The cause of toxic pulmonary edema is damage to the pulmonary membrane by toxic substances. The result of exposure to poisons is inflammation with further development edema lung tissue. Refers to a severe form of chemical lung damage. Most often pathological condition occurs when carbon monoxide, FOS, concentrated vapors of acids and alkalis or other chemicals with a suffocating effect. Edema also develops if aggressive chemicals enter the digestive tract, causing a burn to the upper respiratory tract.
Symptoms of toxic pulmonary edema
The development of toxic pulmonary edema occurs in several stages:
- Reflex.
- Hidden.
- stage with bright severe symptoms toxic pulmonary edema.
- Stage of recovery or reverse development.
In the initial stage (reflex), the patient exhibits the first signs:
- pain in the eyes;
- sore throat;
- lacrimation;
- heaviness in the chest;
- difficulty breathing;
- decreased breathing.
Subsequently, the victim's discomfort, however, breathing problems persist. This stage is called hidden or imaginary well-being. Its duration can be up to a day. During this period, pathological processes occur in the lungs, which manifest themselves with the following symptoms:
- wheezing;
- bubbling breathing;
- painful cough;
- discharge of foamy sputum from the patient’s mouth;
- increasing respiratory failure;
- blueness of the skin (cyanosis).
The patient's arterial pressure, the face becomes gray, the mucous membranes also acquire an earthy tint. If the victim is not provided with medical assistance, toxic pulmonary edema will result in death.
Diagnosis and treatment of toxic pulmonary edema
Patients with suspected pulmonary edema are advised to undergo an X-ray examination, blood and urine tests. The x-ray will reveal unclear and blurred contours of the lungs. In the blood - leukocytosis, increased hemoglobin, excess blood clotting parameters.
Treatment of patients with respiratory failure due to poisoning occurs in intensive care units and includes:
- Artificial ventilation.
- Oxygen therapy.
- Detoxification of the body.
- Prevention of infections.
If there is no spontaneous breathing, the patient is intubated and connected to the apparatus artificial ventilation lungs. At acute poisoning Treatment of toxic edema begins with the administration of a dehydrating drug, lyophilized urea. The medicine increases the osmotic pressure of the blood and promotes the absorption of fluid from the lungs, improves the function of the lung tissue, and prevents the congestion of other vital important organs. After administration of the drug, the patient’s heart muscle function improves. The diuretic Furosemide has almost the same effect.
Advice! If it is not possible to transport the patient to the hospital, in order to prevent the increase in edema and reduce the load of the small circle, bloodletting up to 300 ml is performed. Another way is to apply venous tourniquets to the limbs.
To reduce the permeability of the vascular wall and the development of edema, victims are administered glucocorticoid drugs (Prednisolone), as well as antihistamines. In combination with this purpose, ascorbic acid in a glucose solution and calcium chloride are prescribed.
Oxygen therapy with inhalation of defoamers, which convert foam into liquid, plays an important role in relieving pulmonary edema. The drugs clear the respiratory surface of the lungs and prevent the development of acute respiratory failure. To the branches intensive care Ethyl alcohol is used successfully.
If the use of diuretics for acute intoxication does not have an effect, it is indicated emergency implementation blood filtration using an artificial kidney apparatus. It is also recommended to enter colloidal solutions(Gelofusin) simultaneously with diuretics (Furosemide).
After rendering emergency care and elimination of pulmonary edema, patients are prescribed oxygen therapy with bronchodilators and glucocorticoids. Oxygen treatment begins with a low concentration. The procedure lasts 10–15 minutes. Patients with are indicated in pressure chambers.
Important! If the victim is affected, such therapy is contraindicated. The chemical, if inhaled, can cause repeated swelling of the lung tissue.
Since the patient after acute chemical poisoning with severe respiratory failure is in a state of stress, he is prescribed sedatives, which help to remove emotional stress. Antipsychotics are administered to reduce shortness of breath and anxiety.
To prevent secondary infection, patients are prescribed antibiotics. Drugs that prevent thrombosis (anticoagulants) are also indicated. For a speedy recovery from hypoxic conditions, patients are administered B vitamins, ascorbic acid, and vitamin P in large doses. Vitamin therapy accelerates tissue regeneration and accelerates redox processes, which is important for toxic lesions.
Find out what to do if it occurs: causes, treatment at home and in a hospital setting.
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Prognosis for patients' lives
Severe forms Pulmonary edema often ends in death if assistance is not provided in a timely manner or the victim is treated inadequately. If the patient received treatment on time and in full, changes in the lung tissue begin to reverse. A person is able to fully restore health within a few weeks.
The recovery period may be complicated by repeated pulmonary edema, infection and the development of pneumonia or thrombosis that occurred against the background of blood thickening in the acute period diseases.
After the patient is discharged from the hospital, later complications associated with the respiratory system and central nervous system may appear: emphysema, pneumosclerosis, autonomic disorders, asthenia. Depending on the concentration of the toxic substance and the degree of damage to the body, the victim is likely to develop problems with the liver and kidneys.
Acute toxic pulmonary edema. This is the most severe form toxic damage lungs.
The pathogenesis of toxic pulmonary edema cannot be considered completely clarified. The leading role in the development of toxic pulmonary edema belongs to the increase in the permeability of capillary membranes, which, apparently, can be facilitated by damage to the sulfhydryl groups of lung tissue proteins. Increased permeability is carried out with the participation of histamine, active globulins and other substances released or formed in the tissue when irritants act on it. Important in the regulation of capillary permeability belongs to nervous mechanisms. For example, the experiment showed 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 pathological 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 precede cellular infiltration.
The development of pulmonary edema causes disruption of gas exchange in the lungs. At the height of 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 and an increase in its viscosity. All these factors lead to insufficient oxygen supply to tissues - hypoxia. Accumulate in tissues sour foods metabolism, reserve alkalinity decreases and the pH shifts to the acidic side.
Clinically, two forms of toxic pulmonary edema are distinguished: developed, or complete, and abortive.
With a developed form, there is a sequential development of five periods:
- 1) initial phenomena (reflex stage);
- 2) latent period;
- 3) period of swelling increase;
- 4) period of completed edema;
- 5) reverse development of edema.
The abortive form is characterized by a change of four periods:
- 1) initial phenomena;
- 2) latent period;
- 3) increase in edema;
- 4) reverse development of edema.
In addition to the two main ones, there is another form of acute toxic pulmonary edema - the so-called “silent edema”, which is detected only by X-ray examination of the lungs, while clinical manifestations of pulmonary edema are practically absent.
The period of initial effects 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 impact on the well-being of the victim and soon pass.
The latent period begins after the subsidence of the phenomena of irritation and may have different duration(from 2 to 24 hours), more often 6-12 hours. During this period, the victim feels healthy, but with 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 lung tissue, therefore the lack of clear clinical manifestations does not yet indicate the absence of emerging pathology.
The period of increasing edema manifests itself clinically, which is associated with the accumulation of edematous fluid in the alveoli and a more pronounced disorder respiratory function. Victims experience increased breathing, it becomes shallow and is accompanied by paroxysmal, painful coughing. Objectively, slight cyanosis is noted. In the lungs, ringing, fine, moist rales and crepitus are heard. During X-ray examination in this period, one can note vagueness and blurriness of the pulmonary pattern, small branches are poorly differentiated blood vessels, there is some thickening of the interlobar pleura. The roots of the lungs are somewhat expanded and have unclear contours.
Identifying signs of increasing toxic pulmonary edema is very important to carry out appropriate treatment and preventive measures to prevent the development of edema.
The period of completed edema corresponds to 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 and pronounced shortness of breath are observed - up to 50-60 breaths per minute. In the distance, bubbling breathing can be heard. Cough with discharge large quantity foamy sputum, often mixed with blood. Upon auscultation, a mass of moist rales of various sizes is detected throughout the pulmonary fields. Tachycardia is noted, blood pressure remains normal or even increases slightly. When examining the blood, its significant thickening is revealed: the hemoglobin content increases to 100-120 g/l, erythrocytes to 6.0-8.0*1012/l, leukocytes to 10-15*109/l. Blood viscosity increases. Coagulability increases. The arterialization of blood in the lungs is impaired, which is manifested by a deficiency in arterial blood oxygen saturation with a simultaneous increase in carbon dioxide content (hypercapnic hypoxemia). Compensated gas 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. The face is covered with cold sweat. Extremities 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 carbon dioxide content (hypoxemia with hypocapnia). The coefficient of oxygen utilization and its arteriovenous difference decreases. The state of “Grey hypoxemia” may be preceded by a period of “blue hypoxemia”. Sometimes the process begins immediately, like “gray hypoxemia.” This can be facilitated by physical activity and long-term transportation of the victim.
Violations of cardio-vascular system in toxic pulmonary edema are caused by impaired blood flow in the pulmonary circulation with overload of the “acute” type pulmonary heart", as well as myocardial ischemia and autonomic changes. Regardless of the type of edema, in the stage of completed edema, an increase in blurring of the pulmonary pattern and the appearance in the lower and middle sections of initially small (2-3 mm) spotty shadows, which subsequently increase in size due to the merging of individual foci, forming vaguely contoured shadows resembling "flakes of melting snow." Areas of darkening alternate with clearing caused by developing foci of bullous emphysema. The roots of the lungs become even wider with unclear contours.
The transition from the period of increasing to full-blown pulmonary edema often occurs very quickly, characterized by a rapidly progressing course. Severe forms of pulmonary edema can lead to death after 24-48 hours. In milder cases and with timely intensive therapy, a period of reverse development of pulmonary edema begins.
During the reverse development of edema, the cough and the amount of sputum produced gradually decrease, and shortness of breath subsides. Cyanosis decreases, wheezing in the lungs weakens and then disappears. X-ray studies indicate the disappearance of first large, and then small focal shadows, only vagueness of the pulmonary pattern and 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 is normalized peripheral blood. Recovery can have significant variability in terms of time - from several days to several weeks.
Most a common complication Toxic pulmonary edema may involve infection and the development of pneumonia. During the period of subsidence of clinical manifestations of edema and improvement general condition, usually on the 3-4th day after poisoning, there is a rise in temperature to 38-39 ° C, the cough intensifies again with the release of sputum of a mucopurulent nature. Areas of fine-bubbly moist rales appear or increase in the lungs. Leukocytosis increases in the blood and ESR accelerates. X-rays reveal small pneumonic foci of the type of small focal pneumonia. To others serious complication Toxic edema is considered to be the so-called “secondary” pulmonary edema, which can develop at the end of the 2nd - middle of the 3rd week, as a consequence of advancing acute heart failure. In long-term follow-up after toxic pulmonary edema, the development of toxic pneumosclerosis and pulmonary emphysema is possible. An exacerbation of previously latent pulmonary tuberculosis and other chronic infections may occur.
In addition to changes in the lungs and cardiovascular system, changes in the nervous system are often found with toxic pulmonary edema. Victims complain about headache, dizziness. Relatively often, instability in the neuro-emotional sphere is detected: irritability, anxiety, the predominance of depressive-hypochondriacal reactions, in some victims - agitation and convulsions, and in severe cases- stupor, drowsiness, weakness, loss of consciousness. In the future, the addition of asthenoneurotic and autonomic disorders is possible.
At the height of toxic edema, diuresis sometimes decreases, up to anuria. Traces of protein, hyaline and granular casts, and red blood cells are found in the urine. These changes are associated with the possibility of developing toxic kidney damage caused by general vascular changes.
With pulmonary edema, liver damage is often observed - some enlargement of the organ, changes in functional liver tests like toxic hepatitis. These changes in the liver can persist for quite a long time, often combined with functional disorders gastrointestinal tract.
Poisoning with poisons is always unpleasant, but among all possible complications toxic pulmonary edema is one of the most dangerous. In addition to a high chance of death, this is a defeat respiratory system has a lot serious consequences. It most often takes at least a year to achieve full recovery from illness.
How does pulmonary edema form?
Pulmonary edema begins in the same way as similar damage to other organs. The difference is that the liquid penetrates freely through the easily permeable tissue of the alveoli.
Accordingly, swelling of the lung, the same as, for example, with edema of the lower extremities, does not occur. Instead, liquid begins to accumulate in internal cavity alveoli, which normally serves to fill with air. As a result, the person gradually suffocates, and oxygen starvation causes serious damage to the kidneys, liver, heart and brain.
The peculiarity of toxic pulmonary edema is that the cause of this disease, instead of the disease, is poison. Toxic substances destroy organ cells, contributing to the filling of the alveoli with fluid. It can be:
- carbon monoxide;
- chlorine;
- and diphosgene;
- oxidized nitrogen;
- hydrogen fluoride;
- ammonia;
- vapors of concentrated acids.
That's it for the list possible reasons toxic pulmonary edema is not limited. Most often, people with this diagnosis end up in the hospital due to non-compliance with safety precautions, as well as in the event of accidents at work.
Symptoms and stages of the disease
Depending on how the disease progresses, there are three types of edema:
- Developed (completed) form. In this case, the disease goes through 5 stages: reflex, latent, period of increasing swelling, completion and reverse development.
- Abortive form. It is distinguished by the absence of the most difficult stage of completion.
- “Silent” edema is a hidden, asymptomatic type of the disease. It can only be determined by chance using an x-ray examination.
After inhaling the poison, the body becomes intoxicated, and the initial period of disease development begins—the reflex stage. It lasts from ten minutes to several hours. At this time, classic symptoms of mucous irritation and poisoning appear:
- cough and sore throat;
- pain in the eyes and lacrimation due to contact with toxic gases;
- the appearance of copious discharge from the nasal mucosa.
Also, the reflex stage is characterized by the appearance of chest pain and difficulty breathing, weakness and dizziness occur. In some cases, they are accompanied by disturbances in the digestive system.
Next comes the hidden period. At this time, the symptoms listed above disappear, the person feels much better, but upon examination, the doctor may note bradycardia, rapid shallow breathing and a drop in blood pressure. This condition lasts from 2 to 24 hours, and the longer it is, the better for the patient.
In severe intoxication, the latent period of pulmonary edema may be completely absent.
When the calm is over, a rapid increase in symptoms begins. Appears paroxysmal cough, breathing becomes very difficult and the person suffers from shortness of breath. Cyanosis, tachycardia and hypotension develop, even greater weakness sets in, and pain in the head and chest intensifies. This stage of toxic pulmonary edema is called the growth period; from the outside it is easy to recognize due to the wheezing that occurs when the patient breathes. At that time chest cavity gradually fill with foamy sputum and blood.
The next period is the end of the swelling. It is characterized by the maximum manifestation of the symptoms of the disease and has 2 forms:
- "Blue" hypoxemia. Due to suffocation, a person rushes about and tries to breathe harder. He is very excited, moans, and his consciousness is clouded. The body reacts to swelling by turning blue, pulsating blood vessels, and secreting pinkish foam from the mouth and nose.
- "Gray" hypoxemia. It is considered more dangerous for the patient. Because of sharp deterioration the activity of the cardiovascular and respiratory systems collapses. The breathing and heart rate noticeably decrease, the body becomes colder, and the skin takes on an earthy tint.
If a person was able to survive toxic pulmonary edema, then last stage– reverse development: gradually cough, shortness of breath and sputum production recede. A long rehabilitation period begins.
Consequences of pulmonary edema
Despite the fact that the disease itself often ends in the death of the patient within 2 days, it can also occur with complications. Among them, the consequences of a toxic lung burn can be:
- Airway obstruction. It occurs when excessive foam is produced and greatly impairs gas exchange.
- Respiratory depression. When intoxicated, some poisons can additionally affect respiratory center brain, negatively affecting lung function.
- Cardiogenic shock. Due to edema, failure of the left ventricle of the heart develops, as a result of which blood pressure drops significantly and disrupts the blood supply to all organs, including the brain. In 9 out of 10 cases, cardiogenic shock is fatal.
- Fulminant form of pulmonary edema. This complication lies in the fact that all stages of the disease are compressed in time to a few minutes due to concomitant diseases of the liver, kidneys and heart. It is almost impossible to save the patient.
Even if a person managed to survive the complication, it is far from certain that everything will end full recovery. The disease may return in the form of secondary pulmonary edema.
In addition, due to the weakening of the body as a result of the stress suffered, other consequences may appear. Most often they are expressed through the development of other diseases:
- Pneumosclerosis. Damaged alveoli become overgrown and scarred, losing their elasticity. If a small number of cells are affected in this way, the consequences are almost unnoticeable. But with the widespread spread of the disease, the gas exchange process greatly deteriorates.
- Bacterial pneumonia. When bacteria enter weakened lung tissue, microorganisms begin to actively develop, causing inflammation. Its symptoms are fever, weakness, shortness of breath, cough with expectoration of blood and purulent sputum.
- Emphysema. This disease develops due to the expansion of the tips of the bronchioles, causing additional damage to the walls of the alveoli. A person's chest swells and makes a boxy sound when tapped. Another characteristic symptom- shortness of breath.
In addition to these diseases, pulmonary edema can provoke an exacerbation of other chronic ailments, including tuberculosis. Also, against the backdrop of deteriorating oxygen supply to tissues, the cardiovascular and central nervous systems, liver and kidneys suffer greatly.
Diagnosis and treatment
After intoxication, the development of the disease is determined by physical examination and radiography. These 2 diagnostic methods provide enough information for treatment, but in the final stages you cannot do without an ECG to monitor the condition of the heart.
If pulmonary edema has been controlled, then laboratory tests of blood (general and biochemical) and urine, and liver tests are taken. This is necessary to determine the damage caused to the body and prescribe treatment.
First aid for toxic pulmonary edema is to ensure rest and sedative injections. To restore breathing, oxygen inhalations are performed through alcohol solution to extinguish foam. To reduce swelling, you can apply tourniquets to the limbs and use the bloodletting method.
For treatment, doctors resort to the following set of medications:
- Steroids;
- Diuretics;
- Bronchodilators;
- Glucose;
- Calcium chloride;
- Cardiotonics.
As edema progresses, tracheal intubation and connection to a device may also be required. artificial respiration. After relief of symptoms, it is important to take a course of antibiotics to prevent bacterial infection. On average, rehabilitation after an illness takes about 1-1.5 months, and the chance of becoming disabled is very high.
Actually, toxic pulmonary edema is associated with damage by toxicants to cells involved in the formation of the alveolar-capillary barrier.
The main cause of disorders of many body functions in case of poisoning with pulmonary toxicants is oxygen starvation. Oxygen starvation that develops when affected by asphyxiants can be characterized as hypoxia mixed type: hypoxic(violation external respiration), circulatory (hemodynamic disturbances), fabric(impaired tissue respiration).
Hypoxia underlies severe disorders of energy metabolism. In this case, organs and tissues with a high level of energy expenditure (nervous system, myocardium, kidneys, lungs) suffer the most. Violations of these organs and systems form the basis of the clinical picture of intoxication of OVTV pulmonary toxic effect.
The mechanism of damage to lung tissue cells by asphyxiating toxic substances with a pulmonary toxic effect is not the same, but the subsequent processes that develop are quite similar (Fig. 2).
Figure 2. Scheme of the pathogenesis of toxic pulmonary edema
Cell damage and death leads to increased barrier permeability and biological metabolic disorders active substances in the lungs. The permeability of the capillary and alveolar parts of the barrier does not change simultaneously. Initially, the permeability of the endothelial layer increases, and vascular fluid sweats into the interstitium, where it temporarily accumulates. This phase of the development of pulmonary edema is called interstitial. During the interstitial phase, lymphatic drainage accelerates compensatoryly. However, this adaptive reaction turns out to be insufficient, and the edematous fluid gradually penetrates the layer of destructively altered alveolar cells into the alveolar cavities, filling them. This phase of the development of pulmonary edema is called alveolar and is characterized by the appearance of distinct clinical signs. “Switching off” part of the alveoli from the gas exchange process is compensated by stretching of intact alveoli (emphysema), which leads to mechanical compression of the capillaries of the lungs and lymphatic vessels.
Cell damage is accompanied by the accumulation in the lung tissue of biologically active substances such as norepinephrine, acetylcholine, serotonin, histamine, angiotensin I, prostaglandins E 1, E 2, F 2, kinins, which leads to an additional increase in the permeability of the alveolar-capillary barrier and impaired hemodynamics in the lungs . The speed of blood flow decreases, the pressure in the pulmonary circulation increases.
The edema continues to progress, fluid fills the bronchioles, and due to the turbulent movement of air in the respiratory tract, foam is formed, stabilized by washed away alveolar surfactant.
In addition to these changes, for the development of pulmonary edema great importance have systemic disorders that are included in the pathological process and intensify as it develops. The most important include: disturbances in the gas composition of the blood (hypoxia, hyper-, and then hypocarbia), changes in the cellular composition and rheological properties (viscosity, coagulation ability) of the blood, hemodynamic disorders in the systemic circulation, dysfunction of the kidneys and the central nervous system.
Pathogenesis. The lung parenchyma is formed a huge amount alveoli Alveoli are thin-walled microscopic cavities that open into the terminal bronchiole. Several hundred alveoli closely adjacent to each other form a respiratory unit - the acinus.
The alveoli carry out gas exchange between inhaled air and blood. The essence of gas exchange is the diffusion of oxygen from the alveolar air into the blood and carbon dioxide from the blood into the alveolar air. The driving force of the process is the difference in the partial pressures of gases in the blood and alveolar air.
The barrier to the path of diffusing gases in the lungs is the aerohematic barrier. The barrier consists of 1) an alveolocyte of the first order, 2) an interstitial space - the space between two basement membranes, filled with fibers and interstitial fluid, and 3) capillary endothelial cells (endotheliocytes).
Alveolar epithelium is formed by cells three types. Type 1 cells are highly flattened structures lining the alveolar cavity. It is through these cells that gases diffuse. Type 2 alveolocytes are involved in the exchange of surfactant, a surfactant contained in the fluid lining the inner surface of the alveoli. By reducing the surface tension of the walls of the alveoli, this substance does not allow them to collapse. Type 3 cells are pulmonary macrophages that phagocytose foreign particles that enter the alveoli.
Water balance fluid in the lungs is normally provided by two mechanisms: regulation of pressure in the pulmonary circulation and the level of oncotic pressure in the microvasculature.
Damage to alveolocytes leads to disruption of the synthesis, secretion and deposition of surfactant, increased permeability of the alveolar-capillary barrier, and increased exudation of edematous fluid into the alveolar lumen. In addition, it should be remembered that one of the “non-respiratory” functions of the lungs is the metabolism of vasoactive substances (prostaglandins, bradykinins, etc.) by capillary endothelial cells. Damage to the endothelial cell leads to the accumulation of vasoactive substances in the microvasculature, which, in turn, causes an increase in hydrostatic pressure. These hemodynamic disturbances in the lungs alter normal ratio ventilation and hemoperfusion.
Depending on the rate of pulmonary edema, pulmonary toxicants are divided into substances that cause “fast type” and “delayed type” edema. It is based on differences in the triggering links of pathogenesis.
Pathogenesis of “slow” type edema. Damage to the airborne barrier leads to increased barrier permeability. The permeability of the capillary and alveolar parts of the barrier does not change simultaneously. Initially, the permeability of the endothelial layer increases, and vascular fluid sweats into the interstitium, where it temporarily accumulates. This phase of the development of pulmonary edema is called interstitial. During the interstitial phase, lymphatic drainage is compensatory, approximately 10 times accelerated. However, this adaptive reaction turns out to be insufficient, and the edematous fluid gradually penetrates the layer of destructively altered alveolar cells into the alveolar cavities, filling them. This phase of the development of pulmonary edema is called alveolar and is characterized by the appearance of distinct clinical signs.
Already in the early stages of the development of toxic pulmonary edema, the pattern (depth and frequency) of breathing changes. An increase in the volume of the interstitial space leads to the fact that less than usual stretching of the alveoli during inspiration serves as a signal to stop inhalation and begin exhalation (activation of the Hering-Breuer reflex). At the same time, breathing becomes more frequent and its depth decreases, which leads to a decrease in alveolar ventilation. Breathing becomes ineffective, hypoxic hypoxia increases.
As the edema progresses, fluid fills the bronchioles. Due to the turbulent movement of air in the respiratory tract, foam is formed from edematous fluid rich in protein and surfactant fragments.
Thus, the pathogenetic essence of pulmonary edema is an increase in hydration of the lung tissue. Pulmonary edema has two phases in its development: 1) the release of blood plasma into the interstitial space - the interstitial phase, and then 2) the alveolar phase develops - fluid breaks into the lumen of the alveoli and the respiratory tract. Foamed edematous fluid fills the lungs, and a condition develops that was previously referred to in therapy as “drowning on land.”
Features of the “fast” type of edema are that the membrane of alveolocytes and endothelial cells is damaged. This leads to a sharp increase in the permeability of the barrier to interstitial fluid, which quickly fills the cavity of the alveoli (the alveolar phase begins faster). Edema fluid with rapid type edema contains more protein and fragments of surfactant, which closes the “ vicious circle": edematous fluid has a high osmotic pressure, which increases the flow of fluid into the lumen of the alveoli.
Significant changes in pulmonary edema are observed in the peripheral blood. As edema increases and vascular fluid enters the interstitial space, the content of hemoglobin increases (at the height of edema it reaches 200-230 g/l) and red blood cells (up to 7-9 1012/l), which can be explained not only by blood thickening, but also exit shaped elements from the depot (one of the compensatory reactions to hypoxia).
Gas exchange in the lungs becomes difficult when any element of the airborne barrier - alveolocytes, endothelial cells, interstitium - is damaged. As a result of gas exchange disturbances, hypoxic hypoxia (oxygen starvation) develops. Impaired gas exchange is the main cause of death in those affected.
Clinic. In severe cases, the course of damage to pulmonary toxicants can be divided into 4 periods: the period of contact, the latent period, the development of toxic pulmonary edema, and in a favorable course - the period of resolution of edema.
During the period of contact, the severity of manifestations depends on the irritant effect of the substance and its concentration. In small concentrations at the moment of contact, irritation usually does not occur. With increasing concentration, unpleasant sensations appear in the nasopharynx and behind the sternum, difficulty breathing, drooling, and coughing. These phenomena disappear when contact is stopped.
The latent period is characterized by a subjective feeling of well-being. Its duration for substances of “slow” action is on average 4-6-8 hours. For substances of “fast” action, the latent period usually does not exceed 1-2 hours. The duration of the latent period is determined by the dose of the substance (concentration and duration of exposure), so possible and a sharp reduction in the latent period (less than 1 hour) and an increase to 24 hours. Pathogenetically latent period corresponds to the interstitial phase.
The main manifestations of intoxication are observed during the period of toxic pulmonary edema, when edematous fluid enters the alveoli (alveolar phase). Shortness of breath gradually increases to 50-60 breaths per minute (normally 14-16). The shortness of breath is inspiratory in nature. A painful persistent cough appears that does not bring relief. Gradually, a large amount of foamy sputum begins to be released from the mouth and nose. Moist rales of various calibers are heard: “bubbling breathing.” As swelling increases, fluid fills not only the alveoli, but also the bronchioles and bronchi. Edema reaches its maximum development by the end of the first day.
Conventionally, two periods are distinguished during edema: the period of “blue” hypoxia and the period of “gray” hypoxia. The skin acquires a bluish color as a result of hypoxia, and in extremely severe cases, as a result of decompensation of the cardiovascular system, the blue color changes to an ash-gray, “earthy” color. Pulse slow. Blood pressure drops.
Pulmonary edema typically peaks 16 to 20 hours after exposure. At the height of the edema, death of the affected people is observed. Mortality during the development of the alveolar stage of edema is 60-70%.
The cause of death is acute hypoxia of mixed origin: 1) hypoxic - a sharp decrease in the permeability of the airborne barrier as a result of edema, foaming of edematous fluid in the lumen of the terminal sections bronchial tree; 2) circulatory - development of acute decompensated cardiovascular failure in conditions of acute myocardial hypoxia (“gray” hypoxia); violation of the rheological properties of blood (“thickening”) as a result of pulmonary edema.
Principles of prevention and treatment. To stop further entry of the toxicant into the body, the affected person puts on a gas mask. It is necessary to immediately evacuate those affected from the outbreak. All persons brought from affected areas by pulmonary toxicants are subject to active medical supervision for a period of at least 48 hours. Clinical diagnostic studies are periodically carried out.
There are no antidotes for pulmonary toxicants.
In case of severe irritation of the respiratory tract, the drug ficillin, a mixture of volatile anesthetics, can be used.
Providing assistance with developing toxic pulmonary edema includes the following areas:
1) reduction of oxygen consumption: physical rest, temperature comfort, prescription of antitussives ( exercise stress, persistent cough, shivering thermogenesis increases oxygen consumption);
2) oxygen therapy - oxygen concentration should be no more than 60% to prevent lipid peroxidation in compromised membranes;
3) inhalation of antifoaming agents: antifomsilan, solution ethyl alcohol;
4) decrease in circulating blood volume: forced diuresis;
5) “unloading” of the small circle: ganglion blockers;
6) inotropic support (stimulation of cardiac activity): calcium supplements, cardiac glycosides;
7) “stabilization” of airborne barrier membranes: inhalation glucocorticoids, pro-oxidants.
Question 20
CHLORINE
It is a greenish-yellow gas with a strong irritating odor, consisting of diatomic molecules. Under normal pressure it solidifies at -101°C and liquefies at -34°C. Density of chlorine gas at normal conditions is 3.214 kg/m 3, i.e. it is approximately 2.5 times heavier than air and, as a result, accumulates in low areas, basements, wells, and tunnels.
Chlorine is soluble in water: about two volumes of it are dissolved in one volume of water. The resulting yellowish solution is often called chlorine water. Its chemical activity is very high - it forms compounds with almost all chemical elements. The main industrial method of production is electrolysis of a concentrated solution sodium chloride. The annual consumption of chlorine in the world amounts to tens of millions of tons. It is used in the production of organochlorine compounds (for example, vinyl chloride, chloroprene rubber, dichloroethane, perchlorethylene, chlorobenzene), and inorganic chlorides. Used in large quantities for bleaching fabrics and paper pulp, disinfection drinking water, How disinfectant and in various other industries (Fig. 1). Chlorine under pressure liquefies even at ordinary temperatures. It is stored and transported in steel cylinders and railway tanks under pressure. When released into the atmosphere, it smokes and contaminates water bodies.
First world war used as a toxic agent with an asphyxiating effect. Affects the lungs, irritates mucous membranes and skin. The first signs of poisoning are sharp chest pain, pain in the eyes, lacrimation, dry cough, vomiting, loss of coordination, shortness of breath. Contact with chlorine vapor causes burns to the mucous membrane of the respiratory tract, eyes, and skin.
The minimum perceptible concentration of chlorine is 2 mg/m3. Irritant effect occurs at a concentration of about 10 mg/m3. Exposure to 100 - 200 mg/m 3 chlorine for 30 - 60 minutes is life-threatening, and more high concentrations can cause instant death.
It should be remembered that the maximum permissible concentrations (MPC) of chlorine in the atmospheric air are: average daily - 0.03 mg/m 3 ; maximum single dose - 0.1 mg/m3; in the working area of an industrial enterprise - 1 mg/m3.
The respiratory organs and eyes are protected from chlorine by filtering and insulating gas masks. For this purpose, filtering gas masks of industrial grade L can be used (the box is painted in Brown color), BKF and MKF (protective), V (yellow), P (black), G (black and yellow), as well as civilian GP-5, GP-7 and children's.
The maximum permissible concentration when using filter gas masks is 2500 mg/m 3 . If it is higher, only self-containing gas masks should be used. When eliminating chemical accidents dangerous objects when the chlorine concentration is unknown, work is carried out only in insulating gas masks (IP-4, IP-5). In this case, you should use protective rubber suits, rubber boots, and gloves. It must be remembered that liquid chlorine destroys the rubberized protective fabric and rubber parts of the insulating gas mask.
In the event of an industrial accident at a chemically hazardous facility, or a leak of chlorine during storage or transportation, air contamination may occur in damaging concentrations. In this case, it is necessary to isolate the dangerous area, remove all strangers from it and prevent anyone from entering without respiratory and skin protection. Near the zone, stay to the windward side and avoid low places.
If there is a chlorine leak or spill, do not touch the spilled substance. The leak should be removed with the help of specialists, if this does not pose a danger, or the contents should be pumped into a working container while observing safety precautions.
For severe chlorine leaks, use a spray of soda ash or water to precipitate the gas. The spill site is filled with ammonia water, lime milk, a solution of soda ash or caustic soda.
AMMONIA
Ammonia (NH 3) is a colorless gas with a characteristic pungent odor (ammonia). Under normal pressure it solidifies at -78°C and liquefies at -34°C. The density of ammonia gas under normal conditions is approximately 0.6, i.e. it is lighter than air. Forms explosive mixtures with air in the range of 15 - 28 volume percent NH.
Its solubility in water is greater than that of all other gases: one volume of water absorbs about 700 volumes of ammonia at 20°C. A 10% ammonia solution is marketed under the name “ ammonia" It is used in medicine and in the household (for washing clothes, removing stains, etc.). An 18 - 20% solution is called ammonia water and is used as a fertilizer.
Liquid ammonia is a good solvent large number organic and inorganic compounds. Liquid anhydrous ammonia is used as a highly concentrated fertilizer.
In nature, NH is formed during the decomposition of nitrogen-containing organic
substances. Currently, synthesis from elements (nitrogen and hydrogen) in the presence of a catalyst, at a temperature of 450 - 500 ° C and a pressure of 30 MPa, is the main industrial method for producing ammonia.
Ammonia water is released when coke oven gas comes into contact with water, which condenses when the gas is cooled or is specially injected into it to wash out ammonia.
World production of ammonia is about 90 million tons. It is used in the production of nitric acid, nitrogen-containing salts, soda, urea, hydrocyanic acid, fertilizers, and diazotype photocopying materials. Liquid ammonia is used as a working substance in refrigeration machines (Fig. 2). Ammonia is transported in a liquefied state under pressure, when released into the atmosphere it smokes, and contaminates water bodies when it enters them. Maximum permissible concentrations (MPC) in the air of populated areas: average daily and maximum one-time - 0.2 mg/m 3 ; the maximum permissible in the working area of an industrial enterprise is 20 mg/m 3 . The odor is felt at a concentration of 40 mg/m3. If its content in the air reaches 500 mg/m 3, it is dangerous for inhalation (possible death). Causes damage to the respiratory tract. Its signs are: runny nose, cough, difficulty breathing, suffocation, while palpitations appear and the pulse rate is disturbed. The vapors strongly irritate the mucous membranes and skin, causing burning, redness and itching of the skin, pain in the eyes, and lacrimation. When liquid ammonia and its solutions come into contact with the skin, frostbite, burning, and possible burns with blisters and ulcerations occur.
Respiratory protection from ammonia is provided by filtering industrial and insulating gas masks and gas respirators. Industrial gas masks of the KD brand can be used (the box is painted in grey colour), K (light green) and respirators RPG-67-KD, RU-60M-KD.
The maximum permissible concentration when using filtering industrial gas masks is 750 MPC (15,000 mg/m!), above which only insulating gas masks should be used. For respirators, this dose is equal to 15 MAC. When eliminating accidents at chemically hazardous facilities, when the concentration of ammonia is unknown, work should be carried out only in insulating gas masks.
To prevent ammonia from getting on your skin, you should use protective rubber suits, rubber boots and gloves.
The presence and concentration of ammonia in the air can be determined by the universal gas analyzer UG-2. Measurement limits: up to 0.03 mg/l - when sucking air in a volume of 250 ml; up to 0.3 mg/l - when sucking 30 ml. The NH concentration is found on a scale indicating the volume of air passed through. The number that coincides with the border of the blue-colored column of powder will indicate the concentration of ammonia in milligrams per liter.
You can also find out whether there is ammonia vapor in the air using chemical reconnaissance devices VPKhR, PKhR-MV. When pumped through a marked indicator tube (one yellow ring) at a concentration of 2 mg/l or higher, ammonia turns the filler light green.
Devices latest modifications such as UPGK (universal gas monitoring device) and photoionization gas analyzer Kolion-1 allow you to quickly and accurately determine the presence and concentration of ammonia.
Toxicological characteristics of nitrogen oxides: physicochemical characteristics, toxicity, toxicokinetics, mechanism of toxic action, forms of toxic process,
Pulmonary toxicants + general toxic effects
Gases are part of explosive gases formed during shooting, explosions, missile launches, etc.
Highly toxic. Inhalation poisoning.
Oxide poisoning: reversible form - methemoglobin formation, shortness of breath, vomiting, drop in blood pressure.
Poisoning with a mixture of oxide and dioxide: suffocating effect with the development of pulmonary edema;
Dioxide poisoning: nitrite shock and chemical burn lungs;
The mechanism of toxic action of nitric oxide:
Activation of lipid peroxidation in biomembranes,
Formation of nitric and nitrous acids when interacting with water,
Oxidation of low molecular weight elements antioxidant system,
Mechanism of toxic action of nitrogen dioxide:
Initiation of lipid peroxidation in the biomembranes of airborne barrier cells,
The denaturing ability of nitric acid formed in the aqueous environment of the body,
Maintenance high level free radical processes in the cell,
The formation of a hydroxyl radical during a reaction with hydrogen peroxide, causing an uncontrolled increase in peroxidation in the cell.
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