Carbon monoxide message on obh. General characteristics of the so. Carbon monoxide. Leak of gas

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Carbon monoxide is a product of incomplete combustion of various types of fuel, wood, garbage, etc. This gas is odorless, colorless, does not irritate the eyes and therefore cannot be felt.

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Why is this gas so dangerous?

It replaces oxygen in the blood. As a result, the blood carries too little oxygen to supply the tissues of the body. Inhaling even a small amount of it can cause severe discomfort and, in some cases, death.

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Know when there is danger

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Carbon monoxide enters the atmospheric air during any type of combustion

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POISONING IS POSSIBLE

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IN THE FIRE

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When you are on or near a busy road for a long time (on major highways, the average gas concentration exceeds the poisoning threshold).

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Having closed the stove damper before burning firewood, coal (in a house with stove heating or a bathhouse).

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In winter, in the cabin of cars with a faulty internal combustion engine, when people are trying to warm up in the cabin, waiting for something. They fall asleep and don't wake up anymore.

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Poisoning is most likely in garages with poor ventilation, in other unventilated or poorly ventilated rooms, tunnels, since this gas is contained in the exhaust of a car.

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At home, if a lamp gas leaks, a faulty gas oven in an unventilated room.

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Carbon monoxide poisoning occurs due to violation of the rules for the operation of gas appliances, stove heating and neglect of basic life safety rules.

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The main signs and symptoms of carbon monoxide poisoning are headache, nausea; dyspnea; confusion; muscle weakness; red complexion; prolonged exposure to carbon monoxide can lead to death.

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immediately get out into fresh air and call an ambulance - check if the gas equipment is turned off and open the windows. Never turn on a light or fire - this may provoke an explosion. -On the street, call the fire department or gas network repair service

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If you are caring for a poisoning victim

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Make sure that you have support (someone is waiting for you on the street and is ready to help you) - entering the premises you can become a victim of poisoning yourself - Entering the premises where the victim is located - open windows and doors, do not turn on lights or fires -Try to take the victim out to the street as soon as possible, put him on his back, free him from tight clothes, let him smell the ammonia. - if the victim is not breathing, urgently start artificial respiration - call an ambulance

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Saint Petersburg State Medical University

named after academician I.P. Pavlova

Department of Mobilization Preparation of Health Care and Extreme Medicine

"Carbon monoxide poisoning"

Completed:

Checked:

St. Petersburg

Introduction 3

General characteristics of CO 5

Pathophysiology 6

Clinical manifestations 13

Laboratory and instrumental diagnostics 15

High-risk patient groups

disability or death due to CO 17 poisoning

First aid for carbon monoxide poisoning 17 Medical aid for CO poisoning 17

Forecast 20

Conclusion 21

References 22

Introduction

“I feel bad, my head is splitting. Look, and the dog is sick. We probably ate something. Nothing, everything will pass. No need to disturb anyone. " These were the last words spoken on September 28, 1902 by the great French writer who died of carbon monoxide poisoning due to a malfunctioning oven in his Paris apartment.

Emil Zola said this to his wife. 1

Carbon monoxide (CO) is one of the most common poisonous gases in nature, polluting the environment in today's energy-intensive world. The main source of CO is incomplete combustion of fossil fuels, especially coal. Exhaust gases are one of the main sources of CO formation in the environment. Its next source is cigarette smoke containing 3-6% CO, which is 8 times higher than its permissible concentration in the air of industrial facilities. People are especially susceptible to CO poisoning in enclosed spaces. Passive inhalation of cigarette smoke contributes to the poisoning of nonsmokers; it is especially dangerous for children and pregnant women.

Carbon monoxide is the most common industrial poison and is found wherever there are processes of incomplete combustion of carbon. The danger of worker CO poisoning exists in blast-furnace, open-hearth, forge, foundry, thermal shops, when working on vehicles (exhaust gases contain significant amounts of CO), in chemical plants where carbon monoxide is a raw material (synthesis of phosgene, ammonia, methanol, etc.) ).

In recent years around the world, due to severe winters and an energy crisis, the number of different household heating sources has increased, which, in the absence of adequate ventilation, significantly increases the possibility of CO poisoning. Such poisoning often occurs in everyday life: while taking a bath, while cooking in dishes with a large bottom surface. With poor oxygen access, incomplete combustion occurs, resulting in the formation of CO from carbon compounds contained in natural gas. There is a belief that natural gas is completely safe and does not emit into the atmosphere during combustion, which means that there is no threat of poisoning. However, combustion does not at all mean that natural gas evolution is impossible. Ventilation pipes can often become clogged, or an extractor hood over the gas stove can be installed.

Carbon monoxide is a ubiquitous product of incomplete combustion of coal and other fuels - gas, gasoline. Since CO is odorless, colorless, tasteless, non-irritating and easily mixes with air, and spreads unhindered, it has been called the “silent killer”. It is very often difficult to recognize the potential danger, therefore, CO poisoning emitted from furnaces (the so-called fumes) is often encountered when the damper is closed prematurely, there are cracks in the furnace, or even as a result of the release of CO from red-hot parts of gas columns.

Carbon monoxide is also a component of various industrial gases that are emitted from blast furnaces in coke plants and electric boilers.

General characteristics with

Carbon monoxide is a colorless and odorless gas, lighter than air (relative density by air 0.97), liquefies at a temperature of -191.5 ° C, freezes at a temperature of -204 ° C. Slightly soluble in water and blood plasma (volume fraction about 2%). Poorly absorbed by activated carbon, silica gel. Carbon monoxide forms an explosive mixture with air (volume fraction in the range of 16.2-73.4%). It can combine with some metals to form carbonyls (Ni (CO) 4), which decompose in the presence of a catalyst with the release of CO and metal. 2

CO is formed during incomplete combustion of almost any carbon-containing substance, including fuel for heating premises, as well as in large quantities during fires in buildings. The peak of CO poisoning is observed in autumn and winter, when heating devices are widely used. Intentional or accidental poisoning by car exhaust gases and inhalation of smoke during residential fires is the second most common cause of CO intoxication.

A unique source of CO is methylene chloride, a solvent found in paint strippers. It is formed from inhaled methylene chloride during metabolism in the liver.

Sources and conditions of the toxic effect of CO:

Smoke from burning organic materials (such as cigarettes)

Defective heating devices (fireplaces, heaters, hot water heaters), which use various types of fuel (wood, coal, fuel oil, kerosene, propane

Emissions from indoor gasoline, diesel, propane fueled devices (power generators, automobiles, forklift trucks, ice filling machines)

Methylene chloride (paint remover).

Carbon monoxide was first produced by the French chemist Jacques de Lasson in 1776 by heating zinc oxide with coal, but was initially mistaken for hydrogen because it burned with a blue flame. The fact that this gas includes carbon and oxygen was discovered in 1800 by the English chemist William Crookshank. Carbon monoxide outside the Earth's atmosphere was first discovered by the Belgian scientist M. Migeotte in 1949 by the presence of the main vibrational-rotational band in the IR spectrum of the Sun.

Carbon monoxide (CO) has never been used as an independent poisonous substance, but no war has passed without poisoning with this gas. Carbon monoxide poisoning also consistently ranks high in the statistics of acute poisoning in the Armed Forces during peacetime. At the end of World War II, the Allies bombed fascist cities with napalm: within literally one night, Hamburg, Dresden, and Kassel were burned to the ground. When they later analyzed the cause of the deaths, it turned out that 60% of the townspeople died from carbon monoxide poisoning.

Pathophysiology

CO has several mechanisms of toxic action. It is capable of disrupting the delivery of oxygen to tissues, its utilization and, possibly, provoking the onset of oxidative stress. High-affinity binding of CO with hemoglobin (and the affinity of hemoglobin for carbon monoxide is 200-250 times higher than for oxygen) leads to: 1) the formation of carboxyhemoglobin (HbCO), 2) the replacement of oxygen in hemoglobin and a decrease in the oxygen-transporting capacity of the blood, and also 3) displacement of the oxyhemoglobin dissociation curve to the left. In addition, CO is able to bind to other heme-containing proteins, for example, myoglobin and some cytochromes, which play a leading role in the production of energy by cells. However, to date, it has not been established how clinically significant such an interaction is. According to the latest experimental data, CO triggers a cascade of reactions, including lipid peroxidation in the brain, which causes temporary and irreversible dysfunction.

A classic example of a damaging effect on blood with a violation of its respiratory function due to the inactivation of the blood pigment - hemoglobin, is the formation of carboxyhemoglobin (HbCO) under the influence of carbon monoxide. The transformation of hemoglobin into HbCO leads to a change in the spectral characteristics of blood, which formed the basis for its quantitative determination in blood. HbCO is formed as a result of the interaction of carbon monoxide (CO) with the iron of hemoglobin, which deprives it of the ability to oxygenate, leads to impaired transport function and, as a result, causes the development of hemic hypoxia. The appearance of HbCO is a consequence of the entry of CO into the lungs with the inhaled air. The formation of HbCO begins from the periphery of erythrocytes already in the pulmonary capillaries. Subsequently, with an increase in the CO content in the inhaled air, HbCO is formed not only in the peripheral parts of the erythrocyte, but also in its central parts. Moreover, the rate of HbCO formation is directly proportional to the CO concentration in the inhaled air, and its maximum in the blood is determined by the contact time. The ability of hemoglobin to bind O 2 and CO is the same, provided that 1 g of hemoglobin can bind 1.53-1.34 ml of O 2.

This dependence is called the Hufner constant. At the same time, the affinity of hemoglobin for CO is 250-300 times higher than for O 2. It is noteworthy that the erythrocyte membrane serves as a kind of protective barrier in the formation of HbCO, since in the suspension of erythrocytes of this derivative of hemoglobin is formed by 20% less than in the solution of hemoglobin. The valence of iron in HbCO remains unchanged, only the rearrangement of the Fe 2+ bonds occurs. All unpaired electrons participate in the formation of HbCO. In parallel with the formation of bonds between CO and Fe 2+, the nature of the bond of iron with globin and porphyrin changes. It loses its ionic character and becomes covalent. Interaction of CO with HbO 2 expressed by mutually conjugated reactions.

HbO 2 + CO → HbCO + O 2

HbCO + O 2 → HbO 2 + CO

The rate of these reactions and the formation of HbCO are determined by the partial pressure of CO and O 2 in air. In this case, the amount of HbCO formed is proportional to the CO pressure in the environment and inversely proportional to the O 2 pressure. Despite the high, as mentioned above, the affinity of CO for hemoglobin, its association with hemoglobin occurs 10 times slower than that with O 2. However, in this case, the dissociation of HbCO proceeds 3600 times slower than the dissociation of HbO 2. For this reason, CO accumulates very quickly in the blood even with a relatively low CO content in the inhaled air. Thus, in addition to turning off part of hemoglobin from oxygen transport, another pathogenetic link in the violation of the respiratory function of the blood against the background of carboxyhemoglobinemia is a slowdown in the dissociation of oxyhemoglobin under the influence of HbCO, which is known as the Holden effect. So, under physiological conditions, an increase in the concentration of CO 2 in the blood promotes the accelerated elimination of O 2 from HbO 2, in the presence of HbCO this balanced process is disturbed. It is generally accepted that the essence of the Holden effect lies in the fact that when CO interacts with hemoglobin, CO entering the blood is combined with only 3 out of 4 iron atoms in the hemoglobin molecule, while O 2 combines with the 4th iron atom, whose affinity for this atom iron increases sharply, which, naturally, complicates the dissociation of oxyhemoglobin. Another causal factor for the inhibition of dissociation of НbO 2 under the influence of CO is a decrease in the level of the intermediate metabolite 2,3-diphosphoglycerate, which is formed during the glycolysis reaction. 2,3-diphosphoglycerate has the ability to enhance the process of dissociation of HbCO due to the conformational changes in hemoglobin caused by it, therefore, it is natural that the deficiency of this metabolite indirectly inhibits the release of O 2 from HbO 2. 3

So, the main triggering mechanism for the development of specific hemic hypoxia in CO poisoning is the formation of HbCO, which loses its ability to carry oxygen in combination with a depressing effect on the dissociation of HbO 2. Irrefutable evidence that carboxyhemoglobinemia is the primary cause of CO intoxication is a direct relationship between the level of HbCO in the blood and the severity of intoxication. So, according to VEHenderson 4, when the content of HbCO in the blood is equal to 10%, only shortness of breath with physical exertion is noted, with 40-50% of HbCO there are clear signs of intoxication: headache, confusion up to its loss, concentration of HbCO in the blood above 60 % leads to death. In any case, in people falling into a coma or dying from acute CO poisoning, the HbCO content is usually at least 50%. but there is not always a direct relationship between the content of НbСО in the blood and the severity of poisoning. Cases are known when a severe form of poisoning developed already at 20% HbCO and, conversely, at 60% HbCO, mild forms of poisoning are encountered. This is largely due to the rather high individual sensitivity to CO, which is associated with a genetic factor.

A real confirmation of oxygen starvation due to carboxyhelobinemia in severe acute CO intoxication is a decrease in the oxygen content in arterial blood to 13.4-12.4 vol.% Compared to 18-20 vol.% In the norm. At the same time, the arterial-venous difference in the content of O 2 falls from 6-7 vol.% To 3.0-2.2 vol.%, The utilization of oxygen by tissues decreases, based on the value of the corresponding coefficient, the content of CO 2 in the blood decreases to 35 vol.%. % in comparison with the norm.

The formation of НbСО under the influence of CO is not the only violation of porphyrin metabolism. So, in case of acute CO poisoning upon inhalation of CO in concentrations of 40-600 mg / m 3, the content of proto- and uroporphyrin in erythrocytes increases, and copro- and uroporphyrinuria develops. Moreover, the growth of coproporphyrins in urine is due to the formation of products of synthesis of CO with iron porphyrins of tissues, which, entering the blood, are then excreted in the urine. In especially severe cases, an increase in the content of porphobilinogen was observed. An increase in the level of methemoglobin and the appearance of sulfhemoglobin in the blood are possible. And finally, under the influence of CO, the content of the key product of hemoglobin synthesis, deltaaminolevulinic acid, increases in plasma and erythrocytes, which, apparently, indicates the inhibition of hemoglobin synthesis under the influence of CO.

For a long time, it was believed that the mechanism of the toxic effect of CO is determined exclusively by a violation of the respiratory function of the blood due to the formation of HbCO. However, over time, this concept was revised. It has been convincingly proven that CO acts on many biologically active systems of the body that contain iron, namely: myoglobin, cytochrome-containing respiratory enzymes, such as cytochrome P-450, cytochrome oxidase (cytochrome a 3), cytochrome c, peroxidase , catalase. 5

When CO interacts with myoglobin, carboxymyoglobin is formed, although the affinity of CO for myoglobin is less than for hemoglobin. At the same time, the affinity of myoglobin for CO, according to various sources, is 25-50 times higher than for oxygen.

Thus, in the case of CO poisoning, along with the formation of HbCO, the formation of carboxymyoglobin also occurs. Moreover, its growth in the muscles proceeds in parallel with the growth of this derivative of hemoglobin in the blood. It is possible that the appearance of carboxymyoglobin in muscles plays a certain role in the pathogenesis of CO intoxication, in any case, muscle damage is unambiguously associated with the effect on myoglobin. There is evidence that the ratio of carboxymyoglobin and HbCO, regardless of the level of CO exposure, is 0.52. In severe poisoning, more than 25% of myoglobin can be associated with CO.

The results of numerous studies indicate that the interaction of CO with the system of cytochromes - iron-containing respiratory enzymes - plays an important role in the pathogenesis of CO intoxication, which leads to inhibition of tissue respiration. As it turned out, the severity of disturbances in the body precisely due to this mechanism significantly exceeds those caused by the banal oxygen deficiency associated with a deficiency of O 2 in the inhaled air.

Until a certain time, the main attention in assessing the toxic effect of CO on the body was paid to acute poisoning arising under the influence of this gas. Despite the fact that the triggering mechanism for the development of acute CO intoxication is its interaction with hemoglobin and other iron-containing biochemical structures, the clinical picture of intoxication is dominated primarily by symptoms of disorders from the central nervous system, the severity of which, as a rule, depends on the HbCO content in the blood.

Considering that the pathogenesis of acute CO poisoning is initially determined by the damaging effect on the blood, it is appropriate to characterize how the morphological and biochemical composition of the blood changes. At the height of intoxication, the number of erythrocytes increases to 5.5 - 6.6 * 10 12 / l, which is caused, on the one hand, by the contraction of the spleen due to reflexes from the carotid sinuses and the entry of deposited erythrocytes into the blood, and on the other hand, by the cause of erythrocytosis there may be a direct stimulation of CO formation of erythropoietin. And finally, hypoxia cannot be ruled out as another causal factor in the increase in the number of red blood cells. Erythrocytosis is most often a temporary phenomenon, but sometimes polycythemia vera develops either immediately after acute intoxication, or as an aftereffect months or even years later. With repeated CO poisoning against the background of lymphocytosis, normoblasts appear in the blood with an increased content of reticulocytes. It is noteworthy that changes in the hemoglobin content during CO intoxication are not very typical.

In some cases, the outcome of red blood damage in CO poisoning is the development of Birmer type anemia in combination with neutropenia. 6

According to A.M. Rashevskaya and L.A. Zorina 7, changes from the side of white blood are more common than those from the side of red. This is manifested by neutrophilic leukocytosis, sometimes up to 20-25 * 10 9 / l with a shift to the left against the background of lympho- and eosinopenia with a decrease in phagocytic activity. It is believed that the mechanism of leukocytosis is associated with stress, and inhibition of phagocytosis - with inhibition of cytochrome oxidase activity in neutrophils. In humans with CO poisoning, an increase in the activity of alkaline phosphatase of neutrophils has been recorded.

As for the bone marrow, its cells undergo degenerative changes during irritation, as evidenced by an increase in nucleated elements with a shift of the formula to the left with apex in the area of myelocytes and metamyelocytes.

Certain changes in the biochemical nature seem to be essential in CO intoxication: an increase in non-hemoglobin iron in the blood (can reach 50%), which is directly related to the state of red blood. In case of repeated acute poisoning, the iron content in the tissues decreases in parallel due to the combination with CO, which is regarded as a detoxification mechanism. Some other biochemical changes in the peripheral blood in acute CO poisoning have also been well studied. So, on the part of carbohydrate metabolism, disorders in the form of hyperglycemia and glucosuria were revealed. According to some authors, these shifts may be a consequence of changes in the central mechanisms of regulation of carbohydrate metabolism, according to others, the reason is in the increased breakdown of liver glycogen due to the intense release of adrenaline. An increase in the content of lactic acid in the blood with an increase in the level of НbСО up to 30% is considered quite natural. Disorders of nitrogen metabolism in acute CO intoxication is reduced mainly to increased accumulation of nitrogenous toxins in the blood, namely urea, which is caused by violations of the antitoxic function of the liver. From the side of lipid metabolism, the stimulation of the oxidation of free fatty acids and a decrease in the production of triglycerides were traced. Electrolyte metabolism is manifested by an imbalance in the content of calcium, magnesium, and especially potassium and sodium in the blood and tissues. The latter leads to disruption of the activity of the heart muscle.

For a long time, the possibility of the development of chronic CO poisoning was questioned. It is now generally accepted that this form of pathology exists. However, due to the fact that it is difficult to differentiate the true chronic exposure to CO from repeated acute poisoning, the issue was unambiguously resolved on the basis of experimental data.

Chronic CO poisoning in humans can occur with prolonged inhalation of air containing CO in a concentration of the order of 10-50 mg / m 3. Usually, in this case, 3-13% HbCO is found in the blood, while in the blood of non-smokers, the HbCO content is 1.5-2 %. From the side of red blood in conditions of chronic CO poisoning, an increase in the content of hemoglobin and erythrocytes, sometimes against the background of reticulocytosis, a shift in the leukocyte formula to the left, more rarely thrombocytosis was observed. In this case, the content of erythrocytes can reach values of 6 * 10 12 / l and above. However, in the later stages of intoxication, and sometimes already at its initial stages, anemia may develop. Even isolated cases of pernicious and hyperchromic anemia with degeneration into paramyeloblastleukemia, which usually ended in death, have been described. It is noteworthy that under conditions of chronic exposure to CO on people with an average HbCO content of 4% in erythrocytes, the content of delta aminolevulinic acid increased to 2.7-6.9 μg / ml in comparison with the initial (0.7-2.5 μg / ml). Subsequently, this was accompanied by a violation of the synthesis of porphyrins and heme. In general, the direct effect of CO on the biosynthesis of heme in the cell cannot be ruled out. To a certain extent, by the content of deltaaminolevulinic acid in erythrocytes, one can judge the sensitivity of the organism to CO. Changes on the part of white blood are characterized by multidirectionality, in particular, both leukocytosis and leukopenia can occur against the background of eosinopenia, lymphocytosis, monocytosis. The toxic granularity of neutrophils has also been described. Under chronic exposure to CO, an increase in DNA and a decrease in RNA was found in neutrophils, provided that the activity of peroxidase in them fell. When studying the effect of CO on a person at concentrations of the order of 10-20 mg / m 3 in a pressurized chamber for 1-3 months, the following regular changes were found: a shift in the acid-base balance towards acidosis, the appearance of HbCO in the blood within the range of 10.5-14 %, an increase in serum non-hemoglobin iron to 149 μg% at 127 μg% in the initial state (in the case of a CO concentration of about 20 mg / m 3) and a decrease in the catalase index. As mentioned above, there is not always a direct relationship between the HbCO content in the blood and the severity of clinical symptoms. However, this phenomenon occurs especially often when analyzing cases of chronic poisoning. This makes it much more difficult to diagnose. The explanation for such facts, when the symptoms of poisoning persist with a progressive decrease in the level of HbCO in the blood up to normal values, is that the CO that has entered the body is fixed by hemoglobin in the form of HbCO and is excreted from the body after its destruction. Studies by a number of authors have shown that CO is able to be fixed in the cells of a number of organs, in particular, the liver, spleen, muscles, and brain. This is combined with an increase in plasma non-hemoglobin iron content in chronic CO poisoning, as a result of which CO is out of touch with hemoglobin for a long time. An increase in the content of the β-globulin fraction of serum proteins, which contains the transport form of iron, transferrin, can also be explained by the growth of non-hemoglobin iron in serum. This assumption is directly confirmed by a series of relevant studies, which showed that in chronic CO intoxication, an increase in the iron content in the serum and protoporphyrinuria are combined with an increase in the β-globulin fraction of serum proteins. eight

It is well known that the clinic of both acute and chronic CO poisoning is replete with symptoms of damage primarily to the central nervous system, as well as other organs and systems, which is explained primarily by the result of the developing hemic hypoxemia and hypoxia, as well as, to a certain extent, by the blockade of enzyme systems containing iron porphyrin structures. Chronic exposure is characterized by disorders of the central nervous system; asthenic syndrome, autonomic dystonia and angiodystonic syndrome with a tendency to angiospasm, as well as changes in the mental sphere. It has been proven that chronic CO intoxication is accompanied by a dysfunction of the cardiovascular system under the condition of varying degrees of damage to the heart muscle due to hypoxia. Possible changes in blood pressure in the direction of hypo- and especially hypertension. Somewhat less natural, but, nevertheless, the occurrence of deviations from the endocrine system, including the genital area, as well as indicators of the functions of the thyroid gland and adrenal glands, is possible.

And, finally, there is evidence of impairments to the sense organs under the influence of chronic CO intoxication. This applies to the organ of hearing (cochlear and vestibular parts of the inner ear), as well as the organ of vision with disorders of convergence, accommodation, color perception, visual acuity, narrowing of the visual fields and, finally, changes in the fundus in the form of vascular pathology of the retina of varying intensity.

Poisoning by combustion products - the main cause (80% of all cases) of deaths in fires. Over 60% of them are accounted for by carbon monoxide poisoning. Let's try to understand and remember knowledge from physics and chemistry.

What is carbon monoxide and how is it dangerous

Carbon monoxide (carbon monoxide, or carbon monoxide, chemical formula CO) is a gaseous compound formed during combustion of any kind. What happens when this substance enters the body?

After entering the respiratory tract, carbon monoxide molecules immediately appear in the blood and bind to hemoglobin molecules. A completely new substance is formed - carboxyhemoglobin, which interferes with the transport of oxygen. For this reason, oxygen deficiency develops very quickly.

The most important danger- carbon monoxide is invisible and in no way perceptible, it has no smell or color, that is, the cause of the ailment is not obvious, it is not always possible to detect it immediately. Carbon monoxide cannot be sensed in any way, which is why its second name is the silent killer. Feeling fatigue, loss of strength and dizziness, a person makes a fatal mistake - he decides to lie down. And, even if he then understands the reason and the need to go out into the air, as a rule, he is not able to do anything. Knowledge could save many symptoms of CO poisoning- knowing them, it is possible in time to suspect the cause of the ailment and take the necessary measures to rescue.

Symptoms and Signs

The severity of the lesion depends on several factors:

health status and physiological characteristics of a person. Weakened, with chronic diseases, especially those accompanied by anemia, the elderly, pregnant women and children are more sensitive to the effects of CO;
the duration of the impact of the CO compound on the body;
the concentration of carbon monoxide in the inhaled air;
physical activity during poisoning. The higher the activity, the faster the poisoning occurs.

Severity

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Mild degree severity is characterized by the following symptoms:

general weakness;
headaches, mainly in the frontal and temporal regions;
knocking at the temples;
noise in ears;
dizziness;

visual impairment - flickering, points in front of the eyes;
unproductive, i.e. dry cough;
rapid breathing;
shortness of breath, shortness of breath;
lacrimation;
nausea;
hyperemia (redness) of the skin and mucous membranes;
tachycardia;
increased blood pressure.

Symptoms medium severity is the preservation of all the symptoms of the previous stage and their more severe form:

clouding of consciousness, loss of consciousness is possible for a short time;
vomit;
hallucinations, both visual and auditory;
violation of the vestibular apparatus, uncoordinated movements;
chest pains of a pressing character.

Severe degree poisoning is characterized by the following symptoms:

paralysis;
long-term loss of consciousness, coma;
convulsions;
dilated pupils;
involuntary emptying of the bladder and intestines;
an increase in the pulse rate up to 130 beats per minute, but at the same time it is weakly felt;
cyanosis (blue discoloration) of the skin and mucous membranes;
breathing disorders - it becomes superficial and intermittent.

Atypical forms

There are two of them - faint and euphoric.

Symptoms of the fainting form:

pallor of the skin and mucous membranes;
lowering blood pressure;
loss of consciousness.

Symptoms of the euphoric form:

psychomotor agitation;
violation of mental functions: delirium, hallucinations, laughter, strange behavior;
loss of consciousness;
respiratory and heart failure.

First aid to victims

It is very important to provide it promptly, since irreversible consequences occur very quickly.

First, it is necessary to take the victim out to fresh air as soon as possible. In cases where this is difficult, then the victim should be put on a gas mask with a hopcalite cartridge as soon as possible, and given an oxygen cushion.

Secondly, it is necessary to make breathing easier - to clear the airways, if necessary, unfasten clothes, lay the victim on his side in order to prevent possible retraction of the tongue.

Thirdly, to stimulate breathing. Bring ammonia, rub the chest, warm the limbs.

And most importantly, you need to call an ambulance. Even if a person at first glance is in a satisfactory condition, it is necessary to be examined by a doctor, since it is not always possible to determine the true degree of poisoning only by symptoms. In addition, timely initiated therapeutic measures will reduce the risk of complications and mortality from carbon monoxide poisoning.

In the serious condition of the victim, it is necessary to carry out resuscitation measures before the arrival of doctors.

Sources of danger

In our time, cases of poisoning happen a little less often than in those days when heating of living quarters was predominantly stove, but there are enough sources of increased risk even now.

Potential Sources of Carbon Monoxide Poisoning Hazards:

houses with stove heating, fireplaces. Improper operation increases the risk of carbon monoxide entering the room, thus, whole families get burned in their homes;
baths, saunas, especially those that heat "black";
garages;
in industries using carbon monoxide;
long stay near major highways;
fire in a closed room (elevator, mine, etc. premises, which cannot be left without assistance).

Only numbers

A mild degree of poisoning occurs even at a carbon monoxide concentration of 0.08% - there is a headache, dizziness, suffocation, general weakness.
An increase in CO concentration up to 0.32% causes motor paralysis and fainting. Death occurs in about half an hour.
At a CO concentration of 1.2% and above, a lightning-fast form of poisoning develops - in a couple of sighs a person receives a lethal dose, a fatal outcome occurs in a maximum of 3 minutes.
The exhaust gases of a passenger car contain from 1.5 to 3% carbon monoxide. Contrary to popular belief, poisoning with the engine running is possible not only indoors, but also outdoors.
About two and a half thousand people in Russia are hospitalized annually with varying degrees of severity of carbon monoxide poisoning.

Carbon monoxide (carbon monoxide) // Harmful substances in industry. Handbook for chemists, engineers and doctors / Ed. N. V. Lazarev and I. D. Gadaskina. - 7th ed. - L .: Chemistry, 1977 .-- T. 3. - S. 240-253. - 608 p.

Carbon monoxide concentration and symptoms of poisoning

Prevention measures

In order to minimize the risks of carbon monoxide poisoning, it is enough to observe the following rules:

operate stoves and fireplaces in accordance with the rules, regularly check the operation of the ventilation system and in a timely manner, and trust the laying of stoves and fireplaces only to professionals;
do not stay near busy highways for a long time;
always turn off the engine of the car in a closed garage. In order for the concentration of carbon monoxide to become lethal, only five minutes of engine operation is enough - remember this;
when you are in the car for a long time, and even more so when you sleep in the car, always turn off the engine;
make it a rule - if you experience symptoms for which you can suspect carbon monoxide poisoning, provide an influx of fresh air as soon as possible by opening the windows, or rather leave the room. Do not lie down feeling dizzy, nauseous, weak.

Remember - carbon monoxide is insidious, it acts quickly and imperceptibly, therefore life and health depend on the speed of the measures taken. Take care of yourself and your loved ones!

Topic: Carbon monoxide. Household gas.

First aid for gas poisoning.

Objectives: to familiarize students with the sources of carbon monoxide, symptoms of gas poisoning "

Learn to provide first aid for gas poisoning.

During the classes.

Organizing time.

Homework check.

What is fire. Causes of the fire.

Fire safety rules.

Fire factors and its effect on the human body.

Rules of conduct in case of fire.

3 Message of the topic of the lesson.

During holidays and festivities, balloons are sold on the streets of the city.

and inflatable toys that must be firmly held in your hands, otherwise they will fly away.

Who knows what balloons and toys are inflated with?

Why are they "behaving" like that?

These toys and balloons are inflated with a special gas that is lighter than air.

Therefore, balls and toys rush upward.

Today we are talking about various gases. We will learn where the gas is used, what harm it can do to a person and how to provide first aid for gas poisoning.

4. Work on the topic of the lesson.

What do you know about this topic?

Carbon monoxide.

The scientific name for carbon monoxide is oxygen oxide.

In addition to its usual name, this gas has others, it is also called "invisible poison" and "humane killer".

Carbon monoxide is emitted during fires, in baths, in country and country houses with stove heating. It turns out as a result of incomplete combustion of fuel in the furnaces, when the furnace valve is closed prematurely.

Carbon monoxide can also be formed in a city kitchen when natural gas is incompletely burned.

Carbon monoxide is very poisonous, it has no color or smell, so it cannot be seen or felt. It is lighter than air, therefore it rushes upward.

That is why, when evacuating in a fire, you should move by bending low or crawling.

Writing in a notebook.

Carbon monoxide, its characteristics.

Lighter than air.

It is colorless and odorless.

Poisonous.

The second gas we encounter on a daily basis is household gas that goes into gas stoves. Household gas has practically no color or smell, but in order to determine its presence in an apartment, micro doses of odoranite are added to it at a gas station to impart a specific smell.

Gas poisoning is dangerous.

Symptoms of gas poisoning.

Severe headache and dizziness.

Noise in ears.

Darkens in the eyes.

Nausea.

Muscle weakness.

Loss of consciousness.

5. Work on the textbook.

Selective Reading and Answering Questions, pages 46-49.

Find and read where else you can get carbon monoxide poisoning?

(This gas is the cause of death in the cold season, falling asleep in a car with the engine running).

Read where underground (ground) gases accumulate, which also have no color or smell ?.

(They accumulate in basements, mines, water and sewer wells, landfills and swamps.)

Read what steps are required to provide first aid for gas poisoning ?.

First aid for gas poisoning.

Remove victim to fresh air.

Rub the body, wrap the patient, put heating pads at the feet.

Short-term inhalation of ammonia.

In case of respiratory arrest, artificial respiration.

Calling an ambulance.

If gas leaks, do not.

Touching electrical switches, ringing electric bells, using the elevator.

Use matches and lighters.

Check for gas leaks with fire (matches). You can use soap suds to check for leaks.

Necessary:

Turn off the gas without turning on the light.

Open windows and doors.

If the cause of the gas contamination is unclear, call the gas service by phone 04.

6. Lesson summary.

Why is carbon monoxide called "invisible poison", "humane killer"?

(A person dies in a dream, does not experience pain and suffering.)

You put in to warm up your lunch. The burner blew out and the kitchen filled with gas. Your actions?

(Hold your breath. Turn off the gas. Open windows and doors for ventilation)

7. Homework.

Tutorial, page 46-49. Answer the questions on page 49.

Notes in a notebook.

reference

Teacher-organizer of OBZH.

Akopdzhanyan Nikolai Ivanovich.

on the topic: "Carbon monoxide and household gas. First aid for gas poisoning.

I used the following materials during the lesson.

OBZH textbook, grade 5,

Methodological manual on life safety,

Used the resources of the Internet,

Microsoft office /

Preview:

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Slide captions:

Topic: Carbon monoxide. Household gas. First aid for gas poisoning Objectives: To familiarize students with the sources of carbon monoxide, the symptoms of gas poisoning ”To teach first aid for gas poisoning.

Carbon Monoxide The scientific name for carbon monoxide is oxygen oxide. In addition to its usual name, this gas has others, it is also called "invisible poison" and "humane killer". Carbon monoxide is emitted during fires, in baths, in country and country houses with stove heating. It turns out as a result of incomplete combustion of fuel in the furnaces, when the furnace valve is closed prematurely. Carbon monoxide can also be formed in a city kitchen when natural gas is incompletely burned. Carbon monoxide is very poisonous, it has no color or smell, so it cannot be seen or felt. It is lighter than air, therefore it rushes upward. That is why, when evacuating in a fire, you should move by bending low or crawling.

Carbon monoxide, its characteristic Lighter than air. It is colorless and odorless. Poisonous.

Symptoms of gas poisoning Severe headache and dizziness. Noise in ears. Darkens in the eyes. Nausea. Muscle weakness. Loss of consciousness.

First aid in case of gas poisoning Remove victim to fresh air. Rub the body, wrap the patient, put heating pads at the feet. Short-term inhalation of ammonia. In case of respiratory arrest, artificial respiration. Calling an ambulance.

In case of gas leakage it is forbidden !!! Touching electrical switches, ringing electric bells, using the elevator. Use matches and lighters. Check for gas leaks with fire (matches). You can use soap suds to check for leaks.

It is necessary to: Cut off the gas without turning on the light. Open windows and doors. If the cause of the gas contamination is unclear, call the gas service by phone 04.

Lesson summary Why is carbon monoxide called "invisible poison", "humane killer"? (A person dies in a dream, does not experience pain and suffering.) You have set the dinner to be warmed up. The burner blew out and the kitchen filled with gas. Your actions? (Hold your breath. Turn off the gas. Open windows and doors for ventilation)

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Carbon monoxide

Carbon monoxide poisoning- an acute pathological condition that develops as a result of the ingress of carbon monoxide into the human body is dangerous to life and health, and without adequate medical care can lead to death.

Poisoning is possible:

· In case of fires;

· In production, where carbon monoxide is used for the synthesis of a number of organic substances (acetone, methyl alcohol, phenol, etc.);

In garages with poor ventilation, in other unventilated or poorly ventilated rooms, tunnels, since the exhaust of a car contains up to 1-3% CO according to standards and over 10% with poor adjustment of the carburetor motor;

· When you are on or near a busy road for a long time. On major highways, the average CO concentration exceeds the toxicity threshold;

At home with a gas leakage and with untimely closed stove dampers in rooms with stove heating (houses, baths);

· When using low-quality air in breathing apparatus.

Symptoms:

In case of light poisoning:

o headache appears,

o knocking at the temples,

o dizziness,

o chest pain,

o dry cough,

o lacrimation,

o nausea,

o visual and auditory hallucinations are possible,

o redness of the skin, carmine-red coloration of the mucous membranes,

o tachycardia,

o increased blood pressure.

In case of moderate poisoning:

o drowsiness,

o possible motor paralysis with preserved consciousness

In case of severe poisoning:

o loss of consciousness, coma

o convulsions,

o involuntary discharge of urine and feces,

breathing disorder that becomes continuous, sometimes of the Cheyne-Stokes type,

o dilated pupils with a weakened reaction to light,

o sharp cyanosis (blue discoloration) of the mucous membranes and facial skin. Death usually occurs at the scene as a result of respiratory arrest and a drop in cardiac activity.

When coming out of a coma, the appearance of a sharp motor excitement is characteristic. Coma may re-develop.

Serious complications are often noted:

Violation of cerebral circulation,

Subarachnoid hemorrhage,

Polyneuritis,

Phenomena of cerebral edema,

Visual impairment,

Hearing impairment,

Possible development of myocardial infarction,

Skin and trophic disorders (blisters, local edema with swelling and subsequent necrosis), myoglobinuric nephrosis are often observed,

· With prolonged coma, severe pneumonia is constantly noted.

First aid

carbon monoxide poisoning man

1. Remove the victim from a room with a high carbon monoxide content. If poisoning occurs while using a breathing apparatus, it should be replaced.

2. In case of weak shallow breathing or stopping it, start artificial respiration.

3. Contribute to the elimination of the consequences of poisoning: rubbing the body, applying a heating pad to the legs, short-term inhalation of ammonia (the tampon with alcohol should be no closer than 1 cm, the tampon should be waved in front of the nose, which is very important, since when the tampon touches the nose, for the powerful effect of ammonia on the respiratory center, its paralysis may occur). Patients with severe poisoning are subject to hospitalization, since complications from the lungs and nervous system are possible at a later date.

Treatment

It is necessary to immediately eliminate the source of polluted air and provide breathing with pure oxygen under an increased partial pressure of 1.5-2 atm or, preferably, with carbogen.

· In the first minutes to the victim, inject intramuscularly a solution of the antidote "Acizol". Further treatment in the hospital.

For the relief of seizures and psychomotor agitation, neuroleptics can be used, for example, chlorpromazine (1-3 ml of a 2.5% solution intramuscularly, previously diluted in 5 ml of a 0.5% sterile solution of novocaine) or chloral hydrate in an enema. Contraindicated: bemegrid, corazole, analeptic mixture, camphor, caffeine.

In case of respiratory failure - 10 ml of 2.4% aminophylline solution into the vein again.

With severe cyanosis (blue in the face), in the 1st hour after poisoning, intravenous administration of a 5% solution of ascorbic acid (20-30 ml) with glucose is indicated. Intravenous infusion of 5% glucose solution (500 ml) with 2% novocaine solution (50 ml), 40% glucose solution in a vein drip (200 ml) with 10 units of insulin under the skin.

Prophylaxis

Carry out work in well-ventilated areas

Check the opening of dampers when using stoves and fireplaces in houses

· Taking the antidote "Acizol" 1 capsule 30-40 minutes before contact with carbon monoxide.

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