Download presentation carbon monoxide poisoning. Carbon monoxide poisoning

Carbon monoxide poisoning Completed by: 5th year student 504 group 1 med Palichuk I. N. State Institution “KGMUim. S.I. Georgievsky" Department of Internal Medicine No. 3 Head. department prof. Khrenov A. A. Teacher Assoc. Kushnir S.P. studentdoctorprofessor. com. ua sdp. net. ua

Carbon monoxide (carbon monoxide) is a colorless, tasteless and odorless gas. Carbon monoxide can form wherever conditions are created for incomplete combustion of carbon-containing substances. It is a component of many gases and aerosols: in generator gases - 9-29%, in explosive gases - up to 60%, in car exhaust gases - on average 6.3%. studentdoctorprofessor. com. ua sdp. net. ua

Carbon monoxide poisoning is possible in boiler rooms, foundries, when testing engines, in garages, on vehicles, in gas plants, in mines, etc.; in everyday life due to improper heating of stoves or improper use of gas stoves. MPC - 20 mg/m 3. studentdoctorprofessor. com. ua sdp. net. ua

Entry and excretion from the body is through the respiratory organs in unchanged form. Due to the high affinity for hemoglobin, it causes blockade of hemoglobin (formation of carboxyhemoglobin) and disruption of oxygen transport. Inhibits the dissociation of oxyhemoglobin, inhibits tissue respiration (mixed hemic-tissue hypoxia), and causes hypocapnia. studentdoctorprofessor. com. ua sdp. net. ua

Carbon monoxide quickly penetrates the blood-brain barrier. The effect on the central nervous system is due to both hypoxia and the direct effect of carbon monoxide. studentdoctorprofessor. com. ua sdp. net. ua

Symptoms Mild degree of carbon monoxide intoxication - headache, mainly in the temples and forehead, “pulsation in the temples,” dizziness, tinnitus, vomiting, muscle weakness. Increased breathing and heart rate. Fainting, especially when performing physical work. studentdoctorprofessor. com. ua sdp. net. ua

One of the earliest symptoms is a decrease in reaction speed and impaired color vision. studentdoctorprofessor. com. ua sdp. net. ua

In case of moderate intoxication, loss of consciousness for several hours or significant memory loss. Loss of criticism. Sharp adynamia. Loss of coordination of movements, trembling. Upon return of consciousness - a pronounced asthenic state studentdoctorprofessor. com. ua sdp. net. ua

Symptoms of severe intoxication: Prolonged coma (up to 5-7 days or more). Brain lesions, rigidity of limb muscles, clonic and tonic convulsions, seizures. Involuntary urination and defecation. Cyanosis of the extremities, general hyperhidrosis. The complexion is bright scarlet (carboxyhemoglobin gives this color). studentdoctorprofessor. com. ua sdp. net. ua

Breathing is intermittent, maybe Cheyne-Stokes type. Pulse 110-120 beats per minute, hypotension, tendency to collapse. Temperature 39 -40°C (possible hypothermia), neutrophilic leukocytosis, low ESR. Possible death from respiratory paralysis. Upon recovery from a coma, there is a long-term state of stunning. Apathy. There may be a short-term delirious state, sudden motor agitation, delirium, and complete retrograde amnesia. studentdoctorprofessor. com. ua sdp. net. ua

The prognosis is determined mainly by the depth and duration of the coma. The increase in the phenomena of depression of the central nervous system on the 2nd day makes the prognosis unfavorable. With moderate and severe degrees of intoxication, mononeuritis of the ulnar, median or common peroneal nerve is possible, paresis and paralysis are possible. studentdoctorprofessor. com. ua sdp. net. ua

Visual impairment Double vision, color blindness; swelling of the optic nerve and retina, optic nerve atrophy (rare). studentdoctorprofessor. com. ua sdp. net. ua

Damage to the skin and hair Trophic lesions of the skin, hemorrhagic rashes, erythematous-bullous forms (the picture of a “thermal burn”), painful dense swelling, most often of the distal limbs, graying, hair loss. studentdoctorprofessor. com. ua sdp. net. ua

Changes in the circulatory and respiratory system From the very first hours of carbon monoxide intoxication, pronounced changes occur in the circulatory and respiratory system. First, functional disorders - tachycardia, pulse lability, extrasystole, and coronary insufficiency may also be observed. In case of moderate and severe poisoning - toxic damage to the myocardium (as a result of both hypoxia and the direct effect of carbon monoxide on the heart muscle) with symptoms of cardiovascular failure. studentdoctorprofessor. com. ua sdp. net. ua

The ECG shows diffuse muscle changes, which after a few days take on a focal character, such as a heart attack. Various conduction disorders, up to partial or complete blockade. Focal changes in the myocardium last up to 1.5 months and often occur in young people (up to 30 years). Coronary insufficiency may not be clinically determined (pain syndrome may be completely absent). Recovery is slow. Exacerbations are possible.

Changes in the bronchopulmonary apparatus Bronchitis, in moderate and severe degrees of intoxication - toxic pneumonia, pulmonary edema, developing within 1 - less than 2 days. Clinical symptoms are very scarce and do not correspond to the severity of radiological data. studentdoctorprofessor. com. ua sdp. net. ua

An X-ray examination of the lungs, taken 10-15 hours after the onset of carbon monoxide intoxication, reveals changes in three forms: 1. Emphysema and increased pulmonary pattern. The shadows of the hilum of the lungs are expanded and consist of small focal and linear formations. After 1-3 days - complete recovery. studentdoctorprofessor. com. ua sdp. net. ua

2. Along with those indicated, changes of a focal nature with unclear contours, occupying the basal region, densely located, without a tendency to merge. On the 3rd -4th day, the normal pulmonary pattern is restored.

3. Diffuse large-focal changes in the lung tissue, irregular in shape, with blurred contours, 1-2 cm in size, merging in places. Emphysema of the bullous type. Despite such extensive anatomical changes, their complete resolution is possible on the 7-10th day from the onset of intoxication. studentdoctorprofessor. com. ua sdp. net. ua

Clinical and radiological data indicate a violation of circulation in the pulmonary circulation from small degrees of stagnation in the pulmonary vessels (in the first of the described forms) to interstitial (in the second form) and alveolar pulmonary edema (in the third form). In a small number of cases, a moderate fever develops in the 2nd week, the general condition worsens again, and upon auscultation, moist and scattered dry rales are detected (the so-called post-carbon pneumonia). These bronchopneumopneumopic changes, with a favorable course, soon disappear, and normal pneumatization of the lungs is restored. sdp. net. ua

Particular attention should be paid to hemodynamic disturbances during carbon monoxide intoxication. In almost half of the victims, an acute total enlargement of the heart with a predominance of the right parts is observed radiographically. Normalization after 3-5 days. Pulmonary edema and acute expansion of the heart sharply aggravate intoxication. For early diagnosis of changes in the lungs and heart, X-ray examination must be performed as early as possible. sdp. net. ua

Blood changes High levels of hemoglobin and red blood cells. With toxic pulmonary edema - neutrophilic leukocytosis, band shift; ESR is not increased (if there is no infection); increased levels of sugar, lactic acid, acetone bodies, urea, transferase activity, decreased alkaline reserve. Sometimes rapid development of anemia. sdp. net. ua

Chronic intoxication Complaints of headaches, noise in the head, dizziness, increased fatigue, irritability, poor sleep, memory impairment, short-term disorientation, palpitations, pain in the heart, shortness of breath, fainting, disorders of skin sensitivity, smell, hearing, vestibular function apparatus, vision (impaired color perception, narrowing of the field of view, impaired accommodation). Nutrition decline. Functional disorders of the central nervous system - asthenia, autonomic dysfunction with angiodystonic syndrome, a tendency to vascular spasms, hypertension, and in the future the development of hypertension is possible. Myocardial dystrophy, angina symptoms. The ECG shows focal and diffuse changes, coronary disorders. sdp. net. ua

Chronic poisoning contributes to the development of atherosclerosis and aggravates the course of the latter if it already existed before intoxication. Endocrine disorders, in particular thyrotoxicosis. sdp. net. ua

Determining the content of carboxyhemoglobin in the blood has some diagnostic value, but there is no parallelism between its amount and the severity of intoxication. The speed of development and severity of acute and chronic intoxications may depend on the individual characteristics of the body and the presence of other diseases. Poisoning is more severe in young people and pregnant women, with diseases of the lungs and heart, circulatory disorders, anemia, diabetes, liver disease, neurasthenia, and chronic alcoholism. sdp. net. ua

When some other toxic substances are present in the air - gasoline, benzene, nitrogen oxides, cyanides, hydrogen sulfide - the toxic effect of SDP is summed up and potentiated. net. ua

The unfavorable effect of carbon monoxide is enhanced by increased physical activity, vibration, noise, decrease and increase in air temperature, and a decrease in the partial pressure of oxygen. sdp. net. ua

First aid and treatment Take the patient in a supine position (even if independent movement is possible) into fresh air. Peace. Be sure to warm up (hot water bottles, mustard plasters on your feet). Early and prolonged inhalation of oxygen. sdp. net. ua

In case of severe carbon monoxide intoxication - emergency hyperbaric oxygen therapy for 1-1.5 hours at a total pressure of 0.3 m Pa (3 kgf/cm2), if necessary, repeat this procedure. Drug therapy is carried out against the background of oxygen therapy. In mild cases - ammonia, tea, coffee. sdp. net. ua

If there is a simultaneous absence of pulse and breathing stops, massage the heart area, artificial respiration. Emergency therapy must be carried out until the function of the cardiovascular and respiratory systems is completely restored. sdp. net. ua

Treatment of chronic poisoning Depending on the underlying syndrome: glucose, vitamin therapy, cardiac, vasodilator, pantothenic acid, ATP, glutamic acid. sdp. net. ua

Examination of work ability After treatment of acute carbon monoxide poisoning in moderate and severe form with release from work (in a hospital) - provision of sick leave. Subsequent careful medical observation. Depending on the presence and severity of complications, work capacity may be permanently limited. At initial signs of chronic intoxication - transfer to another job (temporarily) for a period of 2 months. If the treatment and preventive measures taken are ineffective or the symptoms of chronic poisoning are severe, a permanent transfer to another job with a possible determination of disability is required. sdp. net. ua

Prevention Sealing equipment and pipelines where carbon monoxide may be released. Systematic monitoring of the concentration of carbon monoxide in the room air and rapid removal of the released gas, automatic signaling of dangerous concentrations of carbon monoxide SDP. net. ua

Presentation on life safety.
Topic: Carbon monoxide poisoning. General poisoning from gaseous combustion products.
Completed by Pavel Vladimirovich Vasiliev.

Slide number 2.

One of the main causes of death in fires (more than 80% of cases) is acute poisoning by gaseous combustion products of various building materials and structures. Rapid poisoning of the body is possible as a result of pollution of the surrounding atmosphere with harmful substances in concentrations that damage the body (toxodoses) or quantities that pose a threat to life and health.

The most toxic combustion products are synthetic polymer materials. When burning, most plastics emit toxic substances: carbon monoxide, hydrogen cyanide, hydrogen chloride, acrolein, nitrogen oxides, various aliphatic and aromatic hydrocarbons, etc. Foam rubber used for making furniture is extremely dangerous in terms of fire, which, when burned, emits a toxic gas containing cyanide compounds. These substances, even in small quantities, are highly toxic and affect the human respiratory and nervous systems. Loss of consciousness and the associated inability to independently exit the fire zone lead to the fact that victims are exposed to harmful substances for a long time.

Slide number 3.

Carbon monoxide (carbon monoxide) is colorless, odorless and tasteless, and does not cause eye irritation in its pure form, which explains the invisibility of the development of acute poisoning in people. Carbon monoxide is formed during incomplete combustion (lack of oxygen) of fuel, solid, liquid or gaseous combustible substances.

Slide number 4.

Carbon monoxide is part of exhaust, powder, and explosive gases and is formed during fires, especially in confined spaces (rooms). Acute carbon monoxide poisoning, as a rule, occurs due to violations of safety precautions when working with internal combustion engines, gas generating units and the operation of technically faulty stoves, heating devices, when working in poorly ventilated rooms when heating them with open fire, etc.

Slide number 5.

A characteristic feature of carbon monoxide, which determines its toxic effect on the body, is its significantly greater ability than oxygen to combine with the hemoglobin of red blood cells (erythrocytes) in the blood. This produces carboxyhemoglobin, which is unable to carry oxygen. In addition to oxygen deficiency, carbon monoxide has a toxic effect directly on tissues, in particular on the central nervous system. Therefore, many of the symptoms observed in acute carbon monoxide poisoning are due to damage to the central nervous system. One of the most vulnerable organs in case of poisoning is the heart muscle, which is more affected if the victim was performing physical work at the time of poisoning. Practice shows that a person doing heavy physical work can be poisoned by half the amount of carbon monoxide in the air than a person at rest. Sensitivity to carbon monoxide also increases with increasing external temperature and humidity.

Mechanism of action of carbon monoxide on humans is that, when it enters the blood, it binds hemoglobin cells. Then hemoglobin loses its ability to carry oxygen. And the longer a person breathes carbon monoxide, the less workable hemoglobin remains in his blood, and the less oxygen the body receives. A person begins to choke, a headache appears, and consciousness becomes confused. And if you don’t go out into the fresh air in time (or don’t take someone who has already lost consciousness out into the fresh air), then a fatal outcome is possible. In the case of carbon monoxide poisoning, it takes quite a long time for the hemoglobin cells to be able to completely clear the carbon monoxide. The higher the concentration of CO in the air, the faster the life-threatening concentration of carboxyhemoglobin in the blood is created. For example, if the concentration of carbon monoxide in the air is 0.02-0.03%, then in 5-6 hours of inhaling such air a carboxyhemoglobin concentration of 25-30% will be created, but if the concentration of CO in the air is 0.3-0.5% , then the lethal content of carboxyhemoglobin at the level of 65-75% will be achieved after 20-30 minutes of a person’s stay in such an environment.

Slide number 6.

Carbon monoxide poisoning can occur suddenly or slowly, depending on the concentration. At very high concentrations, poisoning occurs quickly, characterized by rapid loss of consciousness, convulsions and respiratory arrest. In blood taken from the region of the left ventricle of the heart or from the aorta, a high concentration of carboxyhemoglobin is detected - up to 80%. With a low concentration of carbon monoxide, symptoms develop gradually: muscle weakness appears; dizziness; noise in ears; nausea; vomit; drowsiness; sometimes, on the contrary, short-term increased mobility; then movement coordination disorder; rave; hallucinations; loss of consciousness; convulsions; coma and death from paralysis of the respiratory center. The heart may continue to contract for some time after breathing has stopped. There have been cases of death from the consequences of poisoning even 2-3 weeks after the poisoning event.

Slide number 7.

Severe complications are often observed:

Cerebrovascular accident

Subarachnoid hemorrhages

Polyneuritis is multiple nerve lesions.

Phenomena of cerebral edema

Visual impairment

Hearing impairment

Possible development of myocardial infarction

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

With a long coma, severe pneumonia is constantly observed.

Slide number 8.

First aid. Initial inspection:

Check the patient's vital signs: breathing, pulse, note the presence or absence of hypotension, signs of shock, level of consciousness.

In case of carbon monoxide poisoning, redness of the skin, carmine-red (blood-red) coloring of the mucous membranes, and tachycardia (increased heart rate from 90 beats per minute) are noted.

Slide number 9.

Hypotension is decreased vascular or muscle tone. Hypotension is often referred to as arterial hypotension, that is, a decrease in blood pressure to 90/50 or lower.

Acute arterial hypotension is manifested by the following symptoms: dizziness, fainting, disturbances of consciousness.

Slide number 10.

Shock (from the English shock - blow, shock) is a pathological process that develops in response to exposure to extreme irritants and is accompanied by a progressive disruption of the vital functions of the nervous system, blood circulation, respiration, metabolism and some other functions. Essentially, this is a breakdown of the body’s compensatory reactions in response to damage.

The diagnosis of shock is made when the patient has the following signs of shock:

decreased blood pressure and tachycardia;

anxiety (erectile phase according to Pirogov) or blackout (torpid phase according to Pirogov);

breathing problems;

decrease in the volume of urine excreted;

cold, moist skin with a pale cyanotic or marbled color.

Slide number 11.

The clinical classification divides shock into four degrees according to its severity.

Shock I degree. Consciousness is preserved, the patient is communicative, slightly inhibited. Systolic blood pressure (BP) exceeds 90 mmHg, the pulse is rapid.

Shock II degree. Consciousness is preserved, the patient is inhibited. Systolic blood pressure 90-70 mmHg, pulse 100-120 beats per minute, weak filling, shallow breathing.

Shock III degree. The patient is adynamic, inhibited, does not respond to pain, and answers questions in monosyllables. The skin is pale, cold, with a bluish tint. Breathing is shallow and frequent. Systolic blood pressure is below 70 mm Hg, pulse is more than 120 beats per minute, thready, central venous pressure (CVP) is zero or negative. Anuria (lack of urine) is observed.

IV degree shock manifests itself clinically as one of the terminal conditions.

Approximately the severity of shock can be determined by the Algover index, that is, by the ratio of the pulse to the value of systolic blood pressure. Normal index - 0.54; 1.0 - transition state; 1.5 - severe shock.

Slide number 12.

Assess the neurological status of the victim - Neurological disorders in acute CO poisoning are observed quite often. The leading manifestations of neurological disorders are headache, dizziness, agitation, stupor, convulsions and coma. Other abnormalities include behavioral disturbances, decreased cognitive ability, gait disturbances, and tics including irritability, strange behavior, and hyperactivity.

In acute poisoning, heaviness in the head, a feeling of squeezing of the forehead (“as if with a hoop or pincers”) are initially noted, and later a severe headache appears with a predominant localization in the forehead and temples, dizziness and tinnitus, trembling, weakness, increased heart rate and vomit.

In more severe cases of poisoning, increasing drowsiness, confusion, irresponsible actions, weakness in the legs, shortness of breath, loss of consciousness or its deep disorder appear. There are seizures resembling epilepsy. Paralysis is possible, as well as involuntary urination and fecal incontinence. Breathing is usually rapid, sometimes irregular. In severe poisoning, the skin and mucous membranes are bright cherry red.

Slide number 13.

First aid for carbon monoxide poisoning and other combustion products is to provide the victim with access to fresh air. That is, take it out or remove it from a smoke-filled or gas-filled room.

If there is no breathing, perform mouth-to-mouth or mouth-to-nose artificial ventilation. However, you should be careful, when poisoned by gas, a person exhales poison! When performing mechanical ventilation, you must use a damp cloth or gauze bandage. When carrying out the procedure, artificial ventilation using the mouth-to-mouth or mouth-to-nose method, draw air away from the victim’s face.

Call an ambulance immediately. Artificial respiration should be performed until paramedics arrive if the victim is not breathing on his own.

Firefighters and rescuers have personal protective equipment, including oxygen cylinders and masks; if rescuers were at the scene before the ambulance arrived, it is necessary to use these means to facilitate breathing for a victim of carbon monoxide.

In case of carbon monoxide poisoning, the patient must be taken to a hospital that has a pressure chamber. Because the only way to save a person is to let him breathe oxygen under high pressure conditions.

Slide number 14.

Remove the victim to fresh air.

If the victim is conscious, provide continuous access to fresh air and short-term inhalation of ammonia, and rub the body.

Call an ambulance.

If the victim is unconscious, it is necessary to immediately begin artificial respiration until he regains consciousness or until the ambulance arrives.

Notify the emergency physician if you suspect carbon monoxide poisoning.

Slide number 15.

Inhalation of carbon dioxide and other toxic combustion products leads to hypoxia.

HYPOXIA - low oxygen content in the blood.

Manifestations of hypoxia:

In adults: anxiety

pale skin

In children: pronounced fear

tearfulness

Sometimes spastic muscle contractions and cramps occur.

Slide number 16.

If you have established that the victim is in a state of hypoxia, then you need to

Take the victim to fresh air and allow him to breathe oxygen.

If the victim is unable to breathe, artificial ventilation is necessary.

Slide number 17.

Artificial respiration is a form of ventilation that provides oxygenation and ventilation (removal of carbon dioxide) to the victim.

Ventilation using the mouth-to-mouth method is carried out as follows. The person providing assistance with one hand placed on the victim’s forehead bends his head back, while simultaneously supporting it with the other hand placed under the neck and back of the head. Use the fingers of the hand on the forehead to close the nose to prevent air leakage. The person providing assistance tightly covers the victim’s mouth with his mouth and exhales into his respiratory tract. The criterion for monitoring effectiveness is an increase in the volume of the victim’s chest. After the chest has expanded, the person providing assistance turns his head to the side and the patient exhales passively. The intervals of respiratory cycles should be within the physiological norm - no more than 10-12 per minute. (1 breathing cycle for 4-5 counts). The volume of exhaled air should be approximately 50% greater than the normal volume.

Slide number 18.

Whenever fire in the building, those present must observe safety precautions. One of the measures is the use of personal respiratory protection when leaving smoke-filled and burning rooms. Timely use of personal protective equipment will protect the respiratory system from toxic combustion products, thereby preserving the health and life of victims.

Self-rescuer insulating fire protection SIP-1 is designed to protect organs breathing, vision and facial skin from harmful substances, regardless of their concentration, during independent evacuation from premises during a fire or in other emergency situations. The insulating fire safety self-rescuer is intended for use by people over 12 years of age.

The self-rescuer SIP-1 is produced ready for use and does not require individual adjustment; it is supplied in hard packaging (case) and in soft fabric packaging (bag). Self-rescuer SIP-1 is a single-use respiratory protection device.

SIP-1 differs from similar isolating self-rescuers by the location of the breathing bag around the neck, and not on the chest, which allows you to carry loads or property, or people who have lost consciousness. The design of the insulating self-rescuer prevents the half mask from being torn off from the face, as well as the loss of breathing mixture from the bag when bending, falling, crawling or colliding with obstacles.

The universal gas and smoke protection kit GDZK-U is a filter protection product designed to protect the human respiratory system, eyes and head from smoke and toxic gases.

The GDZK-U set consists of a fire-resistant hood with an observation window, a half mask with an exhalation valve, a filtering and absorption box, an adjustable headband, a sealed bag and a bag on which a instructions for use is placed; in the pocket of the bag there is an instruction manual.

The GDZK-U kit provides protection for at least 30 minutes at high concentrations of the main toxic combustion products and hazardous chemical substances of various classes.

The kit provides protection at ambient temperatures from 00 to 600 C and retains protective properties after short-term exposure to a temperature of 200 0 C for 1 minute and an open flame with a temperature of 850 0 C for 5 seconds.

Universal protective hood KZU

The advanced protective hood is a disposable filter protection device and is designed to protect the human respiratory system, eyes and scalp from gases, vapors and aerosols of hazardous chemicals and toxic combustion products, as well as briefly from exposure to open flames. It can be used to evacuate people from zones of chemical contamination as a result of man-made accidents, as well as from buildings, structures and objects for various purposes in case of smoke.

Operates in all climatic zones at temperatures from -30°C to +40°C with a free oxygen content in the air of at least 17% by volume.

Slide number 19.

Compliance with fire safety rules, careful attention to your behavior, the behavior of children and adolescents, as well as elderly people and smokers, equipping your apartment with fire alarms, smoke detectors, fire extinguishing equipment, fire-safe behavior will help you save your life and property.

Gas is colorless and odorless. Molecular weight 28.01. Boiling point 190 o C, density 0.97. It does not dissolve in water and burns with a bluish flame. It is found wherever conditions exist for incomplete combustion of substances containing carbon. Carbon monoxide

In wartime, poisoning can occur from explosions of rockets, mines, shells, volumetric explosion ammunition, from shooting from enclosed spaces, from persons located in areas engulfed in large fires as a result of the enemy’s use of incendiary mixtures. In peacetime, the most typical situations causing carbon monoxide poisoning are malfunctions or violations of operating rules of heating systems, malfunctions of internal combustion engines or their operation in enclosed spaces (garages, boxes, hangars). In military personnel, poisoning may also be associated with violations of the operation of military equipment (vehicles, tanks, artillery systems, aircraft).

Refers to substances with general toxic effects. Poisoning occurs by inhalation. Acute carbon monoxide poisoning occupies a leading place among inhalation poisonings, and in terms of the number of deaths they account for 17.5% of the total number of fatal poisonings. The maximum permissible concentration of carbon monoxide in the air of working premises is 20 mg/m3. The toxicity of carbon monoxide is determined primarily by its concentration in the air and the duration of exposure. However, the severity of intoxication is largely determined by other factors: the initial state of health (more severe with anemia, hypovitaminosis), the functional state of the body (more severe with psycho-emotional stress, physical activity), age (more severe in children and the elderly).

When inhaling air contaminated with it, it easily overcomes the pulmonary capillary membrane of the alveoli and enters the blood. There it interacts with the hemoglobin of red blood cells, forming carboxyhemoglobin, which is unable to carry oxygen. The nature of the interaction of CO with hemoglobin has much in common with the interaction of oxygen with Hb. Carbon monoxide binds to both the oxidized and reduced forms of hemoglobin. Analysis of the association and dissociation curves of oxyhemoglobin and carboxyhemoglobin indicates that the increased affinity of carbon monoxide does not mean an increase in the rate of addition of the poison to hemoglobin. It has been established that the rate of addition of CO to hemoglobin is not higher, but is approximately 10 times lower than the rate of addition of oxygen. At the same time, the dissociation rate of carboxyhemoglobin is approximately 3600 times less than the corresponding rate for oxyhemoglobin. The ratio of these rates is defined as the relative affinity of CO to Hb and is approximately 360. This determines the rapid formation of carboxyhemoglobin in the blood at a low content of carbon monoxide in the inhaled air. MECHANISM OF ACTION AND PATHOGENESIS.

For a long time it was believed that in case of carbon monoxide poisoning, the development of hypoxia associated with the inactivation of hemoglobin is the only mechanism for the development of intoxication. Currently, data have been obtained indicating a certain significance in the development of intoxication of the interaction of carbon monoxide with myoglobin, cytochrome oxidase, cytochrome P-450, cytochrome C, and possibly with other iron- and copper-containing biochemical systems. Myoglobin in the body acts as a depot of oxygen, which is transferred to working muscles. The interaction of carbon monoxide with myoglobin occurs in the same way as with hemoglobin. As a result, carboxyhemoglobin is formed and the supply of oxygen to working muscles is disrupted. This explains the development of severe muscle weakness in those poisoned with carbon monoxide. Consequently, in case of carbon monoxide poisoning, both the transport of oxygen to the tissues and its deposition are disrupted. The possibility of interaction (in divalent form) of the cytochrome system with carbon monoxide, in particular cytochrome oxidase, cannot be excluded. All of the above leads to disruption of tissue respiration and redox processes. Thus, hypoxia is also tissue in nature. Undoubtedly, everything taken together leads to dysfunction of the central nervous system, cardiovascular, respiratory and others, which creates a clinical picture of poisoning.

General cerebral disorders are expressed in complaints of headaches in the temporal and frontal regions, often of a girdling nature, dizziness, and nausea. Vomiting occurs, sometimes repeatedly. Loss of consciousness develops up to deep coma. Violation of mental activity is manifested by agitation or stupor. Neuropsychic disorders can be expressed by symptoms characteristic of organic psychosis: memory impairment, disorientation regarding place and time, visual and auditory hallucinations, persecution mania, painful interpretation of surrounding reality and hallucinations. Stem-cerebellar disorders are characterized by miosis, mydriasis, anisocoria, but in most cases the pupils are of normal size and have a lively reaction to light. Unsteadiness of gait, impaired coordination of movements, tonic convulsions, and spontaneous myofibrillations are noted. Pyramidal disorders concern increased muscle tone of the limbs, increased and expanded zones of tendon reflexes, and the appearance of Babinski and Oppenheimer symptoms. Particular attention should be paid to the development of hyperthermia, which is of central origin and is considered one of the early signs of toxic cerebral edema, which is the most severe complication of acute carbon monoxide poisoning. When patients emerge from a comatose state and in the long-term period, long-term and persistent damage to the peripheral nerves is observed, such as cervicobrachial plexitis, damage to the radial, ulnar or median nerves, or a picture of polyneuritis involving the auditory, optic and other nerves. The development of asthenovegetative syndrome, toxic encephalopathy, and the phenomena of Korsakoff amnestic syndrome is possible. PSYCHONEUROLOGICAL DISORDERS

One of the leading symptoms of carbon monoxide poisoning is inspiratory dyspnea of ​​central origin. Fire victims often have impaired patency of the upper respiratory tract as a result of bronchorrhea and hypersalivation. Patients complain of difficulty breathing, sore throat, lack of air, and hoarseness. Many people experience a cough with sputum containing soot, and various wheezes are heard in the lungs. Swelling of the mucous membranes of the nasopharynx, acute nasopharyngitis and tracheobronchitis are noted due to the combined effects of smoke and high temperature of inhaled air, burns of the upper respiratory tract. Pathological processes in the lungs (pneumonia) are secondary and are caused by impaired airway patency. Impaired external respiration function is accompanied by impairment of CBS with the development of respiratory and metabolic acidosis. DISTRIBUTION OF EXTERNAL RESPIRATORY FUNCTION

When carbon monoxide is inhaled in high concentrations at the scene of an accident, sudden death may occur due to respiratory arrest and primary toxic collapse. In some cases, a picture of exotoxic shock develops. Hypertensive syndrome with severe tachycardia is often observed. ECG changes are nonspecific, usually these are signs of myocardial hypoxia and coronary circulation disorders: the R wave decreases in all leads, especially in the chest leads, the S-T interval shifts below the isoelectric line, the T wave becomes biphasic or negative. In severe cases, the ECG shows coronary circulatory disorders resembling myocardial infarction. These changes usually disappear quickly as the general condition of patients improves, but with prolonged exposure to CO, they can persist for up to 7-15 days. DISORDERS FUNCTION OF THE CARDIOVASCULAR SYSTEM

Trophic disorders often occur in those who are poisoned by car exhaust fumes. This is explained by the fact that most of these victims are found at the scene in an unconscious state, lying in an awkward position, with their limbs tucked and compressed (positional trauma). Victims report numbness, pain, and limited function of the affected part of the body. In the early stages of trophic skin disorders, bullous dermatitis with hyperemia of skin areas and swelling of subcutaneous tissues is observed. Sometimes trophic disorders take the form of ischemic polyneuritis, expressed in atrophy of individual muscle groups, impaired sensitivity and limited function of the limbs. In more severe cases, necrotizing dermatomyositis develops, when compactions and infiltrates are noted in areas of hyperemic skin with the further formation of tissue necrosis and deep ulcers. In especially severe cases of dermatomyositis, the development of mineral syndrome and acute renal failure due to myoglobinuric nephrosis of varying severity is possible. If poisoning has occurred recently, then the skin and visible mucous membranes are scarlet (the scarlet color is due to carboxyhemoglobin). The skin of patients in a state of severe hypoxia is cyanotic. TROPHIC DISORDERS AND DISORDERS OF RENAL FUNCTION

Depending on the concentration of the poison and the time it acts on the body, the severity of carbon monoxide intoxication is determined. Currently, toxicologists define two variants of the course of acute CO intoxication: slow - with a typical form of clinical course, which distinguishes degrees of severity (mild, moderate, severe) and fulminant - apoplexy and syncope forms. CLINICAL PICTURE OF POISONING

First, let's look at the clinical course of a typical form of poisoning. In case of mild poisoning, victims complain of a headache, a feeling of beating in the temples, tinnitus, palpitations, flashing before the eyes, dizziness, general malaise, muscle weakness, which is initially felt mainly in the legs, and the gait becomes unsteady. Poisoned people may experience general anxiety and fear. Euphoria and inappropriateness of actions often appear. Possible shortness of breath, nausea, vomiting. Objectively: there is a slight blush on the cheeks and cyanosis of the mucous membranes, consciousness is preserved, reflexes are increased, tremor of outstretched arms, there is a slight increase in breathing, pulse and a moderate increase in blood pressure. There is from 10 to 30% carboxyhemoglobin in the blood. After stopping contact with CO, the clinical manifestations of intoxication quickly subside, even without treatment, and after a few hours, less often 1-2 days, completely disappear.

With moderate poisoning, all of the above symptoms intensify, especially muscle weakness and adynamia (despite the life-threatening danger, patients are unable to independently overcome even a short distance). Coordination of movements is impaired, drowsiness and indifference to the environment appear. With further contact with the poison, a state of stupor occurs and there may be a short loss of consciousness. The skin and visible mucous membranes acquire a pinkish-reddish color. Shortness of breath is more pronounced. After an increase, blood pressure begins to decrease. Fibrillar contractions of individual muscle groups may be observed. In the blood, carboxyhemoglobin reaches 30-40%.

Severe intoxication is characterized by the development of the previously described picture with the transition to a prolonged comatose state (up to several days). The skin and mucous membranes are initially bright scarlet, later acquiring a cyanotic tint. Trophic skin lesions in the form of erythema, blisters, hemorrhagic and infiltrative formations may occur on the torso, and more often on the extremities. The pupils are dilated and do not respond to light. Tonic-clonic, trismus of the masticatory muscles, and stiff neck are periodically observed. Tendon reflexes are first increased, then decreased. There is involuntary urination and defecation. Breathing is shallow, irregular, often of the Cheyne-Stokes type. Pulse is frequent, weak filling; blood pressure is low. The heart increases in size. The first tone at the apex is weakened, and a systolic murmur is heard here. The ECG reveals diffuse and focal muscle changes, extrasystole, intracardiac conduction disturbances, and symptoms of acute coronary insufficiency. A clinical blood test reveals erythrocytosis and neutrophilia with a shift to the left. Carboxyhemoglobinemia reaches 40-50% or more. Particularly severe intoxications are observed when exposed to high concentrations of carbon monoxide. In this case, the clinical picture develops extremely rapidly - the so-called fulminant forms of poisoning. These include apolexic and syncope forms. In both cases, death occurs almost instantly. Those affected lose consciousness, fall, and then, after short-term convulsions or immediately stop breathing. In the syncope form, severe collapse or shock primarily develops, due to which the skin of the poisoned person acquires a gray-ash color (“white asphyxia”).

Deaths most often occur from damage to the respiratory center. If the coma lasts more than two days, the prognosis is usually unfavorable. If the patient comes out of a coma, psychomotor agitation, hallucinations, and retrograde amnesia are often observed. Subsequently, an asthenic state may remain for a long time. In extremely severe cases, after emerging from a coma, persistent organic changes in the nervous system are observed (until complete decortication). Memory impairment, decreased hearing and vision, paralysis, and psychosis may remain for a long time (and sometimes for life).

Treatment measures begin with removing the victim from the area with an increased concentration of carbon monoxide. Subsequently, specific and symptomatic therapy is carried out, including measures to restore external respiration (toilet of the oral cavity and upper respiratory tract, reflex stimulation of breathing, artificial ventilation), oxygen therapy, restoration of blood circulation, functions of the central nervous system, water-electrolyte and acid underlying conditions, as well as correction of metabolism. In case of carbon monoxide poisoning, the central place among therapeutic measures is occupied by oxygen therapy, which at the beginning of intoxication (toxigenic phase) can be considered as specific (antidote), and as the clinical picture of poisoning develops (somatogenic phase) - as symptomatic, aimed at eliminating the hypokic state. The reduction of carboxyhemoglobin to non-toxic concentrations occurs most rapidly with hyperbaric oxygen therapy. This most effective method of treating CO poisoning is applied (once or repeatedly) using both stationary and portable compression oxygen chambers (the lecturer can go into more detail on the types of pressure chambers, operating modes, etc.). To a certain extent, some authors include, along with oxygen therapy, treatment with cytochrome C in mg doses as pathogenetic therapy in order to compensate for its tissue deficiency and correct certain aspects of metabolism with its help. To accelerate the removal of CO from the body, iron and cobalt preparations are used. TREATMENT

The main provisions for providing medical care at the stages of evacuation are: bringing medical care as close as possible to the injured; early use of oxygen therapy; timely use of resuscitation measures. First aid in an outbreak includes putting a gas mask on the poisoned person. Then evacuation outside the outbreak is carried out. Those affected in an unconscious state and in the convulsive stage of intoxication need to be evacuated while lying down. First aid is carried out outside the outbreak, which allows you to remove the gas mask. Anticyan is administered - 1 ml intramuscularly, if necessary, cordiamine, mechanical ventilation.

First medical aid. Restoration of external respiration using breathing devices and service inhalers. The use of analeptics to stimulate breathing is unacceptable due to the ineffectiveness of the therapeutic dose and the increased danger to the body. Measures are being taken to prevent and relieve complications such as collapse, acute heart failure, convulsive syndrome, psychomotor agitation, cerebral edema, etc. Evacuation of moderate and severe victims is carried out lying on a stretcher with oxygen therapy along the way.

Qualified help. Carrying out hyperbaric oxygenation and a fuller range of resuscitation measures, including mechanical ventilation using breathing and oxygen equipment, as well as symptomatic therapy; prevention and treatment of acute hemodynamic disorders, administration of cardiac glycosides, vasoconstrictors, antiplatelet agents; for cerebral edema - craniocerebral hypothermia, lumbar puncture, administration of osmotic diuretics, etc.; for pulmonary edema - large doses of diuretics, ganglion blockers, alpha-blockers, calcium preparations; oxygen therapy with antifoam agents; correction of CBS and water-electrolyte status; relief of psychomotor agitation (sedatives, anticonvulsants, administration of lytic mixtures); prevention and treatment of pneumonia; correction of tissue metabolism (vitamins, hormones, biostimulants, etc.).

1. Gembitsky E.V., Alekseev G.I. and others. Military field therapy. -L., VMedA, S; Luzhnikov E.A. Clinical toxicology. - M.: Medicine S Literature

First aid for poisoning

Teacher of Makeevka Lyceum No. 2 “Prestige”

Pershina Inna Georgievna

Poisoning. Causes of poisoning.

A poison is any substance that, when ingested, causes poisoning, illness or death. The consequences of poisoning depend on various factors:

Type of toxic substance (or substances);

Amount of toxic substance;

The time when the poisoning occurred;

Duration of contact with a toxic substance;

Physiological characteristics of the victim (age, weight);

Method of entry into the body.

Ways of toxic substances entering the human body:

• digestive tract;
• Airways;
• skin (dermal method);
• as a result of injection.

Poisoning through the digestive tract:

Poisoning through the digestive tract occurs when toxic substances enter the body through the mouth or when these substances come into contact with the lips or mucous membranes of the mouth. These could be: medications, detergents, pesticides, mushrooms and plants. Many substances in small quantities are not poisonous and only lead to poisoning when taken in a significant dose.

Inhalation poisoning:

Gaseous or inhaled toxic substances enter the body through inhalation. These include gases and vapors, such as carbon monoxide coming from a car exhaust pipe or entering a room due to poor exhaust in a furnace or heating device, nitrous oxide (laughing gas) and substances used in manufacturing.

Dermal method of poisoning:

Toxic substances that penetrate the skin may be contained in some plants, solvents, and insect repellents. Injectable toxic substances enter the body through bites or stings from insects, animals, and snakes, or through syringe injection of medications or drugs.”

Signs and symptoms of poisoning:

The most important thing is to determine that poisoning has occurred. Look for anything unusual at the scene, such as a foul odor, flames, smoke, open or overturned containers, an open first aid kit, or an overturned or damaged plant.

The main signs and symptoms of poisoning include:

General painful condition or appearance of the victim; signs and symptoms of a sudden attack of illness;

Nausea, vomiting;

chest or abdominal pain;

Breathing disorders;

Sweating;

Salivation;

Loss of consciousness;

Muscle twitching;

Convulsions;

Burns around the lips, on the tongue or on the skin;

Unnatural skin color, irritation, wounds;

Strange behavior of the victim.

Principles of first aid:

Follow basic first aid principles for any emergency situation involving poisoning. Interview the victim or witnesses and try to find out:

What type of toxic substance was taken;

In what quantity?

How long ago.

If the toxic substance is unknown, collect a small amount of vomit for subsequent medical examination.

First aid for oral poisoning (when a toxic substance is ingested through the mouth)

Call an ambulance immediately. Find out the circumstances of the incident (in case of drug poisoning, present the medicine wrappers to the arriving medical worker).

If the victim is conscious

Provide gastric lavage. Let's drink a glass of clean water at a temperature of 18-20 C. For one liter of water, it is advisable to add a dessert spoon of salt (10 g) and a teaspoon of baking soda (5 g). After drinking every 300-500 ml of water, you should induce vomiting by touching the root of the tongue with your fingers. The total volume of liquid taken during gastric lavage should be at least 2500-5000 ml. Gastric lavage is carried out until “clean lavage waters”. If you are unconscious, do not rinse your stomach!

If the victim is conscious

Dissolve 10-20 tablets of activated carbon in a glass of water until it becomes a paste. Give the victim something to drink (as an absorbent).

Determine the presence of a pulse in the carotid arteries, the reaction of the pupils to light, and spontaneous breathing.

If the victim is unconscious

If there is no pulse, breathing, or pupillary response to light, begin CPR immediately.

If the victim is unconscious

Place the victim in a stable lateral position.

If the victim is unconscious

Wrap the victim in warm blankets and clothes. Call (on your own or with the help of others) an ambulance and ensure that the victim is transported to a medical facility.

First aid for inhalation poisoning (when a toxic substance enters through the respiratory tract)

Signs of carbon monoxide poisoning:

• pain in the eyes;
• tinnitus;
• headache;
• nausea;
• vomit,;
• loss of consciousness;
• redness of the skin.

Signs of household gas poisoning:

• heaviness in the head;
• dizziness;
• noise in ears;
• vomit;
• severe muscle weakness;
• increased heart rate;
• drowsiness;
• loss of consciousness;
• involuntary urination;
• paleness (blue discoloration) of the skin;
• shallow breathing;
• convulsions.

First aid:

Make sure that neither you nor the victim is in danger, take the victim to a safe place or open the windows and ventilate the room. Call an ambulance.

First aid:

Determine the presence of a pulse in the carotid arteries, the presence of pupillary reaction to light, and spontaneous breathing.

First aid:

If there is no pulse, breathing or reaction of the pupils to light, immediately begin cardiopulmonary resuscitation.

First aid:

When spontaneous breathing and heartbeat are restored, place the victim in a stable lateral position. Call (on your own or with the help of others) an ambulance and ensure that the victim is transported to a medical facility.

In the autumn season, cases of mushroom poisoning become more frequent. What to do if this does happen? Depending on the nature of the poisonous nature inherent in certain mushrooms, three types of poisoning are distinguished:

• the first species is associated with a group of mushrooms from the fly agaric genus - toadstool and related varieties containing amanithemolysin, amanitotoxin, and phalloidin.
• the second type is associated with the consumption of red, panther, porphyry and other varieties of fly agarics containing muscarine, mycoatropine, mycotoxin and other poisons.
• the third type is poisoning with strings that contain helvella acid, which destroys blood cells (hemoglobin) and the liver.

Toadstool poisoning

In recent years, the pale toadstool has come to be called a real killer, because until its “umbrella” cap opens, it is mistaken for a semi-edible or edible mushroom. This is the most poisonous of all mushrooms. The poison amanite, contained in the toadstool, decomposes liver cells. If timely assistance is not provided, the person quickly dies. All other mushrooms are small fry compared to this pale monster. Even cadaveric poison is much weaker than the poison of the pale grebe. Up to 90% of those poisoned by this mushroom die. This occurs, as a rule, due to the external similarity of this mushroom to edible mushrooms - russula, rows and champignons. For serious poisoning, it is enough to eat half or even a third of the mushroom, especially for children who are hypersensitive to mushroom poisons.

Toadstool poisoning

In the clinic of acute poisoning with toadstool, 4 periods can be distinguished.

1. The latent period lasts from 8 to 24 hours after eating mushrooms. All this time, the person feels practically healthy, although the poisons are already absorbed into the blood, making their way to vital centers.

2. During this period, lasting from one day to 6 days, the poison affects the gastrointestinal tract. The body begins to quickly lose water due to nausea and vomiting. There are stomach pains, frequent and loose stools, sometimes mixed with mucus and blood. In children, this period is very difficult, since the poison quickly penetrates the liver, from which they can die against the background of acute liver failure.

3. Impaired function of both the liver and kidneys. This usually happens on days 5–6. If during this period the patient does not have time to receive the entire complex of antitoxic therapy, then most often death occurs. If effective assistance was provided, then the 4th period begins.

4. The recovery period, when all body functions are gradually restored.

symptoms of toadstool poisoning :

• the appearance of sudden pain in the abdominal area,
• vomit,
• diarrhea (sometimes cholera-like type - “rice water”),
• severe general weakness,
• cyanosis (cyanosis) of the skin and mucous membranes,
• decrease in body temperature,
• convulsions.
• jaundice and liver enlargement may occur.
• The pulse is thread-like, weakly filled, up to 120-140 beats per minute.
• Blood pressure is significantly reduced.
• Possible loss of consciousness.

Fly agaric poisoning

Main signs of poisoning : nausea, vomiting, watery diarrhea, profuse sweating, salivation and lacrimation. Signs of neuropsychic disorders appear quite quickly: dizziness, confusion, hallucinations, delirium. The pupils are dilated. In severe cases, a coma with loss of consciousness develops.

Stitch and morel poisoning

Strings and morels belong to the category of conditionally edible mushrooms. They are poisonous to those who do not know how to handle them. Toxicity is destroyed with appropriate processing. These spring mushrooms contain helvella acid, a poison that can cause fatal poisoning. But boiling for 10–20 minutes completely neutralizes the poison, since helvella acid passes into the decoction. Stitches are also rendered harmless by drying; in this case, helvelic acid is oxidized by air and inactivated. Poisoning occurs when they are eaten unprocessed, undercooked or underdried.

Symptoms of poisoning develop after 6-10 hours of the incubation period: weakness, pain in the epigastric region, nausea, vomiting mixed with bile, and occasionally diarrhea. In severe cases, on the second day signs of jaundice appear, an enlarged liver and spleen, severe headaches, loss of consciousness, stupor, and convulsions are observed. Red blood cells are destroyed, that is, hemolysis occurs, in which hemoglobin leaves the red blood cells. As a result, the blood becomes transparent red (“lacquer blood”).

Symptoms of poisoning

develop after 6-10 hours of incubation period:

• weakness occurs
• pain in the epigastric region,
• nausea,
• vomiting mixed with bile,
• occasional diarrhea.
• in severe cases, on the second day signs of jaundice appear, an enlargement of the liver and spleen is observed,
• severe headaches,
• loss of consciousness,
• numbness,
• convulsions.
• red blood cells are destroyed, that is, hemolysis occurs, in which hemoglobin leaves the red blood cells. As a result, the blood becomes transparent red (“lacquer blood”).

External signs of poisoning:

Signs of poisoning are detected several hours after eating. Initial manifestations:

• stomach ache;
• nausea, vomiting;
• loose stools;
• headache and dizziness.

If poisoning with toadstool occurs, then on the second day the body temperature may rise, the liver may enlarge, and jaundice may develop. Symptoms such as rapid heartbeat and low blood pressure cannot be excluded. The most common causes of death are acute liver failure and damage to other vital organs.

First aid:

• First you need to make sure that it is really mushroom poisoning. At the first sign of it, you should immediately cleanse and rinse the gastrointestinal tract. Several tablets of activated carbon should be given internally to bind poisons. It is better to give it in the form of an aqueous suspension. After rinsing the stomach, the patient must be put to bed, after doing a cleansing enema. If for some reason it was not possible to administer a cleansing enema, you can limit yourself to a laxative - castor oil or bitter salt. With any poisoning, the patient loses a lot of fluid (with vomiting, diarrhea), and along with it, mineral compounds necessary for the normal course of metabolic processes are washed out of the body. Therefore, the loss of fluid and salt must be replenished, for which the victim is given small sips of salted water or strong tea. They also reduce the feeling of nausea and vomiting. Even with a clear improvement in the condition, the patient should not be allowed to drink alcohol. Alcohol in any concentration promotes faster dissolution and absorption of poisons into the body. Typically, those suffering from poisoning need cardiovascular medications. You can introduce camphor (2 ml of a 20% oil solution), cordiamine (1 ml). For convulsions, it is recommended to give one of the sedative medications. In all cases of mushroom poisoning, bed rest is required; in severe conditions, hospitalization is indicated.
• If poisoning is suspected or the first symptoms appear after eating mushrooms, it is necessary to induce vomiting and perform gastric lavage. To do this, drink a large amount of liquid and irritate the root of the tongue with your fingers, which will lead to reflex vomiting. After repeating the washing, you need to take activated carbon or carbolene orally. You can take white clay, milk, saline laxative. Lay the victim down and warm his legs with heating pads. Give plenty of fluids (tea, water are suitable for this). It is necessary to call an ambulance team and hospitalize the victim, as the condition may worsen.

First aid in case of poisoning household chemicals

First aid for poisoning by mouth.

Induce vomiting by sticking your finger down your throat. Vomiting should not be induced if the victim:

• is unconscious;
• is in a state of convulsions;
• pregnant woman;
• swallowed a caustic substance (acid or alkali) or a product containing petroleum (kerosene or gasoline);
• has heart disease.

When vomiting, only part of the ingested toxic substance is eliminated, therefore:

After vomiting, give the victim 5-6 glasses of water to reduce the concentration of the toxic substance in the stomach;

If necessary, induce vomiting again;

Call an ambulance.

First aid for poisoning by gaseous inhaled toxins:

• Make sure the scene of the accident is safe.
• Isolate the victim from exposure to gas or vapors. In this case, you need to take the victim out into fresh air and call an ambulance. Monitor airway, breathing and pulse and provide first aid if necessary.
• Help the victim get into a comfortable position until the ambulance arrives.

First aid for skin poisoning

First aid for poisoning through the skin from contact with poison is to thoroughly rinse the damaged area with water for 20 minutes. First of all, remove clothing contaminated with a toxic substance and try not to touch it until it is washed. If there is a wound, such as a burn, apply a clean or sterile, moist dressing.

Help at later stages after contact with a poisonous plant includes the following:

1. If a rash or blisters form on the skin, wash the affected area with a solution of baking soda for 20 minutes to reduce itching.

2. If the victim's condition worsens or a large area is damaged, consult a doctor who can prescribe medication.

First aid for skin contact with dry or liquid chemicals:

• Remove dry chemicals. Try not to damage the skin. Avoid contact of chemicals with your eyes and skin.
• Rinse the damaged area under running water. Although dry chemicals may cause a reaction when they come into contact with water, generous and prolonged rinsing under running water will quickly remove them from the skin.
• Wear protective gloves when providing assistance.

First aid for poisoning through food or air:

Respiratory cessation as a result of contact with a highly toxic substance occurs when it enters the human body through food or air. In this case, it is not recommended for the first aid provider to perform mouth-to-mouth artificial ventilation. The rescuer can only do the following:

1. Carry out artificial ventilation of the lungs

"mouth to nose", which can be somewhat

reduce the risk of infection.

2. Wait for the ambulance team to arrive,

which will apply special

ventilation device.

First aid for poisoning with acids and caustic alkalis:

Poisoning with acids and caustic alkalis (acetic essence, soldering liquid, bath washing liquid, carbolic, oxalic acid, caustic soda, ammonia). Signs of poisoning are burns of the lips, oral mucosa, pain in the larynx, excessive salivation, and bloody vomiting. Before the ambulance arrives, saliva and mucus should be removed from the victim’s mouth. To do this, wipe the oral cavity with a piece of gauze or napkin wrapped on a teaspoon. If signs of suffocation appear, begin artificial respiration. Usually the mouth-to-nose method is used, since the mucous membrane of the mouth is burned. Victims often vomit blood. Since this can lead to acid or alkali entering the respiratory tract, which will worsen the condition, the victim should be given 2-3 glasses of water (no more) to drink to reduce the concentration of the caustic liquid and reduce its destructive effect. You should not try to neutralize the poisonous liquid with soda, as this leads to the formation of a large amount of carbon dioxide, which stretches the stomach, increases pain and bleeding.

Poisoning with industrial fluids usually develops after ingestion in large quantities. Signs of poisoning are agitation, redness and then paleness of the face, the smell of alcohol on the breath, dizziness, nausea, vomiting, unconsciousness, and sometimes convulsions. If the patient is conscious, then you should immediately clear his stomach by giving him a drink of either water or a weak solution of baking soda (1 teaspoon per 1 glass), then induce vomiting. In the future, if there is no nausea and vomiting, the victim is offered to drink strong tea or coffee. Poisoning with alcohol substitutes such as methyl alcohol and ethylene glycol is very dangerous. In these cases, the victim is given to drink, if he is conscious, 100 - 150 ml of vodka, which in this case is an antidote. However, this is not enough to save the patient; since the vital functions of the body are subsequently disrupted, the patient must be urgently taken to a medical facility.

• Signs: first, excitement, redness of the face, the smell of alcohol on the breath, then delirium, paleness of the face, unconsciousness. It is necessary to carefully sniff ammonia. After gastric lavage, cover the patient with heating pads. Drink plenty of hot drinks (strong coffee).

In case of poisoning with industrial poisons.

Such poisons include many drugs and liquids used for technical purposes (for example, antifreeze). In agriculture, various metal salts and mineral fertilizers are used. It must be borne in mind that chemicals, especially those containing potassium, are poisonous. You cannot work with them without following special instructions. In all cases where there is a suspicion of industrial poisoning, you should resort to gastric lavage, enemas and immediate medical attention. Arsenic poisoning is characterized by continuous vomiting and diarrhea, which leads to cramps and bluish extremities. It is necessary to do gastric lavage and call an ambulance.

First aid for insecticide poisoning

Since insect control is carried out by spraying from a spray bottle or a vacuum cleaner, the air is saturated with larvae of these poisons and easily enters the respiratory tract, onto the mucous membranes of the eyes, mouth and skin. Therefore, it is necessary to use them strictly following the instructions. If the poison gets on the skin, it can cause ulcers; damage to the mucous membranes of the eyes leads to severe eye diseases and partial loss of vision. In case of poisoning with vapors of t and ophos or chlorophos, headache, dizziness, muscle pain, and loss of appetite appear. After a few days, these symptoms may subside, but if the vapor concentration is high, damage to the central nervous system may occur.

First aid for poisoning with household chemicals in a child

Poisoning by household chemicals in a child can be very dangerous if it is acetone, chlorophos, rodent control agents, aniline dyes, naphthalene. In this case, the child needs emergency medical care. Less toxic are cosmetics, shoe polish, purple and red ink, watercolor and oil paints, paraffin candles, shaving cream, and shampoo. In case of poisoning with any household substances, it is necessary to immediately induce vomiting in the child by pressing a finger or the handle of a spoon on the root of the tongue, give plenty of fluids and seek medical help.

Prevention of poisoning

It is best, of course, to prevent the occurrence of poisoning. But people are often not careful enough. For example, most cases of poisoning in children occur when there are no adults nearby to supervise them. Children are curious by nature and can get to something they are interested in in a matter of seconds. Many substances found in or around the home are toxic. Children are at greater risk of poisoning because they often put everything in their mouths. Many household items and indoor plants contain dangerous toxic substances. To prevent cases of poisoning, follow some general rules:

• Keep all medications, household products, poisonous plants and other hazardous substances away from children. Use cabinets with a lock. Treat all household and medicinal substances as potentially hazardous.
• Never call medicine candy when giving it to your child.
• Store all products in their original, labeled containers.
• Never store household items in food or drink containers.
• Use special symbols for toxic substances and teach children what they mean.
• Unusable or expired food should be thrown away. At the same time, make sure that they do not reach children.
• The use of potentially hazardous chemicals should be carried out in a well-ventilated area and only strictly according to the instructions.

Prevention of poisoning

• In areas where there are a lot of ticks, wear light-colored, but not very bright clothing, which makes it easier to see small insects or ticks on them. Wear a long-sleeved shirt and long pants. Tuck the ends of your trousers into your socks or boots. Tuck your shirt into your trousers.
• When hiking in the forest or field, try to follow the path. Avoid bushes or tall grass.
• When you return home, examine yourself carefully. Pay special attention to the hairy part of the body (back of the neck and hair on the head).
• Collect only those mushrooms that you know well and are sure that they are not poisonous.
• Never pick mushrooms that have a tuberous thickening or collar at the base of the stem.
• Take mushrooms only with stems - this will help avoid encounters with toadstool (especially when collecting russula).
• Do not taste raw mushrooms.
• Do not eat overripe, slimy, flabby, wormy or spoiled mushrooms.
• Do not eat mushrooms from jars that are hermetically sealed at home due to the risk of botulism.

References:

1. Arustamov E.A., Voronin V.A., Zenchenko A.D., Smirnov S.A. Life safety: Textbook. – M.: Publishing and trading corporation "Dashkov and K". 2005.

2. Life safety: Textbook for students / Ed. Ed. S.V. Belova. – 3rd ed., rev. and additional – M.: Higher. school . 2003.

3. Hwang T.A., Hwang P.A. Life safety. Series "Textbooks and teaching aids". – Rostov-on-Done: “Phoenix”. 2001.

4. Hwang T.A., Hwang P.A. Life safety. Series "Textbooks and teaching aids". Rostov-on-Done: "Phoenix". 2002.

5. Mikryukov V.Yu. . Ensuring life safety. In 2 books. Book 1. Personal safety: Proc. Benefit – M.: Higher. school . 2004.

BMST named after Academician N. M. Amosov Presentation on the topic: “Carbon monoxide poisoning” Prepared by students of group 1fr11:
Kozel Veronica, Nikiforova Svetlana,
Mameev Ivan, Pozdnyak Marina,
Nikiforova Daria, Kondrikova Victoria,
Panin Igor, Minok Christina

Plan:

What is carbon monoxide?

At-risk groups

At-risk groups

Impact on humans

Clinic

Signs and symptoms

symptoms:

Treatment

First aid for carbon monoxide poisoning

Let's summarize what to do in case of carbon monoxide poisoning.

Antidote

Pharmacological properties.

Indications for use.

Indications for use.

Overdose and side effects.

Storage conditions for Acizol.