Causes and consequences of pulmonary edema: this knowledge can save a life. Clinic of acute lung lesions with toxic substances Clinical signs of toxic pulmonary edema

The intake of various aggressive substances in the body is fraught with the occurrence of a variety of health problems. In this case, drugs, poisons, heavy metal salts, decay products of certain substances and toxins produced by the body itself in response to the development of some diseases can act as aggressors. Such poisoning can be fatal or cause serious dysfunction of vital organs: heart, brain, liver, etc. Among these disorders is toxic pulmonary edema, the symptoms and treatment of which will be considered in a little more detail.

Toxic pulmonary edema can develop as a result of inhalation of certain aggressive substances, represented by nitric oxide, ozone, ammonia, chlorine, etc. It can be caused by some infectious lesions, for example, pneumonia, leptospirosis and meningococcemia, as well as endotoxicosis, for example, sepsis, peritonitis, pancreatitis etc. In some cases, such a condition is provoked by severe allergic diseases or poisoning.
Toxic pulmonary edema is characterized by a number of intense clinical manifestations, especially severe course and often poor prognosis.

Symptoms

If aggressive substances are inhaled, the patient may experience a slight cough, a feeling of tightness in the chest, a feeling of general weakness, headaches, and frequent shallow breathing. High concentrations of toxic elements provoke suffocation and cyanosis. It is impossible to prevent the possibility of further pulmonary edema at this stage. After half an hour or an hour, the unpleasant symptoms completely disappear, a period of latent well-being may begin. But the progression of pathological processes leads to the gradual appearance of negative symptoms.

The initial sign of toxic pulmonary edema of any etiology is a feeling of general weakness and headache, a feeling of weakness, heaviness and tightness in the chest. The patient is disturbed by a feeling of slight shortness of breath, coughing, breathing and pulse become more frequent.

With a sharp pulmonary edema, shortness of breath occurs abruptly, and with a slow development, it is of a constant progressive nature. Patients complain of a pronounced feeling of lack of air. Shortness of breath increases and turns into suffocation, it intensifies both in the supine position and with any movements. The patient tries to take a forced position: sitting with an inclination forward, in order to at least slightly ease breathing.

Pathological processes cause a feeling of pressing pain in the chest area, they cause an increase in heart rate. The patient's skin is covered with cold sweat and is painted in cyanotic or gray tones.

The victim is worried about coughing - at first dry, after - with the separation of frothy sputum, colored pink (due to the presence of blood streaks in it).

The patient's breathing becomes frequent, and as the swelling increases, it becomes bubbling and audible at a distance. Developing edema causes dizziness and general weakness. The patient becomes frightened and agitated.

If pathological processes develop according to the type of "blue" hypoxemia, the victim begins to moan and rush about, he cannot find a place for himself and tries to greedily catch air with his mouth. A pinkish foam comes out of his nose and mouth. The skin turns blue, blood vessels pulsate in the neck, and consciousness becomes clouded.

If pulmonary edema leads to the development of "gray" hypoxemia, the patient's activity of the cardiovascular and respiratory systems is sharply disrupted: a collapse occurs, the pulse becomes weak and arrhythmic (may not be felt), and breathing is rare. The skin becomes earthy gray tones, the limbs become cold, and the facial features become pointed.

How is toxic pulmonary edema corrected, what is its effective treatment?

When symptoms of developing pulmonary edema appear, emergency medical care is immediately needed, the history of which keeps many thousands of cases of saving patients. The victim should be kept calm, he is shown sedatives and antitussives. As a first aid, doctors can also inhale an oxygen-air mixture by passing it through defoamers (alcohol). To reduce blood flow to the lungs, they resort to bloodletting or the imposition of venous tourniquets on the limbs.

To eliminate the onset of toxic pulmonary edema, doctors administer to the victim steroidal anti-inflammatory drugs (usually prednisone), as well as diuretics (most often furosemide). Also, treatment involves the use of bronchodilators (aminophylline), oncotic active agents (plasma or albumin), glucose, calcium chloride and cardiotonic drugs. If progression of respiratory failure is observed, tracheal intubation and mechanical ventilation (artificial ventilation of the lungs) are carried out.

To prevent pneumonia, doctors use broad-spectrum antibiotics at the usual dosage, and anticoagulants are used to prevent thromboembolic complications. The total duration of therapy can reach one and a half months.

The prognosis and survival of toxic pulmonary edema depends on the factor that provoked this disorder, on the severity of the edema, and on how quickly and professionally medical care was provided. Toxic pulmonary edema at the acute stage of development often causes death, and in the long term often becomes the cause of disability.

Additional Information

Patients who have had toxic pulmonary edema can benefit from a variety of herbal and home remedies. They can be used for recreational purposes and only after consulting a doctor.

So an excellent effect is given by treatment with oats, recipes for which (some) have already been given earlier. Brew a glass of such raw materials with half a liter of milk and evaporate on a fire of minimum power until the volume of the broth is reduced by half. At the same time, do not forget to stir the prepared medicine from time to time. Then wipe the oats through a sieve. Drink the resulting mixture at one time before a meal. Take it three times a day.

The feasibility of using traditional medicine should be discussed with the doctor without fail.

This is the most severe form of lung toxicity.

The pathogenesis of toxic pulmonary edema cannot be considered definitive. The leading role in the development of toxic pulmonary edema belongs to an increase in the permeability of capillary membranes, which, apparently, can be facilitated by damage to the sulfhydryl groups of lung tissue proteins. The increase in permeability is carried out with the participation of histamine, active globulins and other substances released or formed in the tissue under the action of stimuli on it. Important in the regulation of capillary permeability belongs to the nervous mechanisms. So, for example, in the experiment it was shown that vagosympathetic novocaine blockade can reduce or even prevent the development of pulmonary edema.

Based on the clinical picture of toxic edema with the presence of leukocytosis and temperature reaction, as well as pathoanatomical data indicating the presence of confluent catarrhal inflammation, in the absence of microbial flora, some researchers consider pulmonary edema as one of the variants of toxic pneumonia, in which exudation processes are ahead of cellular infiltration.

The development of pulmonary edema causes a violation of gas exchange in the lungs. At the height of the edema, when the alveoli are filled with edematous fluid, the diffusion of oxygen and carbon dioxide is possible only due to the solubility of gases. At the same time, hypoxemia and hypercapnia gradually increase. At the same time, there is a thickening of the blood, an increase in its viscosity. All these factors lead to insufficient supply of tissues with oxygen - hypoxia. Acidic metabolic products accumulate in tissues, reserve alkalinity decreases and pH shifts to the acid side.

Clinically distinguish two forms of toxic pulmonary edema: developed, or completed, and abortive.

At developed form there is a consistent development of five periods: 1) initial phenomena (reflex stage); 2) hidden period; 3) the period of increase in edema; 4) the period of completed edema; 5) reverse development of edema.

Abortive form characterized by a change of four periods: 1) initial phenomena; 2) hidden period; 3) increase in edema; 4) reverse development of edema.

In addition to the two main ones, another form of acute toxic pulmonary edema is distinguished - the so-called " silent swelling”, which is detected only by X-ray examination of the lungs, while the clinical manifestations of pulmonary edema are practically absent.

The period of initial phenomena develops immediately after exposure to a toxic substance and is characterized by mild irritation of the mucous membranes of the respiratory tract: a slight cough, sore throat, chest pain. As a rule, these mild subjective disorders do not have a significant effect on the well-being of the victim and soon disappear.

The latent period follows the subsidence of irritation and can have a different duration (from 2 to 24 hours), more often 6-12 hours. During this period, the victim feels healthy, but with a thorough examination, the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis , pulse lability. It has been experimentally proven that in this "hidden" period from the very beginning it is possible to detect histological changes corresponding to edema of the interstitial tissue of the lung, so the absence of clear clinical manifestations does not yet indicate the absence of an emerging pathology.

The period of increasing edema is clinically manifested, which is associated with the accumulation of edematous fluid in the alveoli and a more pronounced violation of the respiratory function. The victims have an increase in breathing, it becomes superficial and is accompanied by paroxysmal excruciating cough. Objectively, slight cyanosis is noted. In the lungs voiced fine bubbling wet rales and crepitus are heard. In X-ray examination in this period, one can note fuzziness, blurring of the pulmonary pattern, small ramifications of blood vessels are poorly differentiated, some thickening of the interlobar pleura is noted. The roots of the lungs are somewhat dilated, have fuzzy contours.

Identification of signs of increasing toxic pulmonary edema is very important for appropriate therapeutic and preventive measures to prevent the development of edema.

The period of completed edema corresponds to the further progression of the pathological process. During toxic pulmonary edema, two types are distinguished: "blue hypoxemia" and "gray hypoxemia". With the "blue" type of toxic edema, pronounced cyanosis of the skin and mucous membranes is noted, pronounced shortness of breath - up to 50-60 breaths per minute. In the distance, bubbling breathing is heard. Cough with large amounts of frothy sputum, often containing blood. During auscultation, a mass of different-sized wet rales is found throughout the lung fields. Tachycardia is noted, blood pressure remains normal or even slightly increased. When examining blood, its significant thickening is revealed: the content of hemoglobin increases. Coagulation is enhanced. The arterialization of blood in the lungs is disturbed, which is manifested by a deficiency in the saturation of arterial blood with oxygen while increasing the content of carbon dioxide (hypercapnic hypoxemia). Compensated gaseous acidosis develops.

With the "gray" type of toxic edema, the clinical picture is more severe due to the addition of pronounced vascular disorders. The skin becomes pale gray in color. Face covered with cold sweat. The limbs are cold to the touch. The pulse becomes frequent and small. There is a drop in blood pressure. The gas composition of the blood in these cases is characterized by a decrease in oxygen saturation and a low content of carbon dioxide (hypoxemia with hypocapnia). The coefficient of oxygen utilization and its arteriovenous difference decrease. The state of "gray hypoxemia" may be preceded by a period of "blue hypoxemia". Sometimes the process begins immediately according to the type of "gray hypoxemia". This can be facilitated by physical activity, long-term transportation of the victim.

Disorders of the cardiovascular system in toxic pulmonary edema are caused by impaired blood flow in the pulmonary circulation with an overload of the "acute pulmonary heart" type, as well as myocardial ischemia and vegetative changes. Regardless of the type of edema, in the stage of completed edema, an increase in the blurring of the lung pattern and the appearance in the lower and middle parts of the first small (2-3 mm) spotted shadows, which later increase in size due to the merger of individual foci, form fuzzy contoured shadows resembling "flakes of melting snow" Areas of darkening alternate with enlightenments due to emerging foci of bullous emphysema. The roots of the lungs become even wider with fuzzy contours.

The transition of the period of increasing to expanded pulmonary edema often occurs very quickly, characterized by a rapidly progressive course. Severe forms of pulmonary edema can be fatal in 24-48 hours. In milder cases and with timely intensive care, a period of regression of pulmonary edema occurs.

During the reverse development of edema, coughing and the amount of sputum discharge gradually decrease, shortness of breath subsides. Cyanosis decreases, weaken, and then wheezing in the lungs disappears. X-ray studies indicate the disappearance of first large and then small focal shadows, only the fuzziness of the lung pattern and the contours of the roots of the lungs remains, and after a few days the normal X-ray morphological picture of the lungs is restored, the composition of the peripheral blood is normalized. Recovery can have significant variability in terms - from several days to several weeks.

The most common complication of toxic pulmonary edema is the addition of infection and the development of pneumonia. During the period of subsiding of the clinical manifestations of edema and improvement of the general condition, usually on the 3rd-4th day after poisoning, there is a rise in temperature to 38-39 ° C, coughing again intensifies with the release of mucopurulent sputum. In the lungs, areas of finely bubbling wet rales appear or increase. In the blood, leukocytosis increases and an acceleration of ESR appears. Radiologically, small pneumonic foci of the type of small-focal pneumonia are noted. Another serious complication of toxic edema is the so-called "secondary" pulmonary edema, which can develop at the end of the 2nd - the middle of the 3rd week, as a result of the onset of acute heart failure. In the long-term follow-up after toxic pulmonary edema, toxic pneumosclerosis and pulmonary emphysema may develop. An exacerbation of previously latent pulmonary tuberculosis and other chronic infections may occur.

In addition to changes in the lungs and the cardiovascular system, changes in the nervous system are often found in toxic pulmonary edema. The victims complain of headache, dizziness. Relatively often, instability in the neuro-emotional sphere is revealed: irritability, anxiety, the predominance of depressive-hypochondriac reactions, in some victims - agitation and convulsions, and in severe cases - stupor, drowsiness, adynamia, loss of consciousness. In the future, the addition of asthenoneurotic and vegetative disorders is possible.

At the height of toxic edema, diuresis sometimes decreases, up to anuria. In the urine, traces of protein, hyaline and granular cylinders, erythrocytes are found. These changes are associated with the possibility of developing toxic kidney damage due to general vascular changes.
With pulmonary edema, liver damage is often noted - a slight increase in the organ, a change in functional liver tests by the type of toxic hepatitis. These changes in the liver can persist for quite a long time, often combined with functional disorders of the gastrointestinal tract.

Acute toxic-chemical damage to the respiratory organs is divided into four periods (phases): the phase of primary reactions, the latent period (latent phase), the phase of detailed clinical reactions, the phase of outcomes. The phase of primary reactions due to exposure to easily water-soluble toxic chemicals is manifested by acute suffocating laryngospasm and bronchospasm, while substances that are hardly water-soluble cause less vivid or even erased reactions that do not cause concern to the victims.
The latent period (after the phase of primary reactions) lasts from 1-2 to 48 hours. It can end at any time (usually at night) with the rapid development of pulmonary edema, which is more typical for exposure to poorly soluble chemicals. Easily soluble substances are less likely to cause the development of acute toxic-chemical pulmonary edema, since they, to a lesser extent, due to acute laryngo- and bronchospasm, reach the bronchial-alveolar (distal) sections of the lung when inhaled. Thus, patients in the latent period are subject to constant medical observation in the emergency room or hospital, otherwise they may die at the prehospital stage.
The period of developed clinical reactions often begins) with acute toxic-chemical pulmonary edema or with acute toxic-chemical tracheobronchitis (when exposed to chemicals that are easily soluble in water). There is an acute toxic-chemical pulmonary edema of blue (with a picture of acute hypoxia and hypercapnia) and gray (with acute hypoxia and hypocapnia) type.
Pulmonary edema of the blue type is characterized by the presence of a pronounced alveolar phase and obstructive syndrome (with damage to the small bronchi) with a predominance of inspiratory dyspnea. Against the background of small bubbling, and then large bubbling rales affecting the receptors of the reflexogenic cough zone, foamy sputum appears, colored pinkish-orange (when nitrogen oxides are exposed to the mucous membranes of the respiratory tract, causing a xantoprotein reaction with the protein content of the bronchial tree).
With toxic-chemical gray-type pulmonary edema with a predominance of the interstitial phase of edema with severe inspiratory dyspnea, the main clinical manifestation is cardiovascular insufficiency. This is a more severe form of pulmonary edema, in which the alveolar-capillary membrane is affected to the full depth.
After relief of pulmonary edema, the clinical picture of acute toxic-chemical alveolitis or pneumonitis remains. In some cases, the development of acute toxic-chemical pneumonia is possible.
In case of acute toxic-chemical injury, substances easily soluble in water, when acute toxic-chemical pulmonary edema was not observed during the period of clinical developed reactions, lesions of the upper respiratory organs (toxic-chemical rhinitis, pharyngolaryngotracheitis), as well as acute bronchitis with predominant damage to the mucous membranes of large bronchial structures.
With a favorable course and treatment of respiratory pathology caused by acute toxic-chemical damage, the total duration of the disease is 2-3 weeks.
An unfavorable prognosis for toxic-chemical damage to the respiratory organs is possible if aseptic inflammation is complicated by bacterial infection: an infectious-inflammatory process accompanied by an increase in body temperature, hematological and biochemical changes. Such a complication is always dangerous and can be observed from the 3-4th day of the lesion. The addition of infectious-inflammatory reactions against the background of toxic-chemical damage to the lungs often leads to persistence of the infection and subsequent chronicization of the pathological process in the lungs, despite carefully conducted anti-inflammatory therapy. This is explained by the fact that in such cases, the infectious-inflammatory process in the lungs is superimposed on destructively altered bronchial-pulmonary structures.

The essence of pulmonary edema is that the pulmonary alveoli are filled with edematous fluid (transudate) due to sweating of blood plasma, as a result of which pulmonary gas exchange is disturbed and acute oxygen starvation develops, pulmonary hypoxia with a sharp violation of all body functions. Toxic pulmonary edema also develops in case of poisoning with other toxic and irritating substances (nitrogen oxides, nitric acid vapors, sulfuric acid, ammonia, lewisite, etc.).

Most researchers consider the main cause of toxic pulmonary edema to be an increase in the permeability of the pulmonary capillaries and alveolar epithelium, a violation of their microstructure, which has now been proven using electron microscopy.

Many theories have been put forward for the development of toxic pulmonary edema. They can be divided into three groups:

Biochemical;

Nervous reflex;

Hormonal.

Biochemical. In pulmonary edema, inactivation of the surfactant system of the lungs plays a certain role. Lung surfactant is a complex of phospholipid substances with surface activity, located in the form of a submicroscopic film thickness on the inner surface of the alveoli. The surfactant reduces the surface tension forces in the alveoli at the air-water interface, thus preventing alveolar atelectasis and exudation of fluid into the alveoli.

With pulmonary edema, capillary permeability first increases, swelling and thickening of the alveolar interstitium appear, then an increase in the permeability of the alveolar walls and alveolar pulmonary edema occurs.

Nervous reflex.

The basis of toxic pulmonary edema is a neuro-reflex mechanism, the afferent path of which is the sensory fibers of the vagus nerve, with a center located in the brain stem; The efferent pathway is the sympathetic division of the nervous system. At the same time, pulmonary edema is considered as a protective physiological reaction aimed at washing off the irritating agent.

Under the action of phosgene, the neuroreflex mechanism of pathogenesis is presented in the following form. The afferent link of the neurovegetative arc is the trigeminal nerve and vagus, the receptor endings of which are highly sensitive to vapors of phosgene and other substances of this group.

Excitation efferently spreads to the sympathetic branches of the lungs, as a result of a violation of the trophic function of the sympathetic nervous system and the local damaging effect of phosgene, swelling and inflammation of the lung membrane and a pathological increase in permeability in the vascular membrane of the lungs occur. Thus, there are two main links in the pathogenesis of pulmonary edema: 1) increased permeability of the pulmonary capillaries and 2) swelling, inflammation of the interalveolar septa. These two factors cause the accumulation of edematous fluid in the pulmonary alveoli, i.e. leads to pulmonary edema.

Hormonal.

In addition to the neuroreflex mechanism, neuroendocrine reflexes, among which antisodium and antidiuretic reflexes occupy a special place. Under the influence of acidosis and hypoxemia, chemoreceptors are irritated. The slowing down of blood flow in the small circle contributes to the expansion of the lumen of the veins and irritation of volumenreceptors that respond to changes in the volume of the vascular bed. Impulses from chemoreceptors and volumenreceptors reach the midbrain, the response of which is the release of aldosterone-tropic factor, neurosecretate, into the blood. In response to its appearance in the blood, the secretion of aldosterone is stimulated in the adrenal cortex. The mineral corticoid aldosterone is known to promote the retention of sodium ions in the body and enhance inflammatory reactions. These properties of aldosterone are most easily manifested in the "place of least resistance", namely in the lungs damaged by a toxic substance. As a result, sodium ions, lingering in the lung tissue, cause an imbalance in osmotic balance. This first phase of neuroendocrine responses is called antisodium reflex.

The second phase of neuroedocrine reactions begins with the excitation of lung osmoreceptors. The impulses sent by them reach the hypothalamus. In response to this, the posterior pituitary gland begins to produce antidiuretic hormone, the "fire-fighting function" of which is to urgently redistribute the body's water resources in order to restore osmotic balance. This is achieved through oliguria and even anuria. As a result, the flow of fluid to the lungs is further enhanced. This is the second phase of neuroendocrine reactions in pulmonary edema, which is called the antidiuretic reflex.

Thus, the following main links of the pathogenetic chain in pulmonary edema can be distinguished:

1) violation of the main nervous processes in the neurovegetative arc:

pulmonary branches of the vagus, brain stem, sympathetic branches of the lungs;

2) swelling and inflammation of the interalveolar septa due to metabolic disorders;

3) increased vascular permeability in the lungs and stagnation of blood in the pulmonary circulation;

4) oxygen starvation of the blue and gray types.

Toxic pulmonary edema(TOL) is a symptom complex that develops in case of severe inhalation poisoning with asphyxiating and irritating poisons, many of which are highly toxic.

Such poisons include vapors of certain acids (sulphuric, hydrochloric), chlorine, hydrogen sulfide, ozone. The occurrence of TOL may be due to inhalation exposure to rocket fuel oxidizers (fluorine and its compounds, nitric acid, nitrogen oxides), intoxication with combustible mixtures (diborane, ammonia, etc.).

There is a pronounced reflex period;

It is combined with signs of chemical edema of the lung tissue, mucous membrane of the respiratory tract;

A combined nature of the lesion is observed, consisting of symptoms of damage to the respiratory organs and manifestations of the resorptive action of the poison.

Main links pathogenesis of toxic pulmonary edema are an increase in the permeability and a violation of the integrity of the pulmonary capillaries with the participation of histamine, active globulins and other substances released or formed in the tissue under the action of stimuli on it, while hypoxemia and hypercapnia gradually increase. Acidic metabolic products accumulate in tissues, reserve alkalinity decreases and pH shifts to the acid side.

Clinic.

There are two forms of toxic pulmonary edema: developed or completed and abortive. With a developed form, a consistent development of five periods is observed:

1) initial phenomena (reflex stage);

2) hidden period;

3) the period of increase in edema;

4) the period of completed edema;

5) the period of reverse development or complications of TOL.

The abortive form is characterized by a change of four periods:

1) initial phenomena;

2) hidden period;

3) the period of increase in edema;

4) the period of reverse development or complications of TOL.

In addition to the two main ones, the so-called "silent edema" is distinguished, which is detected only with an X-ray examination of the lungs.

1. The period of reflex disorders develops immediately after exposure to a toxic substance and is characterized by mild irritation of the mucous membranes of the respiratory tract: a slight cough, chest pain. In some cases, a reflex stop of breathing and cardiac activity may occur. As a rule, bilateral symmetrical shading, increased bronchopulmonary pattern, and expansion of the roots of the lungs are observed on the radiograph (Fig. 10).

Figure 10. Chest X-ray showing signs of bilateral toxic pulmonary edema.

2. The period of subsiding of the phenomena of irritation(latent period) can have a different duration (from 2 to 24 hours), more often 6-12 hours. During this period, the victim feels healthy, but with a thorough examination, the first symptoms of increasing oxygen deficiency can be noted: shortness of breath, cyanosis, systolic blood pressure.

3. The period of increasing pulmonary edema manifested by severe respiratory failure. In the lungs voiced fine bubbling wet rales and crepitus are heard. There is an increase in temperature, neutrophilic leukocytosis, and collapse may develop. In X-ray examination in this period, one can note fuzziness, blurring of the pulmonary pattern, small ramifications of blood vessels are poorly differentiated, some thickening of the interlobar pleura is noted. The roots of the lungs are somewhat expanded, have fuzzy contours (Fig. 11).

4. The period of completed edema(observed only in the advanced form of pulmonary edema) corresponds to the further progression of the pathological process, during which two types are distinguished: “blue hypoxemia” and “gray hypoxemia”.

With the "blue" type of TOL, pronounced cyanosis of the skin and mucous membranes is noted, pronounced shortness of breath - up to 50-60 breaths per minute. Cough with large amounts of frothy sputum, often containing blood. Auscultation reveals a mass of various wet rales. With the aggravation of the state of "blue hypoxemia", a detailed picture of "gray hypoxemia" is observed, which is more severe due to the addition of pronounced vascular disorders. The skin becomes pale gray in color. Face covered with cold sweat. The limbs are cold to the touch. The pulse becomes frequent and small. There is a drop in blood pressure. Sometimes the process can begin immediately according to the type of "gray hypoxemia". This can be facilitated by physical activity, long-term transportation of the victim. On the part of the cardiovascular system, the phenomena of myocardial ischemia and vegetative changes are observed. Bullous emphysema develops in the lungs. Severe forms of pulmonary edema can be fatal within one to two days.

Figure 11. X-ray signs of an increase in toxic pulmonary edema.

5. Regression period or complications. In mild cases of TOL and with timely intensive therapy, a period of regression of pulmonary edema occurs. During the reverse development of edema, coughing and the amount of sputum discharge gradually decrease, shortness of breath subsides. Cyanosis regresses, weaken, and then wheezing in the lungs disappears. On x-ray examination - blurred lung pattern and contours of the roots of the lungs. After a few days, the usual x-ray picture of the lungs is restored, the composition of peripheral blood is normalized. Recovery can have considerable variability in terms from several days to several weeks. When exiting TOL, secondary pulmonary edema may develop due to acute left ventricular failure. In the future, the development of pneumonia and pneumosclerosis is possible. In addition to changes in the pulmonary and cardiovascular systems, TOL often reveals changes in the nervous system. With pulmonary edema, there is often damage and some enlargement of the liver, an increase in the level of liver enzymes, as in toxic hepatitis. These changes can persist for quite a long time, often combined with functional disorders of the gastrointestinal tract.

Treatment TOL should be aimed at eliminating emergency impulses, removing the irritating effect of toxic substances, eliminating hypoxia, reducing increased vascular permeability, unloading the pulmonary circulation, maintaining the activity of the cardiovascular system, eliminating metabolic disorders, preventing and treating infectious complications.

Removal of irritation of the respiratory tract is achieved by inhalation of an anti-smoke mixture, soda, the appointment of codeine-containing drugs to suppress cough.

The impact on the neuro-reflex arc is carried out by vagosympathetic novocaine blockades, neuroleptanalgesia.

Elimination of oxygen starvation is achieved by oxygenation, improvement and restoration of airway patency. Oxygen is given for a long time in the form of a 50-60% mixture under slight pressure (3-8 mm of water column). For the purpose of defoaming, oxygen inhalation is carried out through ethyl alcohol, an alcohol 10% solution of antifomsilan, an aqueous 10% solution of colloidal silicone. Aspirate fluid from the upper respiratory tract. If necessary, intubation and transfer of the patient to mechanical ventilation is possible.

The impact on the respiratory center is achieved by the use of drugs. Morphine preparations reduce shortness of breath associated with cerebral hypoxia and excitation of the respiratory center. This leads to a decrease and deepening of breathing, i.e. to its greater efficiency. Repeated administration of morphine is possible according to indications.

Reducing the permeability of the pulmonary capillaries is achieved by intravenous administration of 10 ml of a 10% solution of calcium chloride, ascorbic acid and rutin, the introduction of glucocorticoids (100-125 mg of hydrocortisone suspension in / in), antihistamines (1-2 ml of 1% solution of diphenhydramine in / m) .

Unloading of the pulmonary circulation can be carried out by intravenous administration of aminophylline, blood deposition (sitting position of the patient, venous tourniquets on the limbs, intravenous administration of 0.5-1 ml of 5% pentamine), the appointment of osmotic diuretics (urea, 15% solution mannitol 300-400 ml IV), saluretics (40-120 mg furosemide IV). In some cases, venous bloodletting in the amount of 200-400 ml can be effective. With low blood pressure, especially collapse, bloodletting is contraindicated. In the absence of contraindications, cardiac glycosides may be administered intravenously.

Metabolic acidosis is often observed in TOL, for which the administration of sodium bicarbonate, trisamine, can be effective.

Antibacterial agents are prescribed for the treatment of infectious complications.

TOL prevention, first of all, it consists in observing the safety regulations, especially in closed (with poor ventilation) rooms during work related to the inhalation exposure to irritating substances.

SUDDEN DEATH

Sudden death may be due to disorders of the heart (in this case, they talk about sudden cardiac death - SCD) or damage to the central nervous system (sudden brain death). 60-90% of sudden deaths are due to SCD. The problem of sudden death remains one of the serious and urgent problems of modern medicine. Premature death has tragic consequences for both individual families and society as a whole.

Sudden cardiac death- unexpected, unforeseen death of cardiac etiology, occurring in the presence of witnesses within 1 hour from the onset of the first signs, in a person without the presence of conditions that could currently be fatal.

About 2/3 of cardiac arrests occur at home. About 3/4 of cases are observed between 8.00 and 18.00 hours. The male sex predominates.

Considering the causes of SCD, it should be noted that most of the sudden deaths do not have severe organic changes in the heart. In 75-80% of cases, SCD is based on coronary artery disease and associated atherosclerosis of the coronary vessels, leading to myocardial infarction. Approximately 50% of SCD cases are the first manifestation of CAD. Also among the causes of SCD should be noted dilated and hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy; genetically determined conditions associated with the pathology of ion channels (long QT syndrome, Brugada syndrome); valvular heart disease (aortic stenosis, mitral valve prolapse); anomalies of the coronary arteries; syndrome of premature excitation of the ventricles (Wolf-Parkinson-White syndrome). Rhythm disturbances leading to SCD are most often ventricular tachyarrhythmias (cardiac fibrillation, polymorphic ventricular tachycardia of the "pirouette" type, ventricular tachycardia with the transition to ventricular fibrillation (VF)), less often - bradyarrhythmias, and also (5-10% of cases) - primary ventricular asystole (mainly due to AV block, SSSU). SCD may be due to a ruptured aortic aneurysm.

Risk factors for SCD: long QT syndrome, WPW syndrome, SSSU. The frequency of development of VF is directly related to an increase in the size of the chambers of the heart, the presence of sclerosis in the conduction system, an increase in the tone of the SNS, incl. against the background of pronounced physical effort and psycho-emotional stress. In families with cases of SCD, the most common risk factors for coronary artery disease are: arterial hypertension, smoking, a combination of two or more risk factors. Individuals with a history of sudden cardiac death have an increased risk of SCD.

Sudden death may be due to neurogenic causes, in particular, rupture of aneurysmal protrusions in the cerebral arteries. In this case, we are talking about sudden brain death. A sudden hemorrhage from the vessels of the brain leads to impregnation of the brain tissue, its edema with a possible wedging of the trunk into the foramen magnum and, as a result, respiratory failure until it stops. With the provision of specialized resuscitation care and the timely connection of mechanical ventilation, the patient can maintain adequate cardiac activity for a long time.