Update: October 2018
Carbon monoxide poisoning refers to acute pathological conditions that develop as a result of a certain concentration of carbon monoxide entering the human body. This condition is life-threatening and without qualified medical assistance can be fatal.
Carbon monoxide (CO, carbon monoxide) is a combustion product and enters the atmosphere in any form. Having no smell or taste, the substance does not demonstrate its presence in the air in any way and easily penetrates walls, soil and filter materials.
Therefore, excess CO concentrations can be detected only with the help of special devices, and in the worst case, in a rapidly developing clinic. In urban air, the main contribution to the concentration of this dangerous substance comes from exhaust gases from automobile internal combustion engines.
Effect on the body
- CO enters the bloodstream 200 times faster than O2 and enters into active contact with hemoglobin in the blood. As a result, carboxyhemoglobin is formed - a substance that has a stronger bond with hemoglobin than oxyhemoglobin (oxygen combined with hemoglobin). This substance blocks the process of oxygen transfer to tissue cells, causing hemic hypoxia.
- CO binds to myoglobin (a protein in skeletal and cardiac muscle), reducing the pumping function of the heart and causing muscle weakness.
- In addition, carbon monoxide enters into oxidative reactions and disrupts the biochemical balance in tissues.
Where are cases of CO poisoning possible?
- On fires.
- In production where CO is used in reactions for the synthesis of substances (phenol, acetone).
- In gasified rooms operating gas equipment (gas stoves, water heaters, heat generators) with insufficient ventilation or insufficient amount of supply air necessary for gas combustion.
- Garages, tunnels and other areas with insufficient ventilation where vehicle exhaust fumes may accumulate.
- When staying near busy highways for a long time.
- At the time of a lighting gas leak at home.
- When the stove doors of a home stove, a stove in a bathhouse, or a fireplace are closed untimely (early).
- Prolonged use of a kerosene lamp in an unventilated area.
- Use of poor quality air in breathing apparatus.
Risk groups (with increased sensitivity to CO)
Signs of poisoning depending on CO concentration
| CO concentration, % | Time of onset of clinical manifestations | Signs |
| Up to 0.009 | 3-5 hours |
|
| Up to 0.019 | 6 hours |
|
| 0,019-0,052 | 2 hours |
|
| Up to 0.069 | 2 hours |
|
| 0,069-0,094 | 2 hours |
|
| 0,1 | 2 hours |
|
| 0,15 | 1.5 h | |
| 0,17 | 0.5 h | |
| 0,2-0,29 | 0.5 h |
|
| 0,49-0,99 | 2-5 min |
|
| 1,2 | 0.5-3 min |
|
Symptoms of carbon monoxide poisoning
Mild poisoning: |
Moderate poisoning: |
Severe poisoning: |
|
|
|
The mechanism of symptoms
Neurological symptoms
- The brain and nerve cells are most sensitive to hypoxia, so headaches, nausea, dizziness, etc. are a signal that nerve cells are suffering from oxygen starvation.
- More severe neurological symptoms (convulsions, loss of consciousness) occur against the background of deep damage to the nervous structures, even irreversible.
Cardiovascular symptoms
The lack of oxygen begins to be compensated by more intense cardiac activity (tachycardia), but the occurrence of pain in the heart indicates that the heart muscle is also experiencing hypoxia. Acute pain indicates a complete cessation of oxygen supply to the myocardium.
Respiratory symptoms
Increased breathing also refers to compensatory mechanisms, but damage to the respiratory center in severe poisoning leads to superficial, ineffective respiratory movements.
Skin symptoms
The red-blue tint of the scalp and mucous membranes indicates increased, compensatory blood flow to the head.
Consequences of carbon monoxide poisoning
In mild to moderate poisoning, the patient may experience headaches, dizziness, decreased memory and intelligence, and emotional instability for a long time, which is associated with damage to the gray and white matter of the brain.
Severe complications are most often irreversible and often lead to death:
- trophic skin disorders (edema followed by tissue necrosis);
- subarachnoid hemorrhages;
- disturbance of cerebral hemodynamics;
- cerebral edema;
- polyneuritis;
- impairment of vision and hearing to complete loss;
- myocardial infarction;
- severe pneumonia complicating coma.
First aid for carbon monoxide poisoning
First aid involves stopping the victim’s contact with poisonous gas and restoring vital functions. Providing first aid for carbon monoxide poisoning should prevent poisoning of the person who is trying to provide this very assistance. Ideally, you should put on a gas mask and only then enter the room where the victim is located.
- Remove or remove the injured person from the room where there is an increased concentration of CO. This is the activity that must be performed first, since with each breath the pathological changes in the body intensify.
- Call an ambulance for any condition of the patient, even if he is joking and laughing. Perhaps this is a consequence of the effect of CO on vital centers of the central nervous system, and not a sign of health.
- In case of mild poisoning, give the person strong, sweet tea, warm him up and provide him with peace.
- In the absence or confusion of consciousness - lay on a flat surface on your side, unfasten the collar, belt, provide a flow of fresh air. Let the cotton wool with ammonia be sniffed at a distance of 1 cm.
- If there is no cardiac or respiratory activity, perform artificial respiration and massage the sternum in the projection of the heart.
What to do if you are poisoned in a fire?
If it so happens that there are people left in the burning building, you cannot try to save them yourself - this will lead to an increase in the number of victims of the emergency and nothing more! You should immediately call the Ministry of Emergency Situations.
Even 2-3 breaths of CO poisoned air can be fatal, so no amount of wet rags or filter masks will protect the person who comes to help. Only a gas mask can protect against the deadly effects of CO!
Therefore, rescuing people in such a situation should be trusted to professionals - the Emergencies Ministry team.
Treatment
If a person is in critical condition, the ambulance team carries out a set of resuscitation measures. In the first minutes, the antidote Acizol 6% is administered by intramuscular injection in a volume of 1 ml. The patient is taken to the hospital (intensive care unit).
In a hospital setting, the patient is provided with complete peace. Organize breathing with pure oxygen with a partial pressure of 1.5-2 atm or carbogen (95% oxygen and 5% carbon dioxide) for 3-6 hours.
Further therapy is aimed at restoring the functioning of the central nervous system and other organs and depends on the severity of the condition and the reversibility of the pathological reactions that have occurred.
Prevention of CO poisoning
- All work associated with the risk of CO poisoning should be carried out only in well-ventilated areas.
- Check stove and fireplace dampers. Never close them if the firewood is not completely burned.
- Install autonomous gas detectors in rooms with a potential risk of CO poisoning.
- In case of possible contact with CO, take 1 capsule of Acizol half an hour before possible contact with the gas. The protection lasts 2-2.5 hours after taking the capsule.
Acizol is a domestic drug, a fast and effective antidote against acute carbon monoxide poisoning in lethal doses. Prevents the formation of carboxyhemoglobin and accelerates the removal of CO from the body. As early as possible, intramuscular administration of Acizol to victims significantly increases their chances of survival and increases the effectiveness of subsequent resuscitation and medical measures.
If poisoning occurs carbon monoxide , then we are talking about a serious pathological condition. It develops if a certain concentration enters the body carbon monoxide .
This condition is dangerous to health and life, and if you do not seek help from specialists in a timely manner, death from carbon monoxide may occur.
Carbon monoxide (carbon monoxide, CO) is a product that is released during combustion and enters the atmosphere. Since poisonous gas has no smell or taste, and it is impossible to determine its presence in the air, it is very dangerous. In addition, it can penetrate through soil, walls, and filters. Many people are interested in the question of whether carbon monoxide is heavier or lighter than air; the answer is that it is lighter than air.
That is why it is possible to determine that the concentration of carbon monoxide in the air is exceeded using special devices. You can also suspect CO poisoning if a person rapidly develops certain symptoms.
In urban environments, the concentration of carbon monoxide in the air is increased by vehicle exhaust gases. But poisoning from car exhaust gases can only occur at high concentrations.
How does CO affect the body?
This gas enters the blood very quickly and actively binds to. As a result, it is produced carboxyhemoglobin , which is more closely related to hemoglobin than oxyhemoglobin (oxygen and hemoglobin). The resulting substance blocks the transfer of oxygen to tissue cells. As a result, it develops hemic type.
Carbon monoxide in the body binds to myoglobin (this is a protein of skeletal muscles and cardiac muscle). As a result, the pumping function of the heart decreases and severe muscle weakness develops.
Also carbon monoxide enters into oxidative reactions, which disrupts the normal biochemical balance in tissues.
Where can carbon monoxide poisoning occur?
There are many situations that can occur in which carbon monoxide poisoning is possible:
- poisoning by combustion products during a fire;
- in rooms where gas equipment is operated, and there is no normal ventilation, there is not enough supply air, which is necessary for normal gas combustion;
- in those industries where CO is involved in the synthesis reactions of substances ( acetone , phenol );
- in places where automobile exhaust gases can accumulate due to insufficient ventilation - in tunnels, garages, etc.;
- at home, when there is a leak of lighting gas;
- when staying near very busy highways for a long time;
- with prolonged use of a kerosene lamp, if the room is not ventilated;
- if the stove damper of a home stove, fireplace, or sauna stove was closed too early;
- when using breathing apparatus with poor quality air.
Who may suffer from hypersensitivity to CO?
- people who have been diagnosed with exhaustion of the body;
- those who suffer;
- future mothers;
- teenagers, children;
- those who smoke a lot;
- people who abuse alcohol.
You should know that organs and systems are more quickly affected by carbon monoxide poisoning in women. The symptoms of poisoning are very similar methane .
Signs of carbon monoxide poisoning
The following describes the symptoms of carbon monoxide poisoning in people depending on the concentration of CO. Symptoms of household gas poisoning and poisoning from other sources manifest themselves differently, and by the way carbon monoxide (not carbon dioxide, as it is sometimes mistakenly called) affects a person, one can assume how strong its concentration in the air was. However, carbon dioxide in high concentrations can also lead to poisoning and the manifestation of a number of alarming symptoms.
Concentration up to 0.009%
Clinical manifestations are observed after 3-5 hours:
- decreased speed of psychomotor reactions;
- increased blood flow in vital organs;
- in people with heart failure in severe form, chest pain is also noted.
Concentration up to 0.019%
Clinical manifestations are observed after 6 hours:
- performance decreases;
- shortness of breath during moderate physical exertion;
- headache , slightly pronounced;
- visual impairment;
- Death may occur in those with severe heart failure, and fetal death may also occur.
Concentration 0.019-0.052%
- severe throbbing headache;
- irritability, instability of emotional state;
- nausea;
- disturbance of attention, memory;
- problems with fine motor skills.
Concentration up to 0.069%
Clinical manifestations are observed after 2 hours:
- vision problems;
- worse headache pain;
- confusion;
- weakness;
- nausea, vomiting;
- runny nose.
Concentration 0.069-0.094%
Clinical manifestations are observed after 2 hours:
- severe motor impairment (ataxia);
- appearance;
- strong rapid breathing.
Concentration 0.1%
Clinical manifestations are observed after 2 hours:
- weak pulse;
- state of fainting;
- convulsions;
- breathing becomes rare and shallow;
- state .
Concentration 0.15%
Clinical manifestations are observed after 1.5 hours. The manifestations are similar to the previous description.
Concentration 0.17%
Clinical manifestations are observed after 0.5 hours.
The manifestations are similar to the previous description.
Concentration 0.2-0.29%
Clinical manifestations are observed after 0.5 hours:
- convulsions appear;
- respiratory and cardiac depression is noted;
- coma ;
- death is likely.
Concentration 0.49-0.99%
Clinical manifestations are observed after 2-5 minutes:
- no reflexes;
- pulse is threadlike;
- deep coma;
- death.
Concentration 1.2%
Clinical manifestations are observed after 0.5-3 minutes:
- convulsions;
- lack of consciousness;
- vomit;
- death.
Symptoms of carbon monoxide poisoning
The table below summarizes the signs that appear at different degrees of poisoning:
Mechanism of symptom development
Various types of symptoms are associated with exposure to carbon monoxide. Let us consider in more detail the symptoms of different types and the features of the mechanisms of their manifestation.
Neurological
Greatest sensitivity to hypoxia demonstrate nerve cells as well as the brain. That is why the development of dizziness, nausea, and headaches indicate that oxygen starvation of cells is occurring. More severe neurological symptoms occur as a result of severe or irreversible damage to nerve structures. In this case, convulsions and impaired consciousness occur.
Respiratory
When breathing quickens, the compensatory mechanism “turns on.” However, if the respiratory center is damaged after poisoning, respiratory movements become superficial and ineffective.
Cardiovascular
Due to the insufficient amount of oxygen, more active cardiac activity is observed, that is, tachycardia . But due to hypoxia of the heart muscle, pain in the heart can also occur. If such pain becomes acute, it means that oxygen has completely stopped flowing to the myocardium.
Skin
Due to the very strong compensatory blood flow to the head, the mucous membranes and skin of the head become blue-red.
If carbon monoxide poisoning or mild or moderate natural gas poisoning occurs, a person may experience dizziness and headaches for a long time. His memory and intellectual abilities also deteriorate, and emotional fluctuations are noted, since poisoning affects the gray and white matter of the brain.
The consequences of severe poisoning are usually irreversible. Very often such lesions end in death. In this case, the following severe manifestations are noted:
- subarachnoid hemorrhages;
- disorders of a skin-trophic nature (edema and tissue);
- cerebral edema ;
- disturbance of cerebral hemodynamics;
- deterioration of vision and hearing up to complete loss;
- polyneuritis ;
- pneumonia in severe form, which is complicated by coma;
Providing first aid for carbon monoxide poisoning
First of all, emergency care for carbon monoxide poisoning involves the immediate cessation of human contact with the gas that poisons the body, as well as the restoration of all important body functions. It is extremely important that the person receiving first aid does not become poisoned during these actions. Therefore, if possible, it is necessary to put on a gas mask, and only after that go to the room where the poisoning occurred.
Before starting PMP, it is necessary to remove or remove the person who was injured from the room in which the concentration of carbon monoxide is increased. You need to clearly understand what kind of gas CO is and how quickly it can harm the body. And since every breath of poisoned air will only intensify the negative symptoms, the victim must be taken to fresh air as soon as possible.
No matter how quickly and professionally first aid is provided, even if the person feels relatively well, it is necessary to call an ambulance. There is no need to be deceived by the fact that the victim is joking and laughing, because such a reaction can be provoked by the effect of carbon monoxide on the vital centers of the nervous system. Only a professional doctor can clearly assess the patient’s condition and understand what to do in case of carbon monoxide poisoning.
If the degree of poisoning is mild, the victim should be given strong tea, warmed up and provided with complete rest.
If there is confusion of consciousness, or there is no confusion at all, you should lay the person on his side on a flat surface, make sure that he receives an influx of fresh air by unfastening his belt, collar, and underwear. Let the ammonia smell, holding the cotton wool at a distance of 1 cm.
If there is no heartbeat and breathing, artificial respiration should be performed and the sternum should be massaged in the projection of the heart.
In an emergency, you should not act rashly. If there are still people in the burning building, you cannot save them yourself, as this may lead to an increase in the number of victims. It is important to call the Ministry of Emergency Situations immediately.
Even after just a few breaths of CO poisoned air, a person can die. Therefore, it is a mistake to believe that a wet rag or gauze mask can protect against the harmful effects of carbon monoxide. Only a gas mask can prevent the fatal effects of CO.
Treatment of carbon monoxide poisoning
Treatment at home after poisoning should not be practiced. A person in such a situation needs the help of specialists.
Provided that the victim is in critical condition, doctors carry out a set of resuscitation measures. Immediately 1 ml of 6% antidote is injected intramuscularly. The victim must be taken to the hospital.
It is important that in such conditions the patient is provided with complete rest. He is provided with breathing pure oxygen (partial pressure 1.5-2 atm.) or carbogen (composition - 95% oxygen and 5% carbon dioxide). This procedure is carried out over 3-6 hours.
Next, it is important to ensure the restoration of the functions of the central nervous system and other organs. The treatment regimen prescribed by a specialist depends on how severe the patient’s condition is and whether the pathological reactions that occurred after poisoning are reversible.
To prevent natural gas and CO poisoning, it is important to carefully follow the rules that will help prevent dangerous situations.
- If there is a risk of carbon monoxide poisoning during certain work, it should only be carried out in well-ventilated areas.
- Carefully check the dampers of fireplaces and stoves, do not close them completely until the wood is burned.
- In rooms where CO poisoning could potentially occur, it is necessary to install autonomous gas detectors.
- If possible exposure to carbon monoxide is anticipated, take one capsule Acizola half an hour before such contact. The protective effect will last up to two and a half hours after taking the capsule.
Acizol is a domestically produced medicine that is an effective and fast-acting antidote against acute CO poisoning. It creates an obstacle in the body to the formation carboxyhemoglobin , and also speeds up the process of removing carbon monoxide.
The sooner Acizol is administered intramuscularly in case of poisoning, the greater the person’s chances of survival. This medicine also increases the effectiveness of those measures that will subsequently be taken for resuscitation and treatment.
conclusions
Thus, carbon monoxide poisoning is a very dangerous condition. The higher the concentration of gas, the more likely the fatal outcome. Therefore, it is very important to be extremely careful in observing all the rules of prevention, and at the first suspicion of such poisoning, immediately call emergency help.
Carbon monoxide poisoning due to inhalation of carbon monoxide gas occupies a leading place in the list of inhalation poisonings, the fourth place among the most commonly observed poisonings (after alcohol, drug and psychoactive substance poisoning).
Mortality in the affected area is about 17.5% of the total number of all fatal poisonings. In particular, according to Russian forensics, this figure ranges from 11.0 to 58.8%. The hospital mortality rate for carbon monoxide poisoning averages 3.8%.
The highest percentage (17.9%) of deaths was registered with carbon monoxide poisoning in combination with thermal inhalation injury, after 4.1% in the group of patients with isolated carbon monoxide poisoning.
Thus, the high mortality rate of carbon monoxide poisoning in Ukraine indicates the importance of constantly updating knowledge about diagnosis and treatment with modern data, which is the purpose of this report.
The insidiousness of carbon monoxide (CO, carbon monoxide, carbon monoxide) lies in the fact that CO poisoning most often occurs unnoticed, since it is a colorless gas that has neither taste nor smell (odor is created only by impurities); CO is lighter than air (at 0 °C, 760 mm Hg), burns with a bluish flame until carbon dioxide (CO2) is formed, releasing heat; a mixture of 2 volumes of CO and 1 volume of O2 explodes when ignited.
CO is released during smoldering and combustion of almost all combustible substances and materials, especially in conditions of insufficient oxygen supply, and is one of the most toxic components of combustion products that make up the smoke.
CO is a component of various industrial and domestic gases. During fires, carbon monoxide easily penetrates through walls and ceilings (while losing odorous impurities) - “filtered gas”, “leaking gas”. CO poisoning is possible due to a leak of household propane gas containing 4-11% CO.
Poisonings can be: accidental, with criminal or suicidal intent. Poisoning is possible both in industrial and domestic conditions:
- in garages, residential premises, bathhouses, cars, buses;
- when testing engines, in engine rooms of motor ships, diesel locomotives, in airplane cockpits;
- in boiler houses, gas generators, blast furnaces, open-hearth and foundries, in sugar and bakeries, in brick, ceramic, cement and other industries;
- as a result of terrorist acts;
- during artillery, mortar and machine gun fire, in tanks, armored vehicles, in the cannon turrets of warships;
- When napalm incendiary mixtures burn, high concentrations of carbon monoxide and carbon dioxide are formed.
Group and mass poisoning with carbon monoxide are possible. Cases of group poisoning are not uncommon in large enclosed spaces, restaurants, nightclubs, indoor skating rinks, and churches, where many dozens of people of all ages become victims of poisoning. CO is one of the main damaging factors during natural disasters, such as large forest fires, volcanic eruptions, etc.
In modern conditions, the likelihood of poisoning people during fires increases significantly due to the use of polymer materials in construction and everyday life. For this reason, the mixture of gases that are released during modern fires due to the admixture of hydrogen cyanide (HCN), hydrogen chloride, nitrogen oxides, acrolein, acetonitrile and other substances becomes even more toxic. The most toxic combustion products of nitrogen-containing polymer materials are cyanide, acrylonitrile and CO.
A constant element of all variants of etiological conditions of CO poisoning is the low ventilation performance of the victim’s area: the formation of CO is quantitatively greater than its removal.
Pathogenesis of CO poisoning
The pathogenesis of CO poisoning consists of several parts. When inhaled, CO quickly penetrates through the alveolar-capillary membrane into the blood, where it reversibly combines with divalent iron in hemoglobin, forming a very stable compound - carboxyhemoglobin (HbCO).
Due to the fact that the affinity of carbon monoxide for human hemoglobin is 220 times higher than that of oxygen, and the dissociation of HbCO is 3600 times slower than the dissociation of HbO2, even small concentrations of CO can lead to the formation of significant amounts of HbCO in the blood.
For example, if the concentration of CO in the air is 0.3-0.5% (3.4-5.7 mg/l), then the lethal content of HbCO at the level of 65-75% will be achieved after 20-30 minutes of a person’s stay in the air. such an environment; at a CO concentration of 14 mg/l, death occurs within 1-3 minutes.
The percentage of HbCO in the blood is directly proportional to the partial pressure of CO (pCO) and inversely proportional to the partial pressure of oxygen (pO2) in the alveolar gas. The half-life of HbCO when inhaling ordinary air is 320 minutes, pure oxygen under a pressure of 1 atm. - 80 min, under pressure 3 atm. - 23 min.
The resulting product, HbCO, cannot add oxygen. In addition, the presence of HbCO reduces the dissociation of oxygen and the remaining oxyhemoglobin (HbO2), which shifts the dissociation constant of HbO2 to the left and reduces the diffusion of oxygen into tissues.
Thus, it develops hemic hypoxia, which poses a real threat to life and can lead to death directly at the scene of the incident, which requires first (emergency) medical care.
A significant part of CO (from 15 to 50%) interacts with other iron-containing biologically active systems of the body (hemoproteins): cytochrome oxidase - cytochrome a3, cytochrome P-450, cytochrome C, catalase, peroxidase, myoglobin, etc.
The dissociation of the resulting compounds is very slow (from 48 to 72 hours), as a result, tissue respiration is blocked, oxidative processes in mitochondria are disrupted, and a violation of oxygen utilization by the cell develops, which causes the appearance of symptoms histotoxic (tissue) hypoxia.
The respiratory pigment of muscle cells (heart, skeletal muscles) - myoglobin, like hemoglobin, binds and releases oxygen, which ensures the supply of oxygen to muscle fibers. The process of interaction between carbon monoxide and myoglobin iron proceeds parallel to the increase in HbCO in the blood and ends with the formation of carboxymyoglobin.
In severe poisoning, more than 25% of myoglobin may be associated with CO. In this case, myoglobin loses its ability to serve as an intermediate link connecting hemoglobin with the oxidative enzymes of the muscular system, and becomes a depot of carbon monoxide in the victim’s body. At the same time, the affinity of myoglobin for CO is 25-50 times higher than for O2.
The attachment of a CO molecule to cardiac myoglobin reduces the functional reserve of the myocardium, which forms a deficiency of inotropic function of the heart, arterial hypotension, and a decrease in cardiac index, which causes the circulatory component of tissue hypoxia.
In clinical settings, CO is removed through the lungs. An insignificant amount of carbon monoxide is released through the skin - 0.007 ml/h, slightly more through the gastrointestinal tract and kidneys. CO is excreted in the urine as a complex compound with iron.
The factors that determine the absorption of CO by the blood and the saturation of hemoglobin include the initial concentration of CO and O2, the amount of ventilation and the quality of the diffusion barrier of the lungs and capillary.
There is evidence of a two-phase decrease in the percentage of HbCO: an initially rapid exponential decrease is associated with redistribution and removal through the lungs. The second phase of slow linear decline is due to the release of carbon monoxide from hemoglobin and myoglobin, pulmonary diffusion and ventilation.
Thus, during CO poisoning, mixed hypoxia is formed, which is due to the total effect
- hypoxic (decrease in the partial pressure of oxygen in the air entering the alveoli),
- hemic (reduction in the amount of oxygen that dissociates from connection with hemoglobin in the microcirculation zone),
- circulatory (reduced perfusion of the microcirculation zone)
- histotoxic (decreased performance of mitochondrial respiratory enzymes) hypoxia.
Additional components of the pathogenesis of CO poisoning are: microthrombosis in the microcirculation zone (including coronary), pathological processes of lipid peroxidation in the brain; hyperglycemia, hyperlactatemia; leukocyte-induced inflammation and demyelination of white matter; stimulation of production of nitric oxide radical by leukocytes and endothelial cells; direct toxic damage to the myocardium. As a result, nervous, myocardial and embryonic tissue is most sensitive to CO.
Associated factors aggravating the course of carbon monoxide intoxication: overwork, past illnesses, blood loss, increased physical activity, vitamin deficiencies, nutritional dystrophy, burn disease, significant changes in environmental factors (high air temperature, simultaneous action of other toxic substances, decreased oxygen content, the presence of carbon dioxide (CO2) in the air, pregnancy, adolescence, severe alcohol poisoning, acute respiratory distress syndrome due to acute thermal injury of the respiratory tract.
Women tolerate intoxication more easily than men. There is increased resistance to carbon monoxide in children under 1 year of age compared to adults.
CO poisoning in pregnant women is a particular problem. In case of carbon monoxide poisoning, the fetus suffers from more pronounced and prolonged tissue hypoxia than the mother's body. In the early stages of pregnancy, fetal hypoxia can lead to miscarriage or developmental defects.
In the later stages, premature birth or the birth of a live child with severe encephalopathy is possible. These changes were recorded when the level of carboxyhemoglobin in the fetus exceeded 15%. The carboxyhemoglobin content in the mother's blood does not reflect the risk of fetal death.
Of greater importance is the rapid decrease in oxygen content in the fetal blood, which develops in a matter of minutes. According to numerous studies, with preserved consciousness and the absence of mental disorders in the mother, the pregnancy outcome is usually favorable.
Diagnosis of acute carbon monoxide poisoning
The diagnosis of acute carbon monoxide poisoning is made on the basis of: laboratory data, characteristic clinical phenomena, toxicological history, study of the conditions of poisoning at the scene of the incident.
Differential diagnosis should be carried out with acute cerebrovascular accident, myocardial infarction, and cyanide poisoning.
It is advisable to test the air in the enclosed space where the victim was found for the presence of carbon monoxide using indicator tubes or other methods.
Outside of cases of CO poisoning, hemolysis and thalassemia increase the level of HbCO, in non-smokers the level of HbCO is 1–2%, in the blood of smokers the HbCO content is 5–10%, while the average daily concentration ranges from 1.5 to 15%.
An absolute indicator of carbon monoxide poisoning is more than 3.0% HbCO found in the blood, but a negative reaction to HbCO does not exclude carbon monoxide poisoning.
The HbCO content cannot serve as a reliable criterion for the severity of the patient’s condition upon admission to the hospital. In most cases, it is very low, and clinical symptoms indicate severe poisoning. This discrepancy is explained by the time that elapsed from the moment the victim was evacuated from an area with an increased concentration of carbon monoxide, during which time his breathing was restored, carboxyhemoglobin dissociated and carbon monoxide was eliminated through the lungs.
The determination of carboxyhemoglobin in blood taken directly at the scene of the incident is of great diagnostic importance.
Clinical picture
According to the severity of carbon monoxide poisoning (Luzhnikov E.A., 1989) they are distinguished: mild poisoning, moderate poisoning, severe poisoning.
For mild cases poisoning appears
- headache in the temporal and frontal regions, often of a girdling nature (the “hoop” symptom), dizziness, tinnitus, nausea, vomiting, minor visual impairment;
- patients complain of general anxiety, fear, difficulty breathing, sore throat, dry cough, feeling of thirst, burning face, discomfort in the heart area;
- characterized by an increase in blood pressure to 150/90 mm Hg, moderate tachycardia;
- loss of consciousness (from the moment of poisoning) is not observed;
- the carboxyhemoglobin content in the blood is 15-30% (on average the threshold level is 20% of total hemoglobin).
Average degree carbon monoxide poisoning:
- nausea, difficulty breathing, feeling of lack of air, shortness of breath are noted;
- disturbance of mental activity is manifested by agitation or stupor, up to coma;
- pathological reflexes, miosis, mydriasis, and occasionally anisocoria appear; in most cases, the pupils are of normal size, with a lively reaction to light;
- The appearance of facial skin hyperemia is noteworthy;
- there must be at least a short-term loss of consciousness from 1-2 to 20 minutes;
- the content of carboxyhemoglobin in the blood is 30-40%.
In severe cases Carbon monoxide poisoning is defined by:
- coma of varying depth and duration - from several hours to a day or more, there may be convulsions, pathological reflexes, paresis, paralysis;
- the skin of the victim at the scene of the incident may be scarlet; upon admission to the hospital in a state of severe hypoxia, their color changes to cyanotic;
- due to the development of acute rhinolaryngitis and tracheobronchitis, breathing problems may occur, including stopping;
- on the part of the cardiovascular system (CVS), signs of acute left ventricular failure are formed, changes on the ECG are not specific and in most cases are manifested by signs of myocardial hypoxia and coronary circulatory disorders: the amplitude of the R wave decreases in all leads, especially in the chest leads, the S-interval T shifts below the isoline, the T wave becomes biphasic or negative;
- when analyzing acid-base balance - metabolic acidosis;
- the content of carboxyhemoglobin in the blood is 50-60%.
Pulse oximetry data in case of CO poisoning attract attention and require correct interpretation. Carboxyhemoglobin absorbs light in much the same way as oxyhemoglobin, so instead of saturating hemoglobin with oxygen, the pulse oximeter in such patients shows the sum of the percentage concentrations of HbCO and HbO2.
For example, if SpO2 = 65% and HbCO = 25%, the pulse oximeter will display an SpO2 value close to 90%. Thus, with pulse oximetry against the background of carboxyhemoglobinemia, the SpO2 indicator turns out to be overestimated.
In some cases, CO poisoning can be combined with a burn of the respiratory tract. As a rule, in these cases, the severity of the patient’s condition is due not so much to CO poisoning (which can be mild or moderate), but rather to a burn to the respiratory tract. In the acute period, acute respiratory failure may develop due to prolonged intractable laryngobronchospasm, and in the next day severe pneumonia develops.
As a concomitant of CO poisoning, such patients may develop compartment syndrome(crash syndrome, positional injury) - develops in cases where the victim remains unconscious in one position for a long time, touching parts of the body with a hard surface or pressing a limb with the weight of his own body.
In this case, the nutrition of muscle and nervous tissue and skin is sharply disrupted, which leads to their death. The affected areas become sharply painful, increased in volume, dense (up to stone density).
As a result of the breakdown of muscle tissue, myoglobin (a protein that is part of muscle tissue) enters the blood; if the injury area is extensive, a large amount of myoglobin affects the kidneys - myoglobinuric nephrosis develops. Thus, the patient develops the so-called myorenal syndrome, characterized by a combination of positional trauma and renal failure.
For moderate and severe carbon monoxide poisoning, a characteristic complication is the rapid development of hypoxic bullous dermatitis and polyneuritis, appearing 10-15 hours after poisoning.
Therapeutic measures
From the literature, the main components of the treatment of carbon monoxide poisoning are known:
- early intensive oxygen therapy with monitoring of ventilation efficiency;
- use of metabolic drugs (acyzole, thiotriazoline, sodium thiosulfate);
- the use of hyperbaric oxygen therapy;
- prevention of cerebral edema;
- prevention of myorenal syndrome;
- compensation for the functioning of the cardiovascular, respiratory, and urinary systems.
Pre-hospital activities medical care is reduced to evacuation of the victim from the area of carbon monoxide-polluted air, carrying out respiratory therapy measures (airway patency, control and prosthetic (if indicated) ventilation of the lungs), maintaining the function of the cardiovascular system, assessing the severity of associated injuries (poisoning, mechanical and thermal trauma, etc.), stabilization of disorders (pain, wound contamination, migration of bone fragments, etc.) caused by concomitant lesions.
The main thing in cases of carbon monoxide poisoning is to provide the victim with the earliest possible and prolonged inhalation of oxygen, which displaces CO from its connection with hemoglobin in the blood. Equally important is the control of pulmonary ventilation, which provides the main route for the elimination of carbon monoxide outside the body. For the first three hours, the victim needs high oxygen concentrations (75-80%, 6-10 l/min), followed by a decrease to 40-50%.
For acute symptoms of bronchospasm - inhalation (beta2-agonists (salbutamol, ventolin) 2-3 mg via inhaler for 5-10 minutes or combined bronchodilators (berodual 1-2 ml).
The drug acyzole is recommended as an antidote therapy for carbon monoxide poisoning. Acizol is a highly effective antidote for acute carbon monoxide poisoning, as well as an effective antihypoxant for oxygen deficiency.
For therapeutic purposes, as an antidote at the prehospital stage, acyzol is administered to adult victims as early as possible, regardless of the severity of the condition, intramuscularly at a dose of 60 mg (1 ml of 6% solution), repeated administration of 60 mg is allowed no earlier than one hour.
For prophylactic purposes, as an antidote at the prehospital stage, adults take acyzol orally 120 mg (one capsule) 30-40 minutes before entering the smoke zone (gas contamination), repeated administration is possible after 1.5-2 hours; or intramuscularly at a dose of 60 mg (1 ml of 6% solution) 20-30 minutes before entering an area with a high risk of poisoning; repeated administration of 60 mg is allowed no earlier than one hour later.
The maximum daily dose for an adult when administered intramuscularly is 240 mg (4 ml of 6% solution); when taken orally - 480 mg (4 capsules).
The protective effect of acyzol lasts for 1.5-2 hours when using an ampoule solution of the drug, and repeated administration is allowed 1 hour after the first administration. When using capsules, the protective effect lasts for 2-2.5 hours, re-taking the drug is allowed after 1.5-2 hours.
Due to interactions with other drugs, simultaneous use with unithiol is not recommended.
You can consider the introduction of metabolic drugs: thiotriazoline, succinic acid drugs, trimetazidine, mildronate. It is advisable to prescribe endotheliotropic and decongestant therapy: T-lysine escinate 30-40 mg (20-40 ml) per day; prednisolone 30-60 mg 2-3 times a day.
Provide warming; when using heating pads, care must be taken, since victims of CO have an increased pain sensitivity threshold and a tendency to burns.
In the first hour of intoxication, in the presence of cyanosis, 20-30 ml of a 5% ascorbic acid solution with 20-50 ml of a 40% glucose solution is administered intravenously.
Hyperbaric oxygenation(HBO) is a specific antidote therapy and can significantly accelerate (10-15 times) the dissociation of HbCO and increase the amount of oxygen freely dissolved in the plasma. HBOT is the method of choice for CO poisoning, accompanied by impaired consciousness such as toxic encephalopathy and the development of coma.
It should be taken into account that immediately after the evacuation of the victim from the affected area, the removal of CO through the respiratory tract begins, and therefore even a small content of HbCO upon admission to the hospital in the presence of characteristic toxic encephalopathy does not cancel HBOT.
Indications for HBOT: coma, focal neurological deficit, myocardial ischemia on ECG, HBCO > 40%, change in consciousness, short-term loss of consciousness, progressive deterioration of condition during normobaric oxygen therapy with Fi021.0 for 4 hours.
On the first day after poisoning, it is advisable to administer HBOT at intervals of 12 hours, and then once every 2-3 days. The working pressure in the hyperbaric chamber should depend on the severity of the poisoning: with moderate severity, the pressure is 1-1.5 ati, in severe cases - up to 2-2.5 ati.
Usually, after the first HBOT session, there is a noticeable improvement in the condition: consciousness is restored or the depth of the coma decreases. Sometimes recovery from a coma may be accompanied by pronounced psychomotor agitation directly in the pressure chamber; for this reason, for prophylactic purposes, it is advisable to administer diazepam, GHB in sub-narcotic doses.
If pathological symptoms do not disappear during an hour-long session of hyperbaric oxygenation, then hypoxic damage and cerebral edema should be suspected, since during this time the concentration of HbCO in the blood decreases on average from 50 to 20%.
If combined poisoning with carbon monoxide and cyanides is suspected, administration is indicated: first - amyl nitrite by inhalation (as a methemoglobin former), then - sodium thiosulfate up to 50 ml of 30% IV solution.
Promising is the use of 2.5-5 g of the injectable form of hydroxocobalamin (from the group of cobalamins; these include cyanocobalamin, hydroxocobalamin), which, when reacting with cyanides, is converted into cyanocobalamin.
Intensive therapy for cerebral edema
Intensive therapy for AGM should begin as early as possible. When transporting such patients, the head end of the stretcher is raised by 35-40°.
To prevent hypoxia, all patients in a coma (GCS score 8 or less) undergo tracheal intubation, sanitation of the tracheobronchial tree and prosthetic functions of external respiration using artificial pulmonary ventilation (ALV) with FiO2 0.5.
At the same time, the increase in intrathoracic pressure is eliminated by sedating the patient and absolute synchronization with the ventilator. For this purpose, sibazon is used in the form of a bolus intravenous infusion of 0.4 mg/kg with a further transition to the drip mode at a rate of 0.1-0.2 mg/kg per hour. It is possible to use sodium thiopental at a dose of 200-300 mg intravenously for 30 seconds, then at a rate of 5-8 mg/kg per hour. These same drugs are also effective for relieving seizures.
In order to influence the metabolic link of regulation of cerebral blood flow and reduce intracranial pressure, mechanical ventilation is carried out in the mode of moderate hyperventilation, which should ensure the maintenance of PaCO2 at a level of 25-30 mm Hg.
Against the background of cerebral edema, provided that diastolic blood pressure is at least 80 mm Hg. the following blood pressure values should be maintained: during stunning, systolic blood pressure should be no lower than 110 mm Hg, during stupor - no lower than 125 mm Hg, coma - no lower than 140 mm Hg. Systolic blood pressure should not be allowed to increase above 160 mmHg.
In case of low systolic blood pressure due to hypovolemia, electrolyte and colloid solutions balanced in composition are prescribed in volumes and ratios corresponding to the hemodynamic and renal status of the patient.
For the treatment of cerebral edema, it is possible to use hyperosmolar solutions of sodium chloride (3 and 7.5%, injection rate - 150-200 ml/h) or mannitol at the rate of 0.25-2 g/kg in the form of 15-25% r- ra for 30-60 minutes. In patients with low body weight or debilitated patients, a dose of 0.5 g/kg may be sufficient.
Hypoosmolar solutions, especially glucose solutions, are excluded! A bolus intravenous injection of 20-40 ml of 40% glucose solution is acceptable to relieve comatose states caused by hypoglycemia.
In the absence of effect from infusion therapy and in cases of normovolemia, vasopressors and inotropic drugs are additionally used for 10 minutes. In this case, dopamine (8-10 mcg/kg per minute) is used alone or in combination with mezatone (0.15-0.2 mcg/kg per minute) or norepinephrine (0.3-0.4 mcg/kg in 1 minute).
Also, for cerebral edema due to arterial hypertension, treatment begins with intravenous administration of a 25% solution of magnesium sulfate. Magnesium sulfate: 20 ml of a 25% solution (5 g) is administered intravenously (drip in a balanced crystalloid solution) over 15-20 minutes.
The use of a solution of L-lysine aescinate is indicated. It is administered intravenously at 30-40 mg per day. Nootropic drugs (piracetam, Cerebrolysin, Actovegin, etc.) are not used in the acute period against the background of cerebral edema.
Prevention of myorenal syndrome
In order to prevent myorenal syndrome, before removing the victim from the rubble, pain relief should be performed - narcotic or non-narcotic analgesics (morphine, omnopon, promedol are contraindicated in cases of traumatic brain injury with hypotension); If possible, it is permissible to use conduction anesthesia techniques.
Application of a tourniquet is indicated only for bleeding from a great vessel. In order to prevent the massive release of endotoxins from areas of crushed muscle masses, the injured limb is bandaged: one rescuer frees the limb, starting from the proximal sections, the other bandages the released sections in the distal direction; Bandaging is indicated only for the period of transportation with constant monitoring of the pulse and condition of the limb.
It is strictly forbidden to rub and massage the limb. Immobilization is carried out using standard splints or improvised means. It is advisable to perform local hypothermia (ice, special cooling packs).
In cases where the limb is already enlarged in size, application of a tourniquet or elastic bandaging is not indicated. A mandatory component of treatment in this case is immobilization and elevated position of the limb, especially during transportation.
If the positional syndrome lasts several days, hyperkalemia develops, and transportation of such a patient becomes dangerous. An ECG is required. Correction of hyperkalemia is carried out by introducing a potassium antagonist - calcium gluconate (or calcium chloride) 10% solution 10-20 ml, 40% glucose solution 20-40 ml, 20% glucose solution with insulin, sodium hydroxybutyrate 2 g, which promote the transition of potassium into the cell. Alkalinization of plasma with a 4% soda solution (0.5-1.5 ml/kg) 2-4 times a day is also effective.
Absolutely indicated, regardless of the severity, is the earliest, as soon as technically possible, infusion therapy. To prevent fat embolism in patients with concomitant fractures of long bones, lipostabil can be administered in a dose of 10 ml or higher.
Carbon monoxide poisoning remains an urgent problem of toxicological care in the conditions of modern development of the human living environment. The consequences of terrorist attacks, fires, and the operation of faulty equipment explain the high prevalence and significant mortality due to this pathology.
Often an inaccessible history of the onset of the disease, the lack of an antidote component of therapy, instrumental, laboratory and technical base complicate the treatment of carbon monoxide poisoning, especially in the case of its combination with other inhalation toxicants (cyanide compounds, nitrogen oxides, acrylonitrile) and associated injuries (burn of the respiratory tract, crash syndrome, etc.).
Taking into account the presented modern data, it is necessary to comply with the specified principles for assessing the patient’s condition and identifying groups of victims of carbon monoxide poisoning who are at risk of life-threatening complications. A comprehensive examination and timely intensive therapy will improve treatment results and avoid death of victims.
Lysenko V.I., Golyanishchev M.A.
The silent killer is the name given to carbon monoxide or carbon monoxide. Due to the lack of color and odor, the gas is not detectable organoleptically.
According to statistics, mortality from carbon monoxide poisoning is 60-70% of the total number of cases of mortality from inhalation poisoning. The UN has assigned carbon monoxide a hazard class of 2.
Carbon monoxide is a major source of air pollution. It is released with vehicle exhaust, as part of tobacco smoke, and during incomplete combustion of natural gas. Faulty hoods, air ducts, and the use of homemade heating devices cause fatal intoxication with carbon (II) monoxide.
The danger of carbon monoxide is that it is produced endogenously and is a signal molecule of gaseous substances in the body, therefore, when it accumulates in a room, protective mechanisms are not activated. The body accepts it as “one of its own” and the danger alarm systems do not work.
If the main source of danger for a rural resident is smoke - carbon monoxide released when the stove damper is closed early, then for a city dweller the most common cause of poisoning is car repair in his own garage.
Already in the amount of 0.08% of the total volume of air, CO causes the first signs of poisoning. If the gas content increases 4 times, then loss of orientation occurs, the ability to move and think logically is lost. At a concentration of 1.2%, death occurs within 3-4 minutes from respiratory arrest.
Do not delude yourself that by switching from wood-burning stoves and stoves to natural gas, a person has completely protected himself from CO2. Even a wide-bottomed pan on the stove causes carbon monoxide to accumulate in the kitchen.
Carbon monoxide has accompanied people from the moment of the first conscious use of open fire to the present day, so it is simply necessary to know how to identify the signs of poisoning and methods of providing first aid.
In the human body, carbon monoxide is synthesized by tissue cells. It plays the role of a neurotransmitter and affects muscle fibers in the walls of blood vessels. Insufficient synthesis of endogenous CO is associated with:
- atherosclerosis;
- hypertension;
- inflammatory processes;
- heart failure.
Carbon monoxide promotes the transmission of nerve impulses, and its role in the formation of long-term memory is especially important. Released into the presynaptic cleft, the gas “returns” the signal to the membrane of the transmitter synapse, which increases its transmitting ability.
Carbon monoxide promotes the formation of a new capillary network. Participation in angiogenesis has a positive effect during tissue regeneration, during the growth of the body, during vascular thrombosis or the formation of scar tissue.
Normally, angiogenesis occurs continuously and is slow. In malignant tumors, angiogenesis occurs more intensely, which causes tumor growth and metastasis.
The study of the role and properties of endogenous carbon monoxide is of great scientific and practical importance. The results of studies have been published in the scientific literature confirming the theory that endogenous CO has cytoprotective and anti-inflammatory properties. Experiments are being conducted using carbon monoxide in the treatment of the following pathologies:
- ischemic stroke;
- myocardial infarction;
- graft rejection;
- sepsis;
- malaria;
- autoimmune pathologies.
Endogenous CO is involved in the regulation of processes occurring in the body. Therefore, the immune and protective systems of cells perceive the gas as a natural component and do not signal the danger of intoxication.
Carbon monoxide, penetrating into the human body, binds to hemoglobin in the blood, forming a stable compound - carboxyhemoglobin. It displaces oxygen from red blood cells as it is less active and leads to several types of oxygen starvation:
- fabric;
- transport (hemic);
- circular (cardiovascular);
- pulmonary;
- exogenous.
Carboxyhemoglobin is a more stable compound than oxyhemoglobin, and the diffusion of CO from the resulting compound is much slower. The gas easily overcomes the blood-brain barrier and penetrates cell membranes, causing organic damage to the central nervous system.
Different tissues react differently to carbon monoxide toxicity. Those in which the blood supply is more intense are most susceptible to pathological changes. Hypoxia affects the nervous tissue of the brain, heart muscle, lung and vascular tissue, and smooth muscle tissue.
The severity of symptoms of intoxication depends on the condition of the organ. First of all, those who already have pathology suffer. The degree of intoxication also depends on the physical activity of the victim at the time of poisoning.
Individual characteristics are also of great importance - low metabolic rate, genetic disorders, susceptibility to toxins, the level of evolutionary complexity of the central nervous system, constitutional characteristics, and quality of nutrition. The degree of intoxication depends on these and other indicators. Even the same concentration of carbon monoxide can cause different symptoms and severity of poisoning.
Intoxication is most severe in children, the elderly and pregnant women. For example, with severe poisoning, irreversible changes can occur in the body or the recovery process can take a long time. 10-30% of victims experience long-term (up to 6 weeks) dysfunction of the nervous system:
- lack of self-criticism;
- decrease in mnestic functions;
- personality change;
- psychoemotional disorders.
Carbon monoxide poisoning during gestation poses a danger not only to the health of the woman, but also to the developing fetus. The impact on all organs and a huge number of aggravating factors cause great differentiation of clinical manifestations.
Signs and manifestations of intoxication
Intoxication of varying degrees of severity is manifested not only by differences in the severity of symptoms, but also in different symptom complexes.
The initial stages of intoxication appear:
- muscle atony;
- dizziness;
- ringing in the ears and the appearance of “flares” or dark “gnats” before the eyes;
- nausea turning into vomiting;
- asthenia or short-term agitation;
- loss of orientation in space;
- difficulty breathing;
- redness of the face;
- rapid heartbeat;
- pain in the chest and head.
Severe poisoning is accompanied by:
- cyanosis;
- delusional;
- hallucinations;
- convulsions;
- coma and death.
When intoxicated with carbon monoxide, a person is not able to critically assess the situation and try to avoid further exposure to the toxic agent. Therefore, correct and timely provision of prehospital care is of great importance.
Providing pre-hospital care to the victim
His health and life depend on how adequately and quickly assistance is provided to the victim. There have been cases of death 1-2 weeks after poisoning due to complications that have developed. The prehospital care algorithm is as follows:
- the patient should be immediately isolated from the source of carbon monoxide - taken to the air;
- loosen parts of the wardrobe that impede free breathing - collar, belt, trouser waistband;
- if there is an oxygen cushion, allow the patient to breathe. Oxygen will relieve signs of hypoxia;
- if the victim is conscious, then the processes of metabolism and detoxification should be stimulated - give him a drink of warm, strong or strong;
- to prevent hypothermia and restore blood supply, it is necessary to rub the limbs, warm the victim with a heating pad or blanket;
- if the patient is unconscious, then it is necessary to lay him on his side, raising his legs higher to prevent aspiration of vomit or tongue;
- clean the oral cavity;
- try to restore consciousness with the help of ammonia;
- carry out resuscitation measures;
- call an ambulance.
Further treatment of intoxication is carried out in a medical institution. If timely assistance is provided, the prognosis for the pathological condition is favorable.
Poisoning that occurs with the participation of carbon monoxide and smoke is quite relevant. The absence of color, gas smell, and a very high percentage of deaths indicate that it is necessary to learn how to provide first aid in case of carbon monoxide poisoning. It is very important to provide emergency assistance and begin treatment in a timely manner in order to avoid serious health problems, as well as death.
Causes of intoxication
CO or carbon monoxide occurs due to oxidation (incomplete combustion), then it enters the blood and quickly comes into contact with hemoglobin. As a result of such processes, carboxyhemoglobin is formed. All this leads to oxygen starvation, which is very dangerous.
Carbon monoxide poisoning can occur in the following emergency situations:
- fire – natural, domestic;
- from exhaust gases;
- car interior or garage while the engine is running;
- use of heating equipment, stoves, chimneys;
- the process of producing certain organic substances - acetone, etc.
Symptoms and signs of damage
Signs of carbon monoxide poisoning are expressed in its negative effect on the human body. Oxygen starvation has a huge impact on a person’s overall health, the state of the nervous system, breathing and blood circulation. The degree of damage depends on the amount of CO in the air, as well as the duration of stay in the hazardous area. When a person breathes air containing 0.02 - 0.03% gas for about six hours, then the following consequences begin to appear:
- vomiting, nausea;
- dizziness and even fainting;
- headache;
- apathy, weakness, general malaise, confusion;
- the functioning of the heart is impaired;
- problems arise with the victim’s respiratory system.
When the concentration of carbon monoxide increases to 0.1 - 0.2%, a coma may develop, which can cause cardiac arrest and death. Poisoning is accompanied by alarming symptoms that signal that terrible damage to all internal organs is occurring.
For mild to moderate carbon monoxide poisoning, symptoms may include:
- severe nausea;
- periodic vomiting;
- lack of oxygen;
- discomfort;
- cardiac dysfunction;
- there is a strong pulsation in the temples;
- dizziness, fainting;
- specific noise in the ears, film before the eyes;
- hearing and vision decrease;
- coordination in time and space is impaired;
- clouding of consciousness;
- pulse quickens.
The severe stage is characterized by the following painful symptoms and signs:
- pulse is about one hundred and thirty beats per minute or very weak;
- loss of consciousness with the formation of a coma;
- convulsions;
- impaired breathing;
- involuntary urination.
The brain is the first to suffer due to its high sensitivity to lack of oxygen. Headache, muscle weakness, irregular breathing, vomiting, and trembling are the main signs of poisoning.
Atypical types of intoxication:
- fainting - there is a sharp and instantaneous drop in blood pressure, which is accompanied by fainting, as well as blanching of the skin or mucous membranes;
- euphoric - psychomotor overexcitation gradually develops, which occurs with hallucinations or delusions, then clouding of reason occurs, the heart stops and death occurs.
Chronic carbon monoxide poisoning associated with prolonged exposure to the gas is considered very dangerous. As a result, problems arise with the endocrine and nervous systems. Timely provision of emergency care and treatment is very important.
First aid
To avoid tragic consequences, it is necessary to urgently begin drug treatment in a hospital. Help if you notice any of the above signs/symptoms:
- urgently call an ambulance;
- try to stop the harmful effects of carbon monoxide - move the victim to fresh air;
- ensure the supply of oxygen - remove tight clothing from the victim, then lay him on his side;
- to bring a person back to consciousness, use the famous ammonia;
- use cold compresses and rubbing to restore and improve blood circulation;
- prepare hot coffee or tea;
- in the absence of breathing, it is necessary to perform indirect cardiac massage and artificial respiration.
When a person has carbon monoxide poisoning, treatment, which is carried out in a hospital, consists of a set of therapeutic procedures and measures:
- symptomatic measures;
- oxygen therapy - for such a procedure an oxygen mask and pure oxygen are used;
- restoration of acid and alkaline balance.
Assistance in case of carbon monoxide poisoning, as well as treatment, should be provided by qualified specialists, since a person’s life is at stake. If the symptoms are severe enough, especially in pregnant women, accompanied by permanent loss of consciousness, urgent measures are necessary. A special procedure is carried out, breathing pure oxygen in a pressure chamber.
In addition to CO poisoning, emergencies occur around the world every ten minutes. As a result, people die from smoke poisoning. Intoxication occurs due to the penetration of smoke into the victim’s respiratory tract. Smoke consists of toxic substances such as:
- hydrogen cyanide (dangerous even in small quantities);
- carbon monoxide.
The main danger is smoke poisoning caused by the combustion of the following substances:
- varnishes;
- plastic;
- rubber;
- foam;
- plywood.
During the combustion process, the above substances produce dioxin, as well as phosgene, which provoke the development of malignant tumors and allergic reactions.
- weakness of the body;
- drowsiness;
- nausea, vomiting;
- noise in ears;
- headache;
- dyspnea;
- heaviness in the head;
The entry of smoke into the human body is accompanied by serious manifestations after three to four hours. There is a high risk and danger to life. First aid when smoke enters the body is similar to that performed in case of a carbon monoxide tragedy. It is necessary to call an ambulance, as well as provide qualified treatment in a hospital.
Preventive actions
To avoid carbon monoxide poisoning, you need to know certain rules:
- use high-quality, serviceable heating equipment;
- if your house has stove heating, then do not forget to clean the chimney;
- ventilate the room regularly;
- Observe safety measures in the car when the engine is running, especially in the cold season;
- be careful around the fire.
Awareness of such a topic will help you avoid tragic incidents and subsequent consequences. Be careful!
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