakness, frequent and shallow breathing are noted; blood pressure drops. The pulse is rapid at first, then slows down, the skin is pale grayish or bluish. With severe hypoxia, loss of consciousness occurs.

Possible myocardial and pulmonary infarction.

Cerebral lesions are caused by gas emboli in the brain. After a short latent period, sharp headaches and weakness occur. In mild cases, the sensitivity of one half of the body disappears, in more severe cases, paralysis occurs: speech is lost, signs of paresis of the facial nerve and pathology of other cranial nerves appear, as well as paraplegia or paraparesis of the lower extremities.

Paralysis of the lower extremities is accompanied by disorders of urination and defecation (anuria and constipation). High tendon and periosteal reflexes are detected.

Particularly severe cases with fatal outcome– massive gas embolism with blockage of blood circulation. Blockage of pulmonary blood flow leads to death from asphyxia. There may be an acute disorder of myocardial nutrition.

Pathological anatomy. When death occurs quickly, severe rigor mortis is often noted. When pressing on the skin, crepitus is observed due to the accumulation of gas in the subcutaneous tissue and the development of emphysema, sometimes covering the face. In some places, the skin has a marbled appearance as a result of uneven distribution of blood in the vessels. Due to asphyxia, the blood of the majority of the deceased remains liquid. Crepitation is found in many organs. The right side of the heart is distended with gas. During microscopic examination, gas bubbles are found in the dilated cavities of the right heart and coronary vessels, the inferior vena cava, vessels of the lungs, brain and spinal cord, their membranes, vessels of the liver, spleen, and small intestine. They are clearly visible in large blood vessels, especially veins: the blood in the vessels takes on a foamy appearance. Severe anemia of tissues and organs is noted. Edema, hemorrhages, and interstitial emphysema are found in the lungs. In the liver, phenomena of fatty degeneration are observed. In the brain and spinal cord, disorders of blood and lymph circulation lead to dystrophic changes in nerve cells and the appearance of ischemic foci of softening of brain tissue with the subsequent development of cysts in these areas. The consequence of changes in the spinal cord and paresis of the pelvic organs can be purulent cystitis and ascending purulent pyelonephritis.

With prolonged exposure to high atmospheric pressure in connection with the emerging circulatory disorders in the long tubular bones, mainly of the lower extremities, foci of rarefaction are found, surrounded by a zone of sclerosis, as well as foci of aseptic necrosis of bone tissue, sometimes with secondary osteomyelitis. Cartilage atrophy occurs in the joints with the development of deforming osteoarthritis and arthritis.

Diagnosis confirms the effectiveness of re-placement of the victim in conditions of increased pressure (recompression); detection on radiographs of bubbles in joint cavities, synovial sheaths of tendons, muscle fascia, as well as damage to bones and joints.

Treatment

In all cases of severe decompression sickness, immediate recompression is necessary.

Prevention

The main preventive measure is strict adherence to the “Safety Rules when working under compressed air (caisson work).” The permissible pressure in the caisson is limited: it should not exceed 4 Atm, which corresponds to a water depth of 40 m. According to these rules, the duration of working time in the caisson and the duration of escape are strictly regulated (the higher the pressure, the shorter the working time and the longer the decompression period).

*Ending. Starts at number 13.

Effect of partial pressure of gases on the body*

The gases that make up the breathing air affect the human body depending on the magnitude of their partial pressure.

Air nitrogen begins to practically have a toxic effect at a partial pressure of 5.5 kg/cm2. Since atmospheric air contains approximately 78% nitrogen, the indicated partial pressure of nitrogen corresponds to an absolute air pressure of 7 kg/cm2 (immersion depth - 60 m). At this depth, the swimmer becomes agitated, ability to work and attentiveness decrease, orientation becomes difficult, and sometimes dizziness occurs. At great depths (80-100 m), visual and auditory hallucinations develop. Almost at depths above 80 m, the swimmer becomes unable to work, and descent to this depth while breathing air is possible only for a very short time.

Oxygen in high concentrations, even under atmospheric pressure, it has a toxic effect on the body. Thus, at a partial pressure of oxygen of 1 kg per cm2 (breathing pure oxygen in atmospheric conditions), inflammatory phenomena develop in the lungs after 72 hours of breathing. When the partial pressure of oxygen is more than 3 kg per cm2, convulsions occur within 15-30 minutes and the person loses consciousness. Factors predisposing to the occurrence of oxygen poisoning are: the content of carbon dioxide in the inhaled air, strenuous physical work, hypothermia or overheating.

With a low partial pressure of oxygen in the inhaled air (below 0.16 kg/cm2), the blood flowing through the lungs is not completely saturated with oxygen, which leads to a decrease in performance, and in cases of acute oxygen starvation - to loss of consciousness.

Carbon dioxide. Maintaining normal carbon dioxide levels in the body is regulated by the central nervous system, which is very sensitive to its concentration. An increased content of carbon dioxide in the body leads to poisoning, a decreased content leads to a decrease in the respiratory rate and ego stop (apnea). Under normal conditions, the partial pressure of carbon dioxide in atmospheric air is 0.0003 kg/cm2. If the partial pressure of carbon dioxide in the inhaled air increases by more than 0.03 kg/cm2, the body will no longer be able to cope with the removal of this gas through increased breathing and blood circulation, and severe disorders may occur.

It should be borne in mind that a partial pressure of 0.03 kg/cm2 on the surface corresponds to a carbon dioxide concentration of 3%, and at a depth of 40 m (absolute pressure 5 kg/cm2) – 0.6%. An increased content of carbon dioxide in the inhaled air enhances the toxic effect of nitrogen, which can already appear at a depth of 45 m. That is why it is necessary to strictly monitor the content of carbon dioxide in the inhaled air.

Saturation of the body with gases. Being under high pressure entails saturation of the body with gases that dissolve in tissues and organs. At atmospheric pressure on the surface in a human body weighing 70 kg, about 1 liter of nitrogen is dissolved. With increasing pressure, the ability of body tissues to dissolve gases increases in proportion to the absolute air pressure. So, at a depth of 10 and (absolute air pressure for breathing 2 kg/cm2) 2 liters of nitrogen can already be dissolved in the body, at a depth of 20 m (3 kg/cm2) - 3 liters of nitrogen, etc.

The degree of saturation of the body with gases depends on their partial pressure, the time spent under pressure, as well as on the speed of blood flow and pulmonary ventilation. During physical work, the frequency and depth of breathing, as well as the speed of blood flow, increase, so the saturation of the body with gases is directly dependent on the intensity of the submarine swimmer’s physical activity. With the same physical activity, the speed of blood flow and pulmonary ventilation in a trained person increase to a lesser extent than in an untrained person, and the saturation of the body with gases will be different. Therefore, it is necessary to pay attention to increasing the level of physical fitness and the stable functional state of the cardiovascular and respiratory systems.

A decrease in pressure (decompression) causes desaturation of the body from indifferent gas (nitrogen). In this case, excess dissolved gas enters the bloodstream from the tissues and is carried by the blood stream into the lungs, from where it is removed into the environment by diffusion. If you ascend too quickly, nitrogen dissolved in the tissues forms bubbles of various sizes. They are carried throughout the body by the blood flow and cause blockage of blood vessels, which leads to decompression sickness.

Gases formed in the intestines of a submariner while he is under pressure expand upon ascent, which can lead to pain in the abdomen (flatulence). Therefore, you need to ascend from depth to the surface slowly, and in case of a long stay at depth, with stops in accordance with the decompression tables.

The effect on the body of holding your breath when diving

A special feature of diving is holding your breath during intense physical activity, when the body does not receive oxygen, which is so necessary for the functioning of the muscles and, most importantly, the brain. At the same time, depending on the load, oxygen consumption increases to 1.5-2 l/min. The cooling effect of water also increases oxygen consumption, causing oxygen deficiency. In addition, holding your breath while inhaling is accompanied by an increase in intrapulmonary pressure to 50-100 mmH2O. Art., which impedes blood flow to the heart and worsens intrapulmonary circulation.

In water during diving, the need to take a breath is not felt for some time. This occurs until the partial pressure of carbon dioxide in the blood reaches the value necessary to excite the respiratory center. But even in this case, with an effort of will you can suppress the need to take a breath and stay under water. With prolonged exposure to carbon dioxide on the respiratory center, its sensitivity decreases. Therefore, the initially unbearable need to take a breath becomes dulled later.

The appearance of the need to take a breath is a signal for the diver to ascend to the surface. If the diver does not surface, then as the reserves of oxygen contained in the air of the lungs are consumed, phenomena of oxygen starvation begin to develop, which are fleeting and end with an unexpected loss of consciousness. Oxygen starvation is the most common cause of death during diving.

At depth, the partial pressure of oxygen is correspondingly higher, which allows the diver to stay under water longer without experiencing signs of oxygen deprivation. For example, at a depth of 30 m (absolute air pressure 4 kg/cm2), when the oxygen content in the air of the lungs decreases to 5%, the diver feels good, since the partial pressure of oxygen is the same as in atmospheric air.

During ascent, the partial pressure of oxygen will begin to fall rapidly, both due to oxygen consumption and mainly due to a decrease in absolute pressure. At a depth of 20 m it will be below 0.15 kg/cm2, at a depth of 10 m - below 0.1 kg/cm2, at the surface - below 0.05 kg/cm2, and such a low partial pressure of oxygen leads to loss of consciousness.

The duration of voluntary breath-holding in a healthy adult at rest is short - on average, after a normal inhalation it is 54-55 seconds, and after a normal exhalation - 40 seconds. But professional divers can hold their breath for 3-4 minutes!

Caisson sickness and decompression

Scuba diving is dangerous because the air contained in the cylinders contains nitrogen, an inert gas that we inhale painlessly all the time. Meanwhile, a scuba diver in good health and mental capacity, trying to break his own diving depth record, may dive and not come back up. At a depth of 30 to 100 meters - this figure varies for different swimmers - he goes crazy and chokes; in essence, he commits suicide in a state of insanity.

The reason for this is nitrogen narcosis, which Cousteau, one of the first to observe this phenomenon, and one of the few who experienced it himself but survived, called “deep intoxication.” At first, the diver feels in seventh heaven, he is happier than ever in his life. He is carefree and carefree. He is a superman, master over himself and over everything that surrounds him. He no longer needs scuba gear. He can, laughing, hold out his mouthpiece to a passing fish. And then die, sinking to the bottom.

This phenomenon is explained by disruption of the brain centers as a result of inhaling nitrogen under high pressure. However, there is something worse. Both scuba divers and divers, and workers working in caissons filled with compressed air face the same danger of nitrogen penetrating into the blood and spreading it to various organs.

At a certain depth, nitrogen begins to penetrate into the human blood under pressure. If the decrease in pressure occurs too sharply, the diver begins to feel something like a tickling sensation. Doesn't feel any other warning signs. The cause of sudden death or paralysis is gas embolism - blockage of an artery by nitrogen bubbles. More often, nitrogen dissolved in tissues begins to be released in joints, muscles and various organs of the human body, causing a person to experience hellish torment. If he is not immediately placed in a decompression chamber, he may become crippled or die.

Cases of such a mysterious death interested the English scientist John Holden, who found a way to save himself from this disease. This method began to be used in the US Navy in 1912. It consists in the fact that the victim is raised to the surface gradually, keeping him at each stop for a certain period of time so that the nitrogen has time to be removed from the diver’s body, getting first into the blood and then into the lungs.

Naturally, Holden's safe ascent table, which provides for such decompression stops, takes into account the time the swimmer is under pressure and the amount of pressure. When descending to great depths, the ascent will take longer than the work. Fatigue and cold, or the urgency of the task, sometimes force swimmers to shorten the decompression period. And this can lead to irreparable consequences.

Well-trained, disciplined combat swimmers strictly adhere to the decompression regime. They strive to reduce risk to a minimum. But sponge catchers still become crippled due to decompression sickness and, as far as is known, careless scuba divers still die from it every year.

In addition to decompression sickness, another danger awaits a diver who rises to the surface too quickly. In the event of unexpected damage to the scuba gear, a swimmer may instinctively hold his breath during an urgent ascent. Then the air in his lungs will expand as the water pressure decreases and damage the lungs. As he rises to the surface, he may begin to convulse and bleed profusely from the mouth and nose. A non-scuba diver does not suffer from pulmonary barotrauma because the air he inhaled before diving was at normal atmospheric pressure.

Of course, a swimmer cannot immediately help his friend on the spot if his lungs are damaged. There are no means to provide such assistance. If, due to damage to the breathing apparatus or for some other reason, a swimmer rises to the surface too quickly and gets decompression sickness, the only way his comrades can help him is to put diving equipment or scuba gear on the victim and, together with him, descend to a sufficient depth for decompression. Using this technique, you can relieve a short but painful attack of decompression sickness, but in more difficult cases, especially if the victim has lost consciousness, it is not suitable. In such cases, as well as in case of pulmonary barotrauma, the swimmer must be quickly placed in a decompression chamber.

Rescue vessels and diving boats designed to carry divers down are usually equipped with such cameras.

All cameras are built according to the same principle. These are large cylinders with several pressure gauges, a telephone set and many instruments. Some cells are so large that several people can stand upright in them. At one end of the chamber there is a vestibule with two doors, reminiscent of a submarine's escape chamber; this allows a person to be admitted or released without changing the pressure in the main compartment. At the other end of the chamber there is a small airlock used to transfer food, drink, and medicines that the patient will need during a long retreat. All safety devices, from pumps to electric lamps, are duplicated in case they fail.

The sick diver is placed in a cell. A doctor stays with him and communicates with the medical staff outside. The doors are closed, air is pumped inside until the nitrogen bubbles in the body decrease in volume and the pain disappears. After this, they begin to reduce the pressure in accordance with the decompression tables. The doctor monitors the patient's condition throughout this procedure.

The doctor and the patient can sometimes remain in captivity for more than a day: Holden’s decompression method is only a preventive measure, while treatment requires more significant “doses”. If the patient dies, the doctor remains in the chamber until decompression is completed, otherwise he himself will become a victim of decompression sickness.

Thus, the underwater swimmer faces two kinds of danger: physical and physiological.

Physical hazards that are possible even at shallow depths (up to 30 meters) include:

Damage to the hearing organs (ruptured eardrums);

Rupture of blood vessels as a result of sudden rarefaction of air in a mask or wetsuit;

Blockage of blood vessels as a result of excess pressure in the lungs;

Hemorrhages in internal organs;

Hypothermia of the body;

Involuntary pushing to the surface due to excess air pressure in the wetsuit.

Physiological hazards are mainly related to the problem of breathing under water. These include:

Suffocation as a result of oxygen starvation;

Poisoning as a result of oversaturation of the body with oxygen;

Asphyxiation due to carbon dioxide poisoning;

- “decompression sickness” (at medium depths, from 30 to 60 meters);

Nitrogen intoxication (at depths of more than 60 meters).

In conclusion, I strongly recommend that novice scuba divers read Ivan Arzamastsev’s book “Adventures under and above water” (Dalnauka publishing house, 2005), which humorously outlines diving safety techniques and recommendations in verse:

Jumped into the water

I didn't blow my mind.

In five minutes

Returned.

A lot of blood,

Little hearing -

This is barotrauma of the ear.

Everything hurts.

There is aching in the bones.

Nitrogen bubbles in the blood.

More into the water

I shouldn't climb

It's decompression sickness.

(From the diving epic)