Carbon monoxide poisoning Completed. Carbon monoxide presentation for the lesson (grade 8) on the topic Signs of household gas poisoning
Presentation on life safety.
Subject: Carbon monoxide poisoning. General poisoning by gaseous products of combustion.
Made 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 affect the body (toxodoses) or quantities that pose a threat to life and health.
The most toxic combustion products are synthetic polymeric materials. Most plastics emit toxic substances during combustion: carbon monoxide, hydrogen cyanide, hydrogen chloride, acrolein, nitrogen oxides, various aliphatic and aromatic hydrocarbons, etc. Foam rubber used for the manufacture of 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, associated with this, the inability to independently exit the fire zone, lead to the fact that the victims are exposed to harmful substances for a long time.
Slide number 3.
Carbon monoxide (carbon monoxide) is colorless, odorless and tasteless, does not cause eye irritation in its pure form, which explains the imperceptibility of the development of acute poisoning of 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 the exhaust, powder, explosive gases, is formed during fires, especially in confined spaces (premises). Acute carbon monoxide poisoning, as a rule, occurs when working with internal combustion engines, gas generators and operating technically faulty furnaces, heating appliances, 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 a much greater ability than oxygen to combine with the hemoglobin of red blood cells (erythrocytes) of the blood. In this case, carboxyhemoglobin is formed, which is not able 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 doing physical work at the time of poisoning. Practice shows that a person doing hard physical work can be poisoned by half the amount of carbon monoxide in the air than a person who is at rest. Sensitivity to carbon monoxide also increases with increasing external temperature and humidity.
The mechanism of action of carbon monoxide on a person is that it, getting into the blood, binds hemoglobin cells. Then hemoglobin loses its ability to carry oxygen. And the longer a person breathes carbon monoxide, the less efficient hemoglobin remains in his blood, and the less oxygen the body receives. A person begins to suffocate, a headache appears, consciousness is confused. And if you do not go out into the fresh air in time (or do not take out the already unconscious person into the fresh air), then a lethal outcome is not ruled out. In the case of carbon monoxide poisoning, it takes a long time for the hemoglobin cells to be completely cleared of 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 for 5-6 hours of inhalation of such air, a concentration of carboxyhemoglobin of 25-30% will be created, 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 reached after 20-30 minutes of a person's stay in such an environment.
Slide number 6.
Carbon monoxide poisoning can appear abruptly or slowly, depending on the concentration. At very high concentrations, poisoning occurs quickly, characterized by rapid loss of consciousness, convulsions and respiratory arrest. In the blood taken from the region of the left ventricle of the heart or from the aorta, a high concentration of carboxyhemoglobin is found - 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 a disorder of coordination of movements; rave; hallucinations; loss of consciousness; convulsions; coma and death from paralysis of the respiratory center. The heart may still beat for some time after breathing has stopped. There have been cases of people dying from the consequences of poisoning even 2-3 weeks after the poisoning event.
Slide number 7.
Severe complications are often noted:
Violation of cerebral circulation
Subarachnoid hemorrhages
Polyneuritis - multiple lesions of the nerves.
Phenomena of cerebral edema
visual impairment
Hearing loss
Possible myocardial infarction
Skin-trophic disorders (blisters, local edema with swelling and subsequent necrosis) are often observed.
With prolonged coma, severe pneumonia is constantly noted.
Slide number 8.
First aid. Initial inspection:
Check the patient's vital parameters: the presence of 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) color of the mucous membranes, tachycardia (increase in heart rate from 90 beats per minute) are noted.
Slide number 9.
Hypotension - decreased tone of blood vessels or muscles. Often hypotension is called 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, impaired consciousness.
Slide number 10.
Shock (from the English shock - blow, shock) is a pathological process that develops in response to exposure to extreme stimuli and is accompanied by a progressive violation of the vital functions of the nervous system, blood circulation, respiration, metabolism and some other functions. In fact, 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:
lowering blood pressure and tachycardia;
anxiety (erectile phase according to Pirogov) or blackout of consciousness (torpid phase according to Pirogov);
respiratory failure;
decrease in the volume of urine excreted;
cold, moist skin that is pale cyanotic or marbled.
Slide number 11.
The clinical classification divides shock into four grades according to its severity.
Shock I degree. Consciousness is preserved, the patient is in contact, slightly retarded. Systolic blood pressure (BP) exceeds 90 mm Hg, pulse is rapid.
Shock II degree. Consciousness is preserved, the patient is inhibited. Systolic blood pressure 90-70 mm Hg, pulse 100-120 beats per minute, weak filling, shallow breathing.
Shock III degree. The patient is adynamic, lethargic, does not respond to pain, answers questions in monosyllables. The skin is pale, cold, with a bluish tint. Breathing shallow, frequent. Systolic blood pressure below 70 mmHg, pulse over 120 beats per minute, thready, central venous pressure (CVP) zero or negative. There is anuria (lack of urine).
IV degree shock manifests itself clinically as one of the terminal conditions.
Roughly, 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, cognitive decline, gait disturbance, tics including irritability, bizarre behavior, and hyperactivity.
In acute poisoning, initially there is heaviness in the head, a feeling of squeezing the forehead (“as if with a hoop or pincers”), and later there is a severe headache with 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 frequent, 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 take it out of a smoky or gassed room.
In the absence of breathing, carry out the procedure of artificial ventilation of the lungs mouth to mouth or mouth to nose. However, care should be taken, poisoned by gas, a person exhales poison! When carrying out IVL, it is necessary to use a damp cloth or gauze bandage. When carrying out the procedure, artificial ventilation by mouth-to-mouth or mouth-to-nose, draw air away from the face of the victim.
Call an ambulance immediately. Artificial respiration should be carried out before the arrival of doctors, if the victim is not breathing on his own.
Firefighters and rescuers have personal protective equipment, including oxygen tanks and masks, if rescuers are at the scene before the arrival of the ambulance, it is necessary to use these means to facilitate breathing for the 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 victim to fresh air.
If the victim is conscious, provide continuous access to fresh air and short-term inhalation of ammonia, rub the body.
Call an ambulance.
If the victim is unconscious, artificial respiration should be started immediately until consciousness is regained or an 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 - reduced oxygen content in the blood.
Manifestations of hypoxia:
In adults: restlessness
pale skin
In children: pronounced fear
tearfulness
sometimes spastic muscle contraction and convulsions occur.
Slide number 16.
If you have established that the victim is in a state of hypoxia, then you need to
remove the victim to fresh air, give oxygen to breathe.
If the victim is not breathing, then it is necessary to make artificial ventilation of the lungs.
slide number 17.
CPR is a form of ventilation that provides oxygenation and ventilation (removal of carbon dioxide) to the victim.
IVL method "from mouth to mouth" is carried out as follows. The person assisting with one hand, placed on the forehead of the victim, bends his head back, while supporting it with the other hand, placed under the neck and back of the head. The fingers of the hand located on the forehead cover the nose so that there is no air leakage. The person providing assistance tightly covers the mouth of the victim 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 straightened out, the assisting person turns his head to the side and the patient passively exhales. Intervals of respiratory cycles should be within the physiological norm - no more than 10-12 per 1 min. (1 respiratory cycle for 4-5 counts). The volume of exhaled air should be approximately 50% more than the usual volume.
slide number 18.
When fire in the building, those present must observe safety measures. One of the measures is the use of personal respiratory protection equipment when leaving smoky and burning rooms. The timely use of personal protective equipment will protect the respiratory organs from toxic combustion products, thereby preserving the health and life of the victims.
Self-rescuer insulating fire-fighting SIP-1 is designed to protect organs breathing, eyesight and facial skin from harmful substances, regardless of their concentration, during self-evacuation from premises during a fire or in other emergencies. Self-rescuer insulating fire-fighting designed for use by people over 12 years old.
The self-rescuer SIP-1 is produced ready for use and does not require individual adjustment, it is supplied in a hard package (case) and in a soft fabric package (bag). The SIP-1 self-rescuer is a disposable respiratory protection device.
SIP-1 differs from similar insulating self-rescuers by the location of the breathing bag around the neck, and not on the chest, which allows you to carry goods or property, or people who have lost consciousness. The design of the self-contained self-rescuer prevents the half-mask from tearing off the face, as well as the loss of breathing mixture from the bag when bending over, falling, crawling or colliding with obstacles.
Gas and smoke protective kit universal GDZK-U - a filtering means of protection designed to protect the respiratory organs, eyes and head of a person from smoke and toxic gases.
The GDZK-U kit consists of a fire-resistant hood with a viewing window, a half mask with an exhalation valve, a filter-absorbing box, an adjustable headband, an airtight bag and a bag with a user manual, there is an instruction manual in the pocket of the bag.
The GDZK-U kit provides protection for at least 30 minutes at high concentrations of the main toxic combustion products and chemically hazardous substances of various classes.
The kit provides protection at ambient temperatures from 00 to 600C and retains its 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.
Hood protective universal KZU
The advanced protective hood is a single-use filtering protective device and is designed to protect the respiratory organs, eyes and scalp of a person from gases, vapors and aerosols of hazardous chemicals and toxic combustion products, as well as for a short time from exposure to an open flame. 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.
It is operated 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 the elderly and smokers, equipping your apartment with fire alarms, smoke detectors, fire extinguishers, fire safety behavior will help you save your life and property.
Completed by: student of the 5th year of 504 group 1 medical Palichuk I.N. State Institution "KSMU im. S.I.Georgievsky "Department of internal medicine №3 Head of the department prof. Khrenov A.A. Lecturer Assoc. Kushnir S.P. studentdoctorprofessor.com.ua sdp.net.ua
slide 2
Carbon monoxide (carbon monoxide) is a colorless, odorless and tasteless gas. Carbon monoxide can be formed wherever conditions are created for the incomplete combustion of carbonaceous substances. It is an integral part of many gases and aerosols: in generator gases - 9-29%, in explosive gases - up to 60%, in vehicle exhaust gases - an average of 6.3%. studentdoctorprofessor.com.ua sdp.net.ua
slide 3
Carbon monoxide poisoning is possible in boiler houses, foundries, when testing motors, in garages, vehicles, gas plants, mines, etc.; in everyday life with improper heating of stoves or improper use of gas stoves. MPC - 20 mg/m3. studentdoctorprofessor.com.ua sdp.net.ua
slide 4
Receipt and excretion from the body - through the respiratory system in unchanged form. Due to its high affinity for hemoglobin, it causes blockade of hemoglobin (formation of carboxyhemoglobin) and impaired oxygen transport. It inhibits the dissociation of oxyhemoglobin, inhibits tissue respiration (mixed hemic-tissue hypoxia), causes hypocapnia. studentdoctorprofessor.com.ua sdp.net.ua
slide 5
Carbon monoxide quickly crosses the blood-brain barrier. The action on the central nervous system is due to both hypoxia and the direct action of carbon monoxide. studentdoctorprofessor.com.ua sdp.net.ua
Slide 6: Symptoms
Mild degree of carbon monoxide intoxication - headache, mainly in the temples and forehead, "throbbing in the temples", dizziness, tinnitus, vomiting, muscle weakness. Increased respiration and pulse. Fainting, especially when performing physical work. studentdoctorprofessor.com.ua sdp.net.ua
Slide 7
One of the earliest symptoms is a decrease in the speed of reactions, a violation of color perception. studentdoctorprofessor.com.ua sdp.net.ua
Slide 8: With moderate intoxication
Loss of consciousness for several hours or significant memory lapses. Loss of criticism. Sharp adynamia. Disturbance of coordination of movements, trembling. Upon the return of consciousness - a pronounced asthenic state studentdoctorprofessor.com.ua sdp.net.ua
Slide 9: Symptoms of a severe form of intoxication
Protracted coma (up to 5-7 days or more). Brain damage, muscle rigidity of the limbs, clonic and tonic convulsions, seizures. Involuntary urination and defecation. Cyanosis of extremities, general hyperhidrosis. The complexion is bright scarlet (this color is given by carboxyhemoglobin). studentdoctorprofessor.com.ua sdp.net.ua
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Slide 10
Breathing is intermittent, maybe of the 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. After leaving the coma - a long state of stunning. Apathy. There may be a short-term delirious state, a sharp motor excitation, delirium, complete retrograde amnesia. studentdoctorprofessor.com.ua sdp.net.ua
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slide 11
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 intoxication, mononeuritis of the ulnar, median or common peroneal nerve is possible, paresis, paralysis are possible. studentdoctorprofessor.com.ua sdp.net.ua
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slide 12 visual impairment
double vision, color blindness; swelling of the nipple of the optic nerve and retina, atrophy of the optic nerve (rarely). studentdoctorprofessor.com.ua sdp.net.ua
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Slide 13: Damage to the skin and hair
Trophic skin lesions, hemorrhagic rashes, erythematous-bullous forms (a picture of a “thermal burn”), painful dense edema, more often of the distal extremities, graying, hair loss. studentdoctorprofessor.com.ua sdp.net.ua
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Slide 14: Changes in the circulatory and respiratory system
From the very first hours of carbon monoxide intoxication, there are pronounced changes in the circulatory and respiratory system. First, functional disorders - tachycardia, pulse lability, extrasystole, and coronary insufficiency can also be observed. In case of moderate and severe poisoning - toxic damage to the myocardium (as a result of both hypoxia and the direct action of carbon monoxide on the heart muscle) with symptoms of cardiovascular insufficiency. studentdoctorprofessor.com.ua sdp.net.ua
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slide 15
On the ECG - diffuse muscle changes, after a few days, taking 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, often occur in young people (up to 30 years). Coronary insufficiency may not be clinically determined (pain may be completely absent). Recovery is slow. Exacerbations are possible.
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Slide 16: Changes in the bronchopulmonary apparatus
Bronchitis, moderate and severe intoxication - toxic pneumonia, pulmonary edema, developing within 1 - less than 2 days. Clinical symptoms are very poor and do not correspond to the severity of x-ray data. studentdoctorprofessor.com.ua sdp.net.ua
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Slide 17: X-ray examination of the lungs, taken 10-15 hours after the onset of carbon monoxide intoxication, changes are found in the form of three forms:
1. Emphysema and increased lung pattern. The shadows of the gates of the lungs are expanded, consist of small-focal and linear formations. After 1-3 days - full recovery. studentdoctorprofessor.com.ua sdp.net.ua
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Slide 18
2. Along with the above, changes of a focal nature with fuzzy contours, occupying the basal region, densely spaced, without a tendency to merge. On the 3-4th day, the normal pulmonary pattern is restored.
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Slide 19
3. Diffuse macrofocal changes in the lung tissue, irregular in shape, with blurry contours, 1-2 cm in size, merging in places. Emphysema of the lungs 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
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Slide 20
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, moderate fever joins on the 2nd week, the general condition worsens again, and when listening, moist and scattered dry rales are determined (the so-called post-burn pneumonia). These broncho-pneumatic changes, with a favorable course, soon disappear, and normal pneumatization of the lungs is restored. sdp.net.ua
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slide 21
Particular attention should be paid to hemodynamic disturbances in carbon monoxide intoxication. Almost half of the victims radiologically observed an acute total increase in the heart with a predominance of the right sections. Normalization after 3-5 days. Pulmonary edema and acute expansion of the heart sharply exacerbate intoxication. For early diagnosis of changes in the lungs and heart, X-ray examination should be performed as early as possible. sdp.net.ua
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slide 22: blood changes
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Slide 23: chronic intoxication
Complaints of headaches, noise in the head, dizziness, increased fatigue, irritability, poor sleep, memory impairment, short-term disorder of orientation, palpitations, pain in the heart, shortness of breath, fainting, disorders of skin sensitivity, smell, hearing, functions of the vestibular apparatus, vision (violation of color perception, narrowing of the field of vision, disturbance of accommodation). Nutritional decline. Functional disorders of the central nervous system - asthenia, autonomic dysfunction with angiodistonic syndrome, a tendency to vascular spasms, hypertension, in the future, the development of hypertension is possible. Myocardial dystrophy, angina phenomena. ECG shows focal and diffuse changes, coronary disorders. sdp.net.ua
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slide 24
Chronic poisoning contributes to the development of atherosclerosis and aggravates the course of the latter, if it already occurred before intoxication. Endocrine disorders, in particular thyrotoxicosis. sdp.net.ua
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Slide 25
Some diagnostic value is the determination of the content of carboxyhemoglobin in the blood, but there is no parallelism between its amount and the severity of intoxication. The speed of development, the severity of acute and chronic intoxications may depend on the individual characteristics of the organism and on 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
The gas is colorless and odorless. Molecular weight 28.01. Boiling point 190 o C, density 0.97. It does not dissolve in water, it burns with a bluish flame. It occurs wherever conditions exist for incomplete combustion of substances containing carbon. carbon monoxide
In wartime, poisoning can occur during explosions of rockets, mines, shells, ordnance of a volumetric explosion, when firing from enclosed spaces, in persons located in a territory engulfed in large fires as a result of the use of incendiary mixtures by the enemy. In peacetime, the most typical situations that cause carbon monoxide poisoning are malfunctions or violations of the rules for operating heating systems, malfunctions of internal combustion engines or their operation in enclosed spaces (garages, boxes, hangars). In military personnel, poisoning can also be associated with violations of the operation of military equipment (cars, tanks, artillery systems, aircraft).
Refers to substances of general toxic action. 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 allowable concentration of carbon monoxide in the air of working premises is 20 mg/m 3. The toxicity of carbon monoxide is primarily due to its concentration in the air and 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 difficult with psycho-emotional stress, physical exertion), age (more difficult in children and the elderly).
When inhaled, the air infected by it easily overcomes the pulmonary-capillary membrane of the alveoli and penetrates into the blood. There it interacts with erythrocyte hemoglobin, forming carboxyhemoglobin, 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 oxidized and reduced forms of hemoglobin. An 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 poison attachment to hemoglobin. It has been established that the rate of addition of CO to hemoglobin is not higher, but approximately 10 times lower than the rate of addition of oxygen. At the same time, the rate of dissociation 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 for 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 hemoglobin inactivation is the only mechanism for the development of intoxication. Currently, data have been obtained indicating a certain importance 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 disturbed. The possibility of interaction (in the divalent form) of the cytochrome system with carbon monoxide, in particular, with cytochrome oxidase, is not ruled out. All of the above leads to disruption of tissue respiration and redox processes. Thus, hypoxia also has a tissue character. Undoubtedly, all taken together leads to dysfunction of the central nervous system, cardiovascular, respiratory and others, which creates a clinical picture of poisoning.
Cerebral disorders are expressed in complaints of headache in the temporal and frontal regions, often of a girdle character, dizziness, and nausea. There is vomiting, sometimes repeated. Loss of consciousness develops up to a deep coma. Violation of mental activity is manifested by excitement or stunning. Neuropsychiatric disorders can be expressed by symptoms characteristic of organic psychosis: memory impairment, disorientation regarding the place and time of being, visual and auditory hallucinations, persecution mania, painful interpretation of the surrounding reality and hallucinations. Stem-cerebellar disorders are characterized by miosis, mydriasis, anisocoria, but in most cases the pupils are of normal size, a live reaction to light. Unsteadiness of gait, impaired coordination of movements, tonic convulsions, spontaneous myofibrillations are noted. Pyramidal disorders relate to an increase in the muscle tone of the limbs, an increase and expansion of tendon reflex zones, the appearance of Babinski's and Oppenheimer's symptoms. Particular attention should be paid to the development of hyperthermia, which is of central origin and is considered as one of the early signs of toxic cerebral edema, which is the most severe complication of acute carbon monoxide poisoning. When patients leave a coma and in the long-term period, long-term and persistent lesions of peripheral nerves are observed according to the type of cervical-brachial plexitis, lesions of the radial, ulnar or median nerves, or a picture of polyneuritis with involvement in the process of auditory, optic and other nerves. Perhaps the development of asthenovegetative syndrome, toxic encephalopathy, the phenomena of Korsakov's amnestic syndrome. PSYCHONEUROLOGICAL DISORDERS
One of the leading symptoms of carbon monoxide poisoning is inspiratory dyspnea of central origin. In fire victims, the patency of the upper respiratory tract is often impaired as a result of bronchorrhea and hypersalivation. Patients complain of shortness of breath, sore throat, lack of air, hoarseness. Many have a cough with sputum containing soot, various rales are heard in the lungs. There are swelling of the mucous membranes of the nasopharynx, acute nasopharyngitis and tracheobronchitis due to the combined effects of smoke and high temperature of the inhaled air, burns of the upper respiratory tract. Pathological processes in the lungs (pneumonia) are secondary and are caused by impaired airway patency. Violation of the function of external respiration is accompanied by a violation of the acid-base balance with the development of respiratory and metabolic acidosis. DISTURBANCE OF EXTERNAL RESPIRATORY FUNCTION
At the moment of inhalation of carbon monoxide in high concentration at the scene, 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, the S-T interval shifts below the isoelectric line, the T wave becomes biphasic or negative. In severe cases, the ECG shows violations of the coronary circulation, resembling a myocardial infarction. These changes usually disappear quickly as the general condition of patients improves, however, with prolonged exposure to CO, they can persist up to 7-15 days. CARDIOVASCULAR DISTURBANCE
Trophic disorders often occur in vehicles poisoned by exhaust fumes. This is due to the fact that most of these victims are found at the scene in an unconscious state, lying in an uncomfortable position, with twisted and squeezed limbs (positional injury). Victims note numbness, pain, limited function of the affected part of the body. In the early stages of skin-trophic disorders, bullous dermatitis is observed with hyperemia of skin areas and swelling of subcutaneous tissues. Sometimes trophic disorders take the form of ischemic polyneuritis, which is expressed in the atrophy of certain muscle groups, impaired sensitivity and limited function of the limbs. In more severe cases, necrotic dermatomyositis develops, when in areas of hyperemic skin there are seals and infiltrates with further formation of tissue necrosis and deep ulcers. In especially severe cases of dermatomyositis, a mineral syndrome and acute renal failure may develop due to myoglobinuric nephrosis of varying severity. If the 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 KIDNEY DISFUNCTION
Depending on the concentration of the poison and the time of its action on the body, the severity of intoxication with carbon monoxide is determined. Currently, toxicologists define two variants of the course of acute CO intoxication: delayed - with a typical form of the clinical course, where they distinguish degrees of severity (mild, moderate, severe) and fulminant - apoplexy and syncopal forms. CLINICAL PICTURE OF POISONING
Let us first consider the clinical course of a typical form of poisoning. In case of mild poisoning, the victims complain of headache, a feeling of pounding in the temples, tinnitus, palpitations, flashing before the eyes, dizziness, general malaise, muscle weakness, which is initially felt mainly in the legs, the gait becomes shaky. Poisoned people may experience general anxiety, fear. Often there is euphoria, inexpediency of actions. Possible shortness of breath, nausea, vomiting. Objectively: there is a slight blush and cyanosis of the mucous membranes on the cheeks, consciousness is preserved, reflexes are increased, tremor of the outstretched arms, a slight increase in respiration, pulse and a moderate increase in blood pressure are noted. In the blood from 10 to 30% carboxyhemoglobin. After cessation of contact with CO, the clinical manifestations of intoxication quickly decrease, even without treatment, and after a few hours, less often 1-2 days, they completely disappear.
In case of moderate poisoning, all the above symptoms increase, especially muscle weakness and adynamia (despite the danger that threatens life, patients are not able to overcome even a short distance on their own). Coordination of movements is disturbed, drowsiness and indifference to the environment appear. Upon further contact with the poison, a state of stupor occurs and there may be a short loss of consciousness. Skin and visible mucous membranes acquire a pinkish-reddish color. Shortness of breath is more pronounced. Blood pressure after the increase begins to decrease. Fibrillar contractions of individual muscle groups can 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 protracted coma (up to several days). The skin and mucous membranes are initially bright scarlet, subsequently becoming cyanotic. On the trunk, and more often on the extremities, trophic skin lesions can occur in the form of erythema, blisters, hemorrhagic and infiltrative formations. The pupils are dilated and do not react to light. Periodically observed tonic-clonic, trismus of masticatory muscles, stiff neck. Tendon reflexes are first increased, then lowered. There is involuntary urination, defecation. Breathing is shallow, irregular, often of the Cheyne-Stokes type. Pulse is frequent, weak filling; blood pressure is low. The heart is enlarged. The first tone at the apex is weakened, a systolic murmur is also heard here. On the ECG, diffuse and focal muscle changes, extrasystole, intracardiac conduction disturbances, and acute coronary insufficiency are determined. In a clinical blood test, erythrocytosis, neutrophilia with a shift to the left are found. 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 lightning-fast forms of poisoning. These include apolexic and syncopal forms. In both cases, death occurs almost instantly. The affected lose consciousness, fall, and then, after short-term convulsions or immediately stops breathing. In the syncopal form, severe collapse or shock primarily develops, due to which the skin of the poisoned person acquires a gray-ashy 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 poor. If the patient comes out of a coma, psychomotor agitation, hallucinations, retrograde amnesia are often observed. Subsequently, an asthenic state may remain for a long time. In extremely severe cases, persistent organic changes in the nervous system (up to complete decortication) are observed after coming out of a coma. For a long time (and sometimes for life) there may be memory impairment, hearing loss and vision loss, paralysis, psychosis.
Therapeutic measures begin with the removal of the victim from the area with a high concentration of carbon monoxide. In the future, specific and symptomatic therapy is carried out, including measures to restore external respiration (toilet of the oral cavity and upper respiratory tract, reflex excitation of breathing, artificial ventilation of the lungs), oxygen therapy, restoration of blood circulation, the function of the central nervous system, water-electrolyte and acid- underlying conditions, as well as correction of metabolism. In case of carbon monoxide poisoning, oxygen therapy occupies a central place among therapeutic measures, 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 way to treat CO poisoning is used (once or repeatedly) using both stationary and portable compression oxygen chambers (the lecturer can dwell in 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 doses of mg to pathogenetic therapy in order to compensate for its tissue deficiency and correct certain aspects of metabolism with its help. Iron and cobalt preparations are used to accelerate the removal of CO from the body. TREATMENT
The main provisions in the provision of medical care at the stages of evacuation are: the maximum approximation of medical care to the injured; early use of oxygen therapy; timely use of resuscitation measures. First aid in the outbreak includes putting on a gas mask on the poisoned person. Then evacuation is carried out outside the outbreak. Affected in an unconscious state and the convulsive stage of intoxication need to be evacuated lying down. First aid is carried out outside the hearth, which allows you to remove the gas mask. Antician is introduced - 1 ml intramuscularly, if necessary, cordiamin, mechanical ventilation.
First aid. Restoration of external respiration using breathing devices and standard inhalers. The use of analeptics to stimulate respiration 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 such complications 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 more complete resuscitation measures, including mechanical ventilation using respiratory and oxygen equipment, as well as symptomatic therapy; prevention and treatment of acute hemodynamic disorders, the introduction of cardiac glycosides, vasoconstrictors, antiplatelet agents; with cerebral edema - craniocerebral hypothermia, lumbar punctures, the introduction of osmotic diuretics, etc.; with pulmonary edema - large doses of diuretics, ganglionic blockers, alpha-blockers, calcium preparations; oxygen therapy with defoamers; correction of CBS and water-electrolyte state; relief of psychomotor agitation (sedatives, anticonvulsants, the introduction of lytic mixtures); prevention and treatment of pneumonia; correction of tissue metabolism (vitamins, hormones, biostimulants, etc.).
1. Gembitsky E.V., Alekseev G.I. etc. Military Field Therapy. -L., VMedA, S; Luzhnikov E.A. Clinical toxicology.- M.: Medicine C Literature
The toxic effect of carbon monoxide on the body is based on its interaction with hemoglobin and the formation of carboxymoglobin (HbCO), unable to carry oxygen, the development of hemic (transport) hypoxia. The erythrocyte membrane prevents the penetration of CO into the cell and the formation of HbCO. The formation of HbCO begins already in the pulmonary capillaries from the periphery of erythrocytes at a minimum concentration of CO in the air. As the content of carbon monoxide in the inhaled air increases, HbCO is formed not only in the peripheral, but also in the central sections of the erythrocyte. The rate of formation of HbCO is directly proportional to the concentration of CO in the inhaled air, its maximum level in the blood is determined by the time of contact with CO. Hemoglobin has the same ability to bind O2 and CO. At the same time, the affinity of hemoglobin for CO is 250-300 times greater than for O2. The valency of iron in HbCO remains unchanged, while the Fe2+ bonds change. All unpaired electrons are involved in the formation
carboxyhemoglobin. The association of CO with hemoglobin occurs 10 times slower than that with O2. The dissociation of carboxyhemoglobin proceeds 3600 times slower than the dissociation of oxyhemoglobin. For this reason, HbCO accumulates very quickly in the blood, even with a relatively small amount of CO in the inhaled air. The formation of HbCO disrupts the transport of oxygen to tissues, which increases the oxygen starvation of the body.
A very high-quality and useful presentation on the safety and civil defense on the topic: "First aid for carbon monoxide poisoning."
The main characteristics of carbon monoxide (CO) are named, such as the absence of color and odor, increased toxicity, the causes of formation and the effect on the body.
It also talks about potentially dangerous places where you can get poisoned. These are some types of industries, garages and tunnels with poor (or no) ventilation, on busy highways, in case of fire, etc.
In addition, the main symptoms that appear in the victim at different stages of carbon monoxide poisoning are named. Naturally, the first aid provided in such cases is also stipulated here. The first step is to take the victim to fresh air, bring to consciousness, with weakened or absent breathing, carry out artificial respiration. When the victim regains consciousness, he must be given strong tea to drink. You also need to call an ambulance.
Download presentation "First help in cases of poisoning with fumes", 15 slides, 3.9 MB.
